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March 15, 2012 | https://www.sciencedaily.com/releases/2012/03/120315145413.htm | Scientists map hotspots for genetic exchange in chimpanzees | Scientists at the University of Oxford and the University of Chicago have constructed the world's first genetic map in chimpanzees of recombination -- the exchange of genetic material within a chromosome that makes us all unique. The study, published March 15 in | Recombination is a biological process that shuffles parental DNA during the production of sperm and eggs. This fundamental process is shared by almost every form of life -- without shuffling, we would all be genetically identical. Natural selection operates on this diversity to drive the 'survival of the fittest', selecting advantageous genetic profiles.The project to investigate how recombination has evolved in recent human and primate history was led by Professors Gil McVean, and Peter Donnelly from the Wellcome Trust Centre for Human Genetics at the University of Oxford, and Dr Molly Przeworski from the Howard Hughes Medical Institute. To study this evolution, they sequenced the entire genomes of ten western chimpanzees and identified differences between their DNA sequences.The researchers observed that in the chimpanzee genome, for every one thousand bases -- the molecules identified by the letters A, C, G and T in DNA -- around one base was different. By analysing these DNA differences, they were able to map where recombination events had shuffled genetic material in the chimpanzees' ancestors and to compare this map to patterns of recombination in humans from other studies.In a previous study, the researchers, together with Dr Simon Myers from the University of Oxford, had shown that in both chimpanzees and humans, recombination only occurs at specific locations of the genome, known as 'recombination hotspots'. Around 40% of these hotspots occur where a particular thirteen letter sequence of DNA is present.In this new study, funded by the Wellcome Trust and the National Institutes of Health, the researchers found that there was no overlap in the location of recombination hotspots between humans and chimpanzees. This was an extraordinarily unexpected finding given the 98.5 per cent similarity between the human and chimpanzee genomes and extensive similarities at the cellular and organism level.Professor McVean explains: "Genetic recombination has been likened to shuffling a deck of cards, which ensures that children are given a different genetic 'hand' than their parents. We know that in many cases recombination occurs where a particular thirteen letter sequence is present -- this is like a run of hearts from ace to king determining where we cut the deck of cards. Because humans and chimpanzees are genetically very similar, we might explain that you can only 'cut the cards' at the same point -- in fact, we find that this is not true."Recent research found that a protein called PRDM9 binds to the 13 letter DNA motif; this protein is thought to play a central role in identifying where recombination events can occur in humans and other species. However, the gene that produces this protein differs significantly between humans and chimpanzees, and even within chimpanzees. The researchers believe this may explain the lack of overlap -- the difference in the PRDM9 gene is likely to lead to the proteins targeting different locations for recombination within the chimpanzee and human genomes.Professor Donnelly says: "This is an exciting difference between humans and chimpanzees. PRDM9 is potentially one of the fastest evolving genes since humans split from chimpanzees 6.5 million years ago. It supports studies which suggest that the gene somehow determines where recombination occurs."PRDM9 has been linked previously to speciation in mice -- two similar animals are defined as separate species if they are unable to mate together to produce viable offspring. When the gene was switched off in mice, they were rendered infertile.Even though the recombination hotspots differ in location between humans and chimpanzees, the rate of recombination events is similar in humans and chimpanzees. However, the process has been disrupted where chromosomes have undergone major rearrangements in evolution -- for example, the human chromosome 2 is a fusion of two separate chimpanzee chromosomes, and this affects the rate of recombination events at this part of the genome.Oliver Venn, a Wellcome Trust DPhil student at the University of Oxford, adds: "This is the first genome-wide study of genetic variation in our closest living relatives. Whilst, the aim of the research is to improve our understanding of recombination and how it has evolved, it may well tell us something about how and why new species arise." | Genetically Modified | 2,012 |
March 12, 2012 | https://www.sciencedaily.com/releases/2012/03/120312192756.htm | Increased honey bee diversity means fewer pathogens, more helpful bacteria | A novel study of honey bee genetic diversity co-authored by an Indiana University biologist has for the first time found that greater diversity in worker bees leads to colonies with fewer pathogens and more abundant helpful bacteria like probiotic species. | Led by IU Bloomington assistant professor Irene L.G. Newton and Wellesley College assistant professor Heather Mattila, and co-authors from Wellesley College and the Netherlands Organisation for Applied Scientific Research, the new work describes the communities of active bacteria harbored by honey bee colonies. The study, which was conducted at Wellesley College in 2010, is also the first to identify four important microbes in bee colonies that have previously been associated with fermentation in humans and other animals: Succinivibrio (associated with cow rumens), Oenococcus (wine fermentation), Paralactobacillus (food fermentation) and Bifidobacterium (yogurt). Newton, who joined the IU College of Arts and Sciences' Department of Biology last year, said the research suggests honey bees may take advantage of these beneficial symbiotic bacteria to convert indigestible material into nutritious food and to enhance protection from pathogens.The research identified, for the first time, important food-processing genera in honey bee colonies: Succinivibrio and Oenococcus were the dominant genera found in the study, and there was 40 percent greater activity of the probiotic genera Bifidobacterium and Paralactobacillus in colonies that were genetically diverse compared to those that were genetically uniform. Genetic diversity is created in a colony when a queen mates with many male bees, an act that is known to improve colony health and productivity."We don't yet know what's causing colony collapse disorder, but colonies that succumb to it suffer from a broad range of problems," Newton said of a phenomenon that the U.S. Department of Agriculture says has taken about 34 percent of the overall U.S. honey bee population each year since 2007. "What we observed in our work was that there was less likelihood of potentially pathogenic bacteria showing up in genetically diverse honey bee colonies compared to genetically uniform colonies."The team was able to sample and then classify over 70,500 genetic sequences for bacterial genera from 10 genetically uniform colonies and 12 genetically diverse colonies by analyzing a specific molecule found in RNA -- a first for examining honey bees and their symbiotic microbes. Their study is the largest of its kind -- the single-largest analysis of newly identified active microbes ever to be identified in honey bees. In addition, they revealed that those microbes were more diverse in genetically diverse colonies (1,105 unique bacterial species) compared to genetically uniform colonies (781 species)."What we found was that genetically diverse colonies have a more diverse, healthful, active bacterial community -- a greater number and diversity of bacterial sequences affiliated with beneficial genera were found in genetically diverse colonies," Newton said. "Conversely, genetically uniform colonies had a higher activity of potential plant and animal pathogens in their digestive tract -- 127 percent higher than workers from genetically diverse colonies."Newton's co-author, Heather Mattila, has been investigating the benefits of genetic diversity for honey bees for years and was thrilled to have Newton's microbial expertise incorporated into the project."This is an exciting result because it gives us insight into how individual bees and their symbionts can enhance the overall health of a colony when it is genetically diverse," Mattila said.It is yet unknown how genetic diversity within a colony generates and maintains more diverse and healthful bacteria. A honey bee colony is a eusocial superorganism -- thousands of worker sisters work together to execute all tasks needed by the whole. Honey bees may benefit from the bacterial symbionts that they host by increased resistance to colonization by pathogens or through the production of nutrients by these microbes. Newton and Mattila believe the work has clear implications not only for how colonies are managed worldwide but also for the evolutionary advantages that polyandry (mating with multiple males) holds for eusocial honey bees."We are particularly interested in these results, and think the public will be too, given the alarming honey bee colony losses in recent years due to colony collapse disorder, as well as the role that these pollinators play in the security of our food supply," Newton said. "From what we've found at this point, I guess you could say that when you are living with 40,000 of your closest relatives, it pays to be genetically diverse."Co-authors with Newton and Mattila were Wellesley undergraduates Daniela Rios and Victoria Walker-Sperling, and Guus Roeselers of the Netherlands Organisation for Applied Scientific Research. Funding was provided by Wellesley's Brachman Hoffman Awards and a grant from the Essex County Beekeepers Association, Massachusetts. | Genetically Modified | 2,012 |
March 7, 2012 | https://www.sciencedaily.com/releases/2012/03/120307132210.htm | What have we got in common with a gorilla? Insight into human evolution from gorilla genome sequence | Researchers have just completed the genome sequence for the gorilla -- the last genus of the living great apes to have its genome decoded. While confirming that our closest relative is the chimpanzee, the team show that much of the human genome more closely resembles the gorilla than it does the chimpanzee genome. | This is the first time scientists have been able to compare the genomes of all four living great apes: humans, chimpanzees, gorillas and orang-utans. This study provides a unique perspective on our own origins and is an important resource for research into human evolution and biology, as well as for gorilla biology and conservation."The gorilla genome is important because it sheds light on the time when our ancestors diverged from our closest evolutionary cousins. It also lets us explore the similarities and differences between our genes and those of gorilla, the largest living primate," says Aylwyn Scally, first author from the Wellcome Trust Sanger Institute. "Using DNA from Kamilah, a female western lowland gorilla, we assembled a gorilla genome sequence and compared it with the genomes of the other great apes. We also sampled DNA sequences from other gorillas in order to explore genetic differences between gorilla species."The team searched more than 11,000 genes in human, chimpanzee and gorilla for genetic changes important in evolution. Humans and chimpanzees are genetically closest to each other over most of the genome, but the team found many places where this is not the case. 15% of the human genome is closer to the gorilla genome than it is to chimpanzee, and 15% of the chimpanzee genome is closer to the gorilla than human."Our most significant findings reveal not only differences between the species reflecting millions of years of evolutionary divergence, but also similarities in parallel changes over time since their common ancestor," says Dr Chris Tyler-Smith, senior author from the Wellcome Trust Sanger Institute. "We found that gorillas share many parallel genetic changes with humans including the evolution of our hearing. Scientists had suggested that the rapid evolution of human hearing genes was linked to the evolution of language. Our results cast doubt on this, as hearing genes have evolved in gorillas at a similar rate to those in humans."This research also illuminates the timing of splits between species. Although we commonly think of species diverging at a single point in time, this does not always reflect reality: species can separate over an extended period of time.The team found that divergence of gorillas from humans and chimpanzees occurred around ten million years ago. The split between eastern and western gorillas was much more recent, in the last million years or so, and was gradual, although they are now genetically distinct. This split is comparable in some ways to the split between chimpanzees and bonobos, or modern humans and Neanderthals."Our research completes the genetic picture for overall comparisons of the great apes," says Dr Richard Durbin, senior author from the Wellcome Trust Sanger Institute, "After decades of debate, our genetic interpretations are now consistent with the fossil record and provide a way for palaeontologists and geneticists to work within the same framework."Our data are the last genetic piece we can gather for this puzzle: there are no other living great ape genera to study."Gorillas survive today in just a few isolated and endangered populations in the equatorial forests of central Africa. They are severely threatened and their numbers are diminishing. This research not only informs us about human evolution, but highlights the importance of protecting and conserving the full diversity of these remarkable species. | Genetically Modified | 2,012 |
March 2, 2012 | https://www.sciencedaily.com/releases/2012/03/120302101706.htm | Nearby chimpanzee populations show much greater genetic diversity than distant human populations | Chimpanzee populations living in relatively close proximity are substantially more different genetically than humans living on different continents, according to a study recently published in | Common chimpanzees in equatorial Africa have long been recognized as falling into three distinct populations, or subspecies: western, central and eastern chimpanzees. A fourth group, the Cameroonian chimpanzee, has been proposed to live in southern Nigeria and western Cameroon, but there has been considerable controversy regarding whether it constitutes a distinct group.Scientists from the Universities of Oxford and Cambridge, the Broad Institute, the Centre Pasteur du Cameroun and the Biomedical Primate Research Centre examined DNA from 54 chimpanzees, measuring the DNA at 818 positions across the genome that varied between individuals. Analysis of patterns in the data showed Cameroonian chimpanzees to be distinct from the other, well-established groups.Intriguingly, a previous conclusion based on earlier studies -- that Cameroonian and western chimpanzees were most closely related -- was shown to be untrue; instead, the closest relationships to Cameroonian chimpanzees are with nearby central chimpanzees.Dr Rory Bowden from the University of Oxford, who led the study, said: "These findings have important consequences for conservation. All great ape populations face unparalleled challenges from habitat loss, hunting and emerging infections, and conservation strategies need to be based on sound understanding of the underlying population structure. The fact that all four recognized populations of chimpanzees are genetically distinct emphasizes the value of conserving them independently."Genomics can also provide tools for use in chimpanzee conservation. Genetic tests could cheaply and easily identify the population of origin of an individual chimpanzee or even a sample of bushmeat."The authors also contrasted the levels of genetic differentiation between the chimpanzees from the different groups with those based on similar data from humans from different populations. Surprisingly, even though all the chimpanzee populations lived in relatively close proximity (with the habitats of two groups separated only by a river), chimpanzees from different populations were substantially more different genetically than humans living on different continents.Professor Peter Donnelly, Director of the Wellcome Trust Centre for Human Genetics in Oxford and a senior author on the study, said: "Relatively small numbers of humans left Africa 50 000-100 000 years ago. All non-African populations descended from them and are reasonably similar genetically."That chimpanzees from habitats in the same country, separated only by a river, are more distinct than humans from different continents is really interesting. It speaks to the great genetic similarities between human populations, and to much more stability, and less interbreeding, over hundreds of thousands of years, in the chimpanzee groups."The conservation implications of the study extend to other species. New techniques such as next-generation sequencing, which have become available since the study was initiated, will allow a catalogue of genetic variation to be obtained cheaply and easily for any species, simply by sequencing even one or two individuals. Such a catalogue could then be used to perform a study like this one, to identify genetically distinct groups, and subsequently to develop simple and cheap tests of population of origin.Dr Nick Mundy, from the University of Cambridge, and the paper's other senior author, said: "Because they are humans' nearest relatives, the structure and origins of chimpanzee populations have long been of wide interest. Future studies will be able to use genome data to uncover the adaptations that are unique to the Cameroonian chimpanzees." | Genetically Modified | 2,012 |
February 23, 2012 | https://www.sciencedaily.com/releases/2012/02/120223103914.htm | How cells brace themselves for starvation | Sugar, cholesterol, phosphates, zinc -- a healthy body is amazingly good at keeping such vital nutrients at appropriate levels within its cells. From an engineering point of view, one all-purpose model of pump on the surface of a cell should suffice to keep these levels constant: When the concentration of a nutrient, say, sugar, drops inside the cell, the pump mechanism could simply go into higher gear until the sugar levels are back to normal. Yet strangely enough, such cells let in their nutrients using two types of pump: One is active in "good times," when a particular nutrient is abundant the cell's environment; the other is a "bad-times" pump that springs into action only when the nutrient becomes scarce. Why does the cell need this dual mechanism? | A new Weizmann Institute study, reported in It had been known for a while that when the levels of phosphate or zinc drop in the surroundings of a yeast cell, the number of "bad-times" pumps on the cell surface soars up to a hundred-fold. When phosphate or zinc becomes abundant again, the "bad-times" pumps withdraw while the "good-times" pumps return to the cell surface in large numbers. In their new study, the scientists discovered that cells which repress their "bad-time" pumps when a nutrient is abundant were much more efficient at preparing for starvation and at recovering afterwards than the cells that had been genetically engineered to avoid this repression. The conclusion: The "good-times" pumps apparently serve as a signaling mechanism that warns the yeast cell of approaching starvation. Such advance warning gives the cell more time to store up on the scarce nutrient; the thorough preparation also helps the cell to start growing faster once starvation is over.Thus, the dual-pump system appears to be part of a regulatory mechanism that allows the cell to deal effectively with fluctuations in nutrient supply. This clever mechanism offers the cell survival advantages that could not be provided by just one type of pump.If these findings prove to be applicable to human cells, they could explain how our bodies maintain adequate levels of various nutrients in tissues and organs. Understanding the dual-pump regulation could be crucial because it might be defective in various metabolic disorders. | Genetically Modified | 2,012 |
February 16, 2012 | https://www.sciencedaily.com/releases/2012/02/120216095032.htm | Goat kids can develop accents | The ability to change vocal sounds (vocal plasticity) and develop an accent is potentially far more widespread in mammals than previously believed, according to new research on goats from Queen Mary, University of London. | Vocal plasticity is the ability of an individual to modify the sound of their voice according to their social environment. Humans benefit from an extreme form of vocal plasticity which allows us to produce a wide range of sounds and accents, but in most other mammals (except, for example, bats and whales) vocalisations were thought to be genetically determined, with very limited flexibility and ability to learn.Dr Elodie Briefer and Dr Alan McElligott from Queen Mary's School of Biological and Chemical Sciences investigated genetic and social effects on goat kid calls.The team studied four groups of pygmy goats, who were all full or half siblings. They were recorded during two socially and ecologically distinct periods: at one week old, when they typically stay hidden from predators with their siblings; and at five weeks old, when they form social groups with animals of the same age, known as 'crèches'.Writing in the journal Dr Briefer explains: "We found that genetically related kids produced similar calls, which is not that surprising. But the calls of kids raised in the same social groups were also similar to each other, and became more similar as the kids grew older. This suggests that goat kids modify their calls according their social surroundings, developing similar 'accents'."The existence of vocal plasticity in mammals such as goats reveals a possible early pathway in the evolution of vocal communication, which eventually led to human language and speech. Dr McElligott explains: "The research also highlights the important cognitive abilities that some of our domestic animals possess, and which have remained undetected until now. Improved knowledge of their behaviour and cognition provides essential information for improving animal welfare." | Genetically Modified | 2,012 |
February 9, 2012 | https://www.sciencedaily.com/releases/2012/02/120209135840.htm | Integrated weed management best response to herbicide resistance | Over-reliance on glyphosate-type herbicides for weed control on U.S. farms has created a dramatic increase in the number of genetically-resistant weeds, according to a team of agricultural researchers, who say the solution lies in an integrated weed management program. | "I'm deeply concerned when I see figures that herbicide use could double in the next decade," said David Mortensen, professor of weed ecology at Penn State.Since the mid-1990s, agricultural seed companies developed and marketed seeds that were genetically modified to resist herbicides such as Roundup -- glyphosate -- as a more flexible way to manage weeds, Mortensen said. About 95 percent of the current soybean crop is modified by inserting herbicide-resistant genes into the plants."We do understand why farmers would use the glyphosate and glyphosate-resistant crop package," Mortensen said. "It is simple and relatively cheap, but we have to think about the longterm consequences."The researchers said that increased use of herbicider is leading to more species of weeds that also are resistant to the chemicals.They report their findings in the current issue of "Several species have developed amazing biochemical ways to resist the effects of the herbicide," said J. Franklin Egan, doctoral student in ecology, Penn State. "If weed problems are addressed just with herbicides, evolution will win."One way the weeds develop resistance is to make an enzyme that is insensitive to the herbicide, but still maintains cellular function, Egan said. Weeds have also developed ways for the plant to move the herbicide away from targeted enzymes."For instance, glyphosate-resistant strains of Conyza canadensis -- horseweed -- sequester glyphosate in leaf tissues that are exposed to an herbicide spray so that the glyphosate can be slowly translocated throughout the plant at nontoxic concentrations," Egan said. "To the horseweed, this controlled translocation process means the difference between taking many shots of whiskey on an empty stomach versus sipping wine with a meal."In response to the increasing number of weeds resistant to current applications, companies are developing new generations of seeds genetically modified to resist multiple herbicides. This continual insertion of more genes into crops is not a sustainable solution to herbicide resistance, according to the researchers. They add that companies are creating a genetic modification treadmill similar to the pesticide treadmill experienced in the mid-20th century, when companies produced increasingly more toxic substances to manage pests resistant to pesticides."Specifically, several companies are actively developing crops that can resist glyphosate, 2, 4-D and Dicamba herbicides," said Mortensen. "Such genetic manipulation makes it possible to use herbicides on these crops that previously would have killed or injured them. What is more troubling is that 2,4-D and Dicamba are older and less environmentally friendly."Egan said there are several problems with the treadmill response. First, weeds will eventually evolve combined resistance to Dicamba, 2, 4-D and glyphosate herbicides. Globally, there are already many examples of weeds simultaneously resistant to two or more herbicides.Increased use of 2, 4-D and Dicamba applied over the growing corn and soybean means much more of these herbicides will be applied at a time of year when many sensitive crops like tomato and grapes are most vulnerable to injury. Such injury results when these herbicides move from the targeted field during or following an application.Overuse of chemical weed killers may increase chances that farmers will use the herbicide during inappropriate or nonrecommended weather conditions, leading to herbicides drifting from the targeted area and killing or harming other plants and crops.Egan also said that if farms become too reliant on herbicides, farmers will find it more difficult to use integrated weed management approaches.Integrated weed management includes planting cover crops, rotating crops and using mechanical weed control methods. Farmers can use herbicides in this management approach, but must use them in a targeted, judicious fashion.The researchers, who also worked with Bruce D. Maxwell, professor of land resources and environmental sciences at Montana State University; Matthew R. Ryan a post-doctoral student at Penn State; and Richard G. Smith, assistant professor of agroecology at the University of New Hampshire; said that in previous studies, integrated weed management had lowered herbicide use by as much as 94 percent while maintaining profit margins for the operations."Integrated weed management is really the path forward," said Egan. "We believe these methods can be implemented, and we already have a lot of show that they're effective and straight forward to incorporate." | Genetically Modified | 2,012 |
February 8, 2012 | https://www.sciencedaily.com/releases/2012/02/120208152340.htm | Transformational fruit fly genome catalog completed | Scientists searching for the genomics version of the holy grail -- more insight into predicting how an animal's genes affect physical or behavioral traits -- now have a reference manual that should speed gene discoveries in everything from pest control to personalized medicine. | In a paper published February 8 in These resources are publicly available to researchers studying so-called quantitative traits, or characteristics that vary and are influenced by multiple genes -- think of traits like aggression or sensitivity to alcohol. Mackay expects the reference panel will benefit researchers studying everything from animal evolution to animal breeding to fly models of disease.Environmental conditions also affect quantitative traits. But studying the variations of these different characteristics, or phenotypes, of inbred fruit flies under controlled conditions, Mackay says, can greatly aid efforts to unlock the secrets of quantitative traits."Each fly line in the reference panel is essentially genetically identical, but each line is also a different sample of genetic variation among the population," Mackay says. "So the lines can be shared among the research community to allow researchers to measure traits of interest."The "Until now, we had the information necessary to understand what makes a fruit fly different from, say, a mosquito," Mackay says. "Now we understand the genetic differences responsible for individual variation, or why one strain of flies lives longer or is more aggressive than another strain."The study was funded by the National Institutes of Health, the National Human Genome Research Institute and the NVIDIA Foundation's "Compute the Cure" program. Dr. Eric Stone, associate professor of genetics at NC State, is also a lead author of the paper, along with colleagues from Baylor College of Medicine and the Universitat Autonoma de Barcelona in Spain. | Genetically Modified | 2,012 |
February 8, 2012 | https://www.sciencedaily.com/releases/2012/02/120208090146.htm | The genetics of rice metabolism | A large-scale study analyzing metabolic compounds in rice grains conducted by researchers at the RIKEN Plant Science Center (PSC) and their collaborators has identified 131 rice metabolites and clarified the genetic and environmental factors that influence their production. | As one of the most important staple crops, rice plays a central role in supplying the nutrients needed to keep the world population healthy. The nutritional value of rice crops is determined by the types and quantities of metabolites they contain, which are strongly affected by environmental and genetic factors. Understanding these factors is crucial to increasing nutritional value, but the complex relationship between genes and plant metabolism makes this a formidable challenge.At the heart of this challenge are so-called quantitative train loci (QTL), stretches of DNA which contain or link to the genes for a phenotypic trait, in this case metabolite levels. To breed lines of rice which produce more of a specific metabolite (for example one that boosts its nutritional value), you have to know which DNA regions are involved and in what role. This is hard because metabolite levels are controlled by many different QTLs and also strongly influenced by the environment.To solve this problem, researchers at the PSC teamed up with their collaborators at the National Institute of Agrobiological Science (NIAS) to analyze rice grain metabolomic QTL (mQTL) using state-of-the-art mass spectroscopy pipelines developed at the PSC. Analysis of 85 experimental lines of rice specially bred for QTL analysis, prepared by the NIAS researchers and harvested in 2005 and 2007, yielded a total of 759 metabolite signals. From these, the team identified 131 metabolites, including amino acids, lipids, and flavonoids, and identified a total of 801 mQTLs around the rice genome.Most important of all, the team showed that while the levels of most metabolites they identified are influenced mainly by environmental factors, genetics can sometimes play a stronger role: coordinated control of amino acids was linked to an mQTL "hotspot" on chromosome 3, while variation of flavenoid levels was linked to genetic factors. Published in The Plant Journal, the findings promise a future of faster, more effective breeding techniques for rice, and mark a major step toward a healthier, better-fed world. | Genetically Modified | 2,012 |
February 6, 2012 | https://www.sciencedaily.com/releases/2012/02/120206122456.htm | Sharp images from the living mouse brain | To explore the most intricate structures of the brain in order to decipher how it functions -- Stefan Hell's team of researchers at the Max Planck Institute for Biophysical Chemistry in Göttingen has made a significant step closer to this goal. Using the STED microscopy developed by Hell, the scientists have, for the first time, managed to record detailed live images inside the brain of a living mouse. Captured in the previously impossible resolution of less than 70 nanometers, these images have made the minute structures visible which allow nerve cells to communicate with each other. This application of STED microscopy opens up numerous new possibilities for neuroscientists to decode fundamental processes in the brain. | Every day a huge quantity of information travels not only over our information superhighways; our brain must process an enormous amount of data as well. In order to do this, each of the approximately hundred billion nerve cells establishes contact with thousands of neighboring nerve cells. The entire data exchange takes place via contact sites -- the synapses. Only if the nerve cells communicate via such contact sites at the right time and at the right place can the brain master its complex tasks: We play a difficult piece of piano, learn to juggle, or remember the names of people we have not seen for years.We can learn most about these important contact sites in the brain by observing them at work. When and where do new synapses form and why do they disappear elsewhere? This is not easy to determine, since details in living nerve cells can only be observed with optical microscopes. Due to the diffraction of light, however, structures located closer together than 200 nanometers (200 millionths of a millimeter) appear as a single blurred spot. The STED microscopy developed by Stefan Hell and his team at the Max Planck Institute for Biophysical Chemistry is a groundbreaking method devised to surpass this resolution limit. They use a simple trick: Closely-positioned elements are kept dark under a special laser beam so that they emit fluorescence sequentially one after the other, rather than simultaneously, and can therefore be distinguished. Using this technique, Hell's team has been able to increase the resolution by approximately tenfold compared to conventional optical microscopes.STED microscopy has already found wide application in fields ranging from materials research to cell biology. Under this microscope, cell cultures and histological preparations have offered unique insights into the cellular nanocosmos. The first real-time video clips from the interior of a nerve cell have demonstrated how tiny transmitter vesicles migrate within the long nerve cell endings.What was only an ambitious vision a year ago has now become reality: to also study higher living organisms at this sharp resolution in the nanometer range. By looking directly into the brains of living mice using a STED microscope, Hell and his team were the first ones to image nerve cells in the upper brain layer of the rodent with resolution far beyond the diffraction limit."With our STED microscope we can clearly see the very fine dendritic structures of nerve cells at which the synapses are located in the brain of a living mouse. At a resolution of 70 nanometers, we easily recognize these so-called dendritic spines with their mushroom- or button-shaped heads," explains Hell. They are the clearest images of these fundamental contact sites in the brain to date. "To make these visible, we take genetically modified mice that produce large quantities of a yellow fluorescing protein in their nerve cells. This protein migrates into all the branches of the nerve cell, even into smallest, finest structures," adds Katrin Willig, a postdoctoral researcher in Hell's department. The genetically modified mice for these experiments originated from the group of Frank Kirchhoff at the Göttingen Max Planck Institute for Experimental Medicine. Images of the nerve cells taken seven to eight minutes apart revealed something surprising: The dendritic spine heads move and change their shape. "In the future, these super-sharp live images could even show how certain proteins are distributed at the contact points," adds Hell. With such increasingly detailed images of structures in the brain, Hell's team hopes to shed light onto the composition and function of the synapses on the molecular level.Such insights could also help to better understand illnesses that are caused by synapse malfunction. Among these so-called synaptopathies are, for example, autism and epilepsy. As Hell explains, "Through STED microscopy and its application in living organisms, we should now be able to gain optical access of such illnesses on the molecular scale for the first time." As one of the two representatives of the Göttingen Research Center Molecular Physiology of the Brain funded by the German Research Foundation, he is committed to collaboration in his further research. Together with neurobiologists and neurologists, he and his team plan to transfer the progress made in imaging technology into fundamental knowledge about the functioning of our brains. | Genetically Modified | 2,012 |
February 1, 2012 | https://www.sciencedaily.com/releases/2012/02/120201104637.htm | Available information on the free release of genetically modified insects into the wild is highly restricted | Genetically modified insects are being developed with a view to suppress insect populations of the same species which spread human diseases, such as malaria and Dengue Fever, or that are agricultural pests destroying crops. The first generation of "designer insects" have been engineered to be fluorescently marked, to be sterile to varying degrees, or both. These insects are released experimentally to develop species-specific and chemical-free ways to reduce the size of insect pest populations. | A team of researchers from the Max Planck Institute for Evolutionary Biology have now investigated the regulatory history of genetically modified insects, with a particular focus on the pre-release information available to the public in the first three countries permitting free releases: the Cayman Islands (mosquitoes, 2009-?), Malaysia (mosquitoes, 2010-2011), and the USA (moths, 2001-2011). The study centres on the US regulatory experience, which is currently being promoted as a global regulatory model for genetically modified insects.The world's first environmental impact statement on genetically altered insects was produced by US authorities in 2008 and has since then been used as a basis for approval of subsequent experiments around the world. The scientists raise some doubts about the scientific value of this environmental impact statement: for example the majority of novel transgenic approaches it endorses are based on just two laboratory studies out of approximately 170 scientific studies cited. These two studies focus only one of the four species covered by the document. Apparently, such deficits do not only apply to the US. "We noted that public access to scientific information is highly restricted throughout the world, particularly information made available before releases start," says Guy Reeves from the Max Planck Institute for Evolutionary Biology.The Cayman Islands was in 2009 the site of the first free release of genetically modified mosquitoes. There were, however, some doubts about the relative strength of the legal safeguards that existed. The Cayman Islands had no enacted legislation specifically mentioning the release or transportation of living genetically modified organisms. In 2009 only 21 of the world's 191 countries also had not updated their existing environmental protection or animal control laws to specifically regulate living genetically modified organisms. While the Cayman Islands is a British overseas territory and consequently not a sovereign state, it is noteworthy that none of these 21 countries is thought to have approved any release of a living genetically modified organism.The first and most obvious question of people living in the release sites of the genetically modified mosquitoes (OX513a) in the Cayman Islands, Malaysia, and Brazil is whether humans can be bittenby genetically modified mosquitoes. In public information available in the Cayman Islands and Malaysian trials, this obvious question is either conspicuously ignored or it is implied that the there is no biting risk, 'as only male mosquitoes are released and they cannot bite'. However, it is clearly detailed by the Max Planck scientists, that it is probable that transgenic daughters of the released males will bite humans. This is because the released males are more accurately described as partially sterile males, rather than the commonly used term sterile males -- or most recently 'sterile' males.A potential concern about the effects of humans being bitten by these genetically modified females is discussed. The context of this discussion is not to suggest that this technology is inherently dangerous. It is to highlight the fact that public confidence in regulators will be eroded, if written discussion of obvious and scientifically plausible concerns is conspicuously absent from all written documents. As far as the authors are aware there are no publically available documents that scientifically consider possible human health impacts of being bitten by transgenic females (beyond unsubstantiated statements in the general media).The general lack of accurate information available before starting releases is problematic. This is because community engagement fundamentally requires that release descriptions be widely circulated before releases start. The need for high-quality community engagement, particularly in early releases, has repeatedly been argued as essential by expert scientists. "It is rather uncontroversial to state that in the absence of meaningful and accurate descriptions being made widely available, community engagement cannot credibly be said to have occurred," says Reeves.If those that conducted the trials cannot produce pre-release written descriptions, then they need to explicitly state why meaningful community engagement and consent might not be necessary for experimental releases into towns and cities. Individuals providing justifications based on the pressing humanitarian need to rush development of this technology, must also explain why the same argument cannot be applied to clinical trials of vaccines.Large numbers of genetically modified mosquitoes are currently being released in Brazil. Further releases are reportedly under evaluation in various countries, including France, Guatemala, India, Mexico, Panama, Philippines, Singapore, Thailand, Vietnam and the UK. Proposed experimental releases are for both human health purposes and to control agricultural pests.Given the enormous human burden of diseases like dengue fever and crop loss from insect attack, it is important that new control techniques are developed. Field trials are an essential step in the evaluation process. "However, we need an informed public to ensure that experimental testing of this potentially valuable technology can be given a fair chance and that testing does not needlessly provoke public mistrust," says Reeves. Avoiding the kind of questionable practices which characterized the commercial development of genetically modified plant is likely to be important. | Genetically Modified | 2,012 |
January 31, 2012 | https://www.sciencedaily.com/releases/2012/01/120131102521.htm | Protein study gives fresh impetus in fight against superbugs | Scientists have shed light on the way superbugs such as MRSA are able to become resistant to antibiotics. Researchers have mapped the complex molecular structure of an enzyme found in many bacteria. | These molecules -- known as restriction enzymes -- control the speed at which bacteria can acquire resistance to drugs and eventually become superbugs.The study, carried out by an international team including scientists from the University of Edinburgh, focused onHowever, the results would apply to many other infectious bacteria.After prolonged treatment with antibiotics, bacteria may evolve to become resistant to many drugs, as is the case with superbugs such as MRSA.Bacteria become resistant by absorbing DNA -- usually from other bugs or viruses -- which contains genetic information enabling the bacteria to block the action of drugs.Restriction enzymes can slow or halt this absorption process.Enzymes that work in this way are believed to have evolved as a defense mechanism for bacteria.The researchers also studied the enzyme in action by reacting it with DNA from another organism.They were able to model the mechanism by which the enzyme disables foreign DNA, while safeguarding the bacteria's own genetic material.Restriction enzymes' ability to sever genetic material is widely applied by scientists to cut and paste strands of DNA in genetic engineering.The study was carried out in collaboration with the Universities of Leeds and Portsmouth with partners in Poland and France.It was supported by the Biotechnology and Biological Sciences Research Council and the Wellcome Trust and published in | Genetically Modified | 2,012 |
January 27, 2012 | https://www.sciencedaily.com/releases/2012/01/120127140013.htm | Making poisonous plants and seeds safe and palatable: Canola now, cannabis next? | Every night millions of people go to bed hungry. New genetic technology can help us feed the world by making inedible seeds more edible, researchers say. | There are roughly about a quarter of a million plant species known on Earth. But we only eat between 5,000 and 10,000 of them. Many are poisonous to us -- such as lily of the valley. And many plants have no human nutritional value -- such as grass."In fact, there are no more than about 100 known species that can be used as important food crops," says Biology Professor Atle Bones at Norwegian University of Science and Technology.But Bones and his research team have made a major discovery. They have figured out how a canola plant can be genetically programmed to reduce the toxic substances it produces in its seeds -- thus making it more palatable.Nobody has done this before, and Bones thinks it could be the beginning of a food revolution."The principle could be used with other plant species and plant parts," he says.Canola, or rape, is one of the fifteen most important crop plants in the world. It contains special cells that produce toxic substances. These "toxic bombs" are part of the plant's defence system and are activated in specific situations -- such as when an insect begins feeding on a leaf. The substance that is released burns like hot mustard, causing animals and insects to move away."These 'toxic bombs' are good for the plant, but undesirable in animal feed and human food," says Bones.When canola seeds are pressed, all the vegetable oil is removed. What is left is a protein-rich flour that can be used in food for animals and humans. But if the seeds pressed in the wrong way, the plant responds by releasing its toxic compounds. The oil is then flavoured with a taste of strong mustard, and the animals that eat the protein flour have stomach problems and troubles with nutrient uptake.The NTNU research group has genetically reprogrammed canola cells so that the toxic bomb cells disappear on their own as the seed matures. But the toxin only fully disappears in the mature seeds.This way, the plant can continue to protect itself, while the toxic compounds are removed from the part of the rapeseed used for food.Thus, the proportion of rapeseed in the concentrate can be increased, and the seeds can be pressed without the risk of contaminating the oil with unwanted flavours and odours.There are almost 7 billion people on Earth. Every day, 25,000 people die of malnutrition -- while 800 million are starving. By 2050 there will be more than 9 billion of us. As people become more prosperous, their per-person calorie consumption will grow. This combination of increased prosperity and population growth means that food production will have to double by 2050.Globally, genetically modified food in production is already cultivated on +130 million hectares. But Bones believes that the production of genetically modified plants will more than double over the next ten years.Today there are 25 countries that use genetically modified plants on a large scale. More than 50 per cent of the world's population lives in these countries.Genetically modified soy already represents 75 per cent of all soybean production. And genetically modified plants are grown in an area that is 40 times the size of Denmark -- mainly in the USA, Argentina, Brazil and China, according to Bones.Genetically modified food is grown in seven European countries. There is already super broccoli that contains higher doses of the healthy substances in normal broccoli. Next year, producers will introduce soybeans enriched with omega-3 fatty acids.Among the plants that could be genetically modified by removing their undesirable chemicals is cannabis.Cannabis is a type of grass that thrives in subtropical and dry climates -- and is best known as the raw material for hashish and marijuana.But it is one of the world's fastest growing plants, and is exceptionally hardy. Its plant fibres can be used for rope and textiles, or as replacements for trees in the paper industry because they are stronger than wood fibre. The seeds can be used for oil."It would be interesting to use our new technology to produce cannabis that does not contain the psychoactive substance THC," says Bones.It is illegal to grow genetically modified food in Norway, and in principle it may not be imported -- not even for animal feed. But there are cracks in this virtual barrier, and small traces of genetically modified food are seeping in. Because Norway does not allow the sales of goods containing genetically modified contents, there is no provision for labelling this food on the grocery store shelves. But it's there.The government has set 0.9 percent as the ceiling for how much genetically modified food may be in foods before they must be labelled. Each year, the Norwegian Food Safety Authority finds genetically modified canola, corn or rice in imported foods, which are promptly branded as illegal immigrants and kicked out of the country.But the test sample size is small -- last year only 131 samples were tested, of which 4 contained genetically modified food.According to the Norwegian Board of Technology, it is difficult to keep Norway completely free of genetically modified ingredients, which is why the 0.9 per cent limit was set.Atle Bones sees many benefits of genetically modified food."Genetically modified plants can be tailored to tolerate different climatic conditions such as drought or hard winters, and to have increased resistance to insects or fungus. These plants can thus be grown with fewer pesticides."This means that farmers are exposed to less pesticides, there are less pesticides in the ecosystem and probably less pesticides in food that is produced," Bones notes."There is nothing wrong or unethical about using genetically modified plants -- because, in fact, all crops are modified. They have also been created from wild plants through comprehensive human-controlled breeding programmes and genetic selection," says Bones.It is no longer possible in the United States to distinguish between ordinary food and genetically modified food, researchers assert.Some researchers describe the American situation as if people are playing Russian roulette with their health. Fear of allergies is one reason. Atle Bones believes that these kinds of worries over possible health effects are greatly exaggerated."It is obviously not possible to give an ironclad guarantee that no one will be allergic to a new gene in canola or corn. Neither is it possible to guarantee that no one is allergic to traditional modified plants. But this would normally be detected before the plants or the product goes into production."The method we have used, however, can remove known allergens, digestive inhibitory substances or toxins in the plant," said Bones.He also believes that genetically modified plants must be assessed in each situation, and like conventionally modified plants, be tested thoroughly before they are approved for production."With our new technology, it is possible to target changes in specific parts of the plant. It is therefore possible to change a strawberry plant without any change in the berry to be eaten. And that is a scientific breakthrough," Bones concludes. | Genetically Modified | 2,012 |
January 27, 2012 | https://www.sciencedaily.com/releases/2012/01/120125172319.htm | Engineered bacteria effectively target tumors, enabling tumor imaging potential in mice | Tumor-targeted bioluminescent bacteria have been shown for the first time to provide accurate 3-D images of tumors in mice, further advancing the potential for targeted cancer drug delivery, according to a study published in the Jan. 25 issue of the online journal | The specially engineered probiotic bacteria, like those found in many yogurts, were intravenously injected into mice with tumors, after which the researchers took full body bioluminescent images. The 3-D images revealed information about the number and location of the bacteria, to the level of precisely revealing where within the tumor the bacteria were living, providing much more information on the interaction of bacteria and tumors than was previously available using similar two-dimensional imaging methods.According to the authors, led by Mark Tangney of University College Cork in Ireland, "before now, researchers used luminescence to provide an approximation of where a test organism was within the body, and would then follow up with multiple further experiments using different techniques to try to find a precise location."This new research suggests that such bacteria can be engineered to contain diagnostic or therapeutic agents that would be produced specifically within the tumor for targeted treatment. | Genetically Modified | 2,012 |
January 26, 2012 | https://www.sciencedaily.com/releases/2012/01/120124140103.htm | Global research consortium presents findings on safety of genetically modified food | A three-year feeding study has shown no adverse health effects in pigs fed genetically modified (GM) maize. The maize, which is a Bt-maize bred for its insect resistant properties, was sourced from Spain. The results were one of the key findings of trials conducted as part of the GMSAFOOD consortium undertaking post market monitoring: long term, generational and food chain studies to test food safety. | The research team conducted short-term (31 days), medium-term (110 days) and generational pig feeding studies where the health of piglets of sows fed Bt-maize is measured. No adverse effects were observed, suggesting that feeding Bt-maize to pigs of different ages is safe. "These findings can offer some assurance to consumers as to the safety of consuming Bt-maize," Peadar Lawlor, senior researcher at Teagasc, Animal and Grassland Research and Innovation Centre, Moorepark, Ireland, said; "The pig is considered to be an excellent model for humans due to similarities in gastrointestinal anatomy and physiology. Similar responses to Bt-maize consumption could be expected in humans," he said.In addition to testing for any unforeseen adverse effects, the researchers were also looking for biomarkers (fragments of DNA) associated with immune responses which could be used for predicting immune response to future genetically modified organisms (GMOs). The GMSAFOOD consortium, funded by the European Commission, brings together researchers from Austria, Ireland, Norway, Hungry, Turkey and Australia.These results and findings from other GMSAFOOD research teams will be presented at the GMSAFOOD conference at the Medical University of Vienna, Austria 6-8 March 2012. | Genetically Modified | 2,012 |
January 18, 2012 | https://www.sciencedaily.com/releases/2012/01/120109155725.htm | New way to learn about -- and potentially block -- traits in harmful pathogens | Researchers at Duke University Medical Center have developed a new way to identify the genes of harmful microbes, particularly those that have been difficult to study in the laboratory. | This new method uses chemicals to create mutant bacteria, followed by genomic sequencing to identify all mutations. By looking for common genes that were mutated in Chlamydia sharing a particular trait, the investigators were able to rapidly "zero in" on the genes responsible for that trait.The approach is versatile and inexpensive enough that it could be applied to study a range of microorganisms, said Raphael Valdivia, PhD, an associate professor of molecular genetics and microbiology at Duke."We were able to learn about genes that allow Chlamydia to flourish in their hosts without the traditional, lengthy process of domesticating the pathogen to accept recombinant DNA," Valdivia said."Our approach marries classical microbiology techniques with 21st century genome-sequencing technologies. If you encounter a new dangerous microorganism and want to determine what genes are important, I think this represents an effective way to learn all we can, as fast as we can."One of the goals in studying microbial pathogens that harm humans and animals is to locate and disrupt the genes required for infection, Valdivia said.The microbe in this study, Chlamydia, is usually sexually transmitted, hides in human cells, and is a type of bacteria that must cause disease to be transmitted from one host to another. Chlamydia is the leading sexually transmitted infection and a risk factor for pelvic inflammatory disease and infertility.Prior to this work, the function of many Chlamydia genes had to be inferred by their similarity to genes from other bacteria. "By isolating mutants that don't grow well inside cells and identifying the underlying mutations, we can learn a lot about how these genes contribute to disease," Valdivia said. "These are the activities we'd like to block.""For us, this significantly accelerates the analysis of Chlamydia and importantly, should be applicable to many other microbes that have been difficult manipulate with recombinant DNA approaches," he said.Valdivia suggested that even microbes associated with our normal intestinal flora, which are notoriously difficult to manipulate, are now open to exploration so that we can learn how their genes influence human health, including dietary disorders and inflammatory bowel disease.The work was published on Jan. 9 in the early edition of the Valdivia also said that the new technique could help to create Chlamydia vaccines that have a combination of mutations that affect the pathogen's virulence. "That way we can cripple some aspects of the bacterium's ability to thrive intact in a host, while still allowing the bacterium to replicate enough to prime the im mune system against it."The lead author was Bidong D. Nguyen of the Duke Department of Molecular Genetics and Microbiology.This work was supported by funds from a Chancellor's Science Council Pilot Projects award from Duke University and funds from the NIH. | Genetically Modified | 2,012 |
January 11, 2012 | https://www.sciencedaily.com/releases/2012/01/120105111946.htm | Mosquito immune system engineered to block malaria | Researchers at the Johns Hopkins Malaria Research Institute demonstrated for the first time that the Anopheles mosquito's innate immune system could be genetically engineered to block the transmission of the malaria-causing parasite to humans. In addition, they showed that the genetic modification had little impact on the mosquito's fitness under laboratory conditions. The researchers' findings were published December 22 in the online journal | "The immune system of the Anopheles mosquito is capable of killing a large proportion -- but not all -- of the disease-causing parasites that are ingested when the mosquito feeds on an infected human," said George Dimopoulos, PhD, senior author of the study and associate professor in the W. Harry Feinstone Department of Molecular Microbiology and Immunology at the Johns Hopkins Bloomberg School of Public Health. "We've genetically engineered this immune system to create mosquitoes that are better at blocking the transmission of the human malaria parasite For the study, Dimopoulos and his team genetically engineered Anopheles mosquitoes to produce higher than normal levels of an immune system protein Rel2 when they feed on blood. Rel2 acts against the malaria parasite in the mosquito by launching an immune attack involving a variety of anti-parasitic molecules. Through this approach, instead of introducing a new gene into the mosquito DNA, the researchers used one of the insect's own genes to strengthen its parasite-fighting capabilities. According to the researchers, this type of genetically modified mosquito could be further developed and used to convert malaria-transmitting to Plasmodium-resistant mosquito populations. One possible obstacle for this approach is the fitness of the genetically modified malaria resistant mosquitoes, since they would have to compete with the natural malaria-transmitting mosquitoes. The researchers showed with their study that the Rel2 genetically modified mosquito strain lived as long, and laid as many eggs, as the non-modified wild type mosquitoes, thereby suggesting that their fitness had not become significantly impaired."Malaria is one of world's most serious public health problems. Mosquitoes and the malaria parasite are becoming more resistant to insecticides and drugs, and new control methods are urgently needed. We've taken a giant step towards the development of new mosquito strains that could be released to limit malaria transmission, but further studies are needed to render this approach safe and fail-proof," said Dimopoulos. Worldwide, malaria afflicts more than 225 million people. Each year, the disease kills approximately 800,000, many of whom are children living in Africa.The Johns Hopkins Malaria Research Institute is a state-of-the-art research facility at the Johns Hopkins Bloomberg School of Public Health. It focuses on a broad program of basic science research to treat and control malaria, develop a vaccine and find new drug targets to prevent and cure this deadly disease.Funding was provided by the National Institutes of Health and the Johns Hopkins Malaria Research Institute. | Genetically Modified | 2,012 |
January 7, 2012 | https://www.sciencedaily.com/releases/2012/01/120107151904.htm | Scientists refute claim that genetically modified corn caused new insect pest | An article in the forthcoming issue of the | In "Genetically Engineered Bt Corn and Range Expansion of the Western Bean Cutworm (Lepidoptera: Noctuidae) in the United States: A Response to Greenpeace Germany," corresponding author William Hutchison, professor and chair of the University of Minnesota Department of Entomology, and his co-authors maintain that the Greenpeace report fails to consider broader ecological and agronomic factors which explain why the WBC's range has expanded. These additional factors include insect biology, synchrony of insect and corn phenology, reduced insecticide use, increases in conservation tillage, soil type, glyphosate-resistant crops, insect genetics, insect pathogens, pre-existing insect population densities, and climate change.The JIPM authors focus on several discrepancies of fact and interpretation in the Greenpeace document, beginning with its title, "Agro-biotechnology: New plant pest caused by genetically engineered corn. The spread of the western bean cutworm causes massive damage in the U.S."Despite the Greenpeace claim, the WBC is neither "new" nor has it caused "massive damage" recently. The WBC was originally collected in Arizona in the 1880s and was considered an economic pest of beans and corn as early as 1915. Over the last decade its range has expanded, but documentation of economically damaging infestations has been relatively limited.The Greenpeace claim that the WBC has historically "been confined to very limited regions and did not cause any major problems in maize crops" is also untrue, according to the authors. Farmers in Nebraska reported major problems as early as 1962, and instead of being "confined to very limited regions," the WBC was documented throughout the western Great Plains from Mexico to Alberta, where it was found in the mid 1950s, despite the Greenpeace claim that it was found in Canada for the first time as recently as 2009.According to the authors, "a curious theme throughout the Greenpeace Germany report, is that Then (2010) ignored the possibility of other influences on western bean cutworm range expansion, including several ecological and agronomic factors." For example, the increasing use of conservation tillage since the mid-1990s favors the survival rate of WBC larvae because less deep plowing minimizes mortality to insect pests that overwinter in the soil. Another possible reason is the reduction or elimination of insecticide applications, which has occurred with increased use of Bt corn over the past decade, likely resulting in increased survival of the WBC. Other possibilities for the WBC range expansion, such as climate change, were also ignored by Greenpeace and Testbiotech.Out of concern that "potential misinterpretation of selected quotes" in the Greenpeace report may lead to confusion among future regulatory decision makers, the authors go on to give specific responses to other claims in the report. | Genetically Modified | 2,012 |
January 6, 2012 | https://www.sciencedaily.com/releases/2012/01/120105175830.htm | Scientists find structure of gene-editing protein | In the two and a half years since Adam Bogdanove, professor at Iowa State University in the Department of Plant Pathology and Microbiology, along with Matthew Moscou, a former graduate student in that department, discovered how a class of proteins from plant pathogenic bacteria find and bind specific sequences in plant genomes, researchers worldwide have moved fast to use this discovery. | Last year it was first shown that the proteins can be fused to DNA modifying enzymes to manipulate genes and gene functions by Bogdanove and colleagues at the University of Minnesota, led by former ISU professor Dan Voytas, and another group led by Iowa State University faculty member Bing Yang, professor in the Department of Genetics, Development and Cell Biology.The fused proteins are called TAL effector nucleases, or TALENs, and can be used to better understand gene function in model plant and animal systems, to improve traits in livestock and plants, and even to treat human genetic disorders, according to Bogdanove.The fact that these proteins can be readily engineered to bind DNA sequences of choice has resulted in a flurry of publications that demonstrate their utility in many different types of cells, including human stem cells.Largely because of the advent of TALENs, the journal Nature Methods last month named gene editing with engineered nucleases as 2011 Method of the Year.Now, Bogdanove and researchers from the Fred Hutchinson Cancer Research Center in Seattle have taken the next step by determining the 3-D structure of a TAL effector bound to DNA.The findings were posted this week on The first author of the study is Amanda Mak, a postdoctoral researcher in the Hutchinson center. Andres Cernadas, a post doctoral researcher in Bogdanove's lab also contributed.By visualizing the shape of TAL effectors and how they physically interact with the DNA double helix, scientists can now better understand the biochemistry that underlies their ability to recognize and stick to specific DNA sequences.This will in turn improve scientists' ability to target the proteins to different locations in a genome and to better predict and prevent their binding to unintended, off-target sites, according to Bogdanove.The structure itself is also interesting from a basic biology standpoint. "It is really quite beautiful," he says, "So far there is nothing else in nature quite like it."To determine the structure, Bogdanove collaborated with Fred Hutchinson scientists Barry Stoddard, an expert in protein DNA interactions, and Phil Bradley, a computational biologist. Led by Stoddard, the group completed the project in just over a year by using a unique combination of traditional X-ray crystallography and novel computer-based modeling method. | Genetically Modified | 2,012 |
January 6, 2012 | https://www.sciencedaily.com/releases/2012/01/120105145844.htm | Scientists 'hijack' bacterial immune system | The knowledge that bacteria possess adaptable immune systems that protect them from individual viruses and other foreign invaders is relatively new to science, and researchers across the globe are working to learn how these systems function and to apply that knowledge in industry and medicine. | Now, a team of University of Georgia researchers has discovered how to harness this bacterial immune system to selectively target and silence genes. The finding, published in the early online edition of the journal "Scientists study bacteria and other microorganisms to understand essential life processes as well as to improve their use in the safe production of foods, biofuels and pharmaceuticals, and to fight those that cause disease," said Michael Terns, a professor in the departments of biochemistry and molecular biology, and genetics in the UGA Franklin College of Arts and Sciences. "And now we have a new way to engineer bacteria to decrease or even eliminate the expression of the genes of our choosing."The bacterial immune system consists of two components. The first is an RNA (a molecule that, like DNA, contains genetic information) that acts as a homing signal to target a virus or another cellular invader. The second component is a complex of proteins that cleaves the invader's genetic material. In a 2009 paper published in the journal Cell, Terns, co-principal investigator Becky Terns and their colleagues were the first to describe how this pathway, known as the Cmr branch of the CRISPR-Cas immune system, works.In their latest study, the researchers further their understanding of the system and use that in-depth knowledge to essentially hijack the bacterial immune system to direct its homing system to a target of their choosing. Using customized CRISPR RNAs with a modified homing signal, the scientists were able to destroy the message for a protein that is responsible for resistance to the most commonly prescribed family of antibiotics, the beta-lactam antibiotics (that includes, for example, amoxicillin).Becky Terns, co-leader of the UGA team, explained, "In this study we identified the key features of the RNAs that the system normally uses, and then showed that using this information we can program the system with engineered 'homing' RNAs to destroy new targets. New targets would go beyond viruses and other invaders to include essentially any gene present in the organism being studied. And because we have defined the components of this system, it is possible that we can introduce it into organisms that do not already possess it to further expand the potential industrial and biomedical applications."She pointed out that most known CRISPR-Cas systems target and cleave DNA. The system that the UGA team studies is the only known example of a CRISPR-Cas system that targets RNA, the molecule that functions as an intermediary between DNA and the proteins that carry out various functions within cells. "Cleaving its own DNA would kill an organism. Silencing specific RNAs allows more sophisticated applications," Terns said.Researchers could systematically shut down the function of individual genes, for example, to discern the role they play in essential cellular processes. Gene expression could be modified in bacteria that are used to break down plant materials for biofuels or that produce medications, such as insulin, to improve quality and production."This detailed biochemical study of a new branch of the CRISPR-Cas defense system-one that targets RNA molecules-has shed light on a powerful weapon in the bacterial arsenal against invading viruses and mobile elements," said Michael Bender, who oversees RNA processing and function grants at the National Institutes of Health's National Institute of General Medical Sciences. "In addition, by defining the key components of the system, Drs. Terns and their colleagues have set the stage for the development of a new tool for targeting specific RNA molecules in diverse cell types, potentially providing biomedical researchers with a valuable new way to analyze gene functions."Michael Terns added, "The possibility of exploiting the CRISPR-Cas system in biotechnology has been discussed since its discovery, and this work begins to realize some of that enormous potential."Additional UGA authors on the paper include postdoctoral researcher and lead author Caryn Hale, graduate students Sonali Majumdar and Joshua Elmore, former undergraduate student Neil Pfister and Associate Professor of Poultry Science Mark Compton. Collaborators from the University of Connecticut are Associate Professor of Genetics and Developmental Biology Brenton Graveley, postdoctoral researcher Sara Olson and graduate student Alissa Resch.The research was funded by the National Institutes of Health, including American Recovery and Reinvestment Act funds. | Genetically Modified | 2,012 |
January 4, 2012 | https://www.sciencedaily.com/releases/2011/12/111225144318.htm | A radar for ADAR: Altered gene tracks RNA editing in neurons | RNA editing is a key step in gene expression. Scientists at Brown University report in | To track what they can't see, pilots look to the green glow of the radar screen. Now biologists monitoring gene expression, individual variation, and disease have a glowing green indicator of their own: Brown University biologists have developed a "radar" for tracking ADAR, a crucial enzyme for editing RNA in the nervous system.The advance gives scientists a way to view when and where ADAR is active in a living animal and how much of it is operating. In experiments in fruit flies described in the journal "We designed this molecular reporter to give us a fluorescent readout from living organisms," said Robert Reenan, professor of biology and senior author of the paper, which appears Dec. 25, 2011. "When it comes to gene expression and regulation, the devil is in the details.""Biologists already know that errors in transcribing RNA from DNA can lead to improper gene expression in the nervous system and might contribute to diseases such as epilepsy, suicidal depression, and schizophrenia. More recently they've gathered evidence that ADAR is associated with disease. For instance in a study in Reenan said that using the new "reporter" tool to look for correlations between ADAR activity levels and behavior or disease might yield new insights into how RNA editing errors lead to such variations. But he also speculated that the mechanics of how he and his research group created the fluorescent ADAR tracking system could be adapted to someday allow therapies based on targeted RNA repair. Their reporter works by requiring ADAR to fix a purposely broken individual letter of RNA on an engineered gene."We're actually repairing RNA at the level of a single informational bit, or nucleotide," Reenan said. "Here we've shown we can take a mutant version of a gene and restore its function, but at the level of RNA rather than DNA."Reenan and third author Kyle Jay began working to create the reporter in 2006 when Jay was an undergraduate student just embarking on what would become a celebrated senior thesis at Brown. They started with a well-known tool of molecular biology: a jellyfish gene that produces a protein that glows green upon exposure to ultraviolet light. The strategy was to intentionally break the gene in a way that ADAR is uniquely suited to fix.First they engineered the gene to include necessary "intron" code that requires a specific splicing operation to take place. Then they inserted the "stop codon" T-A-G in place of T-G-G, which causes transcription to cease, effectively preventing production of the green fluorescent protein. But before splicing occurs and when ADAR finds the stop codon U-A-G in the RNA transcript, it edits the A to an I, which restores the correct information, and translation of the whole gene proceeds as if there were no stop mutation in the DNA. So when splicing and ADAR editing occurs, neurons with the gene reporter glow green.To see where ADAR editing and splicing were occurring, compared to just splicing alone, they also rigged up an engineered gene with the splicing requirement, but not the T-A-G codon. That would produce yellow fluorescent protein when splicing alone occurred.Armed with their new ADAR reporter, Reenan and lead author James Jepson set out to make some biological observations in flies. One was that ADAR activity is more pronounced in certain parts of the brains of developing larvae than it is in the brains of adults. The team also found wide variation in ADAR activity in the brains of flies of similar ages from individual to individual. This was a surprise, Reenan said, because all the flies were essentially genetically identical.Reenan said he is confident that the ADAR reporter could be useful in more organisms than the fruit fly. The idea of creating the reporter grew out of his lab's studies of comparative genomics in a number of species. ADAR, meanwhile, is found in both invertebrates and vertebrates. In fact, in the paper the researchers describe testing the flexibility of their engineering by inserting into their engineered jellyfish gene -- destined as it was for a fruit fly -- the splicing intron of a moth."Thus it was, a jellyfish-moth gene chimera was crippled by mutation, and repaired by a fruit fly enzyme," Reenan said. "Rube Goldberg would be proud."Reenan said he plans to use the ADAR reporter in flies to continue the investigation of the genes associated with Fragile X and is eager for someone who works on the disorder in mice to give it a try.The idea of adapting this method to direct ADAR to fix mistranscribed RNA or reverse DNA damage at the RNA level in a therapeutic fashion is farther into the future. But in a sense, at least ADAR is now on the radar.In addition to Reenan, Jepson, and Jay, the paper's other author is Yannis A. Savva. Jepson is also affiliated with Thomas Jefferson University in Philadelphia and Jay now works at the University of California-San Francisco.An Ellison Medical Foundation Senior Scholar award funded the research. | Genetically Modified | 2,012 |
December 14, 2011 | https://www.sciencedaily.com/releases/2011/12/111213190237.htm | 'Pep talk' can revive immune cells exhausted by chronic viral infection | Chronic infections by viruses such as HIV or hepatitis C eventually take hold because they wear the immune system out, a phenomenon immunologists describe as exhaustion. | Yet exhausted immune cells can be revived after the introduction of fresh cells that act like coaches giving a pep talk, researchers at Emory Vaccine Center have found. Their findings provide support for an emerging strategy for treating chronic infections: infusing immune cells back into patients after a period of conditioning.The results are published this week in the The first author of the paper is Rachael Aubert, a student in Emory's Immunology and Molecular Pathogenesis program who completed her doctorate in 2009. Senior author Rafi Ahmed, PhD, is director of the Emory Vaccine Center and a Georgia Research Alliance Eminent Scholar.Ahmed's laboratory has extensive experience studying mice infected with lymphocytic choriomeningitis virus (LCMV). Immune responses against LCMV are driven by CD8 or "killer" T cells, which destroy virus-infected cells in the body. But a few weeks after exposure to LCMV, the mice develop a chronic infection that their immune systems cannot shake off, similar to when humans are infected by viruses like HIV and hepatitis C.Aubert and her co-workers examined what happened to mice chronically infected with LCMV when they infused CD4 or "helper" T cells from uninfected mice. After the infusion, the CD8 cells in the infected mice revived and the levels of virus in their bodies decreased by a factor of four after a month. Like coaches encouraging a tired athlete, the helper cells drove the killer cells that were already in the infected mice to emerge from exhaustion and re-engage.The cell-based treatment was especially effective when combined with an antibody that blocks the molecule PD-1, which appears on exhausted T cells and inhibits their functioning. The antibody against PD-1 helps the exhausted T cells to revive, and enhances the function of the helper cells as well: the combination reduced viral levels by roughly ten-fold, and made the virus undetectable in some mice."We have not seen this sharp of a reduction in viral levels in this system before," says co-author Alice Kamphorst, a postdoctoral fellow.The helper cells were all genetically engineered to recognize LCMV, a difference between mouse experiments and potential clinical application. However, it may be possible to remove helper T cells from a human patient and stimulate them so that all the cells that recognize a given virus grow, Kamphorst says."This is an active area of research and several laboratories are looking at how best to stimulate T cells and re-introduce them," she says.In addition, she and her co-workers are examining what types of hormones or signaling molecules the helper cells provide the killer cells. That way, that molecule could be provided directly, instead of cell therapy, she says.The molecule PD-1 was previously identified by Ahmed and colleagues as a target for therapy designed to re-activate exhausted immune cells. Antibodies against PD-1 have been undergoing tests in clinical studies against hepatitis C and several forms of cancer.Collaborators from Harvard Medical School/Dana Farber Cancer Institute contributed to the paper. The research was supported by the National Institutes of Health and the Cancer Research Institute. | Genetically Modified | 2,011 |
December 12, 2011 | https://www.sciencedaily.com/releases/2011/12/111209123216.htm | Beating superbugs with a high-tech cleanser | According to the World Health Organization, antibiotic-resistant bacteria are one of the top three threats to human health. Patients in hospitals are especially at risk, with almost 100,000 deaths due to infection every year in the U.S. alone. | Now Dr. Udi Qimron of the Department of Clinical Microbiology and Immunology at Tel Aviv University's Sackler Faculty of Medicine has developed an efficient and cost-effective liquid solution that can help fight antibiotic-resistant bacteria and keep more patients safe from life-threatening infections. The solution is based on specially designed bacteriophages -- viruses that infect bacteria -- that can alter the genetic make-up of antibiotic-resistant bacteria. "We have genetically engineered the bacteriophages so that once they infect the bacteria, they transfer a dominant gene that confers renewed sensitivity to certain antibiotics," explains Dr. Qimron.The solution, recently detailed in the journal Applied and Environmental Microbiology, could be added to common antibacterial cleansers used on hospital surfaces, turning resistant bacteria into sensitive bacteria. It's easy to prepare, easy to apply, and non-toxic, Dr. Qimron notes. He estimates that one liter of the growth medium -- the liquid in which the bacteriophages are grown -- will cost just a few dollars.The research was done in collaboration with Ph.D. student Nir Friedman, lab technician Shahar Mor, and Dr. Rotem Edgar of the Ichilov Medical Center.Certain antibiotics are designed to target and bind to a part of the bacteria cell called a ribosome -- the protein factory of the cell. But after continual and frequent exposure to antibiotics, the bacteria "learn" to change components in the ribosome itself so that the antibiotics are unable to bind.Dr. Qimron and his colleagues set out to determine whether they could make resistant bacteria sensitive to antibiotics again by re-introducing a component of the ribosome, a gene called Added to cleansers, Tellurite represents the second step in a two-part process. A Tellurite compound, which is toxic to bacteria, would also be spread on all surfaces to wipe out the bacteria that had not been rendered sensitive, and thus the entire population of the surface bacteria would be sensitized. The combination is designed to first disarm, and then kill dangerous bacteria.Next, the solution will be tested in pre-clinical animal trials to ensure its safety before being made available for wider use at hospitals. Once its safety is guaranteed, the solution will come in a bottle, says Dr. Qimron, and easily added to a bucket or spray. | Genetically Modified | 2,011 |
December 9, 2011 | https://www.sciencedaily.com/releases/2011/12/111208092715.htm | How Salmonella forms evil twins to evade the body's defenses | An unusual regulatory mechanism that controls the swimmer/non-swimmer option in genetically identical Salmonella also impacts the bacteria's ability to cause infection. | University of Washington scientists reported the discovery this week in the As Salmonella divides into genetically identical clones, either of the two forms of the bacteria can emerge. Some individuals sport flagella -- thin, whip-like projections that propel the bacterium. Others do not. When grown in a lab dish, both types appear.Salmonella is a common food-poisoning bacteria. It can survive and take hold in hostile environments -- like inside of people who are protected by hoards of infection-fighting cells. In immunocompromised individuals, it causes blood stream infections."In an unpredictable world," said Dr. Brad Cookson, professor of microbiology and laboratory medicine, and division head of Clinical Microbiology at the UW, "Salmonella have evolved to hedge their bets." Each guise has its own advantages and drawbacks in invading a host and evading defenses, depending on the situation.Cookson explained that being genetically the same but differing in appearance and function is useful for a population of disease-causing bacteria. Even though the bacteria might be identical clones, varying characteristics of the individuals -- some of whom are mobile and some of whom are stationary -- allows the population to colonize a host and establish an infection."Diversity," Cookson noted, "improves the chance that some of the clones will thrive in fluctuating environments." To infect an animal, swallowed Salmonella breaches the protective mucous of the gut, colonizes the lymph tissues, and then builds a niche inside germ-killing cells. These cells are co-opted into ferrying the Salmonella to the spleen and other organ system tissues."The ability to swim," Cookson said, "is presumably a critical survival trait." In an intestinal infection, for example, motile Salmonella bacteria grow faster than their non-motile counterparts because they are able to migrate to the nutrient-rich layers of the intestinal lining. Inside of macrophages, however, non-motile Salmonella have the upper hand.That is because the protein needed to make flagella, called flagellin, provokes the body's defenses. When Salmonella bacteria secrete flagellin, their macrophage ferry interprets this as a danger signal, and kills itself -- and the Salmonella on board -- in a self-destructive, pro-inflammatory response called pyroptosis: to go up in flames.As a countermeasure, Salmonella restricts the production of flagellin to avoid tripping the macrophage alarm. This helps Salmonella avoid inciting an inflammatory response that would lessen its chances of colonizing its host.Cookson's team of researchers, led by Dr. Mary Stewart from the UW Department of Microbiology, identified the genetic regulation for the "ON" and "OFF" production of flagellin. This genetic regulation pathway is behind the uncanny ability of genetically identical Salmonella to generate physically distinct subgroups.They discovered that a protein that is almost in a class by itself --YdiV -- determines whether a Salmonella cell will produce or not produce flagellin. This protein can prevent certain parts of the Salmonella genome from being read to manufacture a substance called a sigma factor. The sigma factor plays a key role in recruiting other biochemical functions that promote the production of flagellin.The sigma factor is repressed in only some of the genetically identical cells. This results in the two kinds of subpopulations: those cells that produce flagellin and those that don't. In a lab dish, both types maintain a stable presence within the Salmonella clonal population. In an animal or human, anatomical location determines which type will fare better during each stage of the infection,The researchers also found that Salmonella strains that lack the YdiV protein are unable to fully repress the production of flagellin. These mutant strains are less infectious. Looking at the other side of the host-pathogen struggle, mutant mice that couldn't launch pyroptosis in response to flagellin were more susceptible to serious Salmonella infections.The research was supported by a University of Washington Cellular and Molecular Biology Training Grant, National Institute of General Medical Sciences Public Health Service National Research Award, and grants from the National Institutes of Health.In addition to Cookson and Stewart, the researchers on the study were Alex B. Berezow from the UW Department of Microbiology, and Lisa A. Cummings, and Matthew L. Johnson from the UW Department of Laboratory Medicine. | Genetically Modified | 2,011 |
December 9, 2011 | https://www.sciencedaily.com/releases/2011/11/111130120112.htm | Researchers develop a way to monitor engineered blood vessels as they grow in patients | Using magnetic resonance imaging (MRI) and nanoparticle technology, researchers from Yale have devised a way to monitor the growth of laboratory-engineered blood vessels after they have been implanted in patients. This advance represents an important step toward ensuring that blood vessels, and possibly other tissues engineered from a patient's own biological material, are taking hold and working as expected. Until now, there has been no way to monitor the growth and progress of engineered tissues once they were implanted. | The research was published in the December 2011 issue of the "We hope that the important findings from our study will serve as a valuable tool for physicians and scientists working to better understand the biological mechanisms involved in tissue engineering," said Christopher K. Breuer, M.D., co-author of the study from the Interdepartmental Program in Vascular Biology and Therapeutics at Yale University School of Medicine in New Haven, CT. "Resulting advances will hopefully usher in a new era of personalized medical treatments where replacement vessels are specifically designed for each patient suffering from cardiac anomalies and disease."To make this advance, scientists used two different groups of cells to make tissue-engineered blood vessels. In the first group, the cells were labeled with the MRI contrast agent. In the second group, the cells were normal and did not have an MRI label. Cells from each group were then used to create separate laboratory-engineered blood vessels, which were implanted into mice. The purpose was to see whether the laboratory-engineered blood vessels made from cells that were labeled with the contrast agent would indeed be visible on MRI and to make sure that the addition of the contrast agent did not negatively affect the cells or the function of the laboratory-engineered vessels. Researchers imaged the mice with MRI and found that it was possible to track the cells labeled with contrast agent, but not possible to track the cells that were not labeled. This suggests that using MRI and cellular contrast agents to study cellular changes in the tissue-engineered blood vessels after they are implanted is an effective way to monitor these types of vessels."This is great news for patients with congenital heart defects, who have to undergo tissue grafting, but that's only the tip of the scalpel," said Gerald Weissmann, M.D., Editor-in-Chief of the | Genetically Modified | 2,011 |
December 8, 2011 | https://www.sciencedaily.com/releases/2011/12/111208141937.htm | Researchers identify key plant immune response in fight against bacteria | Researchers at the University of Missouri have found a key process in a plant's immune system response that may help future crops fight off dangerous diseases. | "We study how Arabidopsis, a common weed related to the mustard plant, fends off infectious agents," said Walter Gassmann, professor of plant sciences and researcher for the Christopher S. Bond Life Sciences Center and Interdisciplinary Plant Group. "We have discovered that a protein within the plant known as Enhanced Disease Susceptibility 1 (EDS1) not only plays a key role in the plant's defense but also contributes to the direct recognition of disease agents. Arabidopsis has a widely known genetic structure, and its bacterial pathogens share many tactics with other pathogens such as fungal rusts and mildews. So, if we can translate Arabidopsis' immune response to other plants, we could eventually help crops, such as soybeans, resist devastating infections."Gassmann compares plant and pathogen interactions to warfare. For example, bacterial speck targets "communication hubs" of the plant immune system to suppress the plant's immune system response long enough to invade and cause disease in tomato and Arabidopsis plant tissue. The present study identified EDS1 as one such hub under attack. Meanwhile, in resistant plants, immune receptors that act as sentinels guarding EDS1 detect the invader's attack and trigger an alarm that leads to a vigorous plant defense response. Gassmann believes that further studies on EDS1 and its sentinels could determine how to add the alarm response to plants missing the protein or amplify the response in plants that have the protein."Farmers know that deploying plants with single sentinels, which commonly only detect a single specific attack strategy, only leads to a boom and bust cycle for disease resistant crop plants," Gassmann said. "Farmers are now to the point where in a crop they must stagger multiple sentinels against each pathogen in order to keep plant diseases from spreading. If we can identify the actual targets in the plant, like EDS1, and manipulate these genes in key crops, we could extend the planting cycles for a longer period of time. We're still a long way from application in the field; however, this addition could ultimately produce more food."While genetically modified plants still cause controversy, Gassmann believes that assisting plants with disease resistance derived from nature is better than the use of fungicides. Gassmann also studies how grape production could be improved by using genes from the Missouri Norton grape, which resists powdery mildew, in an effort to alleviate chemical use."If we understand the deeper level of plant immunity, we can develop a smarter way of breeding plants that are generally resistant to devastating diseases," Gassmann said.Gassmann's paper, "Pathogen effectors target Arabidopsis EDS1 and alter its interactions with immune regulators," has been accepted by the journal | Genetically Modified | 2,011 |
November 30, 2011 | https://www.sciencedaily.com/releases/2011/11/111125161023.htm | Transplanted cells repair the brain in obese mice | Without neurons reacting to the blood leptin level, the brain does not control the feeling of hunger and fullness. This type of genetic defects results in severe obesity in humans and animals. Scientists from Harvard University (HU), Massachusetts General Hospital (MGH) and the Nencki Institute of Experimental Biology of the Polish Academy of Sciences (Nencki Institute) in Warsaw have demonstrated in their experiments on mice that it is possible to restore brain functions by transplantation of small numbers of new neurons into the damaged area of the brain. | "A spectacular effect in the brain repair that we were able to achieve was significantly reduced weight of genetically defective obese mice and further significant reduction of adverse symptoms accompanying diabetes," says Dr. Artur Czupryn (Nencki Institute, HU, MGH), first author of a paper published in the latest issue of Already for some time medicine has attempted to repair damaged brain fragments through transplants of stem cells. These interventions are risky. Transplanted cells often develop in an uncontrolled manner, which frequently leads to cancer.The aim of the research carried out for the past five years at HU, MGH and the Nencki Institute was to show that transplantation of small numbers of cells could restore the missing neuronal circuits and restore the lost brain functions. Genetically defective mice, deficient in leptin receptor, have been used in these experiments. Leptin is a protein secreted from cells of the fat tissue into the blood when eating. When it reaches the hypothalamus, it reacts with specific neurons and its presence or its low level cause the feeling of fullness or hunger, respectively. Leptin receptor deficient mice do not know the feeling of fullness. They weigh up to twice more than healthy individuals and suffer from advanced diabetes.The team from Harvard University and Nencki Institute focused on the transplants of immature neurons (neuroblasts) and progenitors, which are specific stem cells with already determined developmental direction. Cells isolated from small regions of developing embryonic brains of healthy mice were used for transplantations. Thus, the probability increased that cells introduced into recipients' brains will transform into neurons or accompanying glial cells.Millions of cells are usually transplanted. In this project, however, scientists injected a suspension of barely several thousand progenitors and neuroblasts into the hypothalamus of mice. About 300 nanolitres of cell suspension was injected into the mouse hypothalamus in the course of low invasive method -- by a thin micropipette with a diameter only several times larger than individual cells."The suspension was introduced into strictly defined region of the hypothalamus of mice, measuring about 200-400 micrometres in length. We were able to locate it thanks to unique high-frequency ultrasound microscopic guidance available at Harvard University. It allowed us to carry out complex non-invasive microtransplants with unprecedented precision, because we were able to carry out high resolution imaging of both the brain structures as well as the introduced micropipette," says Dr. Czupryn.All transplanted cells have been marked with a fluorescent protein, which made possible to follow them in the recipients' brains. Observations carried out 20 or more weeks after the procedure have shown that almost half of transplanted cells transformed into neurons with typical morphology, producing proteins characteristic for normal neurons. By applying sophisticated research techniques, it was possible to demonstrate that the entire range of missing types of neurons was restored in the brain centre for controlling hunger and fullness. Moreover, the new neurons have already formed synapses and communicated with other neurons in the brain, as well as reacted properly to changes in levels of leptin, glucose, and insulin.The final proof for restoration of proper functioning of the hypothalamus in mice was brought by measurements of body weight and blood metabolic factors. Unlike control population of genetically defective obese mice, the weight of mice with transplanted neurons resembled normal weight. Reversal of unfavourable changes of the blood metabolic parameters has also been observed."Many attempts have been described in the literature to date of transplanting cells into the brain. We have shown that a really small transplant of neuroblasts and progenitors was able to reconstitute damaged brain areas and influence the whole organism. We have shown that it is possible to introduce new neurons, which function properly, integrate well into the recipient nervous tissue and restore missing brain functions. Moreover this method turned out to be low invasive and safe, since it did not lead to tumour formation," sums up Dr. Czupryn.Results achieved by the group from Harvard University and the Nencki Institute define a promising research direction, which could lead to the development of new repair therapies. This novel method could help, for example, eliminate the effects of stroke or improve the treatment of Parkinson's disease, which is associated with dysfunction within a defined brain area. Scientists emphasize however that long years of experiments, research, and tests are needed before therapies based on their ideas end up in the clinics and hospitals. | Genetically Modified | 2,011 |
November 21, 2011 | https://www.sciencedaily.com/releases/2011/11/111121114757.htm | Mutants with heterozygote disadvantage can prevent spread of transgenic animals | Genetically modified animals are designed to contain the spread of pathogens. One prerequisite for the release of such organisms into the environment is that the new gene variant does not spread uncontrollably, suppressing natural populations. Scientists at the Max Planck Institute for Evolutionary Biology in Plön, Germany, have now established that certain mutations are maintained over an extended period if two separate populations exchange individuals with one another on a small scale. The new gene variant may remain confined to one of the two populations. The migration rate between the populations determines how long the new gene variant is expected to survive in the environment. | These new findings may help to achieve greater safety when conducting release experiments involving genetically modified animals.Genetically modified organisms must not be allowed to spread uncontrollably. Scientists are therefore keen to take advantage of a mechanism that will localise the spread of mutants. Mutants with a heterozygote disadvantage, as it is known, reduce the evolutionary fitness of their carriers to varying degrees if they are only available to one gene copy (heterozygote) or exist in both gene copies (homozygote). In their study, the Max Planck scientists assumed a fitness loss of 50 percent (compared to wildtypes) for mutant heterozygotes and a 10 percent fitness loss for mutant homozygotes.A mutant with a heterozygote disadvantage can be maintained in a population if it occurs frequently enough for sufficient homozygote offspring to be produced. Above this value, it can suppress the non-mutated gene variant completely and the mutated form becomes extinct. Populations containing mutants with heterozygote disadvantage develop into one of two stable states. These mutant types therefore seem to be well-suited for the safe release of genetically modified organisms. After all, as soon as sufficient numbers of mutants exist in the environment, these replace the natural variant in a local population. If such genes are joined to resistance genes to combat pathogens, mosquito populations could be rendered resistant to Malaria, for example. By releasing the wildtype at a later stage, the transgenic animals can therefore also be removed again more easily from the environment. In population genetics this is known as underdominance.The researchers then analyzed computer-based simulations showing the effect of mutants with heterozygote disadvantage on two populations of equal size, which, as in nature, are subject to statistical fluctuations. In doing so, they paid particular attention to the gene flow arising from the mobility of the individuals. At times, such a mutation can survive in a stable state in a population. However, this only happens if the migration rate is less than 5 percent. "Our calculations have also shown that mutants are best released into both populations even if the goal is to establish the new genetic variant in only one of them in the long term. If, for example, 75 percent of transgenic animals are distributed to the target population and the remaining 25 percent to a neighbouring population, the transgenic individuals may find it easier to gain traction on a long-term basis in the target population," explains Philipp Altrock from the Max Planck Institute for Evolutionary Biology.Scientists in the USA, Brazil, Malaysia and the Cayman Islands have been conducting field experiments on the use of genetically modified animals for several years. These include, for example, experiments involving genetically modified mosquitoes, to protect against infectious diseases such as malaria or dengue fever, and transgenic plant pests. Similar experiments are planned in another nine countries. To date, the males from various insect species, which are generally infertile, are released. In this way, the effective size of the wild population is limited. "One of the disadvantages of this method is that it needs to be repeated very frequently as the transgenic animals cannot reproduce," says Arne Traulsen from the Max Planck Institute in Plön. In addition, in the case of mosquitoes, a few parent individuals can already have a large share of the next generation.In contrast, mutants with heterozygote disadvantage can survive for many generations. Resistance genes linked to such mutants would therefore be more efficient. The safety aspect also increases, as proliferation across a target population is very unlikely. "Nevertheless, the fitness of the transgenic animals, the population sizes, and the migration rates must be known. These factors can most likely be determined for release experiments on maritime islands," says Arne Traulsen. | Genetically Modified | 2,011 |
November 21, 2011 | https://www.sciencedaily.com/releases/2011/11/111121104509.htm | Tweaking a gene makes muscles twice as strong: New avenue for treating muscle degeneration in people who can't exercise | An international team of scientists has created super-strong, high-endurance mice and worms by suppressing a natural muscle-growth inhibitor, suggesting treatments for age-related or genetics-related muscle degeneration are within reach. | The project was a collaboration between researchers at the Salk Institute for Biological Studies, and two Swiss institutions, Ecole Polytechnique Federale de Lausanne (EPFL) and the University of Lausanne.The scientists found that a tiny inhibitor may be responsible for determining the strength of our muscles. By acting on a genome regulator (NCoR1), they were able to modulate the activity of certain genes, creating a strain of mighty mice whose muscles were twice a strong as those of normal mice."There are now ways to develop drugs for people who are unable to exercise due to obesity or other health complications, such as diabetes, immobility and frailty," says Ronald M. Evans, a professor in Salk's Gene Expression Lab, who led the Salk team. "We can now engineer specific gene networks in muscle to give the benefits of exercise to sedentary mice."Johan Auwerx, the lead author from EPFL, says molecules such as NCoR1 are molecular brakes that decrease the activity of genes. Releasing the brake by mutation or with chemicals can reactivate gene circuits to provide more energy to muscle and enhance its activity.In an article appearing in the journal In the absence of the inhibitor, the muscle tissue developed much more effectively. The mice with the mutation became true marathoners, capable of running faster and longer before showing any signs of fatigue. In fact, they were able to cover almost twice the distance run by mice that hadn't received the treatment. They also exhibited better cold tolerance.Unlike previous experiments that focused on "genetic accelerators" this work shows that suppressing an inhibitor is a new way to build muscle. Examination under a microscope confirmed that the muscle fibers of the modified mice are denser, the muscles are more massive, and the cells in the tissue contain higher numbers of mitochondria -- cellular organelles that deliver energy to the muscles.Similar results were also observed in nematode worms, allowing the scientists to conclude that their results could be applicable to a large range of living creatures.The scientists have not yet detected any harmful side effects associated with eliminating the NCoR1 receptor from muscle and fat tissues. Although the experiments involved genetic manipulations, the researchers are already investigating potential drug molecules that could be used to reduce the receptor's effectiveness.The researchers say their results are a milestone in our understanding of certain fundamental mechanisms of living organisms, in particular the little-studied role of corepressors -- molecules that inhibit the expression of genes. In addition, they give a glimpse at possible long-term therapeutic applications."This could be used to combat muscle weakness in the elderly, which leads to falls and contributes to hospitalizations," Auwerx says. "In addition, we think that this could be used as a basis for developing a treatment for genetic muscular dystrophy."He added that if these results are confirmed in humans, there's no question they will attract interest from athletes as well as medical experts. | Genetically Modified | 2,011 |
November 16, 2011 | https://www.sciencedaily.com/releases/2011/11/111115180317.htm | Engineered, drug-secreting blood vessels reverse anemia in mice | Patients who rely on recombinant, protein-based drugs must often endure frequent injections, often several times a week, or intravenous therapy. Researchers at Children's Hospital Boston demonstrate the possibility that blood vessels, made from genetically engineered cells, could secrete the drug on demand directly into the bloodstream. In the Nov. 17 issue of the journal | The technology could potentially be used to deliver other proteins such as Factor VIII and Factor IX for patients with hemophilia, alpha interferon for hepatitis C and interferon beta for multiple sclerosis, says the study's principal investigator, Juan Melero-Martin, PhD, of the Department of Cardiac Surgery at Children's.Such drugs are currently made in bioreactors by engineered cells, and are very expensive to make in large amounts. "The paradigm shift here is, 'why don't we instruct your own cells to be the factory?'" says Melero-Martin, also an assistant professor at Harvard Medical School.The researchers created the drug-secreting vessels by isolating endothelial colony-forming cells from human blood and inserting a gene instructing the cells to produce EPO. They then added mesenchymal stem cells, suspended the cells in a gel, and injected this mixture into the mice, just under the skin. The cells spontaneously formed networks of blood vessels, lined with the engineered endothelial cells. Within a week, the vessels hooked up with the animals' own vessels, releasing EPO into the bloodstream.Tests showed that the drug circulated throughout the body and reversed anemia in the mice, both induced by radiation (as often occurs in cancer patients) and by loss of kidney tissue (modeling chronic kidney failure). Mice with the vessel implants had significantly higher hematocrits (a measure of red blood cell concentration) and recovered from anemia more quickly than controls.The system also had a built-in on/off control: the inserted EPO-encoding gene was linked to a repressor protein that prevented it from being turned on unless the mice were given the oral drug doxycycline (added to their drinking water). Doxycycline disabled the repressor protein, allowing EPO to be made. When doxycycline was added to the water on a weekly on/off schedule, the animals' hematocrit fluctuated accordingly. When hematocrit reached a normal level, the system could be switched off by simply giving them plain water.Melero-Martin and colleagues are looking at ways to deliver doxycycline through the skin to avoid exposing the whole body to an antibiotic. There are also other ways to design the genetic on/off control, using synthetic systems or even regulatory elements used naturally by the body -- sensing blood oxygen levels and stimulating EPO production when oxygen levels dip.A traditional barrier to gene therapy has been getting the genetically altered cells to engraft and stay in place. Blood-vessel implants are an ideal platform technology for gene therapy applications whose goal is systemic drug delivery, says Melero-Martin."Blood vessels are one of the few tissues where we have good control over engraftment," he says. "Endothelial cells are easily isolated from blood, are good at assembling themselves into blood vessels, and are ideal for releasing compounds into the bloodstream, since they line the blood vessels."The lab is interested in trying this system with other therapeutic proteins, and is also exploring ways to get cells to release therapeutics at a moment's notice by getting accumulating stores in advance that could be released upon the proper signal, as beta cells in the pancreas do with insulin, for example.In addition, Melero-Martin wants to explore regenerative medicine applications, creating blood vessels with genetic instructions to produce factors that attract stem cells or induce cells to differentiate.The study was funded by the National Institute of Biomedical Imaging and Bioengineering (NIBIB) of the National Institutes of Health and the Children's Hospital Boston Department of Cardiac Surgery. Ruei-Zeng Lin, PhD, a research fellow in the Department of Cardiac Surgery at Children's, was first author on the paper. | Genetically Modified | 2,011 |
November 9, 2011 | https://www.sciencedaily.com/releases/2011/11/111108201544.htm | 'Noise' tunes logic circuit made from virus genes | In the world of engineering, “noise” – random fluctuations from environmental sources such as heat – is generally a bad thing. In electronic circuits, it is unavoidable, and as circuits get smaller and smaller, noise has a greater and more detrimental effect on a circuit’s performance. Now some scientists are saying: if you can’t beat it, use it. | Engineers from Arizona State University in Tempe and the Space and Naval Warfare Systems Center (SPAWAR) in San Diego, Calif., are exploiting noise to control the basic element of a computer – a logic gate that can be switched back and forth between two different logic functions, such as AND\OR – using a genetically engineered system derived from virus DNA. In a paper accepted to the AIP’s journal Chaos, the team has demonstrated, theoretically, that by exploiting sources of external noise, they can make the network switch between different logic functions in a stable and reliable way.This proof-of-concept work offers the possibility of exploiting noise in biologic circuits instead of regarding it as a laboratory curiosity or a nuisance, the researchers say. | Genetically Modified | 2,011 |
November 8, 2011 | https://www.sciencedaily.com/releases/2011/11/111104091654.htm | Biologists use flies and mice to get to the heart of Down syndrome | A novel study involving fruit flies and mice has allowed biologists to identify two critical genes responsible for congenital heart defects in individuals with Down syndrome, a major cause of infant mortality and death in people born with this genetic disorder. | In a paper published in the November 3 issue of the open access journal Down syndrome, the most common genetic cause of cognitive impairment, is a disorder that occurs in one in 700 births when individuals have three, instead of the usual two, copies of human chromosome 21."Chromosome 21 is the shortest human chromosome and intensive genetic mapping studies in people with Down syndrome have identified a small region of this chromosome that plays a critical role in causing congenital heart defects," said Ethan Bier, a biology professor at UC San Diego and one of the principal authors of the study. "This Down syndrome region for congenital heart disease, called the 'DS-CHD critical region,' contains several genes that are active in the heart which our collaborator, Julie Korenberg, had suspected of interacting with each other to disrupt cardiac development or function when present in three copies. But exactly which of these half dozen or so genes are the culprits?""Identifying the genes within the DS-CHD critical region contributing to congenital heart defects is challenging to address using traditional mammalian experimental models, such as mice," added Bier, "since the number of possible genetic combinations that would need to be generated and tested is very large."To simplify their search, the scientists turned to fruit flies, a simpler and rapidly reproducing biological system with many of the same genes as mice and humans. With help from collaborators Amir Gamliel,Geoff Rosenfeld and Kirk Peterson at the UC San Diego School of Medicine, Rolf Bodmer and Karen Ocorr at the Sanford-Burnham Medical Research Institute, and Julie R. Korenberg at the University of Utah, biologist Tamar Grossman in Bier's lab devised a sequential genetic approach to untangle the problem."First, fruit flies were used to test for all possible pairwise genetic interactions between these genes that might disrupt the function of the simple fluid pumping fly heart," said Bier." These comprehensive genetic studies pointed to a particular pair of genes known as DSCAM and COL6A2 that resulted in the most severe defects when over-produced together."Then the researchers tested the effects of increasing the levels of these genes in the hearts of experimental mice. They first generated genetic lines of mice having elevated activity of each of these genes in the heart and then genetically crossed these mice to create offspring that over-produced both genes together. The parental mice as well as their offspring were then tested for heart function and visible heart defects.Mice having elevated levels of each gene separately were largely normal. But the offspring with extra levels of both genes suffered from severe cardiac defects. These heart defects were of two kinds. The first resembled one of the salient features of Down syndrome cardiac patients, in which blood shunts between the two atrial chambers of the heart through small holes in a septum that normally isolates these two chambers. The second defect, which is not frequently observed in Down syndrome patients, but is a common and very serious condition in the general population, was a thickening of the heart wall -- referred to medically as cardiac hypertrophy."Such thickening of the heart wall greatly reduces heart function and can lead to fatal heart attacks, which indeed was observed among some of the more seriously affected DSCAM and COL6A2 over-producing mice," said Bier.Bier added that the tiered genetic approach, using fruit flies, then mice, could be useful in identifying genes involved in other common genetic disorders that are thought to be caused by multiple genes."These conditions arise due to a surprising variation in the copy number of small intervals of human chromosomes that are carried by virtually all people," he said. "Depending on which small regions of the chromosome have extra or fewer copies of genes, various conditions can result including obesity, autism, and schizophrenia. Typically in these diseases, as in Down syndrome, the difficult puzzle is which of the possible genes with altered copy number are involved in causing the disease."Funding for the research project was provided by grants from the National Institutes of Health. | Genetically Modified | 2,011 |
November 3, 2011 | https://www.sciencedaily.com/releases/2011/11/111102161056.htm | Tactic to delay age-related disorders | Researchers at Mayo Clinic have shown that eliminating cells that accumulate with age could prevent or delay the onset of age-related disorders and disabilities. The study, performed in mouse models, provides the first evidence that these "deadbeat" cells could contribute to aging and suggests a way to help people stay healthier as they age. | The findings appear in the journal "By attacking these cells and what they produce, one day we may be able to break the link between aging mechanisms and predisposition to diseases like heart disease, stroke, cancers and dementia," says co-author James Kirkland, M.D., Ph.D., head of Mayo's Robert and Arlene Kogod Center on Aging and the Noaber Foundation Professor of Aging Research. "There is potential for a fundamental change in the way we provide treatment for chronic diseases in older people."Five decades ago, scientists discovered that cells undergo a limited number of divisions before they stop dividing. At that point the cells reach a state of limbo -- called cellular senescence -- where they neither die nor continue to multiply. They produce factors that damage adjacent cells and cause tissue inflammation. This alternative cell fate is believed to be a mechanism to prevent runaway cell growth and the spread of cancer. The immune system sweeps out these dysfunctional cells on a regular basis, but over time becomes less effective at "keeping house."As a result, senescent cells accumulate with age. Whether and how these cells cause age-related diseases and dysfunction has been a major open question in the field of aging. One reason the question has been so difficult to answer is that the numbers of senescent cells are quite limited and comprise at most only 10 to 15 percent of cells in an elderly individual."Our discovery demonstrates that in our body cells are accumulating that cause these age-related disorders and discomforts," says senior author Jan van Deursen, Ph.D., a Mayo Clinic molecular biologist and the Vita Valley Professor of Cellular Senescence. "Therapeutic interventions to get rid of senescent cells or block their effects may represent an avenue to make us feel more vital, healthier, and allow us to stay independent for a much longer time.""Through their novel methodology, the research team found that deletion of senescent cells in genetically engineered mice led to improvement in at least some aspects of the physiology of these animals. So, with the caveat that the study involved a mouse model displaying accelerated aging, this paper provides important insights on aging at the cellular level," says Felipe Sierra, Ph.D., Director of the Division of Aging Biology, National Institute on Aging, National Institutes of Health.Dr. van Deursen and colleagues genetically engineered mice so their senescent cells harbored a molecule called caspase 8 that was only turned on in the presence of a drug that has no effect on normal cells. When the transgenic mice were exposed to this drug, caspase 8 was activated in the senescent cells, drilling holes in the cell membrane to specifically kill the senescent cells.The researchers found that lifelong elimination of senescent cells delayed the onset of age-related disorders such as cataracts and muscle loss and weakness. Perhaps even more importantly, they showed that removing these cells later in life could slow the progression of already established age-related disorders.The findings support a role of senescent cells in the aging process and indicate that chemicals secreted by these cells contribute to age-related tissue dysfunction and disease.Other co-authors of the article are: Darren Baker, Ph.D., Tamar Tchkonia, Ph.D., Nathan LeBrasseur, Ph.D. and Bennett Childs, all of Mayo Clinic; and Tobias Wijshake and Bart van de Sluis, Ph.D., both of Groningen University, The Netherlands. The Ellison Medical Foundation, the Noaber Foundation, the Robert and Arlene Kogod Center on Aging, and the National Institutes of Health funded the study. | Genetically Modified | 2,011 |
October 28, 2011 | https://www.sciencedaily.com/releases/2011/10/111025143522.htm | Rising to a global health challenge, students coax yeast cells to add vitamins to bread | Any way you slice it, bread that contains critical nutrients could help combat severe malnutrition in impoverished regions. That is the goal of a group of Johns Hopkins University undergraduate students who are using synthetic biology to enhance common yeast so that it yields beta carotene, the orange substance that gives carrots their color. When it's eaten, beta-carotene turns into vitamin A. | The students' project is the university's entry in iGEM, the International Genetically Engineered Machine competition. After a regional judging earlier this month, the undergraduates' project, called VitaYeast, has advanced to the iGEM finals, scheduled for Nov. 5-7 at the Massachusetts Institute of Technology. In the annual iGEM contest, students from around the world present projects based on synthetic biology, a burgeoning field in which researchers manipulate small bits of DNA and other biological material to make cells carry out new tasks.The Johns Hopkins participants say that no matter what happens at the iGEM finals, they will continue to tout their enhanced bread as a relatively simple way to help hundreds of thousands of people who are suffering from malnutrition.Team member Arjun Khakhar, a junior biomedical engineering major, grew up in Bombay, India, where he saw widespread poverty and malnutrition. "The major problem in developing countries right now is Producing a new food to save malnourished people around the globe may sound like an audacious goal for a group of 15 to 20 students who haven't yet picked up their college diplomas. But Arjun doesn't think so. "How do I get the idea in my mind that I want to change the world?" he said. "I would ask, How can you To curb global malnutrition, Arjun and his teammates envisioned an enhanced starter dough that could be shared easily and cheaply among large groups of impoverished people. The bread baked from this dough could avert health problems that occur when vitamins and other nutrients are missing from their diets. Such health problems can be serious. The World Health Organization has described vitamin A deficiency as the leading cause of preventable blindness in children.Yeast, which helps make bread rise, does not normally produce vitamins. To make this happen, the students, representing a variety of science majors, had to genetically tweak the single-cell microbes. The team members figured out how to add to yeast cells certain DNA sequences that triggered a series of biochemical reactions that produced beta carotene. They presented that development at the iGEM regional contest and are continuing to work on yeast that also produces Vitamin C, another crucial nutrient needed in impoverished areas.As they worked on the VitaYeast project, the students were advised by Johns Hopkins faculty members, including Jef Boeke, a leading yeast expert who is a professor of molecular biology and genetics at the School of Medicine. "One of the great things about iGEM teams, which are mostly made up of undergraduates, is that those students, frankly, will not believe that something is impossible," Boeke said. "If you tell them that something is impossible, they will go off and do it. I find that to be very exciting."Working in lab space provided by Boeke and other faculty members, the iGEM students solved the science challenges and produced samples of their enhanced dough. But would VitaYeast yield bread that looks and smells good enough to eat? As all good cooks know, the proof is in the pudding -- or, in this case, the bread basket. To find out, the students purchased a bread-making machine, found a simple recipe online and turned their lab into a makeshift kitchen. "We wanted to simulate the process that a regular person might go through to bake bread," said team member Steffi Liu, a junior biomedical engineering major from Edison, N.J. "The only thing that's different in the recipe is that we substituted our vitamin A yeast for the normal dry packaged yeast."The resulting bread, she said, "looks exactly the same as normal bread. Definitely the same smell! The lab smelled amazing after we baked the bread. Everybody wanted a bite of it. But obviously we can't do that."Because the lab bread contains a genetically engineered ingredient that has not undergone safety testing or received approval from government regulators, the students are not permitted to eat it. But they are encouraged by the tempting aroma and traditional breadlike texture and appearance.In recent years, some genetically engineered foods have been rejected by malnourished people merely because they did not look, smell or taste like the familiar food staples. The Johns Hopkins students are banking on greater success, partly because they are thinking small. "VitaYeast is a tiny component -- it gets killed in the bread," said Noah Young, a senior biomedical engineering major from Irvine, Calif. "We're not genetically modifying the wheat. We're not genetically modifying the flour or the water. We're genetically modifying something like 1 percent of the bread recipe. When you bake VitaYeast bread and you look at it, it looks like normal bread."As part of the project, team member Ashan Veerakumar, a senior neuroscience major from Toronto, will survey Baltimore area residents about whether they would eat genetically modified food, particularly if it could improve their health. "The thing we're trying to find out here," Ashan said, "is whether our project is something the public will accept."He and some of the other team members are also looking for outside funding to continue pushing the VitaYeast project forward. Yet before VitaYeast bread can make its way to malnourished people, it must overcome many hurdles, including animal testing and rigorous regulatory reviews.Still, faculty adviser Boeke is not betting against his student scientists. "Could this notion of releasing a genetically modified organism in a Third World country ever happen?" he asked. "Personally, I think the answer is yes." Some of the iGEM students, Boeke said, "were ready to rush off and do it right away, and we had to restrain their enthusiasm." Another faculty member, who is a bioethicist, was called in to urge the students to be more patient in pressing toward their goal. "She's helped the students understand what the steps are needed to get to that point," Boeke said. "That will certainly be a multiyear process, at best. But I think it could happen."VitaYeast website: An online video about this project can be viewed at: | Genetically Modified | 2,011 |
October 27, 2011 | https://www.sciencedaily.com/releases/2011/10/111027112520.htm | Natural intestinal flora involved in the emergence of multiple sclerosis, study finds | Multiple sclerosis is caused by a combination of genetic and environmental factors. For a long time, pathogens were believed to be such external influences. According to scientists from the Max Planck Institute of Neurobiology in Martinsried, however, it is apparently not harmful bacteria that trigger multiple sclerosis, but beneficial ones -- specifically, the natural intestinal flora, which every human being needs for digestion. The researchers discovered that genetically modified mice develop an inflammation in the brain similar to the human disease if they have normal bacterial intestinal flora. The microorganisms begin by activating the immune system's T cells and, in a further step, the B immune cells. | The findings, published in the journal The human intestine is a paradise for microorganisms: it is home to roughly 100 billion bacteria made up from 2,000 different bacterial species. The microorganisms of the intestine are not only indispensable for digestion, but also for the intestine's development. Altogether, this diverse community comprises between ten and one hundred times more genes than the entire human genome. Scientists therefore frequently refer to it as the "extended self." However, the intestinal bacteria can also play a role in diseases in which the immune system attacks the body itself. Intestinal bacteria can thus promote autoimmune disorders such as Crohn's disease and rheumatoid arthritis.On the one hand, the likelihood of developing multiple sclerosis, a disease in which proteins on the surface of the myelin layer in the brain activate the immune system, is influenced by genes. On the other, however, environmental factors have an even greater impact on the disease's development. Scientists have long suspected that it is caused by infectious agents. The Max Planck researchers now assume that multiple sclerosis is triggered by the natural intestinal flora.This astonishing finding was made possible by newly developed genetically modified mice. In the absence of exposure to any external influences, inflammatory reactions arise in the brains of these animals which are similar to those associated with multiple sclerosis in humans -- however, this only occurs when the mice have intact intestinal flora. Mice without microorganisms in their intestines and held in a sterile environment remained healthy. When the scientists "vaccinated" the animals raised in sterile conditions with normal intestinal microorganisms, they also became ill.According to the Martinsried-based researchers, the intestinal flora influence immune systems in the digestive tract; mice without intestinal flora have fewer T cells there. Moreover, these animals' spleen produces fewer inflammatory substances, like cytokines. In addition, their B cells produce few or no antibodies against myelin. When the researchers restored the intestinal flora to the mice, their T cells and B cells increased their cytokine and antibody production."It appears that the immune system is activated in two stages: to begin, the T cells in the lymph vessels of the intestinal tract become active and proliferate. Together with the surface proteins of the myelin layer, these then stimulate the B cells to form pathogenic antibodies. Both processes trigger inflammatory reactions in the brain which progressively destroy the myelin layer -- a process that is very similar to the way multiple sclerosis develops in humans," says Gurumoorthy Krishnamoorthy from the Max Planck Institute of Neurobiology. Thus, the disease is caused by changes in the immune system and not by disturbances in the functioning of the nervous system. "Multiple sclerosis research has long been preoccupied with this question of cause and effect. Our findings would suggest that the immune system is the driving force here," says Hartmut Wekerle, Director at the Max Planck Institute in Martinsried.The scientists are certain that the intestinal flora can also trigger an overreaction of the immune system against the myelin layer in persons with a genetic predisposition for multiple sclerosis. Therefore, nutrition may play a central role in the disease, as diet largely determines the bacteria that colonise the intestines. "Changing eating habits could explain, for example, why the incidence of multiple sclerosis has increased in Asian countries in recent years," explains Hartmut Wekerle.Precisely which bacteria are involved in the emergence of multiple sclerosis remains unclear. Possible candidates are clostridiums, which can have direct contact with the intestinal wall. They are also a natural component of healthy intestinal flora but could possibly activate the T cells in persons with a genetic predisposition. The scientists would now like to analyse the entire microbial genome of patients with multiple sclerosis and thereby identify the differences in the intestinal flora of healthy people and multiple sclerosis patients. | Genetically Modified | 2,011 |
October 27, 2011 | https://www.sciencedaily.com/releases/2011/10/111023135717.htm | Bio-engineered protein shows promise as new hemophilia therapy | A genetically engineered clotting factor that controlled hemophilia in an animal study offers a novel potential treatment for human hemophilia and a broad range of other bleeding problems. | The researchers took the naturally occurring coagulation factor Xa (FXa), a protein active in blood clotting, and engineered it into a novel variant that safely controlled bleeding in mouse models of hemophilia. "Our designed variant alters the shape of FXa to make it safer and efficacious compared to the wild-type factor, but much longer-lasting in blood circulation," said study leader Rodney A. Camire, PhD, a hematology researcher at The Children's Hospital of Philadelphia."The shape of the variant FXa changes when it interacts with another clotting factor made available following an injury," added Camire. "This increases the functioning of the protein which helps stop bleeding." Camire is an associate professor of Pediatrics in the Perelman School of Medicine at the University of Pennsylvania.The study appears online in In hemophilia, an inherited single-gene mutation impairs a patient's ability to produce a blood-clotting protein, leading to spontaneous, sometimes life-threatening bleeding episodes. The two major forms of the disease, which occurs almost solely in males, are hemophilia A and hemophilia B, characterized by which specific clotting factor is deficient. Patients are treated with frequent infusions of clotting proteins, which are expensive and sometimes stimulate the body to produce antibodies that negate the benefits of treatment.Roughly 20 to 30 percent of patients with hemophilia A and 5 percent of hemophilia B patients develop these inhibiting antibodies. For those patients, the conventional treatment, called "bypass therapy," is to use drugs such as factor VIIA and activated prothrombin complex concentrates (aPCCs) to restore blood clotting capability. But these agents are costly (as much as $30,000 per treatment) and not always effective. Camire added that, in the current animal study, they were able to show the variant protein is more effective at a lower dose than FVIIa.The range of options for hemophilia patients could improve if the study results in animals were to be duplicated in humans. "The variant we have developed puts FXa back on the table as a possible therapeutic agent," said Camire. Naturally occurring (wild-type) FXa, due to its particular shape, is not useful as a therapy because normal biological processes shut down its functioning very quickly.By custom-designing a different shape for the FXa protein, Camire's study team gives it a longer period of activity, while limiting its ability to engage in unwanted biochemical reactions, such as triggering excessive clotting. "This potentially could lead to a new class of bypass therapy for hemophilia, but acting further downstream in the clot-forming pathway than existing treatments," said Camire, who has investigated the biochemistry of blood-clotting proteins for more than a decade.When infused into mice with hemophilia, the FXa variant reduced blood loss after injury, as it safely restored blood clotting ability. Further studies are necessary in large animal models to determine whether this approach can become a clinical treatment for hemophilia patients who have developed inhibitors, or even more broadly as a drug for uncontrolled bleeding in other clinical situations.Funding support for this research came from the National Institutes of Health, Pfizer Inc., and the National Hemophilia Foundation. The first author of the study was Lacramioara Ivanciu, PhD, of The Children's Hospital of Philadelphia. Other co-authors with Camire were from Children's Hospital, Pfizer Inc., and the Perelman School of Medicine of the University of Pennsylvania. | Genetically Modified | 2,011 |
October 20, 2011 | https://www.sciencedaily.com/releases/2011/10/111020024712.htm | New bacteria toxins against resistant insect pests | Toxins from | Scientists have therefore modified the molecular structure of two Bt toxins, Cry1Ab and Cry1Ac, in order to overcome resistance. The novel toxins, Cry1AbMod and Cry1AcMod, are effective against five resistant insect species, such as the diamondback moth, the cotton bollworm, and the European corn borer. Cry1AbMod and Cry1AcMod can be used alone or in combination with other Bt toxins for plant protection.New insights into the mechanisms of action of Cry1Ab and Cry1Ac served as the basis for development of the modified Bt toxins. The primary question had been why the Cry proteins, which naturally occur in "When we studied the new Bt toxins in twelve resistant and non-resistant strains of five major pest species, the results of our experiments were encouraging but surprising. The new toxins are also effective against strains whose Bt resistance is not based on cadherin mutations," says David G. Heckel, director of the Department of Entomology at the Max Planck Institute for Chemical Ecology in Jena, Germany, and co-author of the study. Especially interesting was the finding that the new toxins were specifically effective against a super-resistant strain of tobacco budworm carrying both the cadherin mutation and another mutation affecting an ABC transporter which was discovered by the Max Planck researchers last year.Particularly striking was the effect of Cry1AbMod and Cry1AcMod on a Bt resistant corn borer and a resistant diamondback moth strain that was 350 times stronger compared to that of the natural toxins. On the other hand, the new toxins had only a weak effect on some strains whose Bt resistance is due to a mutated cadherin.If both novel Bt toxins prove to be useful in agriculture, they can be used in combination with different Bt toxins to guarantee a reliable effect on herbivorous pests. Biologists also agree that measures to reduce the occurrence of resistant insect pests must be strictly adhered to and that farmers should be informed in detail. Such measures would mainly include the use of different pesticides, crop rotation, and simultaneous sowing of non-Bt plants in fields, where transgenic Bt varieties are grown. | Genetically Modified | 2,011 |
October 17, 2011 | https://www.sciencedaily.com/releases/2011/10/111017102547.htm | Genetic study of cave millipedes reveals isolated populations and ancient divergence between species | The | The southern Cumberland Plateau in Tennessee and Alabama, USA is known for its high cave density. In addition, it has the highest cave biodiversity of any region in North America. Millipedes of the genus The authors used genetic techniques to compare | Genetically Modified | 2,011 |
October 11, 2011 | https://www.sciencedaily.com/releases/2011/10/111011112310.htm | Improved method for detecting mutant DNAs | Molecular DNA testing methods offer clinicians powerful tools that serve to confirm or identify disease diagnoses. High sensitivity and high specificity, however, are frequently a challenge to achieve with these methods. In a study scheduled for publication in the November issue of | A group of researchers in Korea describe a simple and inexpensive enrichment technique that they have termed mutant enrichment with 3′-modified oligonucleotides (MEMO). This oligonucleotide blocks extension of the normal gene but enables extension of the mutated gene, allowing for increased detection sensitivity."The potential applications of MEMO include all situations in which minority alleles of clinical significance are present and sensitive detection is required," commented lead investigators Seung-Tae Lee MD, PhD, and Chang-Seok Ki, MD, PhD, Department of Laboratory Medicine and Genetics, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea. "In addition to the application of MEMO to detect cancer mutations, it can be used in other situations, such as variant strain identification in infectious diseases (for example, the YMDD mutation in hepatitis B virus infection and antiviral drug-resistant variants in human immunodeficiency virus infection), minor mutant allele detection in patients with low-level somatic mosaicism or mitochondrial heteroplasmy, and characterization of fetal mutations from maternal plasma samples."Using genomic DNA extracted from cancer-derived cell lines containing Compared to preexisting methods, MEMO was shown to provide an improved diagnostic performance so that the method can be easily applicable in various medical fields, where molecular assays are important for disease diagnosis or treatment monitoring, and thus may help to improve patient outcomes. | Genetically Modified | 2,011 |
October 11, 2011 | https://www.sciencedaily.com/releases/2011/10/111007102111.htm | Gene technology can help food crops must to withstand harsher weather | Rapid population growth and a swiftly changing climate compound the challenges of ensuring a secure global food supply. Genetically modified plants could help to solve the problem, believes a Norwegian crop researcher. | Over 90 per cent of the global food supply consists of either plants or meat from production animals raised on plant-based feeds. By 2050, 70 per cent more food will need to be produced worldwide on roughly the same area of farmland to keep up with global population growth. At the same time, major changes in climate are expected to occur.Although a quarter million plant types exist, global food production today is based on only about 100 of them. Wheat, corn and rice account for over 60% of all production."We depend completely on the success of these few crops. But I am convinced that the fitness of current plant varieties will not last forever. All it will take to trigger a famine is one year of badly reduced yields for just one of the three main crops," warns Atle Bones, Professor of Biology at the Norwegian University of Science and Technology (NTNU) in Trondheim.Professor Bones and his colleagues have received funding for their research from a number of programmes at the Research Council of Norway, including the Large-scale Programme on Functional Genomics in Norway (FUGE).Professor Bones believes that in order to ensure a secure global food supply, we will have to use every existing means -- including genetically modified organisms (GMO).Genetically modified plants are created by adding, removing or modifying one or more genes in order to breed plants with desired traits. Currently, most genetically modified food is in the form of plants with traits added to make them more resistant to insects and chemical weed killers (herbicides).Professor Bones envisions a future when plants will need extra-strong resistance to the effects of phenomena such as floods, cold spells, droughts and ultraviolet radiation.According to Professor Bones, there are thousands of plants that could be cultivated for food once they are bred to remove toxic compounds or undesirable traits.Rapeseed is one of the world's 15 most important crops. Professor Bones and his colleagues have figured out how to genetically instruct the rapeseed plant to remove toxins from its seeds."Rapeseed is currently used for producing cooking oil and animal feed, but it has certain limitations," he explains. "Our technique could make it possible to utilise this plant to an even greater extent, and the principle could well be applied to other plant species or plant parts."In Norway, the Norwegian Biotechnology Advisory Board assesses all applications from companies seeking approval for a GMO product.The board's assessment guidelines are based on the precautionary principle, which postpones implementing any measure until its threat to human health or the environment has been ruled out.Are we actually certain that genes from genetically modified food do not enter or alter human DNA, or that genetically modified organisms, once released into nature, will not negatively affect the ecosystem?According to Professor Bones, "Opponents of GMOs see the worst case scenario as organisms turning out to be toxic or spreading into nature in undesired ways. To me, the worst case scenario would be a global food shortage because we squandered our chance to carry out research on introducing traits that enable plants to withstand the coming challenges."The biologist agrees that the benefits must be weighed against the risks, case by case. When it comes to GMOs, he says, there is no single truth but many."As of today, not a single report of GMOs having damaged health or the environment has been verified." He stresses, however, that it is extremely difficult to prove specific effects of food, since a diet consists of many foods that have a combined effect."Furthermore, genetically modified food is now checked far more thoroughly than any other food."Conventional plant breeding, in which the best traits of a plant are selectively bred over time, is still a useful solution in many instances. But it is a method limited in its precision and speed and is restricted to certain species."Using gene technology," continues Professor Bones, "we could in theory create a new product in the course of a few months, with a variety of traits added or altered, and tailored to different farming zones. Genetic modification can also be key for increasing the nutritional value of vegetable foods.""I don't believe that gene technology or GMOs alone will save the world, but they will be part of the solution in certain areas," concludes the crop researcher. "Some changes, such as climatic ones, are going to happen rapidly, so we don't have time to wait the many years it would take with conventional selection to introduce the desired traits into our crop varieties." | Genetically Modified | 2,011 |
October 7, 2011 | https://www.sciencedaily.com/releases/2011/10/111004180106.htm | Lungfish provides insight to life on land: 'Humans are just modified fish' | A study into the muscle development of several different fish has given insights into the genetic leap that set the scene for the evolution of hind legs in terrestrial animals. This innovation gave rise to the tetrapods -- four-legged creatures, and our distant ancestors -- that made the first small steps on land some 400 million years ago. | A team of Australian scientists led by Professor Peter Currie, of the Australian Regenerative Medicine Institute at Monash University, and Dr Nicolas Cole, of the University of Sydney, report their results October 4 in online, open access journal Scientists have long known that ancient lungfish species are the ancestors of the tetrapods. These fish could survive on land, breathing air and using their pelvic fins to propel themselves. Australia is home to three species of the few remaining lungfish -- two marine species and one inhabiting Queensland's Mary River basin.There are big gaps in our knowledge, however. Most conclusions have previously been drawn from fossil skeletons, but the muscles critical to locomotion cannot be preserved in the fossil record. The team used fish living today to trace the evolution of pelvic fin muscles to find out how the load-bearing hind limbs of the tetrapods evolved. They compared embryos of the descendants of species representing key turning points in vertebrate evolution to see if there were differences in pelvic fin muscle formation. They studied "primitive" cartilaginous fish -- Australia's bamboo shark and its cousin, the elephant shark -- as well as three bony fishes -- the Australian lungfish, the zebrafish and the American paddlefish. The bony fish and in particular the lungfish are the closest living relative of the tetrapods' most recent common ancestor with fish."We examined the way the different fish species generated the muscles of their pelvic fins, which are the evolutionary forerunners of the hind limbs," said Professor Currie, a developmental biologist. Currie and his team genetically engineered the fish to trace the migration of precursor muscle cells in early developmental stages as the animal's body took shape. These cells in the engineered fish were made to emit a red or green light, allowing the team to track the development of specific muscle groups. They found that the bony fish had a different mechanism of pelvic fin muscle formation from that of the cartilaginous fish, a mechanism that was a stepping stone to the evolution of tetrapod physiology."Humans are just modified fish," said Professor Currie. "The genome of fish is not vastly different from our own. We have shown that the mechanism of pelvic muscle formation in bony fish is transitional between that in sharks and in our tetrapod ancestors." | Genetically Modified | 2,011 |
May 6, 2021 | https://www.sciencedaily.com/releases/2021/05/210506174114.htm | Swiping, swabbing elevates processing plant food safety | By swiping surfaces in commercial food processing plants with specially designed rapid-testing adenosine triphospate (ATP) swabs -- which produce a light similar to the glow of fireflies in the presence of microorganisms -- spoilage and foodborne illness could diminish, according to a new study from Cornell University food scientists. | During food production, routine cleaning and surface sanitation are keys to help prevent microbial contamination in the end food products. Without such a sanitation regime, food from processing plants can become more vulnerable to spoilage, and people who eat that food may face greater risk with illness or death from foodborne pathogens."Food scientists know that for processing plants, visual inspection is not a reliable indicator of cleaning-protocol success," said Randy Worobo, professor of food science in the College of Agriculture and Life Sciences (CALS) and faculty fellow at the Cornell Atkinson Center for Sustainability. "All food factory 'ecosystems' are prone to niches where microorganisms can hang out or where food residues can persist. We need to find them."Worobo is senior author of the study, "Implementation of ATP and Microbial Indicator Testing for Hygiene Monitoring in a Tofu Production Facility Improves Product Quality and Hygienic Conditions of Food Contact Surfaces: A Case Study," which published on Feb. 12 in Each year more than 48 million Americans get sick from foodborne pathogens; more than 120,000 are hospitalized and about 3,000 die, according to the U.S. Centers for Disease Control and Prevention.Examining the efficacy of an environmental monitoring program using the 3M Clean-Trace Hygiene Monitoring and Management system for ATP monitoring, in combination with 3M Petrifilm Plates, for microbiological enumeration -- Worobo and lead author Jonathan H. Sogin, a doctoral student in food science, in partnership with 3M Food Safety microbiologists, spent nine months testing samples collected from the processing environment in a commercial tofu manufacturing facility.Worobo, Sogin and the 3M Food Safety team assembled a custom-designed plan to use an ATP swab test to check dozens of critical points in the plant after it had been cleaned. Following use, the ATP swab is placed in a luminometer instrument, where the bioluminescence of contaminants is detected.The amount of light is transformed in the luminometer to relative light units, where this value is displayed on the instrument. If it exceeds a defined threshold value, the surface would be considered dirty and may indicate that cleaning operations were not performed properly.Results show that targeted cleaning -- demonstrated by ATP monitoring, and verified by further microbiological tests -- can improve the environmental hygiene of food-processing facilities."If a plant supervisor is responsible for the cleaning crew and the supervisor says, 'That's not clean enough,' there might be an employee who thinks that the supervisor is picking on them," Worobo said. "Instead, if you have luminometer, like the 3M Clean-Trace system, that device removes the bias so that the cleaning crew itself can see the numbers. These methods become a quantitative way to ensure that they're doing a good job."ATP monitoring and microbiological enumeration can verify and improve the efficacy of cleaning and sanitation practices, which can have a positive impact not only for the facility, but for product quality, Sogin said."This test can not only verify that the plant's equipment and food-contact surfaces are cleaned and sanitized before starting food preparations, it can identify problematic situations. It helps you become a sleuth," Worobo said. "But as a standard, the industry should be using this method to verify cleaning and sanitation programs. It's key."In addition to Worobo and Sogin, contributors included Maro Çobo, technician, Cornell AgriTech; and technical applications specialists Cari Lingle and Gabriela Lopez-Velasco, technical sales manager Burcu Yordem, and global scientific affairs manager John M. David, all of 3M.This study was supported by a 3M-sponsored research contract, with additional funding by the U.S. Department of Agriculture and the College of Agriculture and Life Sciences. | Microbes | 2,021 |
April 27, 2021 | https://www.sciencedaily.com/releases/2021/04/210427122428.htm | Exposure to high heat neutralizes SARS-CoV-2 in less than one second, study finds | Arum Han, professor in the Department of Electrical and Computer Engineering at Texas A&M University, and his collaborators have designed an experimental system that shows exposure of SARS-CoV-2 to a very high temperature, even if applied for less than a second, can be sufficient to neutralize the virus so that it can no longer infect another human host. | Applying heat to neutralize COVID-19 has been demonstrated before, but in previous studies temperatures were applied from anywhere from one to 20 minutes. This length of time is not a practical solution, as applying heat for a long period of time is both difficult and costly. Han and his team have now demonstrated that heat treatment for less than a second completely inactivates the coronavirus -- providing a possible solution to mitigating the ongoing spread of COVID-19, particularly through long-range airborne transmission.The Medistar Corporation approached leadership and researchers from the College of Engineering in the spring of 2020 to collaborate and explore the possibility of applying heat for a short amount of time to kill COVID-19. Soon after, Han and his team got to work, and built a system to investigate the feasibility of such a procedure.Their process works by heating one section of a stainless-steel tube, through which the coronavirus-containing solution is run, to a high temperature and then cooling the section immediately afterward. This experimental setup allows the coronavirus running through the tube to be heated only for a very short period of time. Through this rapid thermal process, the team found the virus to be completely neutralized in a significantly shorter time than previously thought possible. Their initial results were released within two months of proof-of-concept experiments.Han said if the solution is heated to nearly 72 degrees Celsius for about half a second, it can reduce the virus titer, or quantity of the virus in the solution, by 100,000 times which is sufficient to neutralize the virus and prevent transmission."The potential impact is huge," Han said. "I was curious of how high of temperatures we can apply in how short of a time frame and to see whether we can indeed heat-inactivate the coronavirus with only a very short time. And, whether such a temperature-based coronavirus neutralization strategy would work or not from a practical standpoint. The biggest driver was, 'Can we do something that can mitigate the situation with the coronavirus?'"Their research was featured on the cover of the May issue of the journal Not only is this sub-second heat treatment a more efficient and practical solution to stopping the spread of COVID-19 through the air, but it also allows for the implementation of this method in existing systems, such as heating, ventilation and air conditioning systems.It also can lead to potential applications with other viruses, such as the influenza virus, that are also spread through the air. Han and his collaborators expect that this heat-inactivation method can be broadly applied and have a true global impact."Influenza is less dangerous but still proves deadly each year, so if this can lead to the development of an air purification system, that would be a huge deal, not just with the coronavirus, but for other airborne viruses in general," Han said.In their future work, the investigators will build a microfluidic-scale testing chip that will allow them to heat-treat viruses for much shorter periods of time, for example, tens of milliseconds, with the hope of identifying a temperature that will allow the virus to be inactivated even with such a short exposure time.The lead authors of the work are electrical engineering postdoctoral researchers, Yuqian Jiang and Han Zhang. Other collaborators on this project are Professor Julian L. Leibowitz, and Associate Professor Paul de Figueiredo from the College of Medicine; biomedical postdoctoral researcher Jose A. Wippold; Jyotsana Gupta, associate research scientist in microbial pathogenesis and immunology; and Jing Dai, electrical engineering assistant research scientist.This work has been supported by grants from Medistar Corporation. Several research personnel on the project team were also supported by grants from the National Institutes of Health's National Institute of Allergy and Infectious Diseases. | Microbes | 2,021 |
April 26, 2021 | https://www.sciencedaily.com/releases/2021/04/210426140741.htm | A new way of rapidly counting and identifying viruses | A Lancaster University professor has introduced a new concept for rapidly analysing for the presence of a virus from colds to coronaviruses. | Based on analysing chemical elements the methodology, which has been adapted from an analytical technique used to identify metallic nanoparticles, is able to detect the presence of viruses within just 20 seconds.Although the tests would need to be performed in a lab, it could be used to quickly identify whether people admitted to hospitals have been infected by a virus -- enabling clinicians to decide treatments and also whether to admit patients into isolation wards.The proposed technique, called 'Single virus inductively coupled plasma mass spectroscopy' (SV ICP-MS) analysis, can be used to quickly determine families of viruses. However, although the concept can identify that someone has a type of coronavirus for example, it would not be able to determine the type of coronavirus, or variants. Additional tests would still be required to find out the specific virus someone was infected with.While SV ICP-MS is not an alternative for tests developed to specifically identify types of Covid-2 infections, it could be used to discriminate if viruses from one family, such as coronaviruses, are present or not. If a virus is found to be present, more specific testing would be needed.The concept, developed by Professor Claude Degueldre, from Lancaster University's Department of Engineering, uses diluted samples of fluids, such as nasal mucus or saliva, from patients. A plasma torch is used to atomise and ionise the virus particles. Measurements of intensities for selected masses of the elements from the viruses provide rapid results to show the presence of a virus or not. This process works on DNA and RNA virus types within seconds.Complementary analysis such as existing sequencing techniques can be tested to complete the identification, though they can take up to two days.Another key benefit is the ability to test a large number of samples quickly.Professor Degueldre said: "What we are proposing here is not a new Covid test but is a new concept to rapidly find out if there are viruses present. This would be useful if people are ill but it is not known if they have a virus or another health condition that is making them sick. This concept would inform the clinical team whether or not there is a virus to inform early treatment actions and other measures such as the need for isolation. More detailed tests would still be required to discover the exact viral infection, but results from these take longer."Another application for the concept is to test water samples from sewage systems or down flow in rivers. The results would enable public health experts to identify areas of cities that have viral outbreaks."The concept is still at an early stage and further research and experiments are needed to further develop the process. | Microbes | 2,021 |
April 20, 2021 | https://www.sciencedaily.com/releases/2021/04/210420183152.htm | Designing healthy diets with computer analysis | A new mathematical model for the interaction of bacteria in the gut could help design new probiotics and specially tailored diets to prevent diseases. The research, from Chalmers University of Technology in Sweden, was recently published in the journal | "Intestinal bacteria have an important role to play in health and the development of diseases, and our new mathematical model could be extremely helpful in these areas," says Jens Nielsen, Professor of Systems Biology at Chalmers, who led the research.The new paper describes how the mathematical model performed when making predictions relating to two earlier clinical studies, one involving Swedish infants, and the other adults in Finland with obesity.The studies involved regular measurements of health indicators, which the researchers compared with the predictions made from their mathematical model -- the model proved to be highly accurate in predicting multiple variables, including how a switch from liquid to solid food in the Swedish infants affected their intestinal bacterial composition.They also measured how the obese adults' intestinal bacteria changed after a move to a more restricted diet. Again, the model's predictions proved to be reliably accurate."These are very encouraging results, which could enable computer-based design for a very complex system. Our model could therefore be used to for creating personalised healthy diets, with the possibility to predict how adding specific bacteria as novel probiotics could impact a patient's health," says Jens Nielsen.There are many different things that affect how different bacteria grow and function in the intestinal system. For example, which other bacteria are already present and how they interact with each other, as well as how they interact with the host -- that is to say, us. The bacteria are also further affected by their environmental factors, such as the diet we eat.All of these variables make predicting the effect that adding bacteria or making dietary changes will have. One must first understand how these bacteria are likely to act when they enter the intestine or how a change in diet will affect the intestinal composition. Will they be able to grow there or not? How will they interact with and possibly affect the bacteria that are already present in the gut? How do different diets affect the intestinal microbiome?"The model we have developed is unique because it accounts for all these variables. It combines data on the individual bacteria as well as how they interact. It also includes data on how food travels through the gastrointestinal tract and affects the bacteria along the way in its calculations. The latter can be measured by examining blood samples and looking at metabolites, the end products that are formed when bacteria break down different types of food," says Jens Nielsen.The data to build the model has been gathered from many years' worth of pre-existing clinical studies. As more data is obtained in the future, the model can be updated with new features, such as descriptions of hormonal responses to dietary intake.Research on diet and the human microbiome, or intestinal bacterial composition, is a field of research that generates great interest, among both researchers and the general public. Jens Nielsen explains why:"Changes in the bacterial composition can be associated with or signify a great number of ailments, such as obesity, diabetes, or cardiovascular diseases. It can also affect how the body responds to certain types of cancer treatments or specially developed diets."Working with the bacterial composition therefore offers the potential to influence the course of diseases and overall health. This can be done through treatment with probiotics -- carefully selected bacteria that are believed to contribute to improved health.In future work, Jens Nielsen and his research group will use the model directly in clinical studies. They are already participating in a study together with Sahlgrenska University Hospital in Sweden, where older women are being treated for osteoporosis with the bacteria Cancer treatment with antibodies is another area where the model could be used to analyse the microbiome, helping to understand its role in why some patients respond well to immunotherapy, and some less so."This would be an incredible asset if our model can begin to identify bacteria that could improve the treatment of cancer patients. We believe it could really make a big difference here," says Jens Nielsen. | Microbes | 2,021 |
April 20, 2021 | https://www.sciencedaily.com/releases/2021/04/210420183138.htm | Food allergies, changes to infant gut bacteria linked to method of childbirth, ethnicity | Researchers have found a causal link between caesarean section birth, low intestinal microbiota and peanut sensitivity in infants, and they report the effect is more pronounced in children of Asian descent than others, in a recently published paper in the journal of the American Gastroenterological Association. | "It's important to know what predicts or increases risk of food sensitivities because they predict which infants will go on to develop asthma and other types of allergies," said Anita Kozyrskyj, pediatrics professor in the University of Alberta's Faculty of Medicine & Dentistry and adjunct professor in the School of Public Health.The research team analysed the gut bacteria of 1,422 infants in the CHILD Cohort Study, by examining fecal samples collected at three or four months of age and again at one year. They identified four typical trajectories for bacterial development, including one in which the infants had persistently low levels of Bacteroides, a type of bacteria known to be critical to immune system development. This profile was most common in babies born by caesarean section.The infants were given skin prick tests at one and three years of age to assess their reaction to a variety of allergens, including egg, milk and peanut. The babies with low Bacteroides levels were found to have a threefold increase in their risk of developing a peanut sensitivity by age three -- and the risk was eight times higher for babies born to mothers of Asian descent.The team did further statistical analysis to look for what are known as "mediation" or causal effects between the exposure and the outcome. "In this case we observed that there was an association between Asian ethnicity and peanut sensitivity, and then the mediation analysis provided additional evidence for the causal association with caesarean section," explained Kozyrskyj, noting it is the first study to identify this link.The researchers also observed that the infants with low Bacteroides also had lower levels of sphingolipids, proteins which are key to cell development and signalling in many parts of the body, including the immune system. Gut microbiota are the main source of these proteins. Children who have this deficiency in their immune cells may be more likely to develop food allergies, Kozyrskyj said."As the gut microbiota are developing so is the gut's immune system, training the gut to react to pathogens and to be tolerant of the food that we require," she explained.Half a million Canadian children have a food allergy, while peanut allergy affects about two in 100 and can lead to severe anaphylaxis. Babies who have food allergies are at greater risk to develop asthma, wheezing, eczema and allergic rhinitis later in life, the study authors reported.The overall rate of allergies is increasing in western countries and is likely linked to environmental factors, said Kozyrskyj, who is principal investigator of the SyMBIOTA (Synergy in Microbiota) laboratory, which studies the impact of maternal and infant antibiotic use, birth mode and breastfeeding on the composition of the intestinal microbiota in infants."In China food allergies are uncommon, but those who immigrate to Canada face a higher risk and more severe form of allergic disease," she said. "It's likely related to a change in diet and environment."The next step for the research is for the results to be replicated in other studies around the world, Kozyrskyj said. She praised her main collaborator Hein Tun, a former post-doctoral fellow at U of A who is now assistant professor of public health at the University of Hong Kong. Their research was funded by the Canadian Institutes of Health Research, Alberta Innovates and the Allergy, Genes, and Environment (AllerGen) Network. Kozyrskyj is a member of the Women and Children's Health Research Institute. Funding partners for the CHILD Cohort Study include the Stollery Children's Hospital Foundation and the Alberta Women's Health Foundation through the Women and Children's Health Research Institute.Previous research by Kozyrskyj and others has shown that babies born by caesarean section do not get the same beneficial transfer of microbiota from mother to child that infants born through vaginal delivery receive. Studies looking to mitigate this by giving C-section babies probiotics or even swabbing them with their mother's vaginal bacteria have not been as successful as hoped, Kozyrskyj said.The best path is to avoid caesarean birth unless it is medically necessary. "With this evidence at hand, the parent and the obstetrician might choose a different birth mode," she said. | Microbes | 2,021 |
April 20, 2021 | https://www.sciencedaily.com/releases/2021/04/210420121428.htm | Overgrowth of gut yeast in newborns may increase asthma risk | An overgrowth of yeast in the gut within the first few months of life may cause changes to the immune system that increase the risk of asthma later on, shows a study published today in | Asthma is a common and sometimes difficult-to-manage, life-long lung condition that affects one in 10 children in developed countries. The findings explain a possible cause of asthma and may help scientists develop new strategies to prevent or treat the condition.The period just after birth is a critical window for the development of a healthy immune system and gut microbiome. Disruptions to gut bacteria that produce anti-inflammatory compounds called short-chain fatty acids (SCFAs) early in life have previously been linked to asthma."We recently showed that overgrowth of a type of gut yeast called Pichia kudriavzevii in newborns in Ecuador is associated with an increased risk of asthma," says first author Rozlyn Boutin, an MD/PhD student in the Department of Microbiology and Immunology at the University of British Columbia, Vancouver, Canada. "In this study, we wanted to see if we could replicate these findings in children from an industrialised setting and identify how fungi of the gut microbiota affect the development of the immune system."Boutin and colleagues began with a study of 123 newborns in Canada, who are part of the CHILD Cohort Study. They again found that an overgrowth of Pichia kudriavzevii in the stools of the newborns during the first three months of life was associated with a higher risk of asthma.To understand how this yeast overgrowth might contribute to asthma later in life, the team applied Pichia kudriavzevii to newborn mice with immature gut microbiota communities. In this mouse model of asthma, the team found that the newborns exposed to the yeast experienced more lung inflammation than those who were unexposed. Applying Pichia kudriavzevii to an adolescent mouse model, however, did not cause this excess inflammation."Our findings show that there is a critical window in early life where disruptions in the gut microbiota caused by Pichia kudriavzevii affect the development of the immune system and increase the risk and severity of asthma later in life," Boutin says.Previous studies have shown that bacterial SCFAs have beneficial effects on immune development that protect against asthma. In this study, the team also showed that anti-inflammatory SCFAs produced by gut bacteria inhibit the growth of Pichia kudriavzevii."Immune responses to gut microbe disruptions early in life have long-term consequences for diseases of the immune system later in life," concludes senior author Brett Finlay, Professor at the Michael Smith Laboratories and the Departments of Biochemistry and Molecular Biology, and Microbiology and Immunology, University of British Columbia. "Our study adds to our understanding of microbiota-associated asthma and suggests that inhibiting yeast overgrowth with SCFAs in early life could be an effective approach to preventing this condition." | Microbes | 2,021 |
April 16, 2021 | https://www.sciencedaily.com/releases/2021/04/210416120127.htm | Experimental antiviral for COVID-19 effective in hamster study | The experimental antiviral drug MK-4482 significantly decreased levels of virus and disease damage in the lungs of hamsters treated for SARS-CoV-2 infection, according to a new study from National Institutes of Health scientists. SARS-CoV-2 is the virus that causes COVID-19. MK-4482, delivered orally, is now in human clinical trials. Remdesivir, an antiviral drug already approved by the U.S. Food and Drug Administration for use against COVID-19, must be provided intravenously, making its use primarily limited to clinical settings. | In their study, published in the journal The same research group, located at Rocky Mountain Laboratories, part of NIH's National Institute of Allergy and Infectious Diseases in Hamilton, Montana, developed the hamster model last year to mimic SARS-CoV-2 infection and mild disease in people. The University of Plymouth in the United Kingdom collaborated on these most recent studies.The project involved three groups of hamsters: a pre-infection treatment group; a post-infection treatment group; and an untreated control group. For the two treatment groups, scientists administered MK-4482 orally every 12 hours for three days. At the conclusion of the study, the animals in each of the treatment groups had 100 times less infectious virus in their lungs than the control group. Animals in the two treatment groups also had significantly fewer lesions in the lungs than the control group.The scientists determined the MK-4482 treatment doses for this study based on previous experiments performed in mouse models of SARS-CoV-1 and MERS-CoV. In those studies, MK-4482 was effective at stopping the viruses from replicating.With funding support from NIAID, Emory University's Drug Innovation Ventures group in Atlanta developed MK-4482 (also known as molnupiravir and EIDD-2801) to treat influenza. Merck and Ridgeback Biotherapeutics are now jointly developing and evaluating MK-4482 as a potential COVID-19 treatment. The drug is in Phase 2 and 3 human clinical studies. | Microbes | 2,021 |
April 15, 2021 | https://www.sciencedaily.com/releases/2021/04/210415090754.htm | Norovirus clusters are resistant to environmental stresses and UV disinfection | Clusters of a virus known to cause stomach flu are resistant to detergent and ultraviolet disinfection, according to new research co-led by Danmeng Shuai, Ph.D., an associate professor of civil and environmental engineering at the George Washington University and Nihal Altan-Bonnet, Ph.D., a senior investigator and the head of the Laboratory of Host-Pathogen Dynamics at the National Heart, Lung, and Blood Institute, part of the National Institutes of Health. The findings suggest the need to revisit current disinfection, sanitation and hygiene practices aimed at protecting people from noroviruses. | Noroviruses are the leading cause of gastroenteritis around the world, with over 21 million cases each year in the United States alone.In 2018, Altan-Bonnet's team found that noroviruses can be transmitted to humans via membrane-enclosed packets that contain more than one virus. In the past, scientists thought that viruses spread through exposure to individual virus particles, but the 2018 study -- and others -- showed how membrane-enclosed clusters arrive at a human cell and release an army of viruses all at once.For the new study, Shuai, Altan-Bonnet and the study's first author Mengyang Zhang, a doctoral student co-advised through a GW/NIH Graduate Partnerships Program, looked at the behavior of these protected virus clusters in the environment. They found that the virus clusters could survive attempts to disinfect with detergent solutions or even UV light. Water treatment plants use UV light to kill noroviruses and other pathogens."These membrane-cloaked viruses are tricky," Shuai said. "Past research shows they can evade the body's immune system and that they are highly infectious. Our study shows these membrane enclosed viruses are also able to dodge efforts to kill them with standard disinfectants."According to the researchers, future studies must be done to find out if certain kinds of cleaning solutions or higher dosages of UV light would degrade the protective membrane and/or kill the viruses inside. Ultimately, the research could be used to devise more effective disinfection methods that could be used to clean surfaces at home, in restaurants and in places where norovirus can spread and cause outbreaks, like cruise ships."Our study's findings represent a step towards providing rigorous guidelines for pathogen control, particularly in our built environment, and public health protection," Altan-Bonnet said. | Microbes | 2,021 |
April 15, 2021 | https://www.sciencedaily.com/releases/2021/04/210415090730.htm | Good dental health may help prevent heart infection from mouth bacteria | Maintenance of good oral health is more important than use of antibiotics in dental procedures for some heart patients to prevent a heart infection caused by bacteria around the teeth, according to a new American Heart Association (AHA) scientific statement published today in the association's flagship journal, | Infective endocarditis (IE), also called bacterial endocarditis, is a heart infection caused by bacteria that enter the bloodstream and settle in the heart lining, a heart valve or a blood vessel. It is uncommon, but people with heart valve disease or previous valve surgery, congenital heart disease or recurrent infective endocarditis have a greater risk of complications if they develop IE. Intravenous drug use also increases risk for IE. Viridans group streptococcal infective endocarditis (VGS IE) is caused by bacteria that collect in plaque on the tooth surface and cause inflammation and swelling of the gums. There's been concern that certain dental procedures may increase the risk of developing VGS IE in vulnerable patients.The new guidance affirms previous recommendations that only four categories of heart patients should be prescribed antibiotics prior to certain dental procedures to prevent VGS IE due to their higher risk for complications from the infection:those who have had a previous case of infective endocarditis;adults and children with congenital heart disease; orpeople who have undergone a heart transplant."Scientific data since the 2007 AHA guidelines support the view that limited use of preventive antibiotics for dental procedures hasn't increased cases of endocarditis and is an important step at combating antibiotic overuse in the population," said Walter R. Wilson, M.D., chair of the statement writing group and a consultant for the Division of Infectious Diseases, Department of Internal Medicine at Mayo Clinic in Rochester, Minn.It has been over a decade since recommendations for preventing infective endocarditis were updated amid concerns of antibiotic resistance due to overprescribing. The American Heart Association's 2007 guidelines, which presented the biggest shift in recommendations from the Association on the prevention of infective endocarditis in more than 50 years, more tightly defined which patients should receive preventive antibiotics before certain dental procedures to the four high-risk categories. This change resulted in about 90% fewer patients requiring antibiotics.The scientific statement writing group reviewed data on VGS IE since the 2007 guidelines to determine if the guidelines had been accepted and followed, whether cases of and mortality due to VGS IE have increased or decreased, and if the guidance might need to be adjusted.The writing committee reports their extensive review of related research found:In a survey of 5,500 dentists in the U.S., 70% reported prescribing preventive antibiotics to patients even though the guidelines no longer recommend it, and this was most often for patients with mitral valve prolapse and five other cardiac conditions. The dentists reported that about 60% of the time the antibiotic regimen was recommended by the patient's physician, and 1/3 of the time was according to patient preference.Since the stricter 2007 antibiotic guidelines, there is no convincing evidence of an increase in cases of VGS IE or increased mortality due to VGS IE.The writing group supports the 2007 recommendation that only the highest risk groups of patients receive antibiotics prior to certain dental procedures to help prevent VGS IE.In the presence of poor oral hygiene and gingival disease, VGS IE is far more likely to develop from bacteria attributable to routine daily activities such as toothbrushing than from a dental procedure.Maintenance of good oral hygiene and regular access to dental care are considered as important in preventing VGS IE as taking antibiotics before certain dental procedures.It is important to connect patients with services to facilitate access to dental care and assistance with insurance for dental coverage, especially in those patients at high risk for VGS IE.It is still appropriate to follow the recommendation to use preventive antibiotics with high-risk patients undergoing dental procedures that involve manipulation of the gum tissue or infected areas of the teeth, or perforation of the membrane lining the mouth.The scientific statement was prepared by the volunteer writing committee on behalf of the American Heart Association's Young Hearts Rheumatic Fever, Endocarditis and Kawasaki Disease Committee; the Council on Lifelong Congenital Heart Disease and Heart Health in the Young; the Council on Cardiovascular and Stroke Nursing; and the Council on Quality of Care and Outcomes Research. | Microbes | 2,021 |
April 14, 2021 | https://www.sciencedaily.com/releases/2021/04/210414100121.htm | A mother's fat intake can impact infant infectious disease outcomes | A team of UBC Okanagan researchers has determined that the type of fats a mother consumes while breastfeeding can have long-term implications on her infant's gut health. | Dr. Deanna Gibson, a biochemistry researcher, along with Dr. Sanjoy Ghosh, who studies the biochemical aspects of dietary fats, teamed up with chemistry and molecular biology researcher Dr. Wesley Zandberg. The team, who conducts research in the Irving K. Barber Faculty of Science, explored the role of feeding dietary fat to gestating rodents to determine the generational effects of fat exposure on their offspring."The goal was to investigate how maternal dietary habits can impact an offspring's gut microbial communities and their associated sugar molecule patterns which can be important in immune responses to infectious disease," says Dr. Gibson, who studies gut health and immunity as well as causes of acute or chronic diseases like inflammatory bowel disease.Their study suggests that the type of fat consumed during breastfeeding could differentially impact an infant's intestinal microbial communities, immune development and disease risk.The three main classes of fatty acids include saturated (SFA), found in meats and dairy products, monounsaturated fats (MUFA), found in plant-based liquid oils, and polyunsaturated fatty acids (PUFAs), found in some nuts, fish and shellfish. PUFAs are further characterized as either n-3 PUFAs or n-6 PUFAs, based on the number and positions of double bonds in the acyl chain.Previous research has determined both n-3 PUFAs and n-6 PUFAs can have a negative impact on intestinal infections such as Enteropathogenic E. coli, Clostridium difficile, salmonella and gastrointestinal illnesses from eating poorly prepared or undercooked food or drinking contaminated water. In contrast, diets rich in MUFAs and SFAs have been shown to be largely protective against these infections.Dr. Gibson's latest research states the beneficial properties of milk fat, or saturated fats, during the pre-and postnatal period might improve protection against infectious intestinal disease during adulthood particularly when a source of n-3 PUFAs are combined with saturated fats."Our findings challenge current dietary recommendations and reveal that maternal intake of fat has transgenerational impacts on their offspring's susceptibility to intestinal infection, likely enabled through microbe-immune interactions," says Dr. Gibson.Global consumption of unsaturated fatty acids has increased significantly between 1990 and 2010, she adds, while people are consuming lower amounts of saturated fats during pregnancy because of recommendations to reduce saturated fat intake."Although it has been known for decades that high-fat diets can directly alter inflammatory responses, recent studies have only just begun to appreciate how fatty acid classes may have discrete effects on inflammation, and can shift host responses to an infection," says Dr. Gibson.Dietary fatty acids can impact inflammatory processes including defensive inflammatory responses following an intestinal infection. This can affect the severity of disease, making dietary fatty acids an important consideration in predicting disease risk, Dr. Gibson explains.Researchers believe it's a combination of dietary fat-host interactions with the intestinal bacteriome that can determine the severity of these infections. The intestinal bacteriome, Dr. Gibson explains, is established during infancy and plays a critical role in aiding immune system maturation and providing a barrier against colonization with potential pathogens.And Dr. Ghosh notes this latest research suggests current health guidelines should be reevaluated."Currently, Canadian dietary guidelines recommend nursing mothers replace foods rich in SFA with dietary PUFAs, with an emphasis on consuming n-6 and n-3 PUFAs," Dr. Ghosh says. "Given that PUFAs worsened disease outcomes in postnatal diet studies, in our views, these recommendations should be reconsidered."While breast milk protein and carbohydrate concentrations remain relatively inert, fatty acid contents vary considerably and are influenced by maternal fat intake."Overall, we conclude that maternal consumption of various dietary fat types alters the establishment of their child's bacteriome and can have lasting consequences on their ability to respond to infection during adulthood," says Dr. Gibson. "At the same time, we show that maternal diets rich in SFA, provide a host-microbe relationship in their offspring that protects against disease."It's important to understand that the intestinal bacteriome is established during infancy because it plays a critical role in aiding immune system maturation which can provide a barrier to potential pathogens, explains Dr. Zandberg. He also notes a healthy bacteriome is dependent on early-life nutrition."Sugars decorate important proteins in the gut," says Dr. Zandberg. "Their patterns are altered in the offspring due to the dietary choices of the mother during gestation and lactation. The change in patterns is associated with changes in the ability of the infant to fight off infectious disease in our model." | Microbes | 2,021 |
April 1, 2021 | https://www.sciencedaily.com/releases/2021/04/210401112526.htm | Gut microbiota in Cesarean-born babies catches up | Infants born by cesarean section have a relatively meager array of bacteria in the gut. But by the age of three to five years they are broadly in line with their peers. This is shown by a study that also shows that it takes a remarkably long time for the mature intestinal microbiota to get established. | Fredrik Bäckhed, Professor of Molecular Medicine at Sahlgrenska Academy, University of Gothenburg, has been heading this research. The study, conducted in collaboration with Halland County Hospital in Halmstad, is now published in the journal Professor Bäckhed and his group have previously demonstrated that the composition of children's intestinal microbiota is affected by their mode of delivery and diet. In the current study, the researchers examined in detail how the composition of intestinal bacteria in 471 children born at the hospital in Halmstad had developed.The first fecal sample was collected when each child was a newborn infant. Thereafter, sampling took place at 4 months, 12 months, 3 years and 5 years. The scientists were thus able to follow the successive incorporation of various bacteria into the children's gut microbiota.At birth, the infant's intestine has already been colonized by bacteria and other microorganisms. During the first few years of life, the richness of species steadily increases. What is now emerging is a considerably more detailed picture of this developmental trajectory.One key conclusion is that the intestinal microbiota forms an ecosystem that takes a long time to mature. Even at 5 years of age, the system is incomplete. The maturation process can look very different from one child to another, and take varying lengths of time.At the age of 4 months, the gut microbiota in the cesarean-born infants was less diverse compared with vaginally born infants. However, when the children were 3 and 5 years the microbiota diversity and composition had caught up and were largely normalized intestinal microbiota."Our findings show that the gut microbota is a dynamic organ, and future studies will have to show whether the early differences can affect the cesarean children later in life," Bäckhed says."It's striking that even at the age of 5 years, several of the bacteria that are important components of the intestinal microbiota in adults are missing in the children," he continues.This indicates that the intestine is a complex and dynamic environment where bacteria create conditions for one another's colonization.According to the researchers, the current study has broadened our understanding of how humans interact with the trillions of bacteria contained in our bodies, and of how these bacteria become established.Lisa Olsson, a researcher at the University of Gothenburg and one of the first authors, adds:"Children learn skills like walking and talking at different rates, and it turns out that the same applies to the maturity of the gut microbiota."Fredrik Bäckhed again:"By investigating and understanding how the intestinal microbiota develops in healthy children, we may get a reference point to explorie if the microbiota may contribute to disease in future studies," he concludes. | Microbes | 2,021 |
March 31, 2021 | https://www.sciencedaily.com/releases/2021/03/210331130910.htm | Sugar not so nice for your child's brain development, study suggests | Sugar practically screams from the shelves of your grocery store, especially those products marketed to kids. | Children are the highest consumers of added sugar, even as high-sugar diets have been linked to health effects like obesity and heart disease and even impaired memory function.However, less is known about how high sugar consumption during childhood affects the development of the brain, specifically a region known to be critically important for learning and memory called the hippocampus.New research led by a University of Georgia faculty member in collaboration with a University of Southern California research group has shown in a rodent model that daily consumption of sugar-sweetened beverages during adolescence impairs performance on a learning and memory task during adulthood. The group further showed that changes in the bacteria in the gut may be the key to the sugar-induced memory impairment.Supporting this possibility, they found that similar memory deficits were observed even when the bacteria, called Parabacteroides, were experimentally enriched in the guts of animals that had never consumed sugar."Early life sugar increased Parabacteroides levels, and the higher the levels of Parabacteroides, the worse the animals did in the task," said Emily Noble, assistant professor in the UGA College of Family and Consumer Sciences who served as first author on the paper. "We found that the bacteria alone was sufficient to impair memory in the same way as sugar, but it also impaired other types of memory functions as well."The Dietary Guidelines for Americans, a joint publication of the U.S. Departments of Agriculture and of Health and Human Services, recommends limiting added sugars to less than 10 percent of calories per day.Data from the Centers for Disease Control and Prevention show Americans between the ages 9-18 exceed that recommendation, the bulk of the calories coming from sugar-sweetened beverages.Considering the role the hippocampus plays in a variety of cognitive functions and the fact the area is still developing into late adolescence, researchers sought to understand more about its vulnerability to a high-sugar diet via gut microbiota.Juvenile rats were given their normal chow and an 11% sugar solution, which is comparable to commercially available sugar-sweetened beverages.Researchers then had the rats perform a hippocampus-dependent memory task designed to measure episodic contextual memory, or remembering the context where they had seen a familiar object before."We found that rats that consumed sugar in early life had an impaired capacity to discriminate that an object was novel to a specific context, a task the rats that were not given sugar were able to do," Noble said.A second memory task measured basic recognition memory, a hippocampal-independent memory function that involves the animals' ability to recognize something they had seen previously.In this task, sugar had no effect on the animals' recognition memory."Early life sugar consumption seems to selectively impair their hippocampal learning and memory," Noble said.Additional analyses determined that high sugar consumption led to elevated levels of Parabacteroides in the gut microbiome, the more than 100 trillion microorganisms in the gastrointestinal tract that play a role in human health and disease.To better identify the mechanism by which the bacteria impacted memory and learning, researchers experimentally increased levels of Parabacteroides in the microbiome of rats that had never consumed sugar. Those animals showed impairments in both hippocampal dependent and hippocampal-independent memory tasks."(The bacteria) induced some cognitive deficits on its own," Noble said.Noble said future research is needed to better identify specific pathways by which this gut-brain signaling operates."The question now is how do these populations of bacteria in the gut alter the development of the brain?" Noble said. "Identifying how the bacteria in the gut are impacting brain development will tell us about what sort of internal environment the brain needs in order to grow in a healthy way."The article, "Gut microbial taxa elevated by dietary sugar disrupt memory function," appears in Translational Psychiatry. Scott Kanoski, associate professor in USC Dornsife College of Letters, Arts and Science, is corresponding author on the paper.Additional authors on the paper are Elizabeth Davis, Linda Tsan, Clarissa Liu, Andrea Suarez and Roshonda B. Jones from the University of Southern California; Christine Olson, Yen-Wei Chen, Xia Yang and Elaine Y. Hsiao from the University of California-Los Angeles; and Claire de La Serre and Ruth Schade from UGA. | Microbes | 2,021 |
March 31, 2021 | https://www.sciencedaily.com/releases/2021/03/210331103557.htm | Preconditions for life present 3.5 billion years ago | Microbial life already had the necessary conditions to exist on our planet 3.5 billion years ago. This was the conclusion reached by a research team after studying microscopic fluid inclusions in barium sulfate (barite) from the Dresser Mine in Marble Bar, Australia. In their publication "Ingredients for microbial life preserved in 3.5-billion-year-old fluid inclusions," the researchers suggest that organic carbon compounds which could serve as nutrients for microbial life already existed at this time. The study by first author Helge Mißbach (University of Göttingen, Germany) was published in the journal | Lüders assesses the results as surprising, although he cautions against misinterpreting them. "One should not take the study results as direct evidence for early life," says the GFZ researcher. Rather, the findings on the 3.5-billion-year-old fluids showed the existence of the potential for just such prehistoric life. Whether life actually arose from it at that time cannot be determined. Based on the results, "we now know a point in time from which we can say it would have been possible," explains Lüders.Fluid inclusions in minerals are microscopic geo-archives for the migration of hot solutions and gases in the Earth's crust. Primary fluid inclusions were formed directly during mineral growth and provide important information about the conditions under which they were formed. This includes the pressure, temperature and the solution composition. In addition to an aqueous phase, fluid inclusions can also contain gases whose chemistry can persist for billions of years. The fluid inclusions examined in this study were trapped during crystallization of the host minerals. The fluid inclusions investigated in this study originate from the Dresser Mine in Australia. They were trapped during crystallisation of the host minerals of barium sulphate (barite). The research team analysed them extensively for their formation conditions, biosignatures and carbon isotopes.In the course of the analyses, it turned out that they contained primordial metabolism -- and thus energy sources for life. The results of Lüders' carbon isotope analysis provided additional evidence for different carbon sources. While the gas-rich inclusions of gray barites contained traces of magmatic carbon, clear evidence of an organic origin of the carbon could be found in the fluid inclusions of black barites."The study may create a big stir," Lüders says. Organic molecules of this type have not yet been found so far in fluid inclusions in Archean minerals. At the same time, however, he says the study is just a first step. Lüders says, "The ever-increasing sensitivity of measuring instruments will provide new tools for the study of solid and fluid micro inclusions in minerals. Measurements of bio signatures and isotope ratios are likely to become increasingly accurate in the near future." | Microbes | 2,021 |
March 30, 2021 | https://www.sciencedaily.com/releases/2021/03/210330121231.htm | Changes in mouth bacteria after drinking beetroot juice may promote healthy aging | Drinking beetroot juice promotes a mix of mouth bacteria associated with healthier blood vessels and brain function, according to a new study of people aged 70-80. | Beetroot -- and other foods including lettuce, spinach and celery -- are rich in inorganic nitrate, and many oral bacteria play a role in turning nitrate to nitric oxide, which helps to regulate blood vessels and neurotransmission (chemical messages in the brain).Older people tend to have lower nitric oxide production, and this is associated with poorer vascular (blood vessel) and cognitive (brain) health.In the new study, by the University of Exeter, 26 healthy older people took part in two ten-day supplementation periods: one with nitrate-rich beetroot juice and another with nitrate-free placebo juice, which they drank twice a day.The results showed higher levels of bacteria associated with good vascular and cognitive health, and lower levels of bacteria linked to disease and inflammation.Systolic blood pressure dropped on average by five points (mmHg) after drinking the beetroot juice."We are really excited about these findings, which have important implications for healthy ageing," said lead author Professor Anni Vanhatalo, of the University of Exeter."Previous studies have compared the oral bacteria of young and older people, and healthy people compared to those with diseases, but ours is the first to test nitrate-rich diet in this way."Our findings suggest that adding nitrate-rich foods to the diet -- in this case via beetroot juice -- for just ten days can substantially alter the oral microbiome (mix of bacteria) for the better."Maintaining this healthy oral microbiome in the long term might slow down the negative vascular and cognitive changes associated with ageing."The researchers ran tests to identify clusters (or "modules") of oral bacteria that tend to thrive together in similar conditions.A module (Prevotella-Veillonella) that has been associated with inflammation was reduced after nitrate supplementation, including a decrease of Clostridium difficile (which can infect the bowel and cause diarrhea).Professor Vanhatalo stressed that more research is needed to confirm the findings and see whether similar effects are found in other groups."Our participants were healthy, active older people with generally good blood pressure," she said. "Dietary nitrate reduced their blood pressure on average, and we are keen to find out whether the same would happen in other age groups and among people in poorer health."We are working with colleagues in the University of Exeter Medical School to investigate interactions between the oral bacteria and cognition to better understand the how diet could be used to delay cognitive decline in older age."Much research has been conducted into the benefits of a healthy gut microbiome, but far less is known about the oral microbial community, which plays a crucial role in "activating" the nitrate from a vegetable-rich diet.The study was funded by the Dunhill Medical Trust, and the research team included Cardiff University. | Microbes | 2,021 |
March 29, 2021 | https://www.sciencedaily.com/releases/2021/03/210329153322.htm | Chronic viral infections can have lasting effects on human immunity, similar to aging | Research from the Buck Institute and Stanford University suggests that chronic viral infections have a profound and lasting impact on the human immune system in ways that are similar to those seen during aging. Results are published in | Using systems immunology and artificial intelligence, researchers profiled and compared immune responses in a cohort of aging individuals, people with HIV on long-term anti-retroviral therapy, and people infected with hepatitis C (HCV) before and after the virus was treated with a drug that has up to a 97% cure rate. Shared alterations in the immune system include T cell memory inflation, upregulation of intracellular signaling pathways of inflammation, and diminished sensitivity to cytokines in lymphocytes and myeloid cells."Chronic inflammation stemming from immune system dysfunction is associated with many of the diseases of aging," says David Furman, PhD, Buck Institute associate professor and senior author of the paper. "Whether chronic viral infection contributes to age-associated immune dysfunction is still an open question, but studies of this type provide a way to start getting answers. At this point it's clear that both aging and chronic viral infections leave profound and indelible marks on immunity."In acute viral infections the body is usually able to clear the offending agent and the immune system (in the best-case scenario) produces antibodies that protect against similar infections -- think of common colds and seasonal flus. But there are viruses, in addition to HIV and HCV, which can remain alive, setting up "host-parasite housekeeping" in the body, in some cases without people being aware of them. Furman says depending on geographic location, 70 to 90% of the population is infected with cytomegalovirus, which is harmless in healthy individuals and is only problematic for pregnant women or those with compromised immune systems. Various herpes viruses (which cause genital herpes, cold sores, chicken pox/shingles, and mononucleosis) can also lead to chronic infections."Each of us has our own virome; it's the collection of the viral infections you have during your lifespan," Furman says. "You probably have been infected by 12 or 15, or even more viruses that you never knew you had. Fortunately technology now exists that allows us to profile these infections in the human population; it is helping us move these types of inquiries forward." Furman says this study is the first to fully incorporate the concept of systems immunology and holistically analyze the immune system using the same technological platforms across different cohorts of patients.The study showed that in patients with HIV, immune system dysregulations were evident despite having been treated with virus-suppressing drugs for over ten years. But clearance of the HCV virus (via the drug sofosbuvir) partially restored cellular sensitivity to interferon-a, which inhibits viral replication. "This plasticity means there is room for intervention in both chronic viral infections and in aging," says Furman. "It's just a matter of identifying and understanding the molecular pathways and networks involved." This paper identified changes in STAT1, the primary transcription factor activated by interferons. STAT1 plays a major role in normal immune responses, particularly to viral, mycobacterial and fungal pathogens.Furman says we are in the midst of an ongoing "living" experiment in regards to the COVID-19 pandemic. He says future studies are needed to determine whether the functional imprinting of the immune system is hardwired to only involve the chronic nature of specific infections, or whether relatively short-lived but vigorous inflammations such as COVID-19 also leave a long-lasting footprint on the immune system. "Has the immune system of those infected with the coronavirus taken a big hit? That's a theory, but we don't know what will happen," says Furman, who is collaborating with Stanford University and the University of California, San Francisco on projects involving COVID-19 and immunity. | Microbes | 2,021 |
March 25, 2021 | https://www.sciencedaily.com/releases/2021/03/210325120838.htm | Combination therapy protects against advanced Marburg virus disease | A new study conducted at the Galveston National Laboratory at the The University of Texas Medical Branch at Galveston (UTMB) has shown substantial benefit to combining monoclonal antibodies and the antiviral remdesivir against advanced Marburg virus. The study was published today in | "Marburg is a highly virulent disease in the same family as the virus that causes Ebola. In Africa, patients often arrive to a physician very ill. It was important to test whether a combination of therapies would work better with really sick people, said Tom Geisbert, a professor in the Department of Microbiology & Immunology at UTMB and the principal investigator for the study. "Our data suggests that this particular combination allowed for recovery when given at a very late stage of disease."Dr. Zachary A. Bornholdt, Senior Director of Antibody Discovery and Research for Mapp Biopharmaceutical and a co-author on the study, said, "Often small molecules and antibodies are positioned to compete with each other for a single therapeutic indication. Here we see the benefit of pursuing both treatment strategies in tandem and ultimately finding synergy upon combining both approaches together."Geisbert, Bornholdt and a large team at UTMB, Mapp Biopharmaceuticals and Gilead have been developing monoclonal antibody (mAbs) therapies to treat extremely dangerous viruses like Marburg and Ebola for several years. The treatments have proven to be highly effective in laboratory studies and emergency use, particularly when delivered early in the disease course.In this study, using a rhesus model, treatment with monoclonal antibodies began six days post infection, a critical point in disease progression. The combination therapy with the antiviral remdesivir showed an 80 percent protection rate, indicating promise for treatment of advanced Marburg infections.The study was supported by the Department of Health and Human Services, National Institutes of Health grant U19AI142785 and UC7AI094660 for BSL-4 operations support of the Galveston National Laboratory. | Microbes | 2,021 |
March 25, 2021 | https://www.sciencedaily.com/releases/2021/03/210325084818.htm | Engineers make filters from tree branches to purify drinking water | The interiors of nonflowering trees such as pine and ginkgo contain sapwood lined with straw-like conduits known as xylem, which draw water up through a tree's trunk and branches. Xylem conduits are interconnected via thin membranes that act as natural sieves, filtering out bubbles from water and sap. | MIT engineers have been investigating sapwood's natural filtering ability, and have previously fabricated simple filters from peeled cross-sections of sapwood branches, demonstrating that the low-tech design effectively filters bacteria.Now, the same team has advanced the technology and shown that it works in real-world situations. They have fabricated new xylem filters that can filter out pathogens such as E. coli and rotavirus in lab tests, and have shown that the filter can remove bacteria from contaminated spring, tap, and groundwater. They also developed simple techniques to extend the filters' shelf-life, enabling the woody disks to purify water after being stored in a dry form for at least two years.The researchers took their techniques to India, where they made xylem filters from native trees and tested the filters with local users. Based on their feedback, the team developed a prototype of a simple filtration system, fitted with replaceable xylem filters that purified water at a rate of one liter per hour.Their results, published today in The researchers are exploring options to make xylem filters available at large scale, particularly in areas where contaminated drinking water is a major cause of disease and death. The team has launched an open-source website, with guidelines for designing and fabricating xylem filters from various tree types. The website is intended to support entrepreneurs, organizations, and leaders to introduce the technology to broader communities, and inspire students to perform their own science experiments with xylem filters."Because the raw materials are widely available and the fabrication processes are simple, one could imagine involving communities in procuring, fabricating, and distributing xylem filters," says Rohit Karnik, professor of mechanical engineering and associate department head for education at MIT. "For places where the only option has been to drink unfiltered water, we expect xylem filters would improve health, and make water drinkable."Karnik's study co-authors are lead author Krithika Ramchander and Luda Wang of MIT's Department of Mechanical Engineering, and Megha Hegde, Anish Antony, Kendra Leith, and Amy Smith of MIT D-Lab.In their prior studies of xylem, Karnik and his colleagues found that the woody material's natural filtering ability also came with some natural limitations. As the wood dried, the branches' sieve-like membranes began to stick to the walls, reducing the filter's permeance, or ability to allow water to flow through. The filters also appeared to "self-block" over time, building up woody matter that clogged the conduits.Surprisingly, two simple treatments overcame both limitations. By soaking small cross-sections of sapwood in hot water for an hour, then dipping them in ethanol and letting them dry, Ramchander found that the material retained its permeance, efficiently filtering water without clogging up. Its filtering could also be improved by tailoring a filter's thickness according to its tree type.The researchers sliced and treated small cross-sections of white pine from branches around the MIT campus and showed that the resulting filters maintained a permeance comparable to commercial filters, even after being stored for up to two years, significantly extending the filters' shelf life.The researchers also tested the filters' ability to remove contaminants such as E. coli and rotavirus -- the most common cause of diarrheal disease. The treated filters removed more than 99 percent of both contaminants, a water treatment level that meets the "two-star comprehensive protection" category set by the World Health Organization."We think these filters can reasonably address bacterial contaminants," Ramchander says. "But there are chemical contaminants like arsenic and fluoride where we don't know the effect yet," she notes.Encouraged by their results in the lab, the researchers moved to field-test their designs in India, a country that has experienced the highest mortality rate due to water-borne disease in the world, and where safe and reliable drinking water is inaccessible to more than 160 million people.Over two years, the engineers, including researchers in the MIT D-Lab, worked in mountain and urban regions, facilitated by local NGOs Himmotthan Society, Shramyog, Peoples Science Institute, and Essmart. They fabricated filters from native pine trees and tested them, along with filters made from ginkgo trees in the U.S., with local drinking water sources. These tests confirmed that the filters effectively removed bacteria found in the local water. The researchers also held interviews, focus groups, and design workshops to understand local communities' current water practices, and challenges and preferences for water treatment solutions. They also gathered feedback on the design."One of the things that scored very high with people was the fact that this filter is a natural material that everyone recognizes," Hegde says. "We also found that people in low-income households prefer to pay a smaller amount on a daily basis, versus a larger amount less frequently. That was a barrier to using existing filters, because replacement costs were too much."With information from more than 1,000 potential users across India, they designed a prototype of a simple filtration system, fitted with a receptacle at the top that users can fill with water. The water flows down a 1-meter-long tube, through a xylem filter, and out through a valve-controlled spout. The xylem filter can be swapped out either daily or weekly, depending on a household's needs.The team is exploring ways to produce xylem filters at larger scales, with locally available resources and in a way that would encourage people to practice water purification as part of their daily lives -- for instance, by providing replacement filters in affordable, pay-as-you-go packets."Xylem filters are made from inexpensive and abundantly available materials, which could be made available at local shops, where people can buy what they need, without requiring an upfront investment as is typical for other water filter cartridges," Karnik says. "For now, we've shown that xylem filters provide performance that's realistic." | Microbes | 2,021 |
March 24, 2021 | https://www.sciencedaily.com/releases/2021/03/210324094729.htm | E. Coli calculus: Bacteria find the derivative optimally | Scientists from the Graduate School of Information Science and Technology at The University of Tokyo calculated the efficiency of the sensory network that bacteria use to move towards food and found it to be optimal from an information theory standpoint. This work may lead to a better understanding of bacterial behavior and their sensory networks. | Despite being single-celled organisms, bacteria such as E. Coli can perform some impressive feats of sensing and adaptation in constantly changing environmental conditions. For example, these bacteria can sense the presence of a chemical gradient indicating the direction of food and move towards it. This process is called chemotaxis, and has been shown to be remarkably efficient, both for its high sensitivity to tiny changes in concentration and for its ability to adapt to background levels. However, the question of whether this is the best possible sensing system that can exist in noisy environments, or a suboptimal evolutionary compromise, has not been determined.Now, researchers from The University of Tokyo have shown that the standard model biologists use to describe bacterial chemotaxis is, in fact, mathematically equivalent to the optimal dynamics. In this framework, receptors on the surface of the bacterium can be modulated by the presence of the target molecules, but this signaling network can be affected by random noise. Once the bacteria determine if they are swimming towards or away from the food, they can adjust their swimming behavior accordingly."E. coli can either move in a straight line or randomly reorient via tumbling. By reducing the frequency of tumbling when it senses a positive attractant concentration gradient, the bacterium can preferentially move toward the food," first author Kento Nakamura says.Using nonlinear filtering theory, which is a branch of information theory that deals with updating information based on a stream of real-time information, the scientists showed that the system used by bacteria is indeed optimal."We find that the best possible noise-filtering system coincides with the biochemical model of the E. coli sensory system," explains senior author Tetsuya J. Kobayashi.The findings of this research may also be applied to sensory systems in other organisms, such as G protein-coupled receptors used for vision. Since all living systems need to be able to sense and react to their environments, this project can help evaluate the efficiency of information filtering more generally. | Microbes | 2,021 |
March 24, 2021 | https://www.sciencedaily.com/releases/2021/03/210324094705.htm | Copper foam as a highly efficient, durable filter for reusable masks and air cleaners | During the COVID-19 pandemic, people have grown accustomed to wearing facemasks, but many coverings are fragile and not easily disinfected. Metal foams are durable, and their small pores and large surface areas suggest they could effectively filter out microbes. Now, researchers reporting in ACS' | When a person with a respiratory infection, such as SARS-CoV-2, coughs or sneezes, they release small droplets and aerosolized particles into the air. Particles smaller than 0.3 µm can stay airborne for hours, so materials that can trap these tiny particles are ideal for use in facemasks and air filters. But some existing filter materials have drawbacks. For example, fiberglass, carbon nanotubes and polypropylene fibers are not durable enough to undergo repeated decontamination procedures, while some further rely on electrostatics so they can't be washed, leading to large amounts of waste. Recently, researchers have developed metallic foams with microscopic pores that are stronger and more resistant to deformation, solvents, and high temperatures and pressures. So, Kai Liu and colleagues wanted to develop and test copper foams to see if they could effectively remove submicron-sized aerosols while also being durable enough to be decontaminated and reused.The researchers fabricated metal foams by harvesting electrodeposited copper nanowires and casting them into a free-standing 3D network, which was solidified with heat to form strong bonds. A second copper layer was added to further strengthen the material. In tests, the copper foam held its form when pressurized and at high air speeds, suggesting it's durable for reusable facemasks or air filters and could be cleaned with washing or compressed air. The team found the metal foams had excellent filtration efficiency for particles within the 0.1-1.6 µm size range, which is relevant for filtering out SARS-CoV-2. Their most effective material was a 2.5 mm-thick version, with copper taking up 15% of the volume. This foam had a large surface area and trapped 97% of 0.1-0.4 µm aerosolized salt particles, which are commonly used in facemask tests. According to the team's calculations, the breathability of their foams was generally comparable to that of commercially available polypropylene N95 facemasks. Because the new material is copper-based, the filters should be resistant to cleaning agents, allowing for many disinfection options, and its antimicrobial properties will help kill trapped bacteria and viruses, say the researchers. In addition, they are recyclable. The researchers estimate that the materials would cost around $2 per mask at present, and disinfection and reuse would extend their lifetime, making them economically competitive with current products.The authors acknowledge funding from the Georgetown Environmental Initiative Impact Program Award, the McDevitt bequest to Georgetown University and Tom and Ginny Cahill's Fund for Environmental Physics at University of California Davis. | Microbes | 2,021 |
March 15, 2021 | https://www.sciencedaily.com/releases/2021/03/210315110259.htm | Bacteria adapt syringe apparatus to changing conditions | Basic, acidic, basic again: for pathogenic bacteria such as Salmonella, the human digestive tract is a sea change. So how do the bacteria manage to react to these changes? A team of researchers from the Max Planck Institute for Terrestrial Microbiology in Marburg led by Andreas Diepold has now provided a possible explanation: pathogenic bacteria can change components of their injection apparatus on the fly -- like changing the tires on a moving car -- to enable a rapid response. | Some of the best-known human pathogens -- from the plague bacterium Yersinia pestis to the diarrhea pathogen Salmonella -- use a tiny hypodermic needle to inject disease-causing proteins into their host's cells, thereby manipulating them. This needle is part of the so-called type III secretion system (T3SS), without which most of these pathogens cannot replicate in the body.Only recently it was discovered that large parts of the T3SS are not firmly anchored to the main part of the system, but are constantly exchanging during function. However, the significance of this phenomenon remained unclear. Researchers in the laboratory of Andreas Diepold at the Max Planck Institute for Terrestrial Microbiology have now discovered that this dynamic behavior allows the bacteria to quickly adapt the structure and function of the injection apparatus to external conditions.Human digestion starts with a neutral to slightly alkaline environment in the mouth and esophagus, which the addition of gastric acids suddenly changes to strongly acidic in the stomach -- an environment that many pathogens do not survive. The actual target of Yersinia enterocolitica, the pathogenic bacteria investigated in the study, is the intestine. Here, pH-neutral conditions are restored.But how do the bacteria manage to adapt so quickly to the changing conditions, and how is this controlled? PhD student Stephan Wimmi, the first author of the study, was able to demonstrate that a protein in the bacteria's membrane acts as a sensor for the pH value. In a collaboration with Ulrike Endesfelder's lab at the Max Planck Institute, he found that this protein becomes more motile at low (= acidic) pH and thus transmits the signal to the T3SS components inside the bacterium.In an acidic environment like the stomach, the mobile components do not bind to the rest of the apparatus (including the needle itself), so that the injection system remains inactive. As soon as the bacteria enter a pH-neutral environment -- as it is found in the intestine -, the dynamic proteins reassemble, so that the T3SS can quickly become active at these sites -- to the possible distress of the infected person.The researchers speculate that the newly discovered effect may allow the bacteria to prevent an energy-consuming "misfiring" of the secretion system in the wrong environment, which could even activate the host's immune response. On the other hand, the mobility and dynamics of the structure allows the system to be rapidly reassembled and activated under appropriate conditions.Protein mobility and exchange are increasingly being discovered in complexes and nanomachines across all domains of life; however, the utility of these dynamics is mostly not understood. The new results from Marburg show how protein exchange allows to respond flexibly to external circumstances -- an immense advantage, not only for bacteria. | Microbes | 2,021 |
March 15, 2021 | https://www.sciencedaily.com/releases/2021/03/210315110254.htm | Surgery should remain as mainstay of treatment for acute uncomplicated appendicitis: Study | An RCSI study conducted in Beaumont Hospital in Dublin has found that surgery, rather than antibiotics-only, should remain as the mainstay of treatment for acute uncomplicated appendicitis. | Published in the Acute uncomplicated appendicitis is a commonly encountered acute surgical condition. Traditional management of the condition has involved surgery to remove the appendix (appendectomy). Antibiotic-only treatment has emerged as a potential alternative option that could offer benefits to patients and hospitals, such as a faster recovery, less scaring, less pain, a better quality of life for patients and reduced demand on operating theatres. There has been a reluctance to adopt antibiotic-only treatment due to previous research that has shown wide variability in failure rates and a lack of evidence regarding the impact on quality of life for patients.In this research, 186 patients with radiological evidence of acute, uncomplicated appendicitis were randomised to two groups. One group received antibiotic-only treatment and patients in the other group were treated with surgery. Patients in the surgery group underwent a laparoscopic appendectomy. In those treated with antibiotics-only, intravenous (IV) antibiotics were administered until there was an improvement in a patient's signs and symptoms and this was followed by five days of oral antibiotics.In the weeks and months following treatment, patients were followed up with questionnaires including a quality of life questionnaire at 1 week, 1 month, 3 months and 12 months. At these points, the patient's pain score, need for additional sick leave, surgical site infections and the development of recurrent appendicitis were recorded.The results from the antibiotic-only group demonstrated that 23 patients (25%) experienced a recurrence of acute appendicitis within one year. In the quality of life questionnaires, it was found that patients in the surgery group experienced a significantly better quality of life score compared with the antibiotic-only group.Professor Arnold Hill, Head of School of Medicine and Professor of Surgery, RCSI, said: 'Antibiotic-only treatment of acute uncomplicated appendicitis has been proposed as an alternative less-invasive treatment option for patients. The COMMA Trial set out to establish if antibiotic-only treatment could replace surgery in some cases, which could offer many benefits for patients and hospitals alike. The results indicate that the treatment protocols should not change. Surgery will deliver the best outcomes for patients in terms of quality of life and recurrence and therefore should remain as the mainstay of treatment for acute uncomplicated appendicitis.' The study was carried out by researchers from RCSI and Beaumont Hospital Dublin. The research was supported by RCSI. | Microbes | 2,021 |
March 11, 2021 | https://www.sciencedaily.com/releases/2021/03/210311123440.htm | Probiotics increase gut bacteria diversity in extremely preterm infants | Extremely preterm infants can suffer from a life-threatening inflammation of the gut. A new clinical study has shown that supplements of a lactic acid bacterium may have positive effects by increasing the diversity of intestinal bacteria in these infants. The study has been led by researchers at Linköping University, Sweden, and published in the scientific journal | A litre of milk weighs a kilogram. Most infants who are born extremely prematurely weigh less than that. An infant who should have developed and grown for three more months in the protective environment of the mother's womb is, of course, extremely vulnerable. As a consequence of advances in neonatal care, many premature infants survive, although one out of four of the extremely premature infants die."Preterm infants can be affected by a very severe inflammation of the intestines, which almost only occurs in such infants. The condition, necrotising enterocolitis (or NEC), leads to parts of the intestine dying. One of three infants who contract the infection die, and those who survive often suffer from long-term complications such as short gut syndrome and neurodevelopmental disabilities," says Thomas Abrahamsson, paediatrician at the neonatal intensive care unit at Crown Princess Victoria Children´s Hospital and associate professor at the Department of Biomedical and Clinical Sciences (BKV) at Linköping University, who has led the study.The bacteria in the intestine of preterm infants differ from those in full-term infants. This has led many people to investigate whether giving probiotic supplements that contain certain bacteria has a positive effect. One finding is that the lactic acid bacterium The study now published is part of a clinical study carried out in Linköping and Stockholm. The researchers looked at 132 infants who had been born extremely prematurely, between week 23 and 28 of pregnancy, i.e. 17 to 12 weeks before the due date. All weighed less than a kilogram at birth. Each infant was randomly assigned to one of two groups: to receive oil drops that contained the probiotic or placebo. The treatment was given daily during the neonatal period. The scientists investigated how the intestinal bacterial flora was influenced by the supplement of "We see that the composition of bacteria in the intestine differs during the first month of the probiotic treatment. During the first week of life, the bacterial groups "The supplemented probiotic Supplementation with probiotics is used in increasing numbers of neonatal clinics. The scientific evidence that supplements of probiotics to preterm infants have a positive effect and can be used safely is considered to be sufficiently strong. | Microbes | 2,021 |
March 9, 2021 | https://www.sciencedaily.com/releases/2021/03/210309153830.htm | A little squid and its glowing bacteria yield new clues to symbiotic relationships | The relationship between the Hawaiian bobtail squid and the bioluminescent bacteria living in its light organ has been studied for decades as a model of symbiosis. Now researchers have used a powerful chemical analysis tool to identify a small molecule produced by the bacteria that appears to play an important role in their colonization of the light organ. | The study, published March 9 in the journal The Hawaiian bobtail squid is a small nocturnal squid, about the size of a thumb, that lives in shallow coastal waters, hiding in the sand during the day and coming out at night to hunt for small shrimp and other prey. The bioluminescent glow from its light organ is directed downward and adjusted to match the intensity of light from the moon and stars, eliminating the squid's shadow and masking its silhouette. This "counterillumination" strategy helps conceal the squid both from bottom-dwelling predators and from its own prey.A juvenile bobtail squid is completely free of bacteria when it first hatches, but within hours its light organ becomes colonized by a very specific type of bacteria called Vibrio fischeri. The baby squid enters an environment teeming with thousands of kinds of bacteria and millions of bacterial cells per milliliter of seawater, of which only a tiny fraction are V. fischeri. Yet only those specially adapted bacteria are able to take up residence inside the light organ."It's a very elegant symbiosis," Sanchez said. "We already knew that not all strains of V. fischeri are the same -- some are better colonizers than others -- and we wanted to know if that's being determined by chemical signals."Sanchez's lab uses a technique called imaging mass spectrometry, which allows researchers to directly visualize the spatial distribution of all kinds of molecules in a sample, such as a squid specimen or a bacterial colony. Most techniques for seeing where specific molecules are in a sample involve labeling the targeted molecules. But imaging mass spectrometry allows untargeted investigations -- in other words, you don't have to know what you're looking for."It's very difficult to visualize the chemistry in an organism," Sanchez explained. "With imaging mass spectrometry, we are directly detecting the chemicals, and we know where in the sample they are."The small molecule identified in this study is a type of diketopiperazine (DKP), a large family of cyclic dipeptides. This particular DKP -- cyclo(D-histidyl-L-proline), or cHP-3 -- was directly detected in the light organs of the colonized squid. It was also produced more abundantly by strains of V. fischeri that showed increased biofilm formation, which correlates with colonization ability. And finally, supplementing bacterial cultures with cHP-3 led to a concentration-dependent increase in bioluminescence."We know that it is produced during the first few hours of colonization when the symbiosis gets established, and we also know that it influences bacterial luminescence, and bioluminescence and colonization are tied together," Sanchez said.The results indicate that cHP-3 is an important chemical signal specific to this symbiosis, but the researchers have not yet determined exactly what its role is or the details of its interactions."We're working on that now. We don't know the mechanisms involved, but there's a lot more going on than we thought there was," Sanchez said. "The next steps for us are to find the gene cluster that produces it, and to find how widely used it is."In addition to Sanchez, the coauthors of the paper include researchers at the University of Illinois at Chicago and the University of Wisconsin, Madison. This work was supported by the National Institutes of Health and the Chicago Biomedical Consortium. | Microbes | 2,021 |
March 9, 2021 | https://www.sciencedaily.com/releases/2021/03/210309132545.htm | Bacterial film separates water from oil | Researchers have demonstrated that a slimy, yet tough, type of biofilm that certain bacteria make for protection and to help them move around can also be used to separate water and oil. The material may be useful for applications such as cleaning contaminated waters. | In the journal "It's really remarkable to think that these little bugs can make this stuff that is so perfect in many ways," said Lucian Lucia, the study's corresponding author and an associate professor of forest biomaterials and chemistry at NC State.The biofilm the bacteria make and release into their environment is made of cellulose, which is the same material that gives plants a sturdy structure in their cell walls. However, when bacteria make cellulose, it has a tightly packed, crystalline structure, researchers said."It's one of the purest, if not the purest, forms of cellulose out there," Lucia said. "It's very well structured. It's very water loving, and it's got a very high crystallinity, so it packs very beautifully. Once you strip out the bacteria, you have this amazingly tough material that has a real robustness, or toughness."The bacteria make the film to protect themselves, the researchers said."If you leave something like an unwashed dish out, it can turn all slimy and gross -- that's a biofilm," said study co-author Wendy Krause, associate professor of textile engineering, chemistry and science at NC State. "Different bacteria make different biofilms. The bacterial film that we're studying is made of cellulose. The bacteria are making it because they live on it and in it. They're making their home."In the experiment, researchers used the bacteria as factories of cellulose nano-fibers. They then removed the bacteria and their non-cellulose residue. Finally, the researchers used the cellulose membrane to see if it could separate water from a solution containing both oil and water.They found the material was effective at removing water, and it was sturdy."The oil doesn't want to go through the membrane; it has a repulsive effect to it," Lucia said. "It's super fat-hating.""If the oil and water were highly mixed, it doesn't matter," Krause added. "You could put an immersion blender into the solution, and the membrane will still separate the water and oil."Researchers see a variety of potential applications for the material in situations where you need to recover water from an oily mixture -- whether it be to clean water contaminated with a textile dye or for environmental remediation. In future work, the researchers want to explore how they can tailor the membrane by chemically modifying it for certain applications. | Microbes | 2,021 |
March 8, 2021 | https://www.sciencedaily.com/releases/2021/03/210308152506.htm | Legume trees key to supporting tropical forest growth | Researchers have found that nitrogen-fixing legume trees can support themselves and surrounding trees not only with increased access to nitrogen, but with other key nutrients through enhanced mineral weathering. | The team, led by the University of Sheffield and the Smithsonian Tropical Research Institute, have published their findings in the journal PNAS which provide new insights into the role of nitrogen-fixing trees in safeguarding the function of tropical forests within the biosphere.The findings may also help inform practitioners and policy makers on how best to approach reforestation on degraded land and help meet climate change mitigation targets.The researchers discovered how the nitrogen-fixing legume trees overcome the constraints of growing on ancient, nutrient-poor tropical soils by accelerating weathering processes, releasing vital nutrients for themselves and surrounding trees in the forest.The trees are able to accelerate mineral weathering processes by locally acidifying the soil and adjusting the carbon to nitrogen ratio of the soil, ultimately changing the microbial community.This change in soil microbes improves access to nutrients and favours a type of bacteria that breaks down iron, releasing iron-bound minerals critical to tree growth.Legume trees are also particularly important in the process of forest recovery because they are able to supply fresh nitrogen into soils, which gets broken down by bacteria and utilised by the legume tree and trees around it.Dr Dimitat Epihov, lead author of the research from the University of Sheffield's Leverhulme Centre for Climate Change Mitigation, said: "Our research shows that legume trees not only provide valuable nitrogen through their symbioses with bacteria that live in their roots, but interact with free-living soil bacteria allowing nutrients to be chemically released."We discovered the abundance of a novel group of acid-loving bacteria, key in liberating minerals locked in iron minerals beneath legume trees, and that those benefits are passed on to nearby trees."Professor David Beerling, Director of the University of Sheffield's Leverhulme Centre for Climate Change Mitigation, said: "By using advanced genomic sequencing techniques we have addressed a long standing puzzle of how fast growing trees access sufficient nutrients to support their growth from nutrient-poor soils."The answer, it turns out, is to exploit specialised consortia of soil microbes whose metabolism allows them to efficiently break down rocks and extract nutrients they contain."The study was carried out in young regrowing forests at the Agua Salud Project in Panama, directed by the Smithsonian Tropical Research Institute. | Microbes | 2,021 |
March 8, 2021 | https://www.sciencedaily.com/releases/2021/03/210308111907.htm | Five days of antibiotics fine for children with pneumonia: Study | Many parents know the struggle of having to make children with pneumonia finish the usual 10-day course in antibiotics despite the child feeling better after a few days of medication. | New research from McMaster University has proven that a five-day course of high-dose amoxicillin will do just as well for children six months to 10 years old with common pneumonia."Several studies have proven that adults with pneumonia do fine with short courses of antibiotics, and now we have proved a short course of antibiotics also works for children," said Dr. Jeffrey Pernica, lead study author, associate professor of pediatrics of McMaster's Michael G. DeGroote School of Medicine and an infectious disease pediatrician for Hamilton Health Sciences.The study, involving 281 Ontario children, found that 85.7% of those who received the short course of antibiotics and 84.1% of those who received the longer course of medication were cured two to three weeks later.The paper was published online by the journal "The dramatic increase in antimicrobial resistance in the world today is driven by overuse of antibiotics -- which has only worsened during the COVID-19 pandemic," Pernica said. "This is why we need these clinical studies -- to figure out how short we can make antibiotic treatment courses for common infections."He said there are other reasons to use the least amount of antibiotics needed to effectively treat bacterial infections, including minimizing the costs of medicine.As well, he noted, a number of conditions including obesity, asthma, and arthritis, have been associated with changes in the human microbiome that can be caused by the use of antibiotics.The research team is recommending that clinical practice guidelines prepared for health professionals consider recommending five days of amoxicillin for pediatric pneumonia.This study was supported by the PSI Foundation, Pediatric Emergency Research Canada and Hamilton Health Sciences.The research is part of Canada's Global Nexus for Pandemics and Biological Threats, an international network based at McMaster, with scientists, clinicians, engineers, social scientists and other experts working collaboratively to prevent future pandemics and mitigate global health threats. | Microbes | 2,021 |
March 8, 2021 | https://www.sciencedaily.com/releases/2021/03/210308084224.htm | Diphtheria risks becoming major global threat again as it evolves antimicrobial resistance | Diphtheria -- a relatively easily-preventable infection -- is evolving to become resistant to a number of classes of antibiotics and in future could lead to vaccine escape, warn an international team of researchers from the UK and India. | The researchers, led by scientists at the University of Cambridge, say that the impact of COVID-19 on diphtheria vaccination schedules, coupled with a rise in the number of infections, risk the disease once more becoming a major global threat.Diphtheria is a highly contagious infection that can affect the nose and throat, and sometimes the skin. If left untreated it can prove fatal. In the UK and other high-income countries, babies are vaccinated against infection. However, in low- and middle-income countries, the disease can still cause sporadic infections or outbreaks in unvaccinated and partially-vaccinated communities.The number of diphtheria cases reported globally has being increasing gradually. In 2018, there were 16,651 reported cases, more than double the yearly average for 1996-2017 (8,105 cases).Diphtheria is primarily caused by the bacterium Corynebacterium diphtheriae and is mainly spread by coughs and sneezes, or through close contact with someone who is infected. In most cases, the bacteria cause acute infections, driven by the diphtheria toxin -- the key target of the vaccine. However, non-toxigenic C. diphtheria can also cause disease, often in the form of systemic infections.In a study published today in By analysing the genomes of 61 bacteria isolated from patients and combining these with 441 publicly available genomes, the researchers were able to build a phylogenetic tree -- a genetic 'family tree' -- to see how the infections are related and understand how they spread. They also used this information to assess the presence of antimicrobial resistance (AMR) genes and assess toxin variation.The researchers found clusters to genetically-similar bacteria isolated from multiple continents, most commonly Asia and Europe. This indicates that C. diphtheriae has been established in the human population for at least over a century, spreading across the globe as populations migrated.The main disease-causing component of C. diphtheriae is the diphtheria toxin, which is encoded by the tox gene. It is this component that is targeted by vaccines. In total, the researchers found 18 different variants of the tox gene, of which several had the potential to change the structure of the toxin.Professor Gordon Dougan from the Cambridge Institute of Therapeutic Immunology and Infectious Disease (CITIID) said: ""The diphtheria vaccine is designed to neutralise the toxin, so any genetic variants that change the toxin's structure could have an impact on how effective the vaccine is. While our data doesn't suggest the currently used vaccine will be ineffective, the fact that we are seeing an ever-increasing diversity of tox variants suggests that the vaccine, and treatments that target the toxin, need to be appraised on a regular basis."Diphtheria infections can usually be treated with a number of classes of antibiotic. While C. diphtheriae resistant to antibiotics have been reported, the extent of such resistance remains largely unknown.When the team looked for genes that might confer some degree of resistance to antimicrobials, they found that the average number of AMR genes per genome was increasing each decade. Genomes of bacteria isolated from infections from the most recent decade (2010-19) showed the highest average number of AMR genes per genome, almost four times as many on average than in the next highest decade, the 1990s.Robert Will, a PhD student at CITIID and the study's first author, said: "The C. diphtheriae genome is complex and incredibly diverse. It's acquiring resistance to antibiotics that are not even clinically used in the treatment of diphtheria. There must be other factors at play, such as asymptomatic infection and exposure to a plethora of antibiotics meant for treating other diseases."Erythromycin and penicillin are the traditionally recommended antibiotics of choice for treating confirmed cases of early-stage diphtheria, though there are several different classes of antibiotics available to treat the infection. The team identified variants resistant to six of these classes in isolates from the 2010s, higher than in any other decades.Dr Pankaj Bhatnagar from the World Health Organization country office for India said: "AMR has rarely been considered as a major problem in the treatment of diphtheria, but in some parts of the world, the bacterial genomes are acquiring resistance to numerous classes of antibiotics. There are likely to be a number of reasons to this, including exposure of the bacteria to antibiotics in their environment or in asymptomatic patients being treated against other infections."The researchers say that COVID-19 has had a negative impact on childhood vaccination schedules worldwide and comes at a time when reported case numbers are rising, with 2018 showing the highest incidence in 22 years.Dr Ankur Mutreja from CITIID, who led the study, said: "It's more important than ever that we understand how diphtheria is evolving and spreading. Genome sequencing gives us a powerful tool for observing this in real time, allowing public health agencies to take action before it's too late."We mustn't take our eye off the ball with diphtheria, otherwise we risk it becoming a major global threat again, potentially in a modified, better adapted, form."The research was funded primarily by the Medical Research Council, with additional support from the NIHR Cambridge Biomedical Research Centre. | Microbes | 2,021 |
March 4, 2021 | https://www.sciencedaily.com/releases/2021/03/210304112452.htm | New model can predict how bacteria develop antibiotic resistance | Using theoretical models of bacterial metabolism and reproduction, scientists can predict the type of resistance that bacteria will develop when they are exposed to antibiotics. This has now been shown by an Uppsala University research team, in collaboration with colleagues in Cologne, Germany. The study is published in the journal | In medical and pharmaceutical research, there is keen interest in finding the answer to how fast, and through which mechanisms, bacteria develop antibiotic resistance. Another goal is to understand how this resistance, in turn, affects bacterial growth and pathogenicity."This kind of knowledge would enable better tracking and slowing of the emergence of resistance, and thereby lengthen the period for which antibiotics are viable as effective treatments of bacterial infections. It would also create potential for new types of antibiotics and therapeutic methods that entail a lower risk of resistance development," says Dan I. Andersson, Professor of Medical Bacteriology at Uppsala University.When genetically adapting to a new environment, an organism undergoes mutations that modify its traits. Other recent studies have shown the difficulty of predicting which mutations will arise when bacteria adapt to new living conditions. For example, if a bacterium migrates to new surroundings with very low nutrient levels, its response will presumably be to evolve towards improved use of the limited resources. On the other hand, predicting the kinds of mutations that bring about this adaptation is much more difficult.In the new study, the scientists generated a theoretical model that links both the degree and the type of resistance developed by the bacterium to its capacity to grow and divide. In their experiments, the researchers were then able to see that the more resistant the bacterium became, the more its ability of nutrient uptake deteriorated. This previously unobserved connection enabled them to predict which kinds of mutation would arise and how much resistance they would confer when the mutated bacteria were exposed to various levels of antibiotics. The results showed that a low antibiotic dose caused a particular sort of mutation to appear, while a high concentration resulted in changes of another kind."Our work is the first step towards developing models that connect bacterial metabolism and growth with mechanisms underlying resistance. That would pave the way for predicting ways in which bacteria change when they are exposed to antibiotics. The results also demonstrate the importance of combining theoretical models with experimental analyses to understand how bacterial metabolism is optimised under various growth conditions," Andersson says. | Microbes | 2,021 |
March 2, 2021 | https://www.sciencedaily.com/releases/2021/03/210302094056.htm | Vaccine development software shows promise in influenza effort, could help defeat coronavirus | A novel computer algorithm that could create a broadly reactive influenza vaccine for swine flu also offers a path toward a pan-influenza vaccine and possibly a pan-coronavirus vaccine as well, according to a new paper published in | "This work takes us a step closer to a pan-swine flu virus vaccine," said Bette Korber, a computational biologist at Los Alamos National Laboratory and a co-author on the paper. "The hope is to eventually be prepared with an effective and rapid response if another swine flu epidemic begins to spread in humans, but this swine flu vaccine could also be useful in a veterinary setting." The immune responses to the vaccine showed very promising breadth against diverse viral variants. "The same basic principles may be applicable to developing a pan-coronavirus vaccine to enable a rapid vaccine response to future coronavirus cross-species jumps," said Korber.The algorithm, Epigraph, has already been used to predict therapeutic HIV vaccine candidates, and it has also shown promising potential as a pan-filovirus vaccine against highly diverse Ebola and Marburg viruses, protecting against disease when tested in an animal model.Vaccination with the Epigraph-designed product led to the development of a strong cross-reactive antibody response in mice, the study showed. In swine, it induced strong cross-reactive antibody and T-cell responses. The research was conducted in close collaboration with researchers from the Nebraska Center for Virology at the University of Nebraska, St. Jude Children's Research Hospital, and Los Alamos National Laboratory."We developed the Epigraph strategy for this kind of problem, and it can, in theory, be applied to many diverse pathogens," said Korber, who created it in partnership with her husband, James Theiler, a Los Alamos Fellow. "The tool creates a cocktail of vaccine antigens designed to maximize efficacy across a highly diverse population."Since 2010, more than 460 swine-flu variant infections have been reported in humans in the United States. Pigs are susceptible to swine, avian, and human influenza viruses, making them the perfect "mixing vessel" for novel reassorted influenza viruses, the authors note. These novel reassorted viruses have significant pandemic potential if zoonosis (transfer from pigs to humans) occurs, as seen with 2009 H1N1 swine flu pandemic. | Microbes | 2,021 |
February 25, 2021 | https://www.sciencedaily.com/releases/2021/02/210225113312.htm | Climate change-driven snowmelt in Alps triggers abrupt seasonal change | Spring snowmelt in the Alps is occurring earlier in the year due to climate change and as a result triggering abrupt deviations in mountain ecosystems. These changes could negatively affect the functioning of these valuable ecosystems. | New research has demonstrated that vitally important microbial communities within Alpine soils are under threat as a direct result of increasing global temperatures caused by ongoing climate change. These belowground microbes critically support aboveground life because they recycle the key nutrients upon which all animals and plants depend, including humans. They also control how much carbon is stored safely in the soil, where it cannot cause further global warming.In winter, Alpine soil microbes depend on snow to act as an insulating blanket, allowing them to continue to work throughout the cold alpine winter. However, it is estimated that the annual Alpine winter snowpack will begin melting over 100 days sooner than currently by the end of this century. Scientists from The University of Manchester demonstrate how this will affect soil microbes, and the critical functions they perform, by using in-the-field experiments and publishing their findings in For scientists, understanding how soil microbes respond to climate change and how this influences biogeochemical cycles, remains a major challenge. This is especially pertinent in Alpine regions where climate change is taking place at double the rate of the global average.Dr Arthur Broadbent from The University of Manchester is a lead author on the new research paper, he said: "Our paper reveals alarming climate change impacts on soil microbial communities, and the biogeochemical cycles that they regulate in mountain ecosystems. Using a high-alpine experiment in the Austrian Alps, we discovered that spring snowmelt triggers an abrupt seasonal transition in soil microbial communities, which is closely linked to rapid shifts in carbon and nitrogen cycling.""Snowmelt is predicted to occur 50-130 days earlier in alpine regions due to climate change by the end of the century. Using experimental manipulations, we demonstrated that earlier snowmelt, of even just 10 days, leads to an earlier seasonal transition in microbial communities and biogeochemical cycling."As a consequence, winter ecosystem functioning will be reduced in seasonally snow-covered ecosystems under future climate change, which threatens carbon retention and plant productivity. This would negatively affect agricultural production and disrupt natural ecosystems. It will also alter annual carbon fluxes in these ecosystems with the potential to cause further climate warming. | Microbes | 2,021 |
February 23, 2021 | https://www.sciencedaily.com/releases/2021/02/210223110656.htm | Mouse study shows bacteriophage therapy could fight drug-resistant Klebsiella pneumoniae | Using viruses instead of antibiotics to tame troublesome drug-resistant bacteria is a promising strategy, known as bacteriophage or "phage therapy." Scientists at the National Institutes of Health have used two different bacteriophage viruses individually and then together to successfully treat research mice infected with multidrug-resistant | Phage therapy has been pursued for about a century, though conclusive research studies are rare and clinical results -- from a handful of reports -- have provided mixed results. In the new paper published in the journal In research conducted in Hamilton, Montana, at Rocky Mountain Laboratories -- part of the NIH's National Institute of Allergy and Infectious Diseases -- and in collaboration with the National Cancer Institute in Bethesda, Maryland, scientists completed a series of studies on research mice infected with ST258. They treated the mice with either phage P1, phage P2, or a combination of the two, all injected at different times following ST258 infection. The scientists had isolated phages P1 and P2 in 2017 from raw sewage that they screened for viruses that would infect ST258 -- an indication that phages can be found just about any place. Phages P1 and P2 are viruses from the order Caudovirales, which naturally infect bacteria.Each of the three experimental treatment regimens helped the mice recover from ST258 infection. The scientists noted that the dose of phage provided was less vital to recovery than was the timing of when the dose was received. Mice treated 1 hour after infection showed the strongest recovery, followed by those treated eight hours after infection and then those treated at 24 hours. Control mice treated with saline all quickly developed severe disease and died.The scientists also checked the blood and tissue of phage-treated mice for the presence of ST258 bacteria and found there were significantly fewer bacteria at all time points regardless of the treatment method used, as compared to control mice.Unfortunately, the scientists also found that ST258 bacteria recovered in the blood and tissue samples of phage-treated mice already had begun developing phage resistance, a finding they are continuing to investigate. The group also is studying how phage therapy results compare between samples of ST258-infected mouse blood and human blood, and are examining whether components of human blood can interfere with phage efficacy.This study represents a first step in evaluating the use of phage therapy for treatment of severe | Microbes | 2,021 |
February 22, 2021 | https://www.sciencedaily.com/releases/2021/02/210222164204.htm | Last-itch effort: Fighting the bacteria that exacerbate eczema with bacteria | In a new study out of University of California San Diego School of Medicine, researchers have identified a universal strain of bacteria derived from healthy human skin that can treat the most common type of eczema, also known as atopic dermatitis. | In the paper published Feb. 22, 2021, in "The main question we wanted to answer was if this was safe. This was a safety study," said Richard Gallo, MD, PhD, Ima Gigli Distinguished Professor of Dermatology and chair of the Department of Dermatology at UC San Diego School of Medicine. "We found exactly what we hoped to find. The eczema of participants who received the bacterial treatment improved and there were no adverse events."Researchers screened more than 8,000 isolates of Staphylococcal bacteria derived from the skin of individuals without eczema, and identified a few strains that inhibited growth of The screening resulted in the identification of a single strain of bacteria called "That's how we found the universal strain. This was one out of 8,000 strains that were tested in a dish for their ability to kill The first tests were performed in animal models where mice were given an experimental version of eczema. Researchers then mixed Success with these animal models led to the Phase I clinical trial using bacteriotherapy to treat 54 trial participants with eczema. Two-thirds of the participants showed a large reduction in "This research is a unique approach to targeting the harmful Healthy human skin is alive with bacteria -- there are more microorganisms living in and on the human body than there are human cells. Most microbes reside on human skin without causing harm, but in some people, bacterial pathogens can negatively alter a person's health.According to the National Eczema Association, nearly 18 million people in the United States have atopic dermatitis, the most common form of eczema, which is a chronic, itchy rash that commonly appears on the arms, legs and cheeks."From our research, we've determined this rational therapeutic approach for atopic dermatitis appears to be safe for people to use to treat their eczema," said Gallo. "And it's easy, too, because it's just a cream and avoids the side effects of steroids and other drugs that target the immune system."Co-authors of the study include: Teruaki Nakatsuji, Tissa R. Hata, Yun Tong, Joyce Y. Cheng, Faiza Shafiq, Anna M. Butcher, Secilia S. Salem, Samantha L. Brinton, UC San Diego; Amanda K. Rudman Spergel, National Institutes of Health; Keli Johnson, Brett Jepson, Agustin Calatroni, Gloria David, Rho Federal Systems Division, Inc.; Marco Ramirez-Gama, and Patricia Taylor, National Jewish Health. | Microbes | 2,021 |
February 11, 2021 | https://www.sciencedaily.com/releases/2021/02/210211144428.htm | Tap water access linked to dengue risk | Dengue virus is among growing number of mosquito-borne viruses that have adapted to spread in urban environments and are spreading with the increasing rate of urbanization. Now, researchers reporting in | It is estimated that 3.5 billion people are at risk of dengue virus, the most widespread arbovirus. While previous attempts at controlling dengue virus with insecticides at egg-laying sites have been successful in the past, new strategies are needed to target hotspots of dengue virus transmission in urban areas.In the new work, Olivier Telle of the French National Centre for Scientific Research (CNRS) in at Paris-Sorbonne, Richard Paul from Institut Pasteur, France, and colleagues conducted surveys across the city of Delhi to analyze social and environmental risk factors for dengue virus. They measured dengue antibodies in 2,107 individuals and mosquito larval prevalence in 18 areas within Delhi as well as socio-economic factors across the city.Across the individuals tested in the city, 7.6% were positive for dengue virus antibodies, indicating a recent or current infection. Colonies with very poor access to tap water, with less than 61% of houses having access, were associated with a higher risk of exposure to the virus (adjusted odds ratio 4.69, 95% CI 2.06-10.67) and were the only type of area to register dengue cases between epidemics. However, despite relatively low mosquito densities, wealthy colonies had a higher risk of recent infection than intermediary colonies (aOR 2.92, 95% CI 1.26-6.72), likely reflecting the import of dengue virus by commuters coming into the high income areas during the day."Improved access to tap water could lead to a reduction in dengue, not only for those directly affected but for the general population," the researchers say. "Targeted intervention through mosquito control in winter in the socially disadvantaged areas could offer a rational strategy for optimizing control efforts." | Microbes | 2,021 |
February 10, 2021 | https://www.sciencedaily.com/releases/2021/02/210210091201.htm | Arizona economic burden of valley fever totals $736 million | A University of Arizona Health Sciences study has estimated total lifetime costs at $736 million for the 10,359 valley fever patients diagnosed in Arizona in 2019, underscoring the economic burden the disease places on the state and its residents. | The prevalence of valley fever, formally known as coccidioidomycosis or cocci, has increased in recent years, from 5,624 cases diagnosed in Arizona in 2014 to 10,359 cases in 2019. There currently are no certain means of prevention or vaccination for the fungal disease, which is caused by spores of Coccidioides, a family of fungi found in soils of the Southwest.The findings highlight the need for a vaccine, better therapeutic options and more consistent use of rapid diagnostic testing -- all areas of focus at the UArizona College of Medicine -- Tucson's Valley Fever Center for Excellence. The study, "Clinical and Economic Burden of Valley Fever in Arizona: An Incidence-Based Cost-of-Illness Analysis," was recently published in the journal "I was overwhelmed by how important this disease is in Arizona and how preventable some of the costs may be," said lead author Amy Grizzle, PharmD, associate director of the Center for Health Outcomes & PharmacoEconomic Research (or HOPE Center) in the UArizona College of Pharmacy. "Because it's kind of an isolated disease, I didn't necessarily think it was that expensive. I'm gratified that this study was able to shed some light on how many people this disease affects and how costly it is, especially taking into consideration some of the long-term complications."Dr. Grizzle said she was surprised by the $736 million total, which can be broken down into direct and indirect costs of $671 million and $65 million, respectively. Among direct costs, she said, are health expenses expected over a person's lifetime, including hospitalization, diagnosis and treatment (chest X-rays, rapid diagnostic tests, medications, surgery, etc.), and follow-up care including skilled nursing facilities for rehabilitation. Indirect costs include short-term work loss and lost earnings due to premature mortality.The study examined the cost-of-illness for valley fever's five primary manifestations:Researchers found that severe cases of valley fever where the disease spreads to other parts of the body, known as disseminated valley fever, resulted in the highest economic burden at nearly $1.4 million per person.The study's estimated lifetime costs are comparable to a 2019 California study that put total lifetime costs for the 7,466 people diagnosed with Valley fever in the Golden State in 2017 at just under $700 million, according to co-author John Galgiani, MD, an infectious diseases specialist with the College of Medicine -- Tucson who also is director of the UArizona Valley Fever Center for Excellence and a member of the BIO5 Institute.Leslie Wilson, PhD, of the University of California San Francisco, led the California study and is a co-author on the Arizona study along with Drs. Grizzle and Galgiani, and David Nix, PharmD, of the UArizona College of Pharmacy.Dr. Galgiani, who founded the Valley Fever Center in 1996, said two-thirds of all valley fever cases reported in the U.S. occur in Arizona, with half in Maricopa County. Only about 5% of U.S. valley fever cases are reported outside of Arizona and California.The primary symptoms of valley fever are respiratory problems similar to bacterial pneumonia, though more serious complications can arise when the infection spreads beyond the lungs to other areas including bones, joints, and the brain and central nervous system.Delays in diagnosis are common because valley fever symptoms can mimic those of the flu or bacterial pneumonia. Such confusion often means ineffective treatment with antibiotics, instead of antifungals like fluconazole, for days or weeks, during which time a patient's condition might deteriorate. The situation has worsened with the emergence of COVID-19, Dr. Galgiani said."Basically, doctors were under-diagnosing valley fever in the springtime, because of several reasons. One, people were being tested for COVID and, when they were negative, they didn't do any more testing," Dr. Galgiani said. "And two, people weren't seeking hospital care for anything if they didn't think it was COVID."Drs. Galgiani and Grizzle say the economic impacts highlighted in the study underscore the value of supporting research into developing more rapid diagnostic tests, better therapies and ultimately a preventative vaccine to address this important public health problem in Arizona."Hopefully, after more treatments and/or a vaccine are available, we can do another cost of illness analysis 10 years from now and see that these medications have greatly reduced the economic burden to Arizona," Dr. Grizzle said. | Microbes | 2,021 |
February 8, 2021 | https://www.sciencedaily.com/releases/2021/02/210208085432.htm | Researchers find peptide that treats, prevents killer citrus disease | New research affirms a unique peptide found in an Australian plant can destroy the No. 1 killer of citrus trees worldwide and help prevent infection. | Huanglongbing, HLB, or citrus greening has multiple names, but one ultimate result: bitter and worthless citrus fruits. It has wiped out citrus orchards across the globe, causing billions in annual production losses.All commercially important citrus varieties are susceptible to it, and there is no effective tool to treat HLB-positive trees, or to prevent new infections.However, new UC Riverside research shows that a naturally occurring peptide found in HLB-tolerant citrus relatives, such as Australian finger lime, can not only kill the bacteria that causes the disease, it can also activate the plant's own immune system to inhibit new HLB infection. Few treatments can do both.Research demonstrating the effectiveness of the peptide in greenhouse experiments has just been published in the The disease is caused by a bacterium called CLas that is transmitted to trees by a flying insect. One of the most effective ways to treat it may be through the use of this antimicrobial peptide found in Australian finger lime, a fruit that is a close relative of citrus plants."The peptide's corkscrew-like helix structure can quickly puncture the bacterium, causing it to leak fluid and die within half an hour, much faster than antibiotics," explained Hailing Jin, the UCR geneticist who led the research.When the research team injected the peptide into plants already sick with HLB, the plants survived and grew healthy new shoots. Infected plants that went untreated became sicker and some eventually died."The treated trees had very low bacteria counts, and one had no detectable bacteria anymore," Jin said. "This shows the peptide can rescue infected plants, which is important as so many trees are already positive."The team also tested applying the peptide by spraying it. For this experiment, researchers took healthy sweet orange trees and infected them with HLB-positive citrus psyllids -- the insect that transmits CLas.After spraying at regular intervals, only three of 10 treated trees tested positive for the disease, and none of them died. By comparison, nine of 10 untreated trees became positive, and four of them died.In addition to its efficacy against the bacterium, the stable anti-microbial peptide, or SAMP, offers a number of benefits over current control methods. For one, as the name implies, it remains stable and active even when used in 130-degree heat, unlike most antibiotic sprays that are heat sensitive -- an important attribute for citrus orchards in hot climates like Florida and parts of California.In addition, the peptide is much safer for the environment than other synthetic treatments. "Because it's in the finger lime fruit, people have eaten this peptide for hundreds of years," Jin said.Researchers also identified that one half of the peptide's helix structure is responsible for most of its antimicrobial activity. Since it is only necessary to synthesize half the peptide, this is likely to reduce the cost of large-scale manufacturing.The SAMP technology has already been licensed by Invaio Sciences, whose proprietary injection technology will further enhance the treatment.Following the successful greenhouse experiments, the researchers have started field tests of the peptides in Florida. They are also studying whether the peptide can inhibit diseases caused by the same family of bacteria that affect other crops, such as potato and tomato."The potential for this discovery to solve such devastating problems with our food supply is extremely exciting," Jin said. | Microbes | 2,021 |
February 2, 2021 | https://www.sciencedaily.com/releases/2021/02/210202113733.htm | Soldiers, snakes and marathon runners in the hidden world of fungi | Researchers at Lund University in Sweden have discovered the individual traits of fungi, and how their hyphae -- that is, the fungal threads that grow in soil -- behave very differently as they navigate through the earth's microscopic labyrinths. | The study was performed in a lab environment, and the underground system constructed synthetically from silicone. Using a microscope, researchers were able to follow seven species and compare their behaviour. How do they react when the maze they grow in turns sharply and forces the hyphae to grow in the direction it came from? What happens when a large space opens up in front of them?"Under a microscope, their behaviour becomes much more personal than you can ever imagine. They become individual characters," says Edith Hammer, one of the researchers behind the study.The research team discovered that the fungi use different strategies when they grow and form their structures, the so-called mycelium. The different characteristics have led the researchers to give the various fungi nicknames such as "the soldier," the marathon runner" and "the snake."The soldier gained its name because it grows with great force, and plows down obstacles in its path, yet it does not get very far. The marathon runner, on the other hand, sends out hypha that act like 'lone fighters', and grow quite far before giving up their search for food. However, this requires that they do not encounter tough obstacles, as this is their weak spot. Unlike the marathon runner, the snake specializes in weaving and growing around obstacles.Examples of obstacles that the hyphae may encounter, and that can delay and confuse them, are zigzag patterns, sharp angles and rounded corners. The study shows that some species simply stop when they end up in a corner.The research is unique because it is the first time that the behaviour of individual hyphae in multiple species has been studied in parallel and in detail. Previous studies have often focused on the mycelium as a whole, as they have not been able to distinguish the behaviour of individual hyphae.So far, however, important pieces of the puzzle are missing on how microscopic soil structures affect the behaviour of fungi, in order for the research to have practical applications in agriculture. | Microbes | 2,021 |
February 1, 2021 | https://www.sciencedaily.com/releases/2021/02/210201103024.htm | Your toothbrush reflects you, not your toilet | Good news: The bacteria living on your toothbrush reflect your mouth -- not your toilet. | After studying microbial communities living on bristles from used toothbrushes, Northwestern University researchers found those communities matched microbes commonly found inside the mouth and on skin. This was true no matter where the toothbrushes had been stored, including shielded behind a closed medicine cabinet door or out in the open on the edge of a sink.The study's senior author, Erica Hartmann, was inspired to conduct the research after hearing concerns that flushing a toilet might generate a cloud of aerosol particles. She and her team affectionately called their study "Operation Pottymouth.""I'm not saying that you can't get toilet aerosols on your toothbrush when you flush the toilet," Hartmann said. "But, based on what we saw in our study, the overwhelming majority of microbes on your toothbrush probably came from your mouth."The study will be published Feb. 1 in the journal Hartmann is an assistant professor of environmental engineering at Northwestern's McCormick School of Engineering. Ryan Blaustein, a former postdoctoral fellow in Hartmann's lab, was the paper's first author. Blaustein is now a postdoctoral fellow at the National Institutes of Health (NIH).To obtain toothbrushes for the study, Hartmann's team launched the Toothbrush Microbiome Project, which asked people to mail in their used toothbrushes along with corresponding metadata. Hartmann's team then extracted DNA from the bristles to examine the microbial communities found there. They compared these communities to those outlined by the Human Microbiome Project, an NIH initiative that identified and catalogued microbial flora from different areas of the human body."Many people contributed samples to the Human Microbiome Project, so we have a general idea of what the human microbiome looks like," Blaustein said. "We found that the microbes on toothbrushes have a lot in common with the mouth and skin and very little in common with the human gut.""Your mouth and your gut are not separate islands," Hartmann added. "There are some microbes that we find both in the human gut and mouth, and those microbes are found on toothbrushes. But, again, those are probably coming from your mouth."During the research, Hartmann's team examined how many different types of microbes lived on the toothbrushes. They found people with better oral hygiene, who regularly flossed and used mouthwash, had toothbrushes with less diverse microbial communities."If you practice good oral hygiene, then your toothbrush also will be relatively clean," Hartmann said. "But it's a small difference. It's not like people who regularly floss, brush and use mouthwash have no microbes and those who don't have tons. There's just a bit less diversity on toothbrushes from people who do all those things."The researchers also found that microbes from toothbrushes of people with better oral hygiene had slightly more antimicrobial-resistance genes. Hartmann said microbes with these genes did not match the human body and were likely from air or dust in the bathroom.Hartmann stresses that there's no need to be alarmed by microbes living on your toothbrush. Unless your dentist recommends otherwise, people should not reach for antimicrobial toothpastes and toothbrushes."By using antimicrobials, you aren't just getting rid of microbes," Hartmann said. "You are pushing the surviving microbes toward antimicrobial resistance. In general, for most people, regular toothpaste is sufficient." | Microbes | 2,021 |
January 26, 2021 | https://www.sciencedaily.com/releases/2021/01/210126105903.htm | Gut microbiota reveals whether drug therapies work in inflammatory bowel diseases | The prevalence of inflammatory bowel diseases has significantly increased both in Finland and globally. These disorders cannot be entirely cured. Instead, they are treated with anti-inflammatory drugs and, at times, through surgery. | If conventional drug therapies based on anti-inflammatory drugs are ineffective, the diseases can be treated using infliximab, a biological TNF-α blocker that is administered intravenously. Infliximab is an antibody that prevents TNF-α, a pro-inflammatory factor, from binding with inflammatory cells in the intestine. It is effective in reducing inflammation and improving the patient's condition, while also controlling the disease well.Although infliximab therapy is often effective, roughly 30-40% of patients either do not respond to the treatment or lose response over time. So far, no reliable tests for predicting treatment response are available."A test for predicting responses would help to choose drug therapies and avoid unnecessary drug use, which would reduce potential adverse effects and save on drug expenses in the healthcare system," postdoctoral researcher Eija Nissilä says.In a collaborative project, the University of Helsinki and the Department of Gastroenterology at the Helsinki University Hospital investigated whether any predictors associated with infliximab therapy could be identified in the gut microbiota. The results were published in the The study revealed that already before treatment the gut microbiota of inflammatory bowel disease patients differed in terms of several bacterial and fungal genera. These differences had a link to infliximab therapy response.The changes that occurred in the gut microbiota during therapy also differed between patients who presented a response to treatment and those who did not. The gut of non-responsive patients had fewer anti-inflammatory bacteria of the Clostridia family and a higher number of pro-inflammatory bacteria and fungi such as Candida. Certain bacteria found in the intestine predicted a good response to infliximab therapy.Based on the results, gut bacteria and fungi could potentially be used as indicators when assessing whether to initiate treatment or not."Such a predictive test would make it possible to choose the appropriate therapy, providing savings in drug therapy costs in healthcare," Nissilä notes. | Microbes | 2,021 |
January 21, 2021 | https://www.sciencedaily.com/releases/2021/01/210121132118.htm | Hope for a vaccination against Staphylococcus areus infections? | <em>Staphylococcus aureus</em> | After decades of research, the Cologne scientists have now published a new promising vaccine strategy against "For the Particularly encouraging is the observation that greater than 97 percent of the more than 35,000 investigated clinical strains of | Microbes | 2,021 |
January 19, 2021 | https://www.sciencedaily.com/releases/2021/01/210119122041.htm | Study in twins identifies fecal microbiome differences in food allergies | A new study out of the University of Chicago and Stanford University on pairs of twins with and without food allergies has identified potential microbial players in this condition. The results were published on Jan. 19 in the | The study grew out of prior research in the Nagler laboratory at UChicago on the fecal microbiota in infants. By transplanting fecal microbes from healthy and food-allergic infants to germ-free mice (who do not possess a microbiome), investigators found that the healthy infant microbiota was protective against the development of food allergies."In this study, we looked at a more diverse population across a large range of ages," said Cathryn Nagler, PhD, the Bunning Family Professor in the Pritzker School of Molecular Engineering, the Department of Pathology and the College at UChicago. "By studying twin pairs, we had the benefit of examining genetically identical individuals who grew up in the same environment, which allowed us to begin to parse out the influence of genetic and environmental factors."After a discussion at a research conference, Nagler and her colleague at Stanford, Kari Nadeau, MD, PhD, decided to collaborate on the project. Nadeau, the Director of the Sean N. Parker Center for Allergy and Asthma Research, had been conducting a study on the epigenetics of food allergies and had already collected fecal samples from study participants. Nagler's lab conducted the sequencing on the samples collected from 13 pairs of twins with and without food allergies, as well as an additional five pairs of twins where both twins had at least one food allergy.The research team looked at which microbes were present in the fecal samples as well as metabolic products (called metabolites), derived not only from the microbes, but also from host and dietary sources."We desperately need biomarkers to understand the immunoregulatory function of intestinal bacteria," said Nagler. "Metabolites give us clues as to what bacteria are doing mechanistically to regulate the immune response."This approach identified 64 distinct sets of bacterial species and metabolites that set apart the healthy and allergic twin groups. Most of these differentially abundant bacteria were members of the Clostridia class, shown to protect against food allergies in several earlier reports from the Nagler lab. Enrichment of the allergy-protective bacteria in the healthy twins, presumably established in early life, persisted into adulthood despite separation and lifestyle changes. In addition, healthy twins showed enrichment for the diacylglycerol metabolic pathway and two specific bacteria: "To narrow down from thousands of bacteria to specific species as candidates for future therapeutic interventions, one dimension of data is not enough -- bringing together data from multiple dimensions is the key," said first author Riyue Bao, PhD, now a Research Associate Professor of Medicine at the University of Pittsburgh. "In our study, we harnessed the benefits of both high-throughput microbiome sequencing and metabolic profiling techniques, and were able to nominate two specific species, each involved in distinct metabolite pathways, that can be prioritized as potential targets for future research and therapeutic interventions in food allergies.""Tons of people will go to Google and they want to know: 'Should I eat yogurt? Should I not eat yogurt? Does my microbiome play a role in my disease?'" said Nadeau. "This research is important as one of key 'bricks' in knowledge of the human microbiome that needs to be laid down to answer these questions. We can't say this is a cause and effect relationship yet, but we can say that there is an association with disease and health. So now we can start to ask, what does this mean?"While the study only included a small group of participants, researchers are excited by the results and how they can be applied to future projects.Future research will investigate the specific roles of these bacteria in food allergies; for example, R. bromii is a keystone species in the degradation of resistant starch -- dietary starch that normally escapes digestion. Nagler plans to investigate how dietary supplementation with resistant starch can affect R. bromii's presence in the fecal microbiome, and in turn whether or not it can boost the response to oral immunotherapy, the only currently available treatment for food allergies.The study, "Fecal microbiome and metabolome differ in healthy and food-allergic twins," was supported by the Sunshine Charitable Foundation, the Moss Family Foundation, NIAID (R56AI134923, R01AI140134) and NHLBI (R01HL118162). Additional authors include Riyue Bao of the University of Chicago (now at the University of Pittsburgh Medical Center), Lauren A. Hesser of UChicago, and Ziyuan He and Xiaoying Zhou of Stanford University. | Microbes | 2,021 |
January 19, 2021 | https://www.sciencedaily.com/releases/2021/01/210119102842.htm | Research establishes antibiotic potential for cannabis molecule | Synthetic cannabidiol, better known as CBD, has been shown for the first time to kill the bacteria responsible for gonorrhoea, meningitis and legionnaires disease. | The research collaboration between The University of Queensland and Botanix Pharmaceuticals Limited could lead to the first new class of antibiotics for resistant bacteria in 60 years.The UQ Institute for Molecular Bioscience's Associate Professor Mark Blaskovich said CBD -- the main nonpsychoactive component of cannabis -- can penetrate and kill a wide range of bacteria including Neisseria gonorrhoeae, which causes gonorrhoea."This is the first time CBD has been shown to kill some types of Gram-negative bacteria. These bacteria have an extra outer membrane, an additional line of defence that makes it harder for antibiotics to penetrate," Dr Blaskovich said.In Australia, gonorrhoea is the second most common sexually-transmitted infection and there is no longer a single reliable antibiotic to treat it because the bacteria is particularly good at developing resistance.The study also showed that CBD was widely effective against a much larger number of Gram-positive bacteria than previously known, including antibiotic-resistant pathogens such as MRSA (methicillin-resistant Staphylococcus aureus) or 'golden staph'.Dr Blaskovich said cannabidiol was particularly good at breaking down biofilms -- the slimy build-up of bacteria, such as dental plaque on the surface of teeth -- which help bacteria such as MRSA survive antibiotic treatments.Dr Blaskovich's team at the Centre for Superbug Solutions mimicked a two-week patient treatment in laboratory models to see how fast the bacteria mutated to try to outwit CBD's killing power."Cannabidiol showed a low tendency to cause resistance in bacteria even when we sped up potential development by increasing concentrations of the antibiotic during 'treatment'.""We think that cannabidiol kills bacteria by bursting their outer cell membranes, but we don't know yet exactly how it does that, and need to do further research.The research team also discovered that chemical analogs -- created by slightly changing CBD's molecular structure -- were also active against the bacteria."This is particularly exciting because there have been no new molecular classes of antibiotics for Gram-negative infections discovered and approved since the 1960s, and we can now consider designing new analogs of CBD within improved properties."Vince Ippolito, the President and Executive Chairman of Botanix, said the research showed vast potential for the development of effective treatments to fight the growing global threat of antibiotic resistance."Congratulations to Dr Blaskovich and his team for producing this significant body of research -- the published data clearly establishes the potential of synthetic cannabinoids as antimicrobials," Mr Ippolito said."Our Company is now primed to commercialise viable antimicrobial treatments which we hope will reach more patients in the near future. This is a major breakthrough that the world needs now."Dr Blaskovich said collaborating with Botanix has sped up the research, with Botanix contributing formulation expertise that has led to the discovery that how cannabidiol is delivered makes a huge difference in its effectiveness at killing bacteria.The collaboration has enabled Botanix to progress a topical CBD formulation into clinical trials for decolonisation of MRSA before surgery."Those Phase 2a clinical results are expected early this year and we hope that this will pave the way forward for treatments for gonorrhoea, meningitis and legionnaires disease."Now we have established that cannabidiol is effective against these Gram-negative bacteria, we are looking at its mode of action, improving its activity and finding other similar molecules to open up the way for a new class of antibiotics."Video: | Microbes | 2,021 |
January 15, 2021 | https://www.sciencedaily.com/releases/2021/01/210115135300.htm | Scientists identify nutrient that helps prevent bacterial infection | Scientists studying the body's natural defenses against bacterial infection have identified a nutrient -- taurine -- that helps the gut recall prior infections and kill invading bacteria, such as | Scientists know that microbiota -- the trillions of beneficial microbes living harmoniously inside our gut -- can protect people from bacterial infections, but little is known about how they provide protection. Scientists are studying the microbiota with an eye to finding or enhancing natural treatments to replace antibiotics, which harm microbiota and become less effective as bacteria develop drug resistance.The scientists observed that microbiota that had experienced prior infection and transferred to germ-free mice helped prevent infection with Taurine helps the body digest fats and oils and is found naturally in bile acids in the gut. The poisonous gas hydrogen sulfide is a byproduct of taurine. The scientists believe that low levels of taurine allow pathogens to colonize the gut, but high levels produce enough hydrogen sulfide to prevent colonization. During the study, the researchers realized that a single mild infection is sufficient to prepare the microbiota to resist subsequent infection, and that the liver and gallbladder -- which synthesize and store bile acids containing taurine -- can develop long-term infection protection.The study found that taurine given to mice as a supplement in drinking water also prepared the microbiota to prevent infection. However, when mice drank water containing bismuth subsalicylate -- a common over-the-counter drug used to treat diarrhea and upset stomach -- infection protection waned because bismuth inhibits hydrogen sulfide production.Scientists from NIH's National Institute of Allergy and Infectious Diseases led the project in collaboration with researchers from the National Institute of General Medical Sciences; the National Cancer Institute; the National Institute of Diabetes and Digestive and Kidney Diseases; and the National Human Genome Research Institute. | Microbes | 2,021 |
January 14, 2021 | https://www.sciencedaily.com/releases/2021/01/210114111914.htm | Scientists artificially infect mosquitoes with human malaria to advance treatment | A vector refers to an organism that carries and transmits an infectious disease, as mosquitoes do malaria. | Lead compounds are chemical compounds that show promise as treatment for a disease and may lead to the development of a new drug.Antiplasmodial lead compounds are those that counter parasites of the genus Plasmodium, which is the parasite that infects mosquitoes and causes malaria in people.The study findings were published in Professor Lizette Koekemoer, co-director of the WRIM and the National Research Foundation SARChI Chair in Medical Entomology and Control, and an honorary member of the Centre for Emerging Zoonotic and Parasitic Diseases, National Institute for Communicable Diseases, co-authored the paper.Koekemoer and her team at WRIM established a unique mosquito malaria infection centre in the Faculty of Health Sciences at Wits University, where the mosquito transmission blocking experiments took place."The WRIM infection centre is the only facility in South Africa and in the southern African region that can artificially infect mosquitoes with the human malaria parasite," says Koekemoer. "The infection centre provided the high level of expertise required to infect mosquitoes with the human malaria parasite, Plasmodium falciparum, and allowed for this unique study to be done."Drugs are used to control human malaria but resistance to these drugs develops rapidly. Furthermore, the drugs mainly target just one stage of the parasite's life cycle and are not good candidates for blocking transmission.To expand drug suitability for malaria elimination strategies, drugs need to be able to act as a chemotype [a chemically distinct entity in a plant or microorganism] that blocks both human-to-mosquito transmission and mosquito-to-human transmission.Koekemoer, with WRIM colleagues and co-authors, Erica Erlank, Luisa Nardini, Nelius Venter, Sonja Lauterbach, Belinda Bezuidenhout, and Theresa Coetzer conducted specialised experiments to measure the reduction of infection in the mosquitoes as well as the "killing effect" [endectocide effect] in the vectors.The scientists screened 400 chemical compounds available in the "Pandemic Response Box," which is supplied by Medicines for Malaria Venture (MMV), to identify the compounds that are most effective across the life stages of the parasite that generally take place in the human host.The Pandemic Response Box contains 400 diverse drug-like molecules active against bacteria, viruses or fungi. It is available free of charge provided that researchers share data resulting from research on the molecules in the box with the public within 2 years of its generation.The compounds that showed a good effect on late-stage gametocytes (those circulating in the blood and being transferred to a mosquito when it feeds on an infected human) were evaluated for their transmission-blocking potential.Mosquitoes were fed infected blood that was treated either with or without the compound. After eight to 10 days, the mosquito guts [stomach] were removed and the number of parasites (called oocysts) counted and compared against those mosquitoes that received only an infected blood meal without treatment.Mass drug administration (MDA) is the administration of antimalarial drugs to target the parasite reservoir in humans, without necessarily testing whether those people are carrying the parasite that causes malaria.The World Health Organization (WHO) recommends MDA for the elimination of the Plasmodium falciparum malaria parasite. However, the effort and cost required to implement MDA on a large scale is prohibitive.Identifying the potential compounds for MDA is amongst the greatest hurdles to overcome and is therefore an intense research pipeline of development.By leveraging the scarce skills and expertise available in different research institutes such as the WRIM, this study published in This opens the door for screening additional chemistry effectively and rapidly to contribute towards the elimination of malaria.Although there were still an estimated 229 million malaria cases in 2019 and 409,000 deaths during this period (compared to some 88 million Covid-19 cases reported), the successes of reducing malaria cases over the past two decades has inspired many countries to commit to eliminating transmission altogether.To date, the WHO has certified 38 countries and territories malaria-free. In southern Africa, eight countries -- including South Africa -- have made the elimination of malaria a policy goal.However, progress towards eliminating transmission has numerous challenges and new drugs and insecticides are urgently needed to combat the development of drug resistance in the parasite and the vector.The WRIM and studies like these are pioneering novel approaches. However, it is still a long road between the laboratory and field operations. But the first steps have been taken. | Microbes | 2,021 |
January 13, 2021 | https://www.sciencedaily.com/releases/2021/01/210113100812.htm | Evolution in a test tube: These bacteria survive on deadly copper surfaces | The descendants of regular wild-type bacteria can evolve to survive for a long time on metallic copper surfaces that would usually kill them within a few minutes. An international research team led by Martin Luther University Halle-Wittenberg (MLU) and the Bundeswehr Institute of Microbiology was able to produce these tiny survivalists in the lab and has been able to study them more closely. The team reports on its findings in | Bacterial infections are usually treated with antibiotics. However, in recent decades many pathogenic bacteria have developed an increasing tolerance to common drugs. So-called multidrug-resistant bacteria are of particular concern as they can no longer be combated with most antibiotics. Copper surfaces -- for example on door handles -- are a good weapon to fight these germs. "Copper surfaces are a sure-fire way to kill bacteria. Most bacteria die within minutes after landing on a copper surface," explains Professor Dietrich H. Nies, a microbiologist at MLU. Copper is a vital trace element for bacteria -- but only in very small quantities. On the copper surfaces, however, the bacteria are literally flooded to death with copper ions because that they can no longer stave them off using their normal defence strategies.Nies' research team wanted to find out if and how quickly two typical species of bacteria, Escherichia coli and Staphylococcus aureus, are theoretically able to adapt to survive on copper surfaces. The team therefore placed the bacteria on the surfaces for only a few minutes before returning them to a normal culture medium where they were allowed to recover. This process was repeated several times, with the survivors gradually being exposed to the deadly surface for longer and longer periods of time. Within three weeks, the researchers had produced bacteria that could survive for more than one hour on a copper surface. "Outside the laboratory, conditions are obviously not as ideal. But if copper surfaces are not cleaned regularly, insulating layers of grease can begin to form on them, which could produce a similar development over time," says Nies.Using comprehensive genetic analyses, the team sought to understand why the bacteria no longer died on the surfaces. "We were unable to find a gene that made them resistant to the deadly effect of metallic copper surfaces," says Nies. Instead, the team observed a phenomenon among the surviving bacteria that was already known for quite some time, although in a slightly different manner: the bacteria's metabolism slowed down to a bare minimum and they fell into a kind of hibernation. Because most antibiotics aim to disrupt the metabolism of growing bacteria, they are almost completely ineffective against these special bacteria, which are also known as "persisters." "No matter how well an antibiotic works, there are always a handful of persisters in every generation," explains Nies. However, these are not considered antibiotic-resistant bacteria, because their offspring are once again susceptible to the drugs.Normally only a tiny proportion of bacteria become persisters. However, in the case of the isolated bacteria, it was the entire population. Although they were able to grow just as fast as their predecessors, they were also able to rescue themselves by switching rapidly into an early state of persistence under adverse conditions. The scientists were concerned one additional thing they observed: "The bacteria also inherited this capability over 250 generations, even though the offspring had not come into contact with a copper surface," says Nies. The team therefore recommends that copper surfaces be cleaned regularly and thoroughly with special agents so that no persister bacteria can develop in the first place. At the same time, Nies points out that the use of copper surfaces is only one of many ways -- including antibiotics -- to effectively combat harmful bacteria. | Microbes | 2,021 |
January 12, 2021 | https://www.sciencedaily.com/releases/2021/01/210112110053.htm | Scientists reveal how gut microbes can influence bone strength in mice | Gut microbes passed from female mice to their offspring, or shared between mice that live together, may influence the animals' bone mass, says a new study published today in | The findings suggest that treatments which alter the gut microbiome could help improve bone structure or treat conditions that weaken bones, such as osteoporosis."Genetics account for most of the variability in human bone density, but non-genetic factors such as gut microbes may also play a role," says lead author Abdul Malik Tyagi, Assistant Staff Scientist at the Division of Endocrinology, Metabolism, and Lipids at Emory Microbiome Research Center, Emory University, Georgia, US. "We wanted to investigate the influence of the microbiome on skeletal growth and bone mass development."To do this, Tyagi and colleagues studied mice that lacked any gut microbes. They transferred fecal material containing a gut microbe called segmented filamentous bacteria (SFB), which stimulates the breakdown of bone, into the animals. Their studies revealed that the offspring of the SFB-treated mice were colonised with these bacteria at birth and had poorer bone structure than identical mice that lacked SFB.Additionally, mice that lived with others carrying SFB became colonised with the bacteria within four weeks, and developed poorer bone structure as a result. "Our work shows that microbes can be either inherited or transmitted between individuals and significantly affects skeletal development in the animals," Tyagi says."Further studies are now needed to determine if the same is true in humans," adds senior author Roberto Pacifici, Garland Herndon Professor of Medicine, and Director of the Division of Endocrinology, Metabolism, and Lipids, at Emory University. "If it is, then it could be possible to develop therapies that change the gut microbiome early in life to allow for healthy skeletal growth."It would also suggest the need for caution in the current use of fecal transplants to treat other conditions in patients, to ensure that bone-weakening bacteria aren't inadvertently introduced," Pacifici concludes. | Microbes | 2,021 |
January 12, 2021 | https://www.sciencedaily.com/releases/2021/01/210112085355.htm | Breakthrough against antibiotic-resistance | A major risk of being hospitalised is catching a bacterial infection. | Hospitals, especially areas including intensive care units and surgical wards, are teeming with bacteria, some of which are resistant to antibiotics -- they are infamously known as 'superbugs'.Superbug infections are difficult and expensive to treat, and can often lead to dire consequences for the patient.Now, new research published today in the journal The strategy involves the use of bacteriophages (also known as 'phages')."Phages are viruses, but they cannot harm humans," said lead study author Dr Fernando Gordillo Altamirano, from the Monash University School of Biological Sciences."They only kill bacteria."The research team investigated phages that can kill the world's leading superbug, "We have a large panel of phages that are able to kill antibiotic-resistant "But this superbug is smart, and in the same way it becomes resistant to antibiotics, it also quickly becomes resistant to our phages," Dr Barr said.The study pinpoints how the superbug becomes resistant to attack from phages, and in doing so, the superbug loses its resistance to antibiotics."A. baumannii produces a capsule, a viscous and sticky outer layer that protects it and stops the entry of antibiotics," said Dr Gordillo Altamirano."Our phages use that same capsule as their port of entry to infect the bacterial cell."In an effort to escape from the phages, The study showed resensitisation to at least seven different antibiotics."This greatly expands the resources to treat "We're making this superbug a lot less scary."Even though more research is needed before this therapeutic strategy can be applied in the clinic, the prospects are encouraging."The phages had excellent effects in experiments using mice, so we're excited to keep working on this approach," said Dr Gordillo Altamirano."We're showing that phages and antibiotics can work great as a team." | Microbes | 2,021 |
January 11, 2021 | https://www.sciencedaily.com/releases/2021/01/210111094309.htm | Probiotic coffee and tea drinks | Good news for those who need a cuppa to start the day. Researchers from the National University of Singapore (NUS) have created new probiotic coffee and tea drinks that are packed with gut-friendly live probiotics. | Supervised by Associate Professor Liu Shao Quan from the Department of Food Science and Technology at the NUS Faculty of Science, the two doctoral students who worked on these two new beverages assert that their drinks have a great taste, and can be stored chilled or at room temperature for more than 14 weeks without compromising on their probiotic viability.Traditional probiotic carriers like yoghurts and cultured milks are dairy-based products. The rise in veganism, along with common health issues like lactose intolerance, high cholesterol, and allergies to dairy proteins, have stimulated the trend in non-dairy probiotic food and beverages."Coffee and tea are two of the most popular drinks around the world, and are both plant-based infusions. As such, they act as a perfect vehicle for carrying and delivering probiotics to consumers. Most commercially available probiotic coffee and tea drinks are unfermented. Our team has created a new range of these beverages using the fermentation process as it produces healthy compounds that improve nutrient digestibility while retaining the health benefits associated with coffee and tea," explained Assoc Prof Liu.To create the new probiotic tea, Ms Wang Rui, a doctoral student from NUS Food Science and Technology, added nutrients into a tea infusion, followed by a careful selection of specific probiotics. The tea mixture is left to ferment for two days, after which it is ready to drink. Any kind of brewed tea can be used in this process, and throughout the fermentation process, the original flavour of the tea is largely retained, with fruity and floral notes introduced."The probiotic tea tastes like fruit tea with a little bit acidity, and a similar mouthfeel to the original tea. Drinkers can add sweeteners and milk, or cream, based on their preferences," said Ms Wang.Many health benefits of tea, such as its antioxidant or anti-inflammatory properties, have been linked to it containing 'polyphenol' molecules. By using the patented fermentation process, the polyphenol contents from the tea are retained, and an additional antibacterial agent -- phenyllactate -- is produced after fermentation. The drink also contains live probiotics which promote gut health.Another doctoral student from the Department, Ms Alcine Chan, created a new probiotic coffee by adding specially selected nutrients to brewed coffee, followed by carefully chosen probiotics. The coffee mixture is left to ferment for a day, and placed in the refrigerator following probiotic fermentation. After this process, the chilled probiotic coffee is ready to drink. Sugar and milk can be added before consumption if desired."The formulation is tricky, especially relating to the type and amount of nutrients added, and the probiotic combination. Not every type of probiotic can grow in coffee brews. Adding too few nutrients will not enable probiotic growth while adding too many nutrients will give an unpleasant taste," shared Ms Chan.Ms Chan concocted several prototypes of the probiotic coffee, and the flavour varies between each one, but all retain the distinctive coffee taste. She explained, "Some of the probiotic coffees give better-balanced acidity, some give better mouthfeels, some have deeper smoky flavours, and some can retain the coffee flavour better after long-term storage."The caffeine content is retained, so people who consume coffee for caffeine can still get their fix. The probiotic coffee also kept the chlorogenic acid content, which has been linked to a lot of the health benefits of coffee.Each serving of probiotic tea and probiotic coffee contains at least 1 billion units of live probiotics. This the daily amount recommended by the International Scientific Association for Probiotics and Prebiotics.Both doctoral students are refining their recipes to enhance the taste and flavour of the two beverages. The NUS team has also filed a patent for the probiotic coffee recipe and hopes to collaborate with industry partners to commercialise the drink. | Microbes | 2,021 |
January 4, 2021 | https://www.sciencedaily.com/releases/2021/01/210104114109.htm | In kefir, microbial teamwork makes the dream work | To make kefir, it takes a team. A team of microbes. | That's the message of new research from EMBL and Cambridge University's Patil group and collaborators, published in "Cooperation allows them to do something they couldn't do alone," says Kiran Patil, group leader and corresponding author of the paper. "It is particularly fascinating how L. kefiranofaciens, which dominates the kefir community, uses kefir grains to bind together all other microbes that it needs to survive -- much like the ruling ring of the Lord of the Rings. One grain to bind them all."Consumption of kefir originally became popular in Eastern Europe, Israel, and areas in and around Russia. It is composed of 'grains' that look like small pieces of cauliflower and have fermented in milk to produce a probiotic drink composed of bacteria and yeasts."People were storing milk in sheepskins and noticed these grains that emerged kept their milk from spoiling, so they could store it longer," says Sonja Blasche, a postdoc in the Patil group and joint first author of the paper. "Because milk spoils fairly easily, finding a way to store it longer was of huge value."To make kefir, you need kefir grains. These can't be artificially made, but must come from another batch of kefir. The grains are added to milk to ferment and grow. Approximately 24 to 48 hours later (or, in the case of this research, 90 hours later), the kefir grains have consumed the nutrients available to them. The grains grow in size and number in this time and the kefir process is complete. The grains are removed and added to fresh milk to begin the process anew.For scientists, however, kefir provides more than just a healthy beverage: it's an easy-to-culture model microbial community for studying metabolic interactions. And while kefir is quite similar to yogurt in many ways -- both are fermented or cultured dairy products full of 'probiotics' -- kefir's microbial community is far larger than yogurt's, including not just bacterial cultures but also yeast.While scientists know that microorganisms often live in communities and depend on their fellow community members for survival, mechanistic knowledge of this phenomenon has been quite limited. Laboratory models historically have been limited to two or three microbial species, so Kefir offered -- as Kiran describes -- a 'Goldilocks zone' of complexity that is not too small (around 40 species), yet not too unwieldy to study in detail.Sonja started this research by gathering kefir samples from several places. While most samples were obtained in Germany, they're likely to have originated elsewhere, since kefir grains have been passed down over centuries."Our first step was to look at how the samples grow. Kefir microbial communities have many member species with individual growth patterns that adapt to their current environment. This means fast- and slow-growing species and some that alter their speed according to nutrient availability," Sonja says. "This is not unique to the kefir community. However, the kefir community had a lot of lead time for co-evolution to bring it to perfection, as they have stuck together for a long time already."Finding out the extent and the nature of the cooperation between kefir microbes was far from straightforward. To do this, the researchers combined a variety of state-of-the-art methods such as metabolomics (studying metabolites' chemical processes), transcriptomics (studying the genome-produced RNA transcripts), and mathematical modelling. This revealed not only key molecular interaction agents like amino acids, but also the contrasting species dynamics between the grains and the milk part of kefir."The kefir grain acts as a base camp for the kefir community, from which community members colonise the milk in a complex yet organised and cooperative manner," Kiran says. "We see this phenomenon in kefir, and then we see it's not limited to kefir. If you look at the whole world of microbiomes, cooperation is also a key to their structure and function."In fact, in another paper from Kiran's group in collaboration with EMBL's Bork group, out today in | Microbes | 2,021 |
December 31, 2020 | https://www.sciencedaily.com/releases/2020/12/201231141454.htm | Asian tiger mosquito poses low risk for Zika virus outbreaks | The Asian tiger mosquito does not pose a major risk for Zika virus epidemics, according to a study published December 31 in the open-access journal | Zika virus has triggered large outbreaks in human populations, in some cases causing congenital deformities, fetal loss, or neurological problems in adults. While the yellow fever mosquito Aedes aegypti is considered the primary vector of Zika virus, the Asian tiger mosquito Aedes albopictus has been shown experimentally to transmit the virus and was involved in several transmissions of the virus in France in 2019. Originating from Southeast Asia, Ae. aegypti is an aggressive biter that has invaded the world and is now present on all inhabited continents, including temperate Europe, due to its ability to endure harsh winter conditions. As the second most important vector of human viral pathogens, Ae. albopictus is displacing Ae. aegypti populations due to competitive advantages. But it is not known if Ae. albopictus could trigger large-scale Zika virus epidemics.To address this question, the researchers exposed Ae. albopictus to Zika virus and assessed infection rates in experiments, modeled the dynamics of Zika virus infection within individual humans, and used epidemiological simulations. The highest risk of transmission occurred during the pre-symptomatic stage of the disease. At this dose, mosquito infection probability was estimated to be 20%, and 21 days were required to reach median systemic infection rates. Despite these unfavorable characteristics for transmission, Ae. albopictus was still able to trigger large outbreaks in a simulated environment in the presence of sufficiently high mosquito densities and biting rates. According to the authors, active surveillance and eradication programs should be implemented in territories occupied by Ae. albopictus to maintain the low risk of Zika virus outbreaks.The authors conclude, "The complementary combination of dose-dependent experimental infection, modeling of intra-human viremia dynamics, and in silico epidemiological simulations confirms the low epidemic potential of Aedes albopictus for Zika virus." | Microbes | 2,020 |
December 23, 2020 | https://www.sciencedaily.com/releases/2020/12/201223125726.htm | With COVID exacerbating superbug threat, researchers ID new weapon | As scientists around the globe wage war against a novel, deadly virus, one University of Colorado Boulder lab is working on new weapons to battle a different microbial threat: a rising tide of antibiotic-resistant bacteria which, if left unchecked, could kill an estimated 10 million people annually by 2050. | "The COVID-19 situation is definitely putting us at risk for increasing resistance to antibiotics, so it's more important now than ever that we come up with alternative treatments," said Corrie Detweiler, a professor of molecular, cellular and developmental biology who has spent her career seeking those alternatives.In a paper published Friday in the journal Along with their other recently published discoveries, the authors say, the finding could lead to a new arsenal for fighting what could be the next big public health threat."If we don't solve the problem of finding new antibiotics or somehow making old antibiotics work again, we are going to see sharply increasing deaths from bacterial infections we thought we had beaten decades ago," said Detweiler. "This study offers a totally new approach and could point the way toward new drugs that work better and have fewer side effects."In the United States alone, 35,000 people die annually from bacterial infections that could not be treated because they've grown resistant to existing drugs. Countless others suffer life-threatening bouts with once-easily treatable illnesses like strep throat, urinary tract infections and pneumonia. By 2050, the authors note, there could be more deaths from antibiotic resistance than from cancer."As our existing antibiotics adapt and work less, we risk essentially going back to a period 100 years ago, when even a minor infection could mean death," said Detweiler.The pandemic has shone even more light on the problem, she notes, as many patients die not from the virus itself but from hard-to-treat secondary bacterial infections.Meanwhile, she and other scholars worry that heightened use of antibiotics to prevent or treat those secondary infections, while at times necessary, may be exacerbating resistance.Most antibiotics in use today were developed in the 1950s, and pharmaceutical companies have since scaled back on research in the field in favor of more profitable ventures.To feed the pipeline, Detweiler's lab developed a technique called SAFIRE for screening for new small molecules which work differently than older drugs.Of 14,400 candidates screened from a library of existing chemicals, SAFIRE identified 70 that hold promise.The new paper centers around "JD1," which appears to be particularly effective at infiltrating what are known as "Gram-negative bacteria."With a tough exterior membrane that prevents antibiotics from accessing the cell, and another interior membrane providing a buffer, these bacteria (including But unlike other drugs, JD1 takes advantage of the host's initial immune assault on that outer bacterial membrane, then slips inside and goes after the inner membrane too."This is the first study to show that you can target a Gram-negative bacteria's inner membrane by exploiting the innate immune response of the host," Detweiler said.In laboratory and rodent experiments, JD1 reduced survival and spread of Gram-negative bacteria called But while it damaged the bacterial cell membranes, it couldn't penetrate the fine layer of cholesterol that lined its mammalian host's cell membranes."Bacteria are vulnerable to JD1 in a way that our cells are not," said Detweiler, noting that for this reason, side-effects would likely be minimal.Further studies are underway to explore JD1 and other compounds like it.Meanwhile, Detweiler has formed a spin-off company to help commercialize other compounds which work by inhibiting pumps, called "efflux pumps," that bacteria use to pump out antibiotics."The reality is, evolution is way smarter than all of the scientists put together and these bacteria will continue to evolve to resist what we throw at them," she said. "We cannot rest on our laurels. We have to keep feeding the pipeline." | Microbes | 2,020 |
December 22, 2020 | https://www.sciencedaily.com/releases/2020/12/201222192939.htm | Light flips genetic switch in bacteria inside transparent worms | Baylor College of Medicine researcher Meng Wang had already shown that bacteria that make a metabolite called colanic acid (CA) could extend the lifespan of worms in her lab by as much as 50%, but her collaboration with Rice University synthetic biologist Jeffrey Tabor is providing tools to answer the bigger question of how the metabolite imparts longer life. | In a study published in "Meng's group discovered that the CA compound could extend lifespan but they couldn't say for sure whether this was a dietary ingredient that was being digested in the stomach or a metabolite that was being produced by bacteria in the intestines," said Tabor, an associate professor of bioengineering and of biosciences at Rice. "We were able to restrict production of CA to the gut and show that it had a beneficial effect on cells in the intestines."For the experiments, Tabor's lab engineered strains of E. coli to make CA when exposed to green, but not red, light. To make sure the bacteria worked properly, the team added genes to make different colors of fluorescent proteins that would show up brightly under a microscope. One color was always present, to make it easy to see where the bacteria were inside the worms, and a second color was made only when the bacteria were producing CA.In collaboration with the Wang lab, Tabor's lab kept the bacteria under a red light and fed them to worms, a species called Caenorhabditis elegans (C. elegans) that's commonly used in life sciences. Researchers tracked the bacteria's progress through the digestive tract and switched on the green light when they made it to the intestines."When exposed to green light, worms carrying this E. coli strain also lived longer. The stronger the light, the longer the lifespan," said Wang, the Robert C. Fyfe Endowed Chair on Aging, a professor of molecular and human genetics at the Huffington Center on Aging at Baylor and a Howard Hughes Medical Institute investigator.In the cells of C. elegans and other higher order life, from humans to yeast, specialized organelles called mitochondria supply most of the energy. Thousands of mitochondria work around the clock in each cell and maintain a dynamic balance between fission and fusion, but they become less efficient over time. As people and other organisms age, the dysfunction of mitochondria leads to functional decline in their cells.In prior experiments with C. elegans, Wang and colleagues showed that CA can regulate the balance between mitochondrial fission and fusion in both intestinal and muscle cells to promote longevity. The worms typically live about three weeks, but Wang's lab has shown that CA can extend their lives to 4.5 weeks -- 50% longer than usual.Tabor said this raises a host of questions. For instance, if CA is produced in the gut, do intestinal cells benefit first? Is the beneficial effect of CA related to its level? And most important, do the mitochondrial benefits spread throughout the body from the intestines?In the "With our technology, we can use light to turn on CA production and watch the effect travel through the worm," Tabor said.He said the precision of the optogenetic technology could allow researchers to ask fundamental questions about gut metabolism."If you can control the timing and location of metabolite production with precision, you can think about experimental designs that show cause and effect," he said.Showing that gut bacteria directly impact health or disease would be a major achievement."We know gut bacteria affect many processes in our bodies," Tabor said. "They've been linked to obesity, diabetes, anxiety, cancers, autoimmune diseases, heart disease and kidney disease. There's been an explosion of studies measuring what bacteria you have when you have this illness or that illness, and it's showing all kinds of correlations."But there is a big difference between showing correlation and causality, Tabor said."The goal, the thing you really want, is gut bacteria you can eat that will improve health or treat disease," he said.But it's difficult for researchers to prove that molecules produced by gut bacteria cause disease or health. That's partly because the gut is difficult to access experimentally, and it's especially difficult to design experiments that show what is happening in specific locations inside the gut."The gut is a hard place to access, especially in large mammals," Tabor said. "Our intestines are 28 feet long, and they're very heterogeneous. The pH changes throughout and the bacteria change quite dramatically along the way. So do the tissues and what they're doing, like the molecules they secrete."To answer questions about how gut bacteria influence our health, you need to be able to turn on genes in specific places and at particular times, like when an animal is young or when an animal wakes up in the morning," he said. "You need that level of control to study pathways on their own turf, where they happen and how they happen."Because it uses light to trigger genes, optogenetics offers that level of control, Tabor said."To this point, light is really the only signal that has enough precision to turn on bacterial genes in the small versus the large intestine, for example, or during the day but not at night," he said.Tabor said he and Wang have discussed many ways they might use optogenetics to study aging."She's found two dozen bacterial genes that can extend lifespan in C. elegans, and we don't know how most of them work," Tabor said. "The colanic acid genes are really intriguing, but there are many more that we'd like to turn on with light in the worm to figure out how they work. We can use the exact technique that we published in this paper to explore those new genes as well. And other people who are studying the microbiome can use it too. It's a powerful tool for investigating how bacteria are benefiting our health." | Microbes | 2,020 |
December 21, 2020 | https://www.sciencedaily.com/releases/2020/12/201221204058.htm | Antibiotics for C-sections effective after umbilical cord clamped | Antibiotics for cesarean section births are just as effective when they're given after the umbilical cord is clamped as before clamping -- the current practice -- and could benefit newborns' developing microbiomes, according to Rutgers co-authored research. | The study, by far the largest of its kind and published in the journal "Most national and international guidelines, including those of the World Health Organization, recommend that women receive antibiotics before the skin incision for cesarean section," said co-author Maria Gloria Dominguez-Bello, Henry Rutgers Professor of Microbiome and Health, professor of microbiology and anthropology, and director of the New Jersey Institute for Food, Nutrition, and Health in the School of Environmental and Biological Sciences at Rutgers University-New Brunswick. "That exposes the baby to antibiotics during birth, affecting the microbiome assembly in the newborn. Early disturbance of bacterial colonization and the developing healthy microbiome may have consequences for immune development, leading to immune malfunctions later in life."A healthy microbiome helps guard against infection and antibiotics disrupt the microbiome, wiping out both bad and good bacteria, according to the U.S. Centers for Disease Control and Prevention. Even stressors perceived as small, such as a hospital birth, can affect the neonatal microbiome, as shown by Dominguez-Bello's group in a 2018 study, and perturbations of the microbiome in early life possibly affect development of immunity and metabolism.Administering antibiotics to prevent infections of the surgical site is common practice and justified to minimize risks. But for cesarean section, the impact of antibiotics on the newborn and its developing microbiome should be considered, as well as the risk of infection, Dominguez-Bello said. Giving mothers antibiotics after clamping avoids additional stressors that impair transmission and colonization of maternal microbes after birth, so the current recommendation for antibiotics before clamping should be revised.The study, led by Rami Sommerstein at Bern University Hospital in Switzerland, covered 55,901 women at 75 hospitals in Switzerland from 2009 to 2018. They include 26,405 patients who received antibiotics before skin incisions for C-sections and 29,496 patients after their umbilical cords were clamped.Of the 846 documented infections after C-sections, 379 (1.6 percent) occurred in women who received antibiotics before incisions and 449 (1.7 percent) occurred in those who received antibiotics after their umbilical cords were clamped, with no statistical differences."That means receiving antibiotics after umbilical cords are clamped to protect against maternal infections is as effective as receiving them before incisions," Dominguez-Bello said. "The guidance on the best timing for antibiotic use should be reevaluated to help promote the development of a healthy microbiome, which is essential for normal immune system development in babies. Bypassing the birth canal is already a stressor that should not be aggravated by the effect of antibiotics in the newborn." | Microbes | 2,020 |
December 21, 2020 | https://www.sciencedaily.com/releases/2020/12/201221121807.htm | Evolution of a killer: How African Salmonella made the leap from gut to bloodstream | University of Liverpool scientists have exploited the combined power of genomics and epidemiology to understand how a type of Salmonella bacteria evolved to kill hundreds of thousands of immunocompromised people in Africa. | Bloodstream infections caused by a drug-resistant type of Salmonella Typhimurium called ST313 are a major public health concern in Africa, where the disease is endemic and causes ~50,000 deaths each year. What was missing was an understanding of the timing of the major evolutionary events that equipped African Salmonella to cause bloodstream infections in humans.In a new paper published in The study was led by Professor Jay Hinton at the University of Liverpool, who has been researching Salmonella for more than 30 years and leads the 10,000 Salmonella Genomes Project -- a worldwide effort to understand the epidemiology, transmission and virulence of invasive non-Typhoidal Salmonellosis.Professor Hinton said: "Through a remarkable team effort we have removed some of the mystery about the evolution of African Salmonella. We hope that by learning how these pathogens became able to infect the human bloodstream we will be better prepared to tackle future bacterial epidemics."In the study, scientists sequenced the genomes of 680 Salmonella isolates, from archives kept by the Malawi Liverpool Wellcome Trust (MLW) clinical research programme and the Institute Pasteur, and used them to uncover the timeline of crucial genetic events responsible for the infection of immunocompromised humans by S. Typhimurium ST313. Mutations that influenced gene function during the evolution of ST313 were identified for the first time.The team also discovered a new antibiotic-susceptible lineage of ST313 that emerged in Malawi in 2016 and is closely related to Salmonella variants that cause stomach infections in the United Kingdom and Brazil. The researchers speculate that changes in antibiotic usage in Malawi between 2002 and 2015 could have created a window of opportunity for the emergence of this new antibiotic-susceptible ST313 lineage.Dr Caisey Pulford, who carried out much of the research as part of her PhD, said: "By combining the power of genomic analysis with epidemiology, clinical observations and functional insights, we have shown the value of using an integrated approach to link scientific research with public health."The study was carried out by researchers from the University of Liverpool, University of Malawi, Queens University Belfast, Institut Pasteur, the Earlham Institute and the Malawi-Liverpool-Wellcome Trust (MLW) Clinical Research Programme. | Microbes | 2,020 |
December 18, 2020 | https://www.sciencedaily.com/releases/2020/12/201218165105.htm | The incredible, variable bacteria living in your mouth | Bacteria often show very strong biogeography -- some bacteria are abundant in specific locations while absent from others -- leading to major questions when applying microbiology to therapeutics or probiotics: how did the bacteria get into the wrong place? How do we add the right bacteria into the right place when the biogeography has gotten 'out of whack'? | These questions, though, have one big obstacle, bacteria are so tiny and numerous with very diverse and complicated populations which creates major challenges to understanding which subgroups of bacteria live where and what genes or metabolic abilities allow them to thrive in these 'wrong' places.In a new study published in "As microbial ecologists, we are fascinated by how bacteria can seemingly divide up any habitat into various niches, but as humans ourselves, we also have this innate curiosity about how microbes pattern themselves within our bodies," said lead author Daniel R. Utter, PhD candidate in the Department of Organismic and Evolutionary Biology, Harvard University.Recent developments in sequencing and bioinformatic approaches have offered new ways to untangle the complexity of bacterial communities. Utter and Colleen Cavanaugh, Edward C. Jeffrey Professor of Biology in the Department of Organismic and Evolutionary Biology, Harvard University, teamed up with researchers at the Marine Biological Laboratory, Woods Hole, University of Chicago, and The Forsyth Institute to apply these state-of-the-art sequencing and analysis approaches to get a better picture of the oral microbiome."The mouth is the perfect place to study microbial communities," according to co-author A. Murat Eren, assistant professor in the Department of Medicine at the University of Chicago. "Not only is it the beginning of the GI tract, but it's also a very special and small environment that's microbially diverse enough that we can really start to answer interesting questions about microbiomes and their evolution."The mouth contains a surprising amount of site-specific microbes in different areas. For instance, the microbes found on the tongue are very different from the microbes found on the plaque on teeth. "Your tongue microbes are more similar to those living on someone else's tongue than they are to those living in your throat or on your gums!" said Eren.The team scoured public databases and downloaded 100 genomes that represented four species of bacteria commonly found in the mouth, "We used these genomes as a starting point, but quickly moved beyond them to probe the total genetic variation among the trillions of bacterial cells living in our mouths," said Utter. "Because, at the end of the day, that's what we're curious about, not the arbitrary few that have been sequenced."Using this recently-developed approach called metapangenomics, which combines pangenomes (the sum of all genes found in a set of related bacteria) with metagenomics (the study of the total DNA coming from all bacteria in a community), allowed the researchers to conduct an in-depth examination of the genomes of the microbes which led to a shocking discovery."We found a tremendous amount of variability," said Utter. "But we were shocked by the patterning of that variability across the different parts of the mouth; specifically, between the tongue, cheek, and tooth surfaces."For example, within a single microbe species the researchers found distinct genetic forms that were strongly associated to a single, different site within the mouth. In many cases, the team was able to identify a handful of genes that might explain a particular bacterial group's specific habitat. Applying metapangenomics the researchers were also able to identify specific ways free-living bacteria in people's mouths differed from their lab-grown relatives."The resolution afforded by these techniques -- via the direct comparison of genomes of "domesticated" and "wild" bacteria -- allows us to dissect these differences gene by gene," notes Cavanaugh. "We were also able to identify novel bacterial strains related to, but different than, those we have in culture.""Having identified some really strong bacterial candidates that could determine adaptation to a particular habitat, we would like to experimentally test these hypotheses," said Cavanaugh. These findings could potentially be the key to unlocking targeted probiotics, where scientists could use what's been learned about each microbe's habitat's requirements to engineer beneficial microbes to land in a specified habitat."The mouth is so easily accessible that people have been working on bacteria from the mouth for a long time," said co-author Jessica Mark Welch, associate scientist at the Marine Biological Laboratory."Every environment we look at has these really complicated, complex communities of bacteria, but why is that?" said Mark Welch. "Understanding why these communities are so complex and how the different bacteria interact will help us better understand how to fix a bacterial community that's damaging our health, telling us which microbes need to be removed or added back in."This study and others like it can provide new insights on the role of oral microbes in human health. "The ability to identify specific genes behind habitat adaptation has been somewhat of a 'holy grail' in microbial ecology," said Utter. "We are very excited for our contributions in this area!" | Microbes | 2,020 |
December 18, 2020 | https://www.sciencedaily.com/releases/2020/12/201218152727.htm | Researchers propose process to detect and contain emerging diseases | A University of Arkansas biologist is part of a global team of researchers developing a strategy to detect and intercept diseases emerging from wildlife in Africa that could eventually infect humans. | Assistant professor Kristian Forbes, along with colleagues from Africa, Europe and North America, have proposed a four-part approach to detect and contain zoonotic diseases, those that begin in animals but spillover into humans, like COVID-19 and HIV."A lot of research effort to prepare against the threat of novel disease emergences of wildlife viruses has been to identify unknown viruses in wildlife that might someday infect humans," Forbes said. "These efforts have been very successful for identifying new viruses; indeed, thousands have been discovered, but we don't currently have the tools to know which of them pose the most immediate risks to human health."To enable fast detection of new zoonotic disease outbreaks, the team proposes a system of procuring and screening samples from hospital patients with fevers of unknown origin, analyzing samples from suspicious fatalities of unknown cause, testing blood serum in high-risk or sentinel groups and analyzing samples that have already been collected and archived. The team outlined their approach in a recent article published in the journal None of these methods are new, Forbes said. But to date they have not been combined into a continent-wide program aimed at rapid detection."Given limitations to the current model for preventing disease emergences, our article focuses on a coordinated and widespread strategy for early detection so that novel disease outbreaks can be intercepted before they potentially become global pandemics." | Microbes | 2,020 |
December 17, 2020 | https://www.sciencedaily.com/releases/2020/12/201217135357.htm | New recipe for antibiotic could prevent deafness | A new method of purifying gentamicin, a widely used antibiotic, reduces the risk that it will cause deafness, according to a Stanford Medicine-led study. | Gentamicin is used in U.S. hospitals to treat a variety of bacterial infections, including infections in newborns and in other susceptible patients, such as those with cystic fibrosis. It's a popular drug in developing countries because it is highly effective and inexpensive. Yet researchers estimate that up to 20% of patients who are treated with it experience some degree of irreversible hearing loss.Now, researchers have found a relatively inexpensive way to reformulate the drug, which belongs to a class of antibiotics called aminoglycosides, to be safer. Their findings were published Dec. 7 in the "When a drug causes hearing loss, it is devastating, and it's especially disturbing when it happens to a young child, as they rely on hearing to acquire speech," said Alan Cheng, MD, a professor of otolaryngology at the Stanford School of Medicine. He shares senior authorship of the study with Anthony Ricci, PhD, also a professor of otolaryngology at Stanford and the Edward C. and Amy H. Sewall Professor II in the School of Medicine. Cheng is the Edward C. and Amy H. Sewall Professor IV in the School of Medicine. Postdoctoral scholar Mary O'Sullivan, PhD, is the lead author."We've developed a simple method of reformulating the drug that should be put to use as soon as possible," Ricci said. The researchers will be writing to the Food and Drug Administration to recommend changes to the organization's requirements for how drug companies make gentamicin."Currently, the FDA's instructions for how to make aminoglycosides are making people go deaf," Ricci said.Aminoglycosides have been in use since the 1950s. The drugs don't need to be refrigerated, which keeps the costs of storing them low. Despite new antibiotics, their use remains commonplace as they are cheap and potent."These drugs are used because they save a lot of lives," Ricci said. "We've stopped paying attention to their toxic side effects because living with hearing loss is better than dying."The gentamicin used in hospitals today is a mixture of five different subtypes of the antibiotic grown together in the same mixture. The mixture also includes as much as 10% impurities. Using methods such as high-performance liquid chromatography and nuclear magnetic resonance imaging, the researchers tried to figure out how to chemically separate each of the subtypes so they could be tested separately. Once the researchers established methods of separating the different parts of the mixture, they tested these various subtypes of gentamicin individually on inner-ear tissues from animals. They identified the least toxic subtype as C2b, and the most toxic as sisomicin. Both C2b and sisomicin showed the same highly effective antimicrobial properties comparable to the mixture as a whole. The researchers also found that by removing impurities from the mixture, toxicity to the ear tissue was reduced."What this study shows is that the formulation that is currently in a hospital bottle of gentamicin is not optimized," Ricci said. The ingredients are required by both federal and international law; one of those is sisomicin, the subtype found to be most toxic to the ear tissue."If we just use the subtype that's less toxic or change the formulation of this bottle, we can make the drug much less ototoxic," Ricci said, referring to harm to the ear. Given that the subtypes are all approved by the Food and Drug Administration, new formulations don't necessarily need to be retested in humans and could get to patients fast.The researchers are also working on plans to create a new aminoglycoside that could further reduce the risk of hearing loss, Ricci said. They've discovered that the inner-ear toxicity of the various subtypes highly correlates with the way they bind to the ion channels that open to the inner ear."This discovery lays the groundwork for the discovery of safer antibiotic alternatives and future drug development," he said. | Microbes | 2,020 |
December 16, 2020 | https://www.sciencedaily.com/releases/2020/12/201216134644.htm | An atlas of S. pneumoniae and host gene expression during colonization and disease | The bacteria Streptococcus pneumoniae colonizes the nasopharynx and can cause pneumonia. Then, it can spread from the lungs to the bloodstream and cause organ damage. This opportunistic pathogen commonly infects young children, those who are immunocompromised and the elderly. In 2015, S. pneumoniae infections worldwide killed an estimated 192,000 to 366,000 children under age 5. | To understand how this pathogen adapts to different locations in the body, and also how the host responds to the invading microbe, researchers at the University of Alabama at Birmingham, the University of Maryland School of Medicine and Yale University School of Medicine measured bacterial and host gene expression at five different sites in a mouse model -- the nasopharynx, lungs, blood, heart and kidneys -- using three genetically different strains of S. pneumoniae.Their resulting in vivo atlas of host-pathogen interactions at disease-relevant anatomical sites is now published in This means the bacterium behaves differently, depending on which site it infects, and that the mouse organs, in turn, also respond differently to the presence of bacteria. Additionally, certain S. pneumoniae genes were found to always be highly expressed by all three strains of bacteria at all anatomical sites, which makes them ideal targets for new vaccines or therapies.This was the first time that gene expression profiles during colonization and at multiple host infection sites were mapped from both the host and the pathogen perspectives."We believe that the atlas of transcriptional responses during host-pathogen interactions presented here," the authors wrote, "will constitute an essential resource for the pneumococcal and microbial pathogenesis research communities and serve as a foundation for identification and validation of key host and pneumococcal therapeutic targets in future studies."Carlos J. Orihuela, Ph.D., professor in the UAB Department of Microbiology, and Hervé Tettelin, Ph.D., professor in the University of Maryland School of Medicine Department of Microbiology and Immunology, are co-senior authors.Besides a descriptive analysis of the transcriptomes, researchers confirmed their findings using bacterial mutants, in vivo challenge experiments and host treatments. In challenge experiments, the researchers found that an interferon beta anti-inflammatory treatment prevented the bacteria from invading vital organs and promoted host survival. This finding offers potentially new therapeutic avenues.Symptoms of pneumococcal infection include fever, cough, shortness of breath, chest pain, stiff neck, confusion, increased sensitivity to light, joint pain, chills, ear pain, sleeplessness and irritability. While advances in antibiotics and the use of pneumococcal conjugate vaccines since 2000 have lowered deaths attributable to S. pneumoniae, the pathogen continues to show an increase in antibiotic resistance, and it also can switch to capsule types that are not covered by the current United States Food and Drug Administration-approved vaccines. Thus, pneumococcal infections continue to be a significant cause of illness and death.Support came from the Merck, Sharpe & Dohme Corp. Merck Investigator Studies Program award IISP ID#: 57329 and from National Institutes of Health grant AI114800. | Microbes | 2,020 |
December 16, 2020 | https://www.sciencedaily.com/releases/2020/12/201216104643.htm | New salmonella proteins discovered | Salmonella are bacteria that can cause food poisoning with severe diarrhea. If they penetrate from the intestine into the blood system, this can lead to sepsis, life-threatening inflammatory reactions in the entire organism. Since salmonellae are also becoming increasingly resistant to antibiotics, new approaches are being sought to combat them. | An international research team, led by scientists from Würzburg, shows how to succeed in this search in the new research journal In a bioinformatic reassessment of the Salmonella genome, the team led by JMU doctoral student Elisa Venturini identified many unknown small proteins that may play a crucial role in infection. As a result, the number of known small Salmonella proteins has grown by 139 to over 600.The small protein MgrB, which consists of 47 amino acids, stood out in the analyses. If the gene containing the blueprint for this protein is switched off, the salmonellae can no longer infect human cells. Although the protein had been studied before, this important function had not been recognised. This has only now been achieved thanks to a new combinatorial approach. Among other things, three data sets that had been generated in earlier infection studies were used for this purpose."Hopefully our approach will provide a blueprint that can also be applied to other organisms for which data sets already exist," says Venturini. The study has clearly shown that the method can still bring new relevant genes to light even in comprehensively studied organisms such as salmonella: The scientific community now has a priority list of previously unknown infection-related small salmonella proteins for further investigation. | Microbes | 2,020 |
December 15, 2020 | https://www.sciencedaily.com/releases/2020/12/201215175758.htm | An avocado a day keeps your gut microbes happy, study shows | Eating avocado as part of your daily diet can help improve gut health, a new study from University of Illinois shows. Avocados are a healthy food that is high in dietary fiber and monounsaturated fat. However, it was not clear how avocados impact the microbes in the gastrointestinal system or "gut." | "We know eating avocados helps you feel full and reduces blood cholesterol concentration, but we did not know how it influences the gut microbes, and the metabolites the microbes produce," says Sharon Thompson, graduate student in the Division of Nutritional Sciences at U of I and lead author on the paper, published in the The researchers found that people who ate avocado every day as part of a meal had a greater abundance of gut microbes that break down fiber and produce metabolites that support gut health. They also had greater microbial diversity compared to people who did not receive the avocado meals in the study."Microbial metabolites are compounds the microbes produce that influence health," Thompson says. "Avocado consumption reduced bile acids and increased short chain fatty acids. These changes correlate with beneficial health outcomes."The study included 163 adults between 25 and 45 years of age with overweight or obesity -- defined as a BMI of at least 25 kg/m2 -- but otherwise healthy. They received one meal per day to consume as a replacement for either breakfast, lunch, or dinner. One group consumed an avocado with each meal, while the control group consumed a similar meal but without the avocado. The participants provided blood, urine, and fecal samples throughout the 12-week study. They also reported how much of the provided meals they consumed, and every four weeks recorded everything they ate.While other research on avocado consumption has focused on weight loss, participants in this study were not advised to restrict or change what they ate. Instead they consumed their normal diets with the exception of replacing one meal per day with the meal the researchers provided.The purpose of this study was to explore the effects of avocado consumption on the gastrointestinal microbiota, says Hannah Holscher, assistant professor of nutrition in the Department of Food Science and Human Nutrition at U of I and senior author of the study."Our goal was to test the hypothesis that the fats and the fiber in avocados positively affect the gut microbiota. We also wanted to explore the relationships between gut microbes and health outcomes," Holscher says.Avocados are rich in fat; however, the researchers found that while the avocado group consumed slightly more calories than the control group, slightly more fat was excreted in their stool."Greater fat excretion means the research participants were absorbing less energy from the foods that they were eating. This was likely because of reductions in bile acids, which are molecules our digestion system secretes that allow us to absorb fat. We found that the amount of bile acids in stool was lower and the amount of fat in the stool was higher in the avocado group," Holscher explains.Different types of fats have differential effects on the microbiome. The fats in avocados are monounsaturated, which are heart-healthy fats.Soluble fiber content is also very important, Holscher notes. A medium avocado provides around 12 grams of fiber, which goes a long way toward meeting the recommended amount of 28 to 34 grams of fiber per day."Less than 5% of Americans eat enough fiber. Most people consume around 12 to 16 grams of fiber per day. Thus, incorporating avocados in your diet can help get you closer to meeting the fiber recommendation," she notes.Eating fiber isn't just good for us; it's important for the microbiome, too, Holscher states. "We can't break down dietary fibers, but certain gut microbes can. When we consume dietary fiber, it's a win-win for gut microbes and for us."Holscher's research lab specializes in dietary modulation of the microbiome and its connections to health. "Just like we think about heart-healthy meals, we need to also be thinking about gut healthy meals and how to feed the microbiota," she explains.Avocado is an energy-dense food, but it is also nutrient dense, and it contains important micronutrients that Americans don't eat enough of, like potassium and fiber."It's just a really nicely packaged fruit that contains nutrients that are important for health. Our work shows we can add benefits to gut health to that list," Holscher says.The paper, "Avocado consumption alters gastrointestinal bacteria abundance and microbial metabolite concentrations among adults with overweight or obesity: a randomized controlled trial" is published in the Authors are Sharon Thompson, Melisa Bailey, Andrew Taylor, Jennifer Kaczmarek, Annemarie Mysonhimer, Caitlyn Edwards, Ginger Reeser, Nicholas Burd, Naiman Khan, and Hannah Holscher.Funding for the research was provided by the Hass Avocado Board and the USDA National Institute of Food and Agriculture, Hatch project 1009249. Sharon Thompson was supported by the USDA National Institute of Food and Agriculture AFRI Predoctoral Fellowship, project 2018-07785, and the Illinois College of ACES Jonathan Baldwin Turner Fellowship. Jennifer Kaczmarek was supported by a Division of Nutrition Sciences Excellence Fellowship. Andrew Taylor was supported by a Department of Food Science and Human Nutrition Fellowship. The Division of Nutritional Sciences provided seed funding through the Margin of Excellence endowment.The Division of Nutritional Sciences and the Department of Food Science and Human Nutrition are in the College of Agricultural, Consumer and Environmental Sciences, University of Illinois. | Microbes | 2,020 |
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