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84,483 | If mitochondria exist at random within a cell, isn't there a possibility that cell division will result in a daughter cell with no mitochondria? If not, what is the process for guaranteeing at least one is present in each daughter cell? If so, what happens to that cell? | Isn't there a possibility that cell division will result in a daughter
cell with no mitochondria? Yes, there is always the possibility. However, there must be a strong negative selection pressure against eukaryotic life that cannot achieve the proper partitioning of mitochondria, so you can imagine that there are mechanisms in place to prevent this case. Mitochondria are both passively and actively partitioned to daughter cells. This is understood to occur through the cytoskeleton and with the control of mitochondrial fusion and fission at key stages of the cell cycle, prior to mitosis and cytokinesis! Here is a great review from several years ago that addresses your question well. | {
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84,525 | This question: Can you get enough water by eating only fish? asks if a person could survive on fish alone. Can a person survive on fish and/ or blood alone of any species if stuck at sea or animal blood as a last resort where there is no water or fire? Obviously if it was a fresh water fish there is water, but there are fresh water mud skippers that can breathe air and the water to tainted to drink in that case a fresh water fish blood maybe safer than the water. https://chemistry.stackexchange.com/questions/115901/what-can-i-eat-that-will-help-metabolize-blood Desalination would be the best way to process the blood but this is in emergency situation scenario. From @PTwr Comment's Link: If you drink blood regularly, over a long period of time the buildup of iron in your system can cause iron overload. This syndrome, which sometimes affects people who have repeated blood transfusions, is one of the few conditions for which the correct treatment is bloodletting. https://what-if.xkcd.com/98/ | Blood is not a good source of water. 1 liter of blood contains about 800 mL of water, 170 grams of protein and 2 grams of sodium (calculated from the composition of lamb blood ). When metabolized, 170 grams of protein yields the amount of urea that requires 1,360 mL of water to be excreted in urine (calculated from here ); 2 grams of sodium requires about 140 mL of water to be excreted (from here ). This means that drinking 1 liter of blood, which contains 800 mL of water, will result in 1,500 mL of water loss through the kidneys, which will leave you with 700 mL of negative water balance. Fish blood can contain less protein, for example, trout (check Table 1) contains about 120 g of protein (plasma protein + hemoglobin) per liter of blood. Using the same calculation as above (1 g protein results in the excretion of 8 mL of urine), drinking of 1 liter of trout blood, which contains about 880 mL of water, will result in 960 mL of urine, so in 80 mL of negative water balance. Turtle blood can contain about 80 g of protein (plasma protein + hemoglobin) and 3.4 g of sodium per liter. Drinking 1 liter of turtle blood, which contains about 920 mL of water, will result in 80 x 8 mL = 640 mL loss of urine due to protein, and ~240 mL due to sodium, which is 880 mL of urine in total. This leaves you with 40 mL of positive water balance (to get 2 liters of water per day you would need to drink 50 liters of turtle blood, which isn't realistic. In various stories ( The Atlantic , The Diplomat , The Telegraph ), according to which people have survived by drinking turtle blood, they have also drunk rainwater, so we can't conclude it was turtle blood that helped them. I'm not aware of any story that would provide a convincing evidence that the blood of turtle or any other animal is hydrating. | {
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84,738 | This cool design was "tattooed" on this leaf. I found it on the windshield of my car. What's up with it? | That is the work of a leaf miner. A leaf miner is the larval stage of an insect that feeds on the inside layer of leaves. Notice how the galleries (tunnels) start small and then get larger as the larva matures? Most leaf miners are moth larvae (Lepidoptera) https://en.wikipedia.org/wiki/Leaf_miner | {
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85,915 | In this paper of the WHO, it is claimed that we should limit our consumption of free sugars: WHO recommends a reduced intake of free sugars throughout the
lifecourse. [...] Free sugars include monosaccharides and
disaccharides added to foods and beverages by the manufacturer, cook
or consumer, and sugars naturally present in honey, syrups, fruit
juices and fruit juice concentrates. At first, I was wondering if the sugars in a fruit can be different from sugars in a juice. According to the answer to my question here , the sugar molecules are exactly the same in both (in the case of a 100% pure juice). So, why this recommendation? Why doesn't our body digest sugars from fresh fruit the same way as sugars from juice? To make it simple, my question only concerns 100% pure juice with no added sugars. I tried to find an answer and, according to the answers of this question , because our body is slow to digest sugars from a fruit, it assimilates it better. Is it right? And, if it is the case, if we eat fiber and starch with our fruit juice, it should be the same as a fresh fruit, right? | Sugars in 100% natural fruit juices are chemically the same as in whole fruits. They mainly include glucose, fructose and sucrose: Apple nutrition data (expand the carbohydrate section) Apple juice nutrition data Sugars in whole fruits are "incorporated" into the fruit, which means the digestive system first needs to physically decompose the fruit and then extract and absorb sugars, which takes some time. In fruit juices, sugars are "free," so they are absorbed quicker than from whole fruits, which results in higher blood glucose levels, which is a risk factor for diabetes type 2 ( Defeatdiabetes , Diabetes.co.uk ). Also, fruit juices are liquid, so they pass through the stomach quicker than whole fruits, so they fill the stomach for a shorter time and may be therefore less satiating. This can make you drink more juice than you intended, which can result in unwanted weight gain. If you eat foods high in fiber along with juice, the fiber will slow down the absorption of sugars from the juice ( Nutrients ). If you eat foods that contain mainly plain starch (white bread, cookies or rice, or potatoes) along with juice, the starch will be quickly digested and absorbed as glucose and will raise the blood glucose even quicker than the sugar from the juice. The effect of nutrients from foods on blood glucose level after meals is expressed as glycemic index (GI): the higher the GI, the higher blood glucose ( Harvard ): Glucose = 100 Cornflakes (mainly plain starch) = 81 Potato, boiled (mainly plain starch) = 78 White bread (mainly plain starch) = 75 White rice (mainly plain starch) = 73 Sucrose = 65 Honey = 61 Apple juice = 41 Apple: = 36 Kidney beans (high in fiber) = 24 Fructose = 15 In conclusion, natural sugars from whole fruits, fruit juices and artificially added sugars are all digested in the same way, but sugars from juices are absorbed quicker, which can result in higher blood glucose levels. Foods that contain mainly plain starch can raise the blood glucose levels much more than fruits and fruit juices. | {
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85,983 | At about 11 pm, I heard a loud impact on the nearby glass door to a second-floor balcony. I thought it might be an acorn but it'd be a very unlikely angle - it'd have to be thrown from below or be a very strange ricochet. So I looked and encountered this rather impressive creature recovering on the balcony: Those planks are six inches wide. I've never seen one of these before. What is it? Are those giant serrated appendages on the front mandibles or antennae? I expect it's not as hazardous as it looks, but is there any risk of it biting people or pets? Do they routinely launch themselves two stories into the air, or would it have crawled up and then just bounded from the balcony floor? Location: Southern Oregon, USA. | Sugars in 100% natural fruit juices are chemically the same as in whole fruits. They mainly include glucose, fructose and sucrose: Apple nutrition data (expand the carbohydrate section) Apple juice nutrition data Sugars in whole fruits are "incorporated" into the fruit, which means the digestive system first needs to physically decompose the fruit and then extract and absorb sugars, which takes some time. In fruit juices, sugars are "free," so they are absorbed quicker than from whole fruits, which results in higher blood glucose levels, which is a risk factor for diabetes type 2 ( Defeatdiabetes , Diabetes.co.uk ). Also, fruit juices are liquid, so they pass through the stomach quicker than whole fruits, so they fill the stomach for a shorter time and may be therefore less satiating. This can make you drink more juice than you intended, which can result in unwanted weight gain. If you eat foods high in fiber along with juice, the fiber will slow down the absorption of sugars from the juice ( Nutrients ). If you eat foods that contain mainly plain starch (white bread, cookies or rice, or potatoes) along with juice, the starch will be quickly digested and absorbed as glucose and will raise the blood glucose even quicker than the sugar from the juice. The effect of nutrients from foods on blood glucose level after meals is expressed as glycemic index (GI): the higher the GI, the higher blood glucose ( Harvard ): Glucose = 100 Cornflakes (mainly plain starch) = 81 Potato, boiled (mainly plain starch) = 78 White bread (mainly plain starch) = 75 White rice (mainly plain starch) = 73 Sucrose = 65 Honey = 61 Apple juice = 41 Apple: = 36 Kidney beans (high in fiber) = 24 Fructose = 15 In conclusion, natural sugars from whole fruits, fruit juices and artificially added sugars are all digested in the same way, but sugars from juices are absorbed quicker, which can result in higher blood glucose levels. Foods that contain mainly plain starch can raise the blood glucose levels much more than fruits and fruit juices. | {
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85,990 | Chromosome 1 is the designation for the largest human chromosome. Humans have two copies of chromosome 1, as they do with all of the autosomes, which are the non-sex chromosomes. Chromosome 1 spans about 249 million nucleotide base pairs, which are the basic units of information for DNA. It represents about 8% of the total DNA in human cells. Why is Chromosome 1 called Chromosome 1? Is being the largest human chromosome the only reason? | Chromosomes were first known about from karyograms (that's the word for chromosome pictures like these) sort of like this one (1)(2): The scientists looking at these chromosomes didn't know much about them at first. They were discovered before anything was understood about genes, but by 1922 it was thought they were the carriers of genes. Without much understanding of the chromosomes, and certainly no understanding of what they carried, scientists needed an easy way to order and compare them. They chose a straight forward option - size - and paired them up and then lined them up biggest to smallest. Because the sex chromosomes didn't fit into this scheme of matching pairs they were left to the end. Hence Chromosome 1 is Chromosome 1 because it is the largest autosomal chromosome . Notes: The actual first karyogram was of a plant, this one is of a human male. The image above is public domain, obtained from Wikipedia, and originally made by the National Human Genome Research Institute. | {
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86,435 | It is well known that UV radiation can damage the DNA and generally harm our skin.
We also know that UV radiation helps on the production of melanin and Vitamin D. From what I could find, the DNA absorption spectrum goes to almost zero for wavelengths higher than 300 nm. This seems to suggest that we would be safe to use UV radiation between 300 and 340 nm in our skin (as long as the power or exposure is not too high/long to make burns), for therapeutic purposes such as the stimulation of Vitamin D production. Is this assumption correct? Are there any evidences that we could use this UV wavelength range safely? | You're talking about long-wave UV, or UV-A radiation. In the 80s, experts claimed that this was a safe wavelength. Protection against UV-A was not part of sunscreen in the early days. Consequently, UV-A was (and still is) used in tanning beds due to its perceived safety over UV-B. However, a lot of research has been done since. UV-A is well understood now to also be unsafe in unreasonable amounts. Currently, UV-A protection is a typical feature of sunscreen and tanning beds are still not a healthy alternative to moderate, healthy doses of sun. Here is a recent review covering some of the aspects comparing different UV range effects on skin. I really suggest you put a search engine to good use here; it makes little sense for us to expound on the literature when it is so clear and easily available. In summary, UVA certainly contributes to the development of skin cancer. UVA penetrates deeper into the skin than UV-B (which is largely responsible for 'burning' of the topmost layer of skin, without directly affecting the deeper layers). For this reason, UV-B is associated primarily with burning and UV-A is primarily associated with aging and aging diseases like cancer. It is important to note that 95% of UV light in every day life is UV-A, because it does not vary seasonally and can penetrate clouds and windows. Therefore, in spite of the fact that short wavelengths carry more energy per photon, the ratios of UV-A and UV-B exposure are far from equal. These are only a few of the explanations as to why we observe an incidence of aging and skin damage and disease upon UV-A exposure. | {
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86,453 | I am a high school student and am currently learning about evolutionary relationship study in biology. My teacher said that a comparative study of amino acid sequences is more useful than a comparative study of nucleotide sequences, because the genetic code is degenerate in nature — several codons may code for the same amino acid. However, I just do not understand the logic. Since several codons may code for the same amino acid, I (as a math person) consider the conversion of a nucleotide sequence to an amino acid sequence as a non-injective function, and thus is information-losing. (Analogy: consider the function $f(x)=x^2$ . Imagine that you have a number, and you plug it into $f(x)$ to get $1$ as the output. You would never know if the original number is $1$ or $-1$ .) Therefore I arrive at the exact opposite conclusion. Is my conclusion correct or not, and why? | You're talking about long-wave UV, or UV-A radiation. In the 80s, experts claimed that this was a safe wavelength. Protection against UV-A was not part of sunscreen in the early days. Consequently, UV-A was (and still is) used in tanning beds due to its perceived safety over UV-B. However, a lot of research has been done since. UV-A is well understood now to also be unsafe in unreasonable amounts. Currently, UV-A protection is a typical feature of sunscreen and tanning beds are still not a healthy alternative to moderate, healthy doses of sun. Here is a recent review covering some of the aspects comparing different UV range effects on skin. I really suggest you put a search engine to good use here; it makes little sense for us to expound on the literature when it is so clear and easily available. In summary, UVA certainly contributes to the development of skin cancer. UVA penetrates deeper into the skin than UV-B (which is largely responsible for 'burning' of the topmost layer of skin, without directly affecting the deeper layers). For this reason, UV-B is associated primarily with burning and UV-A is primarily associated with aging and aging diseases like cancer. It is important to note that 95% of UV light in every day life is UV-A, because it does not vary seasonally and can penetrate clouds and windows. Therefore, in spite of the fact that short wavelengths carry more energy per photon, the ratios of UV-A and UV-B exposure are far from equal. These are only a few of the explanations as to why we observe an incidence of aging and skin damage and disease upon UV-A exposure. | {
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86,613 | All humans have the same sort of proteins in our bodies. Take haemoglobin for example. Is the gene coding for haemoglobin in my body identical to everyone else's gene or is there slight variations in the nucleotide sequence? Are there examples of proteins that are always completely conserved at the population level? | Humans have many variants There is variation. The project I use to help understand this natural variation is gnomAD . Using VarMap and a slightly out of date gnomAD file, I counted
16007805 protein-coding variants across the human genome. This number will only go up over time. Indeed, the 1000 Genome project found that on average each person has between 250-300 loss of function protein variants that are not found in their parents ( The 1000 Genomes Project Consortium, 2010 ). This is an important concept for human health. ClinVar is one of many projects that aims to catalogue and study when these variations lead to disease in a clinical context.
Another is the 100,000 genome project by Genomics England which studies NHS patient data in cases of rare disease and cancer. Haemoglobin has variants, including disease variants At the time of writing, HBA1 (haemoglobin alpha subunit gene) has 183 gnomAD variants and 17 pathogenic variants in ClinVar ( sourced from gnomAD ).
Again, both of these numbers are likely to increase because the data will cover more people. Constraints on highly important proteins But the underlying question is, I think, "are there some proteins that are so important, that life keeps them highly constrained" i.e any variation will lead to an invalid cell or a disease phenotype.
gnomAD attempts to add "constrained" metrics to each protein record, and some are more constrained than others. For example: Haemoglobin scores a pLI of 0.01 (higher scores are more intolerant to variation, specifically loss of function variation). p53 is a gatekeeper of the cell cycle, mutants of which are common in cancer cells. It has a pLI score of 0.53 which means it is very intolerant to variation compared to haemoglobin. Ribosomal protein L5 has a pLI of 0.998 implying it can tolerate little if any variation.
The ribosome is critical in protein production, hence altering it may cause a complete breakdown of cellular life. Variation and Evolution There is an almost philosophical difference between human variation and human evolution. Variation is a static snapshot of our protein sequence from individual to individual. Evolution in the sense of a Dayhoff Matrix requires looking back millions or billions of years by comparing similar protein sequences across many species. | {
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88,338 | It is an often-repeated claim that human, and in fact all animal blood is salty because we evolved from aquatic organisms, and that blood has a similar concentration of salts as ocean water, or at least as primordial ocean water. Is any of that true? Does science know what the salinity of the oceans was billions of years ago, and was it indeed similar to the blood of today's organisms? Does that knowledge prove anything about evolution and the origin of life? I am wondering, because I tried to Google for the answers, and unfortunately all I could find were creationists referencing each other how it couldn't possibly be true because evolution is a lie in the first place etc., and they claim that there is no empirical research that would compare salinity levels of organims' cells and ocean water. | Short answer Early sea water had a very different osmolality than blood plasma. Background The reference range of serum osmolality is 275–295 mosm/kg (mmol/kg) ( MedScape ). The osmolarity of sea water is about 1000 mOsm/l ( Wikipedia ), but it can vary substantially between different seas, namely between 642 and 1,480 mOsm/kg ( Ninawe & Banik, 1998 ). Nonetheless, the range of osmolalities are substantially higher than that of serum. That's why we cannot consume sea water, without losing more water than gaining it ( NOAA ). According to Astro Biology Magazine , the salinity of early oceans 3.5 billion years ago, when life first developed, was even higher. So popular accounts that they are the same and that this has important evolutionary consequences are likely far-fetched. Reference - Ninawe & Banik, J. Mar. Biol. Ass. India (1998); 53 (2): 230-36 | {
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88,473 | Does sleeping fewer hours than needed cause the common cold? If so, how? | There have been some studies directly linking sleep deprivation to increased risk of catching a cold ("Behaviorally Assessed Sleep and Susceptibility to the Common Cold Sleep". 2015;38:1353–9.). Colds are caused by a family of viruses. There is pretty solid evidence that sleep deprivation has a significant weakening effect on your immune system . Given a weakened immune system, it would be more likely that you would catch a cold if you are exposed to one of the cold-causing viruses. | {
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89,120 | For instance, after starting zidovudine monotherapy against HIV, resistance develops against the drug because of a point mutation in the RNA transcriptase enzyme to which the drug binds. So how does the virus ‘know’ to mutate this particular enzyme? | It doesn't. Viruses don't "know" anything. Mutations occur at random. Most of them don't do anything, or have a slight negative effect on the ability of the virus to infect and reproduce . However, there are billions and billions of viruses. Once in a while a random mutation will offer a significant advantage like immunity to an anti-viral drug. The viruses that have that beneficial mutation will then massively out-reproduce the viruses that don't have it. Eventually the population of viruses will consist mostly of individual viruses that have that mutation. | {
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89,123 | What Im getting at is something totally impossible, but im making some mental experiences. Assuming I have a machine that can produce a living being just from a DNA code (like in the movie The Fly). If I make a DNA sequnce, that has mothers and fathers cromosomes identical, would such a being be a monstrosity or a human being when it got out of the machine. For such a person, when DNA recombination between 2 eqal cromosomes is done, it will just be creating clones if itself. Now we introduce a new monstrosity, a male twin male version of the identical-cromosome woman, that only hase the Y Chromosome altered. His sperm cells too will all be the same. when theese 2.people mate, it will produce a clone. EDIT:
To clarify my question number one.. Chromosome pair 1 has 2 chromosomes, one from father, one from mother. If theese two would be identical. | It doesn't. Viruses don't "know" anything. Mutations occur at random. Most of them don't do anything, or have a slight negative effect on the ability of the virus to infect and reproduce . However, there are billions and billions of viruses. Once in a while a random mutation will offer a significant advantage like immunity to an anti-viral drug. The viruses that have that beneficial mutation will then massively out-reproduce the viruses that don't have it. Eventually the population of viruses will consist mostly of individual viruses that have that mutation. | {
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89,218 | I've heard of parasites that can live in the human body and do a lot of damage to the host. There are even safer forms of worm-like parasites inside the intestine, but some parasites can live in the blood vessels or even in the brain or eyes. Parasites are, in my opinion, the most disgusting creatures there are, so I wondered if they could be killed with intoxication.
Would it be possible to get rid of worm parasites in the blood by increasing the amount of alcohol in the blood to a level that humans can tolerate but parasites can't?
Could you also eliminate brain parasites with hangover-related brain dehydration? That the dead parasites remain in the body may not be good or advisable. In addition, eggs, which are usually a little more resilient, should rather be removed from the body by antibiotics or proper medication. But is it at least theoretically possible to do something with alcohol against parasites? | In summary, there is no convincing evidence to say that alcohol intoxication helps to treat or prevent parasites in humans. 1) The evidence from in vivo human studies does not support the idea that alcohol consumption helps in treating parasites. Alcoholism and Strongyloides stercoralis: Daily Ethanol Ingestion Has a Positive Correlation with the Frequency of Strongyloides Larvae in the Stools (PLoS, 2010) : The frequency of Strongyloides was significantly higher in alcoholic
patients than in control group (overall prevalence in alcoholic 20.5%
versus 4.4% in control group; p = 0.001). 2) Even a strong alcohol beverage gets diluted when it reaches the intestine. Ethanol concentrations in the human gastrointestinal tract after intake of alcoholic beverages (European Journal of Pharmaceutical Sciences, 2016) : In a cross-over study, five fasting volunteers were asked to drink two
standard consumptions of commercially available alcoholic beverages,
including beer (Stella Artois®, 500 mL, 5.2% ethanol), wine (Blanc du
Blanc®, 200 mL, 11% ethanol) and whisky (Gallantry Whisky®, 80 mL, 40%
ethanol). The median gastric ethanol Cmax (min–max) for the beer, wine and
whisky conditions amounts to 4.1% (3.1–4.1), 4.1% (2.6–7.3) and 11.4%
(6.3–21.1), respectively...Median duodenal ethanol Cmax (min–max) for
beer, wine and whisky are 1.97% (0.89–4.3), 2.39% (2.02–5.63) and
5.94% (3.55–17.71), respectively. So, the maximal ethanol concentration in the duodenum after drinking 80 mL of whisky was 17.7%. Most of ethanol is absorbed in the first part of the small intestine ( Scandinavian Journal of Gastroenterology ), so it does not reach the more distant parts and does not likely kill the parasites there. 3) Even strong intoxication is associated with low blood alcohol concentration. In strong intoxication, your blood alcohol concentration would be only 0.2-0.3%. In one study (Table 1) , the 50% lethal concentration (LC50) of ethanol, which killed 50% of the bloodstream forms of the parasites Trypanosoma brucei, was 10.6%. 4) Alcohol intoxication and brain dehydration Alcohol intoxication or hangover are not automatically associated with dehydration. Anyway, even in severe dehydration, you still have a lot of water in your body, including the brain, so the parasites living there do not necessarily get dehydrated as a result of your dehydration. In general, dehydration increases the risk of infections, because it dries mucous membranes, for example in the urinary tract ( BMJ Open Quality, 2019 ). | {
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89,508 | My intuition tells me that organic mercury compounds are absolutely toxic. Unimaginably, fundamentally, extremely and uncompromisingly toxic. I know that is not true for all doses. Thiomersal is the organomercury compound that was used in vaccines as preservative. It's use has been controversial outside of the scientific community. I am not asking whether the use in vaccines is dangerous, to be clear: The use of mercury as Thiomersal in vaccines it is not dangerous. That is well-established beyond reasonable doubt. Far beyond. My intuition tells me that any organomercury compound it so mind-blowingly toxic that I feel cognitive dissonance if I try to accept that, at some dose, it's not. I'm totally aware that toxicity depends on dose, that the compound is toxic at higher doses, and the dose used is just low enough that it is not toxic. But the dose used is still antiseptic and antifungal, and having anything in my body that contains mercury and carbon in a dose high enough to kill a form of life feels just not right. I would not worry at all to get vaccinated with a vaccine containing Thiomersal, and if a physician would ask me whether I prefer a vaccine with or without it, I would answer "Whatever you think is best." But still, on the abstract level, the feeling of "That can't be right" to have an organomercury compound in my body it pretty strong. I know it is not dangerous, but: How is that even possible? | Thiomersal is broken down into two compounds, thiosalicylate and ethylmercury (Ensink 2015). The thiosalicylate it is relatively non-toxic, and there is even some evidence that this compound could counteract some of the effects of mercury poisoining (Asadi et al 2010), though the mechanism of this inhibition has yet to be elucidated. Although they have similar names, methylmercury and ethylmercury have very different levels of toxicity. Methylmercury has long been known to be highly toxic, producing high levels of cell death in the brain, particularly in the cerebellum and the visual cortex (Ceccatelli et al 2010). Unlike methylmercury, ethylmercury appears unable to cross the blood-brain barrier as fast as it is eliminated in the stool. Consequently, small quantities of ethylmercury have been shown to be non-toxic, resulting in the relative non-toxicity of thiomersal (Pichichero et al 2002). Sources: Asadi S, Zhang B, Weng Z, Angelidou A, Kempuraj D, Alysandratos KD, Theoharides TC. 2010. Luteolin and thiosalicylate inhibit HgCl(2) and thimerosal-induced VEGF release from human mast cells. Int J Immunopathol Pharmacol 23(4): 1015-1020. Ceccatelli S, Daré E, Moors M. 2010. Methylmercury-induced neurotoxicity and apoptosis. Chemico-Biological Interactions 188(2): 301-308. doi:10.1016/j.cbi.2010.04.007 Ensink E. 2015. Preservative or poison? The science behind Thimerosal. The Substrate (online): http://substrate.asbmb.org/2015/05/15/preservative-or-poison-the-science-behind-thimerosal/ Pichichero ME, Cernichiari E, Lopreiato J, Treanor J. 2002. Mercury concentrations and metabolism in infants receiving vaccines containing thiomersal: a descriptive study. The Lanclet 360(9347): 1737-1741. doi:10.1016/S0140-6736(02)11682-5 | {
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89,585 | I was reading this article on researching bacteria resistance to silver by removing some of their genes. Researchers then used "colony-scoring" software to measure the differences in growth and size of each plate's bacterial colony. E. coli strains with genes deleted involved in producing sensitivity, or toxicity, to silver grew larger colonies. Strains with genes deleted involved with resistance grew smaller colonies. Once you end up with some resistant bacteria and you're done researching it, you can't just flush it down the toilet. How do you safely dispose those colony plates in a way that ensures those bacteria don't get out into the wild and reproduce? | You are absolutely right, flushing down the toilet (or the sink) or simply throwing them into the normal waste doesn't work for biosafety reasons. And it is also not allowed, depending on the country you would do this in, this can lead to hefty fines. Biologically contaminated lab waste can be inactivated (=all potential dangerous organisms are destroyed) by two ways: Either by heat or chemically. Which ways is used, depends on the kind of waste. The most commonly used way is autoclaving, meaning treating the waste with steam at high temperatures at higher pressure. The temperature used here is usually 121°C, the exposure time depends on the volume of the waste, since the temperature needs to be reached and kept for at least 20 minutes. See the references for more details. Liquid wastes (like culture media) can also be inactivated chemically by adding chlorine bleach to decompose the cells. Bleach can also be used to decontaminate surfaces, although here more often alcoholic solutions (70% Ethanol or Isopropanol) are used. After chemical inactivation, the remaining solutions should not be autoclaved as the emerging fumes are either unhealthy (bleach) or explosive (alcoholic solutions) and this is unnecessary, too.
Liquid wastes can also be autoclaved to inactivate them. Autoclaving has the main advantage that it is rather simple (put the waste into the autoclave, close it and run a appropriate program), the waste can afterwards simply be discarded as normal waste, which may not be the case for chemically inactivated waste, which may need special precaution for disposal. References: Decontamination and Sterilization Decontamination of laboratory microbiological waste by steam
sterilization. TECHNIQUES FOR STEAM STERILIZING LABORATORY WASTE Decontamination of Laboratory Microbiological Wasteby Steam Sterilization | {
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89,709 | It's my understanding that the majority of symptoms associated with the common cold (runny nose, inflamed sinus, slight fever) are essentially the result of the immune system's response. I've never heard of someone dying of the common cold (unlike influenza), even in immune compromised people. As such, what damage would the cold virus inflict if there was no immune response? Would it be catastrophic? | Can someone die of the common cold? No.
The common cold is a clinical syndrome restricted to upper respiratory tract involvement. By clinical syndrome, I mean it is the constellation of symptoms (rather than the consequence of a specific pathogen). As you mention, these symptoms are the result of the immune response, rather than tissue damage or compromised function as a direct effect of a pathogen or its toxin (e.g., the watery diarrhea in cholera). As defined (see, e.g., Cecil Medicine Ch. 369), this clinical syndrome cannot lead to death. The common cold is an upper respiratory syndrome of rhinorrhea and nasal obstruction, frequently accompanied by sore throat, sneezing, and cough. Can the viruses that cause the common cold cause death? Yes. Many viruses that cause the common cold also cause other clinical syndromes that can cause death. This occurs when viral replication moves to the lower respiratory tract. As an example, influenza viruses are responsible for 25 - 30% of common colds (see Bennett, Principles and Practice of Infectious Disease, Ch.58). When it moves beyond the upper respiratory tract, influenza is responsible for substantial mortality . Other virus families that are responsible for both a common cold syndrome and lower respiratory tract syndrome in immunocompetent individuals (e.g., bronchiolitis, pneumonia) include parainfluenza virus, metapneumovirus, adenovirus, and (rarely) coronavirus. Rhinovirus, responsible for 40-50% of common cold cases, is uniquely unsuited to lower respiratory tract involvement, because of its preference for the cooler environment of the nasal mucosa, replicating best at 33 C (Murray Medical Microbiology, Ch 56). However, in individuals with Severe Combined Immunodeficiency (SCID), lower respiratory tract involvement does occur. There are a number of case series reporting death due to lower respiratory rhinovirus. This is an example. Can the common cold lead to serious illnesses other than lower respiratory tract involvement? Yes. Other morbidity can occur as a result of the immune response that produces the common cold syndrome. Rhinorrhea and congestion can progress to a viral rhinosinusitis, a separate syndrome with its own complications, or a secondary bacterial infection, which can lead to bacterial sinus involvement and/or bacterial lower respiratory tract infection. Otitis media is another common complication, especially in children, and has its own potential complications. Asthma (and, generally speaking, most lung diseases) can also be exacerbated by what would otherwise be a simple common cold and predisposes to lower respiratory tract involvement. Asthma does deserve special mention, because rhinovirus associated exacerbations can be fatal , but this is a consequence of asthma rather than a common cold syndrome. Further discussion of these syndromes are beyond the scope of the question, but are discussed briefly in the chapters referenced above. | {
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89,837 | My friend caught a strange looking animal and he's saying it is an axolotl. I keep telling him it's almost impossible, since they are almost extinct in their natural environment and he caught it in St-Larent River (Quebec, Canada) Anyone have any idea what it is ? | Based on the size and location that appears to be a Common mudpuppy ( Necturus maculosus ) . (Photo © Brian Gratwicke — CC BY) The four toes visible on the front foot are also consistent with this identification. This species is found throughout eastern North America and you can learn more about them from the Canadian herpetological society and iNaturalist . | {
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89,943 | I'm not a biology student at all, but I'm trying to get a clearer picture on what is meant by "virus cannot survive after a certain period". To my understanding, a virus cannot be killed it can only be inactivated (for example, by means of heat and lowered pH). So I really don't understand how can virus get inactivated by just being on a certain surface for an extended period. I've come across numerous articles which told me virus won't survive on a surface. They usually focus on comparing the survival time between different types of surfaces but never touch on how the virus gets inactivated. Can someone help me understand the "how"? | Many important viruses are coated with a lipid envelope and rely on this to enter the host cell. This envelope is fragile - it's similar to a soap bubble - and it can be disrupted in many ways. Lipids will oxidize in air over time and this will degrade their ability to maintain an envelope. Surfactants such as soap or solvents such as alcohol will disrupt an envelope quickly. Even if the genome inside survives, if the envelope is disrupted the virus won't be able to infect cells.
The exact mechanism of inactivation likely varies a lot from virus to virus, and hasn't been studied extensively.
This paper found that Hepatitis C virus RNA survived alcohol treatment, but lost infectivity, presumably due to envelope disruption. In contrast, heat treatment (80°C) destroyed both the envelope and the RNA. Another paper found enveloped viruses survived being dried out a shorter time than non-enveloped viruses. (5 days vs. weeks) Speaking generally, the environment outside a body is hostile! If you were taken out of your home and dropped somewhere in the wilderness, there's many different ways you could die, and it's more remarkable if you survive. A similar situation arises for viruses. | {
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90,095 | A number of countries are using test kits for detecting new cases of nCoV (2019-Coronavirus) and apparently China is running low. What exactly is in a nCoV "Test Kit" — How does it work? (Surely they also differ, so in which way do they differ?) | The CDC has made available online its nCoV test kit . Briefly,the kit contains primers and probes for real-time reverse-transcriptase PCR, as well as instructions for appropriate use and (critically) controls and guidelines to avoid false positives and negatives. Kits from different countries may use slightly different primers and probes, though since they are all working from the same sequences and the same principles they should be broadly quite similar. Explaining how quantitative PCR works and the details of the primers and probes is out of the scope of this SE. A layman's introduction was written by John Timmer at Ars Technica . | {
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90,433 | This is going to sound really stupid or as a joke, but... Ever since I was a little kid, I have been confused about the following: Humans need air/oxygen to breathe in order to live. Plants/trees/bushes/flowers produce this oxygen, and are thus crucial for humans to survive. Plants/trees/bushes/flowers need "carbon dioxide" to survive, just like humans need oxygen. Plants/trees/bushes/flowers MAY also need some oxygen/air? (I assume so.) Cars (traditional ones) output "carbon dioxide"... yet they are... not good for nature? I don't understand how this fits together. It seems as if nature should absolutely thrive in the middle of highways and nearby, if they get so much nice carbon dioxide from the cars! Yet cars are instinctively seen (also by me) as "evil nature-polluting machines of death". Car exhaust seems to be the opposite of what a plant or tree wants, yet it's full of carbon dioxide, so... why? Can somebody explain this once and for all? | There are at least two separate answers to your question. First, with respect to plants needing CO2, they have evolved to deal with the limited amounts of CO2 normally in the atmosphere. That's really all they need, or "want": adding more doesn't really benefit them. Think of it this way: you need water to live, right? And drink a certain amount of it every day. But drinking large amounts of water can kill you https://en.wikipedia.org/wiki/Water_intoxication and holding you under water for a few minutes certainly will. (As in the comment above, and even better example would be oxygen: we need it to live, but too much can cause all sorts of problems: https://en.wikipedia.org/wiki/Oxygen_toxicity ) Likewise, plants need nitrates, but applying too much can kill them. So extra CO2 in the air is of little or no benefit to plants. The second answer has nothing to do with plants. It's that atmospheric CO2 traps solar heat, causing the Earth to be warmer than it otherwise would. Without the extra CO2 from fossil fuels, Earth maintained a comfortable temperature, one that we'd all (and I mean not just humans, but all life) had gotten used to. Add more CO2, and more solar heat is trapped, making the Earth uncomfortably warm, to the point that many plants & animals can't live where they are, and generally can't migrate. So you wind up with a lot of dead plants and animals. Of course there's more going on than this, things that are feedbacks from and side effects of the increased CO2, such as ocean acidification. If you really want to know more, here's a good starting place: https://history.aip.org/climate/index.htm | {
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90,793 | A couple of colleagues suggested in a discussion that the virus that causes COVID-19 appears to be made by humans, since nature could not have produced such an efficient virus — that spreads so fast and whose patients are contagious quite some time before showing signs of infection. Since my knowledge of biology is very limited, my only counterargument for such a conspiracy theory was along the following lines: there is a consensus that the most probable source of the first infection was in an animal market in China. since that animal market was actually composed of a plethora of animals belonging to various species (mixed with humans), a virus had a bigger chance of evolving a mutation that might infect an individual from another species (a thing that is way less unlikely in the wild since many of those animals do not sit close to each others or next to humans). Clearly, I have made a little story that might be quite far away from how SARS-CoV-2 infected humans, so I am interested in a scientific arguments to support my cause. Question: What are the main scientific arguments that can be used to debunk COVID-19 being engineered by humans? Answers that also include explanations more accessible to laymen are greatly welcomed. | At the moment, there is very little scientific literature about this, but I found two papers that address the problem and are fairly easy to understand. You can find them in the references. Reference 1 is probably the most interesting and is the basis for this answer.
Edit: It is also interesting to read reference 2 on the origin of SARS-CoV-2; the article also addresses some of the conspiracy theories. As far as I can see, there are a few major points taken up by conspiracy theories. 1. SARS-CoV-2 leaked from a lab in which research on the Bat CoV (RaTG13) was done: Unlikely, since the viruses share only around 96% sequence homology, which translates into more than 1100 sites where the sequence of SARS-CoV-2 viruses is different from RaTG13. The mutations are distributed throughout the viral genome in a natural evolutionary pattern, making it highly unlikely that SARS-CoV-2 is a direct descendant from RaTG13. For comparison, the original SARS-CoV and the intermediate host palm civet SARS-like CoV from which it originated shared 99.8% sequence homology, showing a much closer relation. 2. The S (spike) protein from bat SARS-CoV cannot be used to enter human cells via the human ACE2 receptor and therefore has been adapted in the lab: This is untrue, since a 2013 study of a novel bat coronavirus was published showing the ability of the virus to enter cells via the ACE2 receptor. See reference 3 for details. 3. The spike protein of SARS-CoV contains a unique inserted sequence (1378 bp) located in the middle of its spike glycoprotein gene that had no match in other coronaviruses: As shown in reference 4, the sequence comparison of the SARS-CoV-2 with closely related other coronaviruses shows that this sequence is not unique to the new virus but is already present in older strains. It shows some difference due to inserted mutations. 4. The claim that SARS-CoV-2 contains four insertions from HIV-1: The paper claiming this has now been retracted due to severe criticism, and additionally a renowned HIV expert published an analysis (reference 5) demonstrating that the HIV-1 claimed insertions are random rather than targeted. 5. The claim that the SARS-CoV-2 virus is completely man-made: To design such a "weapon grade" virus in the lab, the design would usually start from a known virus backbone and then introduce logical changes (for example, complete genes from other viruses). This cannot be seen in the genome of the virus; rather, you see randomly distributed changes throughout the genome coming from virus evolution and not directed cloning. It is more likely that this virus originates from the recombination of a bat CoV (to which it is closely, but not directly related) and another, not yet known CoV in an intermediate host, like the palm civet for the 2003 CoV. References: No credible evidence supporting claims of the laboratory engineering
of SARS-CoV-2 The proximal origin of SARS-CoV-2 Isolation and characterization of a bat SARS-like coronavirus that
uses the ACE2 receptor Is SARS-CoV-2 originated from laboratory? A rebuttal to the claim of
formation via laboratory recombination HIV-1 did not contribute to the 2019-nCoV genome | {
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90,821 | From my basic understanding: The viruses causing Ebola, Sars and Covid-19 are all the result of a zoonosis, meanings that the viruses have passed from animals to humans. So my question is: Are all recently (let's say 100 years) emerged viral diseases, with potential for a global epidemic, the result of a zoonosis? | To my knowledge, yes. A partial list of recently emerged/emerging viral diseases (I certainly could have missed some), with probable reservoir hosts: Chikungunya * (birds, rodents) coronaviruses (SARS [bats], MERS [camels], COVID-19 [?? bats ?? pangolins ??]) Ebola and other filoviruses (Marburg): (bats?) Hendra , Nipah (bats) Ross river virus * (various mammals) HIV (primates) influenza (H1N1, avian) (birds/pigs) monkeypox (monkeys, duh; also rodents ) West Nile virus* (birds) Zika * (? "a wide range of animals in West Africa" ) Starred examples are vector-borne (so perhaps of slightly lower concern - might not fit your criterion of "capable of causing a global pandemic"). Omitted: older zoonotic viruses (rabies, dengue, hepatitis, ...) non-viral zoonoses (malaria, plague, anthrax) A list of zoonoses ; another from US CDC More generally, the only other place an emerging virus could come from would be from mutation or recombination of existing human viruses. I'm not aware of such an example. | {
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90,962 | Can one be immune to the new coronavirus? Another question is what is the exact definition of "being immune". Does it mean that even when the virus enters my system, it cannot multiply? | It is hypothesized that exposure to and recovery from SARS-CoV-2 (as with other coronaviruses in humans) would generally result in short-term immunity to this strain, but we do not yet have data on this: However, according to Dr Stephen Gluckman, an infectious diseases physician at Penn Medicine and the medical director of Penn Global Medicine, who spoke to the outlet, it seems likely that having the disease once results in immunity in most individuals - as is seen with other coronaviruses. “Coronaviruses aren’t new, they’ve been around for a long, long time and many species - not just humans - get them,” he explained. “So we know a fair amount about coronaviruses in general. For the most part, the feeling is once you’ve had a specific coronavirus, you are immune. We don’t have enough data to say that with this coronavirus, but it is likely.” This means that people who initially recovered are more likely to relapse rather than get reinfected with the virus. According to one study, people with mild infections can test positive for the virus by throat swabs “for days and even weeks after their illness”. But, that doesn’t mean it isn’t possible to contract the disease again, especially in those who are immunocompromised. “The immune response to Covid-19 is not yet understood,” the Centers for Disease Control and Prevention (CDC) explains. “Patients with MERS-CoV infection are unlikely to be reinfected shortly after they recover, but it is not yet known whether similar immune protection will be observed for patients with Covid-19.” Coronavirus: Can You Get Covid-19 Twice Or Does It Cause Immunity? It is also hypothesized (in humans) that previous exposure to coronaviruses may enable immunity to certain other highly related strains: These data indicate that challenge immunity to coronaviruses is strong, but highly virus strain-specific. Virus strain specificity of challenge immunity to coronavirus. , Archives of Virology (1989) But these are all examples of adaptive immunity - not innate. | {
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92,356 | I am curious if there has ever been a (modern) clinical study where a healthy volunteer was purposefully infected with a pathogen in order to test the effectiveness of a therapeutic or preventative measure (like a vaccine)? If not, would the FDA allow for ethical exceptions in cases where there is an extreme case of urgency (like in a pandemic)? Obviously these would be willing volunteers who signed waivers, etc. So Nazi experimentation, the Tuskegee trial, and other studies without total consent from the participants wouldn't qualify here. Edit: Self-experimentation wouldn't qualify here either because the bioethics of self-experimentation are different than testing on others. | This is a great biological question! It asks a lot about how empirical science is done in the field of modern biology. I'm glad we encourage such questions from curious people who want to learn more. One can't easily separate ethics from how biology is done, as much as some people have tried. (Though I suppose some have made bioethics into a separate and successful media career, so it can be done in that way.) In addition to the comment-answer about the Tuskegee Study , Nazi doctors in Germany performed experiments without consent, which included infecting concentration camp prisoners with the bacteria that cause tuberculosis. Your question is about volunteerism, however, and the victims of the United States and Nazi Germany did not give full — or any — consent to experimentation. In this week's issue of Nature , there is a news article which interviews bioethicist Nir Eyal about a recent preprint , of which he is a primary author. In this interview and in the preprint, your very question about coronavirus vaccine research, specifically, is discussed, as it concerns the matters of consent, ethics, and safety of doing accelerated biological research about this virus in a time of emergency. In answer to your first question about modern clinical studies, Dr. Eyal notes: Are there any precedents for infecting healthy people with a pathogen? We do human-challenge studies for less deadly diseases quite frequently. For example, for influenza, typhoid, cholera and malaria. There are some historical precedents for exposure to very deadly viruses. The thing that demarcates the design that we propose from some of these historical instances is that we feel there is a way to make these trials surprisingly safe. As an example, there was a challenge trial for malaria performed in 2012. Healthy individuals were bitten by mosquitoes carrying the malaria parasite and then treated with antimalarial therapies. Clinical trials are done under the aegis of government agencies with review and approval processes, some of which are described on the FDA web site. IRBs or Institutional Review Boards provide oversight: Under FDA regulations, an IRB is an appropriately constituted group that has been formally designated to review and monitor biomedical research involving human subjects. In accordance with FDA regulations, an IRB has the authority to approve, require modifications in (to secure approval), or disapprove research. This group review serves an important role in the protection of the rights and welfare of human research subjects. History does guide us to worry about the ethical issues surrounding medical trials, especially under exploitative regimes that leave people to fend for themselves during a time of global crisis: Do you worry that countries with authoritarian governments could conduct such studies on vulnerable groups, such as prisoners or members of persecuted minorities? We would only recommend conducting the studies in an ethical fashion, with fully informed consent. Vaccine makers want to sell their product to other countries. They want to publish their scientific articles in prestigious journals and there would be many obstacles if their trial doesn’t adhere to widely accepted standards. But in the modern age, in non-corrupt regimes, science does aim, for the most part, to do the right thing, and there are methods and regulatory mechanisms in place to try to enforce societal standards that move us past the days of Tuskegee and Nazi concentration camps. | {
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92,378 | Interstitial fluid is the fluid between cells in tissues - forming the medium between cells and capillaries. From what I gather, the typical human has 5L of blood and 11L of interstitial fluid. This raises an interesting question. If I get cut, why do I not bleed interstitial fluid? When humans are cut, generally their capillaries open and blood comes out. But this should also allow the interstitial fluid to come out - so why don't we see it? | For fluid to flow from a wound there needs to be a significant pressure gradient between where it is now and the outside of the body. Your skin generally does not have a strong compressive effect, which is why a deep cut exposing fat will not lead to the fatty tissue being expulsed from the body any more than the interstitial fluid is. Blood, however, flows. For it to circulate there needs to be a pressure gradient between where it is now and where it is going. Since veins (including the vena cava, which channels blood back into the heart) do not have vascular walls strong enough to create a suction effect (i.e. lower pressure than the surrounding tissue), you can conclude that the pressure of blood vessels is always higher than that of surrounding tissues, and thus higher than the pressure outside of your body. This is why all blood vessels, including veins, will bleed, whereas less pressurized systems such as interstitial fluid will not. | {
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92,383 | On GISAID they classified the corona using 4 clades(S, G, V, Other). I would like to know exactly how these genomes were classified for my research. So how do you classify a coronavirus genome as belonging to one of the clades. | For fluid to flow from a wound there needs to be a significant pressure gradient between where it is now and the outside of the body. Your skin generally does not have a strong compressive effect, which is why a deep cut exposing fat will not lead to the fatty tissue being expulsed from the body any more than the interstitial fluid is. Blood, however, flows. For it to circulate there needs to be a pressure gradient between where it is now and where it is going. Since veins (including the vena cava, which channels blood back into the heart) do not have vascular walls strong enough to create a suction effect (i.e. lower pressure than the surrounding tissue), you can conclude that the pressure of blood vessels is always higher than that of surrounding tissues, and thus higher than the pressure outside of your body. This is why all blood vessels, including veins, will bleed, whereas less pressurized systems such as interstitial fluid will not. | {
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92,770 | No vaccine or cure has been found for SARS-CoV or MERS-CoV yet the world is not too concerned about them. How can it be? Did all people who had those viruses die or do viruses just randomly decide to stop being infectious at some point? | Infections spread in a population when the number of new infections caused by an infected person is greater than or equal to 1. If each infected person spreads the virus to less than 1 person, eventually no one will be infected, without a need for any sort of cure. Of course, the longer a deadly infectious disease spreads in a population, the more people will die during this process. Ideally you want to get the number of transmissions as close to zero as possible as quickly as possible. SARS and MERS are each a bit different, but share some similar characteristics. Compared to COVID-19 caused by SARS-CoV-2, both are more severe in a larger fraction of the people infected (note: all three viruses are closely related betacoronaviruses ). This made it easier for public health officials to identify and isolate infected individuals. The MERS virus is really not gone at all: it lives on in animal reservoirs, like camels (so it is primarily only a concern in places where those reservoirs live). Cases continue to occur sporadically. However, MERS is usually not that transmissible between people, having a natural transmission rate that is already less than 1: that means that most people who get it get it directly from an animal, and don't continue to spread it to others besides occasional infection of individuals with close-contact, like a family member. There have been exceptions where isolated incidents involved substantial human-to-human transmission. Some of these incidents were associated with "super-spreaders": particular individuals who got infected and spread the virus to way more people than the average. See https://wwwnc.cdc.gov/eid/article/26/2/19-0697_article for more. SARS caused by the original SARS-CoV virus indeed seems to be gone, with no cases reported since 2004. The elimination of SARS from the human population occurred via controlling the human-to-human spread through isolation and contact tracing. See https://apps.who.int/iris/handle/10665/70863 for a report on the epidemic and how cases and spread in different locations were handled. Viruses don't have any agency: they can't decide to do anything. However, humans can, and our best response to outbreaks of novel diseases is to trace the spread and try to limit transmission as much as possible. | {
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92,794 | Remdesivir is metabolized into a nucleotide analogue. It is incorporated in the viral genomes causing either termination of transcription or a dysfunctional genome. Thus, the new viral particles produces within infected cells are dysfunctional. However, how does Remdesivir intefere with human transcription, or does it? I'd imagine that a nucleotide analogue could be incorporated into a human mRNA. Can it? edit: The mithocondria are discussed below. I would also be interested in usual, i.e. nucleic transcription. Is Remdesivir transported into the nucleus? Does human RNA polymerase accept it? | Infections spread in a population when the number of new infections caused by an infected person is greater than or equal to 1. If each infected person spreads the virus to less than 1 person, eventually no one will be infected, without a need for any sort of cure. Of course, the longer a deadly infectious disease spreads in a population, the more people will die during this process. Ideally you want to get the number of transmissions as close to zero as possible as quickly as possible. SARS and MERS are each a bit different, but share some similar characteristics. Compared to COVID-19 caused by SARS-CoV-2, both are more severe in a larger fraction of the people infected (note: all three viruses are closely related betacoronaviruses ). This made it easier for public health officials to identify and isolate infected individuals. The MERS virus is really not gone at all: it lives on in animal reservoirs, like camels (so it is primarily only a concern in places where those reservoirs live). Cases continue to occur sporadically. However, MERS is usually not that transmissible between people, having a natural transmission rate that is already less than 1: that means that most people who get it get it directly from an animal, and don't continue to spread it to others besides occasional infection of individuals with close-contact, like a family member. There have been exceptions where isolated incidents involved substantial human-to-human transmission. Some of these incidents were associated with "super-spreaders": particular individuals who got infected and spread the virus to way more people than the average. See https://wwwnc.cdc.gov/eid/article/26/2/19-0697_article for more. SARS caused by the original SARS-CoV virus indeed seems to be gone, with no cases reported since 2004. The elimination of SARS from the human population occurred via controlling the human-to-human spread through isolation and contact tracing. See https://apps.who.int/iris/handle/10665/70863 for a report on the epidemic and how cases and spread in different locations were handled. Viruses don't have any agency: they can't decide to do anything. However, humans can, and our best response to outbreaks of novel diseases is to trace the spread and try to limit transmission as much as possible. | {
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93,262 | Is it possible for a virus to be a descendant of a bacterium that was not through horizontal gene transfer? How I think this could happen: Suppose a species of bacteria lives in an environment where it gets all the resources it needs to reproduce (and let's assume that there will be no major changes in the environment). That is, if it loses a gene that synthesizes some substance (or regulates some process), it will not be at an evolutionary disadvantage. Because it can achieve this from the environment. Even depending on the gene, it can even be an evolutionary advantage, as it can become more efficient when it comes to reproducing. And I have seen that an experiment was carried out related to this question , it was shown that viruses can lose some genes in an environment where it can naturally find the protein that is associated with those genes. Thus, there is a chance that this species will become so simple, that it will end up becoming a virus. | This virology site has a post about a 2017 paper about membrane-vesicled plasmids that act in ways that are theorized to be precursors to how viruses work: It is likely that the plasmid-containing membrane vesicles are precursors of what we know today as virus particles. It is thought that viruses originated from selfish genetic elements such as plasmids and transposons when these nucleic acids acquired structural proteins (pictured; image credit). Phylogenetic analyses of the structural proteins of many enveloped and naked viruses reveal that they likely originated from cell proteins on multiple occasions ( link to paper ). The membrane-encased Archaeal plasmid seems well on its way to becoming a virus, pending acquisition of viral structural proteins. Though plasmids are not viruses and are not bacteria, bacteria are hosts for plasmids, and plasmids add indirectly to the genetic constitution of bacteria. Expression of plasmid genes can help bacteria survive hostile or extreme environments, and they reproduce along with bacterial chromosomes. Via the Wikipedia link: Unlike viruses, which encase their genetic material in a protective protein coat called a capsid, plasmids are "naked" DNA and do not encode genes necessary to encase the genetic material for transfer to a new host; however, some classes of plasmids encode the conjugative "sex" pilus necessary for their own transfer. | {
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93,274 | My OL biology textbook says that one of the functions of the pleural fluid between lungs and pleural membrane is that it ensures no air between lungs and rib cage. But I wonder why air there would cause any problems. I was told that it'd build up there and exert pressure on the lungs but why would it build up there in first place, couldn't it just go out through the mouth or nose? And in case that's really the answer, how does it manage to prevent any oxygen or other gases from getting into the fluid, after all, the pleural fluid touches the pleural membranes cells which require oxygen, won't oxygen diffuse from around them into the fluid? | This virology site has a post about a 2017 paper about membrane-vesicled plasmids that act in ways that are theorized to be precursors to how viruses work: It is likely that the plasmid-containing membrane vesicles are precursors of what we know today as virus particles. It is thought that viruses originated from selfish genetic elements such as plasmids and transposons when these nucleic acids acquired structural proteins (pictured; image credit). Phylogenetic analyses of the structural proteins of many enveloped and naked viruses reveal that they likely originated from cell proteins on multiple occasions ( link to paper ). The membrane-encased Archaeal plasmid seems well on its way to becoming a virus, pending acquisition of viral structural proteins. Though plasmids are not viruses and are not bacteria, bacteria are hosts for plasmids, and plasmids add indirectly to the genetic constitution of bacteria. Expression of plasmid genes can help bacteria survive hostile or extreme environments, and they reproduce along with bacterial chromosomes. Via the Wikipedia link: Unlike viruses, which encase their genetic material in a protective protein coat called a capsid, plasmids are "naked" DNA and do not encode genes necessary to encase the genetic material for transfer to a new host; however, some classes of plasmids encode the conjugative "sex" pilus necessary for their own transfer. | {
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94,024 | With social-distancing measures being implemented in many countries I would expect other viruses, like the ones that cause seasonal flus, to have also a hard time propagating in these circumstances. Are there any estimates or research (epidemiological models) I can check, about the possibility we are winning by accident a war against many other less alarming viruses? | Yes, this helps as well with other infectious diseases. A good example is the flu, which season was measurably shorter this year than in other years on record. See the figure from the reference 1 for comparision: Reference 2 shows that this is also true for other respiratory diseases (figure 2): This shows very well that the isolation measures and the social distancing work very well to control such transmissable diseases. References: How coronavirus lockdowns stopped flu in its tracks Monitoring respiratory infections in covid-19 epidemics | {
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94,096 | My 9 year old niece asked me this when I was explaining some stuff to her about the coronavirus. She asked "What does this virus taste like? Can I tell whether my sandwich is contaminated for example?" That sounded like a silly question and I immediately responded by saying that they are too small to have any taste, and even if you manage to eat a whole lot of viruses it would taste like water. The day after, I searched a bit just to make sure that I haven't fed the wrong information to the kid. As I expected, there wasn't a single page mentioning this question (except this quora post with a vague answer). Now it may sound like I am overthinking and the question is too naive and isn't worth the time, but then again, I thought what's the harm in asking? Has there been any research on the likely taste or maybe smell of a specific virus or bacteria? | As you could imagine, a systematic cataloguing of bacterial or viral flavor profiles would violate a number of biosafety protocols. However, in a laboratory setting, different bacteria definitely have distinct odors . In some cases, the odor is even included in guidelines for laboratory identification of an organism. However, that odor is typically not a result of smelling bacteria directly, as very few bacteria are aerosolized from a lab culture . More likely, the odors of bacteria are a result of volatile chemical metabolites produced by the organisms. For example, the spoiled milk smell comes from a number of odiferous compounds produced by bacteria. Sometimes these bacterial metabolites have rather colorfully descriptive names, such as putricine or cadaverine . Viruses are different though. They don't generate new metabolites on their own (outside of an infected cell) and they are incredibly tiny, even compared to a single cell. The human sense of taste is sensitive enough to detect some compounds in the low parts per million range . To even approach that range, you'd have to cram around 100 billion virus particles into a single milliliter of water (based on back of the envelope calculation). That's about 100,000 times more virus than most COVID19 positive clinical specimens , so I don't think you'll have to worry about tasting it under most circumstance. However, some research has been done to see if dogs can sniff out viral infections (likely by detecting volatile compounds produced by the infected cells, not by detecting the virus directly). Of course, they're trying to train them to detect the novel coronavirus as well. | {
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94,172 | There are countless sources, both peer-reviewed and popular, explaining how overuse and misuse of antibiotics is breeding a new generation of antibiotic-resistant "superbugs" such as MRSA (Methicillin-resistant Staphylococcus aureus) and MDR-TB (multidrug-resistant Tuberculosis). Over in the animal kingdom, the opposite seems to be happening - species after species is becoming endangered and/or extinct as humans destroy or alter their habitat through increased hunting, farming, construction, etc. Are there any non-human animals that have been found to have evolved resistance to human encroachment into or alteration of their habitat in a way analogous to how bacteria have evolved resistance to human attempts to get rid of them? For example, this could consist of: an animal that has adapted stronger bones to better survive collisions with vehicles an animal that has significantly increased its blood coagulation rate to survive gunshot wounds from hunters an animal that has developed better vision to see in urban environments an animal that has evolved a skin pigment change that enables them to not take as much damage when they are sprayed with agricultural pesticides One answer that came to mind is domestic animals - the horse and dog in prehistory, the cat in ancient Egypt, etc. That seems too obvious on one hand, and on the other hand may not really be an answer, as there seems to be no indication that pre-domestic animals were endangered by humans in any meaningful way. Are there animals that have significantly adapted themselves to surviving as wild animals in human-influenced environments? | Note: This is an answer to the last line of your question. A classical example of animals adapting to the influence of humans on their environment is the adaption of the Peppered Moth . Here is a brief summary: The peppered moth was originally a mostly unpigmented animal (<1800) . During the industrial revolution in the southern parts of the UK a lot of coal was burned. This led to soot blackening the countryside. Soon afterwards, a fully pigmented variety was first observed. Only a hundred years later, in 1895, this pigmented variety almost completely displaced the unpigmented variety. It has been shown that the pigmentation is under strong selective pressure as birds hunt these moths. Since birds rely on their visual system to detect their prey, the variety that blends in with its environment (=camouflage) has a selective advantage over the variety that stands out. As pointed out by Tim in the comments, since the 1970s there has been a rapid reversal with unpigmented animals being more abundant. As far as I understand , it is accepted that this reversal is due to a decrease in human induced air pollution leading to less sooty barks on trees which makes the unpigmented variety harder to prey upon. Addendum: genetic basis of adaption In a beautiful recent study , the causal mutation for the pigmented, or melanic, variety was identified: A ~9kb transposon insertion in the first intron of the gene cortex . The authors calculate that this mutation happened in the year 1819, a few years after the industrial revolution was in full swing. The interpretation is that due to sooty tree bark this mutation, causing pigmented moth, was under strong selection. | {
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94,683 | From my understanding, cancer is not contagious, and if a cancerous cell from a patient is introduced to a healthy person, then the immune system of the latter can destroy this cell. In such a case, why are internal organs from cancer patients not used for donation? Is this because there is a small probability of the immune system failing? Isn't there any other way to make these organs usable again? | There are different reasons why cancer patients are mostly excluded from donating organs. Although the probability of transmitting cancer is small, it is not zero. Also tumors tend to form metastases over time, which spread throughout the body. It is possible that a cancer has formed metastases in other, distant organs, which are too small to detect. Since recipients of organs have to take strong immune suppressing medication to prevent the rejection of the transplant, the immune system might not be able to fight the cancer cells anymore. Because of this medication, transplant patients already have a higher chance of getting cancer, because their immune system does not capture cells when they go rogue. See reference 1 for a more general description and 2 for the detailed report, reference 3 for the higher cancer risk of transplant patients. Tumors can go dormant when they are treated with chemotherapeutics to evade destruction, but these dormant cells can re-wake. If this happens after the transplantation of an organ, this is obviously bad for the recipient. See reference 4 for details on mechanisms. Cancer patients who died from the disease have often been treated with agressive drugs like chemotherapeutics. While these attack mostly the fast dividing cells of the tumor, they also have more or less strong side effects on the body. A lot of organs are simply not in the state (or have a strong chance of being in this state) anymore to be transplanted. Nobody wants to transplant a dysfunctional organ. See reference 5 for details. References: Cancer Spreads from Organ Donor to 4 People in 'Extraordinary' Case Transmission of breast cancer by a single multiorgan donor to 4
transplant recipients Cancer in the Transplant Recipient Tumor dormancy as an alternative step in the development of
chemoresistance and metastasis - clinical implications Long-Term Side Effects of Cancer Treatment | {
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94,746 | I have read that during the Second World War, some mosquitoes got trapped in the London underground railway system. The mosquitoes never got out and eventually they became a new species by themselves. I had a similar thought. In the next few centuries, if humans could, in theory, colonize other planets like Mars, Proxima Centauri and beyond, then the environments there are not the same as Earth. So, in the long term, humans who would be born and who would grow up on Mars, for example may become more and more suited to Martian conditions than Earths. Now, when early humans explored and ventured into new geographical areas, they did change characteristics, but we are still one species Sapiens . But living extraterrestrial, is a whole new thing. The gravity alters, the entire atmospheric composition does. So that is going to have some significant changes on humans. So, my question is: is it possible that in millions or even billions of years, if humans expand to space, there may arise separate species of humans? And would this new emergence of human species actually result in humans moving one step up the taxonomical ladder: becoming a genus? EDIT: To avoid confusion and create speculations at the answers, I should specify that I am talking about a very particular case: if Sapiens are living in different planets, then is there a chance that Sapiens will become a new genus, and that Homo can be taken one step higher in the taxonomical order? There would still be Sapiens on Earth, but considering the environmental changes that could happen here too, humans then can be drastically different from humans now. So the question is: can ' Sapiens ' become a genus? Thanks to @tyersome and @jamesqf for pointing this out. | The concept you are referring to is speciation and it has been well studied in a wide variety of different natural organisms. I suppose here we are talking about the biological species concept . The overall answer is yes it is possible, but critically depends on a few different factors. The reality of speciation in the wild is very complex, but these are some things to consider: Genetic isolation If two groups, such as your Martian colony and humans on earth isolate from one another, then for speciation to occur, there needs to be a significant level of genetic differentiation between them. This means substantial differences in the kinds of genetic variants found at positions along the genome. Genetic differences are eroded by post-isolation gene flow – in your example, that might mean a spaceship flying back to Earth with Martian colonists, who then have offspring with people on Earth. Although there is plenty of evidence that speciation with gene flow can occur, the general rule of thumb is that increased gene flow means a longer divergence time is required to fully speciate. In nature, this is often caused by some kind of geographic barrier to gene flow, such as mountains or rivers forming, but it can also be caused by morphological differences, such as variation in sexual appendages. Of course, in our example, this barrier to gene-flow would be the large and difficult to traverse distance between the Earth and Mars. Divergence time You alluded to some kind of separation time, and you are right to be talking on the scale of millions of years. Speciation can occur extremely quickly; in Lake Tanganyika cichlids, it has occurred probably within the last 15,000 years . Humans have created whole new species of crops, such as maize, within the past 10,000 years . There is even evidence of some fish speciating in 3000 generations . However speciation is often a much longer process. For example humans and chimps were thought to speciate in 4.5 millions years . Of course, there is an interaction with several other factors. All other things being equal, less post-isolation gene flows results in a shorter time to speciation and vice versa. Stronger selective pressure between the different environments leads to a more rapid accumulation of genetic differences. As Konrad Rudolph correctly points out, divergence time is strongly related to generation time, with all other things being equal, a shorter generation time, results in faster speciation. Selection pressures & differing environments I think the last main factor governing speciation is how different the Martian colonists environment was from that on Earth. Different environments can lead to natural selection occurring in opposing directions in the two populations, leading to ecological speciation . Speciation can proceed without differing environments, where neutral drift in allele frequencies can eventually cause speciation, but this will be a long process. Speciation will occur much more rapidly if there is a start difference in environment and selection pressures between the two groups. So in conclusion, given enough time, genetic isolation and differential selection pressures (or some combination of the above), it is plausible that a new species of human could form. However, given the time-scales required, it seems a bit unlikely to me. EDIT I think it is worth pointing out what @Jaquez said in the comments. If current terrestrial humans split from an extraterrestrial source to form another species, it would be named as another species within the Homo , such as Homo extraterrestrialis , for example. The addition of a new species does not move the group Homo up to become an e.g. Tribe or Family. | {
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96,016 | I researched about it by searching on Google and reading some bacteriological articles, but I did not get any answer. I also asked some of my teachers, and they were also a bit confused. Some said that it is possible and others said not. So the question remains: Can a bacterium infect another bacterium? If so, how? | Bdellovibrio bacteriovorus (BV) “infects” other bacteria: Similar to a virus, BV attacks bacteria such as Escherichia coli ( E. coli ) by attaching to and entering its prey, growing and replicating within the cell, and then suddenly bursting out, releasing its progeny into the surrounding environment. — How bacteria hunt other bacteria | {
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96,941 | In the last few weeks, Pfizer/BionTech, Moderna and AstraZeneca have each released preliminary estimates of the efficacy of their SARS-COV-2 vaccines. But what do their respective efficacy percentages actually mean? Is the Pfizer/BioNTech vaccine 95% effective in any person? Or is the success of provoking the desired immune response limited to 95% of the population? Put very simply: is it 100% effective in 95% of the population, or 95% effective in 100% of the population? | Vaccine efficacy Pfizer's target measures for efficacy (see the study on clinicaltrials.gov ) seem to be: Confirmed COVID-19 in Phase 2/3 participants without evidence of infection before vaccination Confirmed COVID-19 in Phase 2/3 participants with and without evidence of infection before vaccination From Pfizer's study plan (VE = vaccine efficacy): VE will be estimated by 100 × (1 – IRR), where IRR is the calculated
ratio of confirmed COVID-19 illness per 1000 person-years follow-up
in the active vaccine group to the corresponding illness rate in the
placebo group from 7 days after the second dose. VE will be analyzed
using a beta-binomial model. (note: they also have other time windows and checkpoints in their analysis plan; which one is reported will shift from press release to press release as they get more data. If you are interested in the details the study plan also describes the planned interim analyses, and some of the press releases discuss deviations they've made from their original interim plans in consultation with regulatory agencies) This measure is called relative risk , and can be written like this: %InfectedPerTime placebo = NInfected placebo / (NStudied placebo * AverageFollowUpTime) %InfectedPerTime vaccine = NInfected vaccine / (NStudied vaccine * AverageFollowUpTime) Efficacy aka VE = %Infected vaccine / %Infected placebo If you assume risks are the same in the placebo and vaccine groups (they "should" be, but might vary if, for example, people who experience vaccine side effects change their behavior) and the average follow-up time is the same (they should be approximately the same, because they are giving the vaccine and placebo to patients enrolled at the same time), this ratio would tell you that a vaccine efficacy of 95% means that if you took 20 people who would have had a positive test after the placebo, you would only expect 1 of them to test positive if they instead got the vaccine. Population vs. individual statistics Put very simply: is it 100% effective in 95% of the population, or 95% effective in 100% of the population? These are population-based measures. They can't say anything about efficacy in particular individuals by these outcome measures. For example, there is no way to know from a study like this whether the vaccine is 100% effective in 95% of the population, or if it raises the infective dose in everyone by some amount which causes the number of people exposed to this critical viral dose in their environment to decrease by 95% (or some other effect with the same end result). Other approaches like challenge studies, where vaccinated individuals (or animal models) are intentionally exposed to a certain dose of the virus, can help understand the individual effects of vaccination, as can indirect measures of immune response like antibody titers. These approaches have other drawbacks, however (safety, translating animal results to humans, translating a given immune response to an infection chance, etc). Beyond just 'vaccine efficacy': disease severity, real-world efficacy These particular outcomes also say nothing about disease severity. It could be that the people who do test positive despite getting the vaccine get just as sick as the sickest people who don't (interpretation would be that the vaccine protects mostly against mild illness). It could also be the reverse, and that people who get the vaccine and still test positive have a milder illness than they would have otherwise. Efficacy defined by this relative risk ratio does not say anything about this, it only compares positive vs negative rates. An additional note: these numbers report efficacy in the trial environment. "Real-world" effectiveness (the same measure of effect, but in real world use rather than under trial conditions) might depend on other factors such as differences in the people enrolling in trials vs the general population (both in terms of things like age and preexisting conditions as well as behavior and exposure risks), failure to administer the vaccine properly (including improper storage), failure to complete both doses in timely fashion, etc. This measure of effectiveness also refers only to "primary" effectiveness. One would expect that if enough people were vaccinated, the effect on the population could far exceed the primary effectiveness, because not only do vaccinated individuals have a lower chance of infection, but everyone else in the population also has a lower risk if there are fewer people available to transmit the infection. | {
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97,076 | The main principle behind a vaccine is to take a deactivated virus, "show" it to the immune system so it can "learn" how it looks like, so if and when the real virus does attack us, our immune system is already prepared for it. Vaccines have been developed using this idea even in the 1880's. If that's the case, why does it take so much time and effort to develop a vaccine, for example, against covid-19? (and why are there several variants with different measures of reliability?) Is it only about balancing how strongly we damage the original pathogen, too much damage and our body might not learn the correct identifiers, and to little damage and it might still be active enough to cause the disease? | Roni Saiba's answer does a good job of explaining what goes into current vaccine development and why it takes so much effort, but I want to directly address the question of why we can't just grow some virus, kill it with UV and have a protective vaccine. The answer is that not all immune responses to viral antigens are helpful in fighting infections of that virus. In some cases it can be harmful; antibodies to dengue virus of one serotype will attach to viral particles of another serotype but aren't able to inactivate them. The attachment of antibodies to active viruses makes their absorption by cells more efficient, and infections where this antibody-dependent enhancement occurs are more severe than first-time dengue infections. Some viruses have evolved mechanisms to capitalize on this. The reason we need to get a new flu shot every year is that influenza viruses present a "knob" at the end of their glycoprotein that can change its structure and still retain function. This part is much more 'visible' to the immune system than parts of the virus that can't tolerate changes, so the immune response to this variable part outcompetes and prevents an immune response that would provide long-lasting protection. Conserved stalk-targeting vaccines are being intensely investigated for this reason. SARS-CoV-2 may have a immune-faking mechanism as well: the "spike" glycoproteins responsible for binding the ACE2 receptor and entering the cell convert to their post-binding form prematurely part of the time. Antibodies that bind the "post-fusion" form of the protein don't inactivate the virus, and this form sticks out more so may serve to compete for immune attention with the pre-fusion form that would provide protection if bound by antibodies. In this last example, we can see that a vaccine made of killed SARS-CoV-2 virus particles would be useless if all of the spike proteins had converted to the post-fusion state. The mRNA vaccines therefore don't encode the natural spike protein, but a mutated version which can't convert to the post fusion state as easily: S-2P is stabilized in its prefusion conformation by two consecutive proline substitutions at amino acid positions 986 and 987 In conclusion, viruses and the immune system are very complicated. Simple vaccines work for some viruses, and don't work for others. When they don't work, the reason is always different, but hopefully I've communicated some general understanding of the background issues. EDITS:
This doesn't relate to the rest of my answer but I want to respond to Ilmari Karonen's and there is not enough room in a comment. Looking at the timeline for SARS-CoV-2 vaccine development gives a very misleading impression of how long it takes generally. This is because ~90% of the development work was already done before COVID-19 was ever identified, in the 18 years since the SARS-CoV-1 outbreak started in 2002. Vaccines against SARS were developed and tested up to phase I trials, but couldn't proceed further since the virus was eliminated. I discussed this in a previous answer to a similar question , but to expand/reformat, here's some of what we knew and had available on March 17th 2020, when the "covid vaccine timeline" begins: Identified the receptor as ACE2, and knew that antibodies targeting the receptor binding domain (RBD) of the spike protein neutralize the virus. Protocols to test that these were also true of SARS-CoV-2 were already developed and validated. Without this there would have been a lot more trial-and-error experimentation and false starts with vaccine candidates that looked promising but didn't pan out in testing. Animal models. There is no naturally-occurring model organism for COVID-19. This is a subtle point because other animals can be infected with the virus, and some develop morbidities because of it. However, these are different enough from what we see in humans that something that protects against the reactions we see in the animal can't be assumed to protect against the reactions that cause problems in humans. For SARS, researchers developed transgenic mice that used the human version of ACE2, and showed that the disease they got from SARS were analogous to the disease humans got. This took several years, and the colony was still available when the virus causing the outbreak in Wuhan was identified as SARS-like and researchers started looking for animal models. As an aside, in an interview on This Week in Virology that I can't find right now, one of the maintainers of that colony said they were months or weeks away from shutting it down and euthanizing all the transgenic mice when the pandemic began, so if funding had been just a bit tighter we probably would not be having this particular conversation now. How to stabilize the pre-fusion form of coronavirus spike proteins had been determined from work on SARS and MERS vaccines. In addition to these, a large amount of miscellaneous knowledge about coronavirus functions and the immune reactions to them had been accumulated, and this sped up development, and increased confidence in results, which allows vaccine candidate production and testing to proceed more aggressively. Historically, vaccine development has taken years or decades of research after the need has been identified. Testing is still longer in many cases, but the current case is very unusual. | {
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97,635 | I was discussing with a colleague about using dark-mode vs. light mode and remembered an article arguing that humans vision is more adapted to light-mode rather than dark-mode: I know that the trend “du jour” is to have a dark mode for pretty much
everything, but look around the world is not dark with a bit of light,
it’s actually the contrary. And as the human has evolved its vision to
adapt to this reality, it’s asking extra efforts on many people. Unfortunately, no reference is provided to support this claim, so I am wondering if this is just an opinion or there are some studies to support this. Wikipedia seems to confirm this somewhat since we are adapting much faster to "light mode" transition than to dark mode one: This adaptation period is different between rod and cone cells and
results from the regeneration of photopigments to increase retinal
sensitivity. Light adaptation, in contrast, works very quickly, within
seconds. Also, some studies confirm that working using light mode is on average more efficient than using dark mode: light mode won across all dimensions: irrespective of age, the
positive contrast polarity was better for both visual-acuity tasks and
for proofreading tasks. I am looking for arguments coming from evolutionary biology to confirm (or not) the assumption that human evolution favors light mode. | A question that requires quite a lot of guts to ask on this site :) Nonetheless, and risking sparking a debate, there are a few arguments that spring to (my!) mind that can support the notion that we thrive better in 'day mode' ( i.e. , photopic conditions). To start with a controversial assumption, humans are diurnal animals , meaning we are probably, but arguably, best adapted to photopic (a lot of light) conditions . A safer and less philosophical way to approach your question is by looking at the physiology and anatomy of the photosensitive organ of humans, i.e. , the retina . The photosensitive cells in the retina are the rods and cones. Photopic conditions favor cone receptors that mediate the perception of color. Scotopic (little light) conditions favor rod activity, which are much more sensitive to photons, but operate on a gray scale only. The highest density of photoreceptors is found in the macular region , which is stacked with cones and confers high-acuity color vision. The periphery of the retina contains mostly rods, which mediate low-visual acuity only. Since highest densities of photoreceptors are situated at the most important spot located at approximately 0 degrees, i.e. , our point of focus, and since these are mainly cones, we apparently are best adapted to photopic conditions Kolb, 2012) . An evolutionary approach would be to start with the fact that (most) humans are trichromats (barred folks with some sort of color blindness), meaning we synthesize our color palette using 3 cone receptors sensitive to red (long wavelength), green (intermediate) and blue (short). Humans are thought to have evolved from apes. Those apes are thought to have been dichromats, which have only a long/intermediate cone and a blue cone. It has been put forward that the splitting of the short/intermediate cone in our ape ancestors to a separate red/green cone was favorable because we could better distinguish ripe from unripe fruits . Since cones operate in the light, we apparently were selected for cone activity and thus photopic conditions (Bompas et al , 2013) . Literature - Bompas et al ., Iperception (2013); 4 (2): 84–94 - Kolb, Webvision - The Organization of the Retina and Visual System (2012), Moran Eye Center Further reading - Why does a light object appear lighter in your peripheral vision when it's dark? | {
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98,252 | Today I read a BBC Report about how Pablo Escobar had once imported 4 hippos (1 male, 3 female) into his estate in Colombia for his private zoo. After his downfall, while other species were shipped out, hippos were considered too big to move and expected to not survive. However, to the surprise of all the hippos are thriving and are so numerous that there have been calls to cull them. From the report: Numbers are projected to only get bigger. [Colombian biologist Nataly] Castelblanco and her
peers say the population will reach over 1,400 specimens as early as
2034 without a cull - all of them descended from the original group of
a male and three females. In the study, they envisaged an ideal
scenario in which 30 animals need to be culled or castrated every year
to stop that happening. My understanding is that since there was only 1 male, the gene pool would be limited and lead to lot of inbreeding in the descendants. This would cause population to not explode because some individuals would be unfit to survive. Why has this not happened in case of hippos? Is it because there are 3 females (probably unrelated to each other) which keeps gene pool large enough? Or can mutations explain this phenomenon? Would results have been different if originally 2 females had been moved and only 1 retained? EDIT - I have just found that current population is maybe less than 100 individuals which though big is not massive . EDIT2 - I have edited the question title to keep focus on the hippos although a general answer would be welcome. | I think one of the important things to understand in thinking about this case is that it just hasn't been that long, generationally. Escobar imported the hippos in the late 1980s . Hippos reach sexual maturity at an average of about 7.5 years old for males and 9.5 years for females , space births about 2 years apart, and live for 40-50 years . Thirty years out, this means that only about 3 generations have passed for females. Moreover, the dominant males are highly territorial, which means that much of the breeding might even now be still coming from the initial male and not his descendants. Still, the initial male breeding with his own daughters would indeed produce a significant inbreeding coefficient. The impact of inbreeding, however, is also affected by the density of deleterious alleles. In geographically restricted species, the higher natural level of inbreeding can result in purging selection that leads to a much lower frequency of accumulated deleterious alleles than in highly social and gregarious species like humans and dogs . Hippos appear likely to be such a species, as well as having overall lower genetic variation than other large African mammals, suggesting a fairly recent expansion. In short: it hasn't been that many generations, and if the inbreeding sensitivity of hippos is indeed fairly low to begin with, it may indeed be that there simply isn't any significant impact from inbreeding at this point in time. | {
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98,613 | I've been working on a protocol standardization project where, among other things, we want protocols to be able to be run equivalently by both humans and robots. Something that I've noticed in doing so is that there's a radically different amount of information typically assumed needed by a human vs. a robot when it comes to pipetting. With a robot, it is generally recommended to understand the nature of the liquid thoroughly, specify the liquid class (which includes information on viscosity, volatility, polarity, etc), and do quite a bit of quality control to make sure than when you want to pipette 100 µL you actually get 100 µL. A typical example is shown on this page by Hamilton . With a human experimenter, however, the protocol pretty much always just says "pipette 100 µL" and assumes that the human can figure out all of the potential issues that we have to be so careful for with robots. Is this actually a safe assumption, or just something that we don't typically check during protocol development for humans? Is it really intuitively obvious for nearly all liquids, or should our protocols be providing more guidance for humans as well? | In my experience it is very rare to see a protocol for humans that describes how to pipette a certain liquid, but I don't have as many years pipetting as others do. In general, it is left to the experimenter to observe the behavior of the liquid and act accordingly. It is quite easy to determine when a liquid is leaking (e.g. ethanol) or when it is very viscous (e.g. glycerol), and determine that a change in technique is required. In this case, I would ask someone else in the lab how to deal with the situation. This is something that robots cannot do. However, not everyone has expert help available, and although it is fairly obvious when a technique isn't working, often the solution is not intuitive. Additionally, the advice of others in the lab could be unhelpful or even inaccurate. For example, I was told to cut the tip off a pipette in order to pipette Tween-20 more easily, however in reading for this answer have discovered that this is not recommended at all! (See eppendorf FAQ linked below). Therefore, I would say that, unless the liquid is to be pipetted in the same way as water, it is always useful to provide information for those who are not knowledgeable or do not have easy access to expert practitioners. For some examples of the sorts of problems that experimenters come up against, and therefore which liquids especially could use instructions in protocols, see this set of FAQs from eppendorf on handling liquids . | {
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100,082 | Why aren't there any competing biologies on Earth? I read sci-books about life based on silicon and I've read an article that said that other structures than DNA can encode genetic information . So does physics allow for many competing biologies? What makes DNA-based biology the dominant biology on earth according to known laws of physics? | There are indeed almost certainly other potential alternatives to DNA-based biology and the RNA-based biology that may have predated it, which could be used to form viable organisms. Many of them likely have some energetic disadvantage relative to DNA and RNA (e.g., requiring a higher bond formation energy, having a less flexible backbone) and those would naturally be expected to be outcompeted. But some probably aren't so different from DNA and could indeed have formed a viable alternative---if nothing else, the opposite chirality molecules are certainly candidates. Why aren't alternatives still around? Surprisingly, it turns out that when time scales are long enough, we should expect a natural loss in the number of different independent lineages . Another more recent example of this is the fact that all modern humans are descended from Mitochondrial Eve and Y-chromosome Adam , despite the fact that these two individuals were members of thriving human populations at entirely unrelated times. Biodiversity is constantly being gained through divergence of existing lines and lost through lines that fail to reproduce. Over many generations of reproduction, this produces a random walk pattern that converges toward elimination of all but a single lineage in a given population even if all lineages are equally fit . Now back to the origin of DNA-based life. If abiogenesis is a rare and difficult event, then we would expect only one or a small number of life models to have emerged billions of years ago. Random fluctuations over all that time will tend to drive all but one toward extinction. With evolution at play as well, any lineage that randomly gains an advantage will be even more likely to outcompete the others. And once there is life of any sort around? Well, potential alternatives to DNA are still nutrients, and therefore will simply be eaten by existing life forms before they have the chance to evolve into something new and interesting. | {
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100,242 | How likely is a lack of DNA match with a distant relative? I have recently gotten interested in ancestry research and have had a DNA analysis performed by a prominent commercial provider. I've been working on my family tree for a few months now and have gotten into contact with a lot of distant relatives of mine, which has generally been quite delightful. In one particular case, we discovered that we actually have a double-relationship about 5-7 generations back in time, depending on how you count (common links go back to about ~1790). We found this quite interesting, and this distant relative had a DNA analysis performed on their own genome as well. Much to our surprise, however, we didn't find any commonalities in our DNA, which seems odd given the double-relation, and the fact that we have what we believe to be original and authentic documents of all the relatives forming the link. Of course, we began speculating about the possible reasons for this. Maybe a misattributed child somewhere in the family tree? However, this seems unlikely, given the double nature of the link - most likely, we would need two misattributed children to explain the lack of any commonalities. The other explanation would of course be that the DNA analysis provided by these companies is less reliable than we think, and that just by random mutations and "unlucky" inheritance, any common DNA might have been lost or scrambled beyond recognition. I would like to calculate the probabilities of this happening in order to judge whether it makes sense to dig further into the original documents to try and clear up this mystery, or whether a mismatch by chance alone is sufficiently likely to explain this oddity. Of course, I don't need super precise numbers, but a back-of-the-envelope estimation would be nice - are we talking a few percent, or one in a billion? Also, I would be curious anyway on how to calculate probabilities like this, given the publicly available data on these tests. What are the relevant quantities for this calculation (number of SNPs, I suppose), and how would one define and calculate a probability like this? About myself I'm a physicist with a strong background in data analysis with some basic understanding of biology and genetics. Don't be afraid to hit me with those numbers and probabilities, but please explain any genetics jargon you're going to use! | First, if you haven't read it already, I highly recommend Carl Zimmer's "She has her mother's laugh." for anyone interested in ancestry/genealogy. In it, he presents the following figure showing the probability of sharing any autosomal DNA with a given ancestor as a function of the number of generations separating you from that ancestor. (notably, this analysis excludes the very real possibility of intermarriage within a family tree). So, for example, if you were to look at one single ancestor from 10 generations before you, there's a little less than a 50% chance that you share any of that ancestor's DNA (remember that at 10 generations you have roughly 1,024 ancestors). So, at 5-7 generations there's still a high probability that you both have at least some genetic material from the same common ancestor(s). But, it's much less likely that you both share the same pieces of that genetic material (probably in the 10-14 range on this graph). Plus, very few (probably none) of the commercial DNA ancestry sites do full genome sequencing for ancestry comparisons. They look at a limited number of specific regions that can help identify familial relations. So, even if you do share common ancestral DNA, it's less likely that it would be detected without whole genome comparison. Image Credit: https://gcbias.org/2013/11/11/how-does-your-number-of-genetic-ancestors-grow-back-over-time/ Edit I just wanted to edit and reference that the above analysis was calculated by Graham Coop and colleagues. I did a little more digging and he's got a blog post ( How many genomic blocks do you share with a cousin? ) with a more relevant analysis for you're specific question, showing the probability of two "cousins" having zero shared DNA blocks as a function of how many generations back the two shared common ancestors. Reference: https://gcbias.org/2013/12/02/how-many-genomic-blocks-do-you-share-with-a-cousin/ | {
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100,321 | The well-known cartoon imagery of porcupines shooting their quills at opponents in a fight is just that: a silly cartoon concept that isn't real. But it makes me wonder, does that mechanism exist elsewhere in nature? Are there any animals whose bodies produce solid projectiles that are used as launched/thrown weapons? (Not looking for liquid ranged weapons such as skunk spray, bombardier beetles, etc.) | A good exemple should be the “harpoon” in cone snails (Conidae), which is created from a modified tooth inside their proboscis. (Cone snail with proboscis, from KQED.org ) The harpoon is launched at prey at close distance, and is used to poison and stun prey, and later to pull them in. According to high-speed camera capture the harpoon is launched in just 200 microseconds, with an acceleration similar to a gun. The “harpoon“ structure is also very similar to a human made harpoon (see picture below) (from KQED.org , Courtesy Manuel Jimenez Tenorio, Universidad de Cádiz) (from KQED.org , Courtesy Joseph Schulz, Occidental College) These harpoons are not re-used, and a cone snail can have up to 20 harpoons at different stages of development (see Cone snail toxicity ). It is also worth noting that the harpoon and its venom is a potent defence weapon also against humans. One cone snail can contain poison to kill about 700 people, and people stung by cone snails can get severely injured or even die (fatality reported to 15-75% according to Kapil et al, see below). If you would include use of tools, in projectile use/shooting animals, apes and elephants are known to use stones as throwing weapons (see wiki-page linked below). Sources : https://www.kqed.org/science/1923898/watch-these-snails-stab-fish-and-swallow-them-whole wikipedia: projectile use by non-human organisms (with other examples of projectile use) Kapil S, Hendriksen S, Cooper JS. Cone Snail Toxicity. [Updated 2020 Sep 3]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. www.ncbi.nlm.nih.gov | {
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100,928 | Both the liver and the kidneys are involved in "cleaning" our blood. But why we have one liver and two kidneys? I can just as well imagine that we have two livers and one kidney. Is this just a coincidence? | Your organs can be grouped into two categories. The digestive tract organs, which are singular. These form from the endoderm. The liver and pancreases are all direct outgrowths from the digestive tract which is again singular. Everything else which comes in pairs. These form from the mesoderm or ectoderm. Even the brain and heart are paired organs, the heart starts as two organs and fused during embryonic development. The whole circulatory system starts perfectly paired, (embryonically and evolutionarily) but then specific parts close off to create the complex circulatory system of "higher" animals so we can have a high pressure section and low pressure section. The spine is also sort of singular but is basically the the line splitting the left from right half of the body. Everything that branches off the spine does so in pairs. The real questions is why you have two lungs and one spleen . They are the only organs that breaks the rules. The lungs are an outgrowth of the digestive tract and the endoderm, but is paired. The spleen is part of the circulatory system, but singular. Now the most primitive lungs are singular, it split later likely as animals got larger and needed more lung capacity and also needed a tight connection with circulatory system (paired). The spleen is the weird one, and likely harkens all the way back to before vertebrates existed, it predates the closed circulatory system, and develops on the midline of the body just like the spine and digestive organs. Just like how the spine is the midline dividing the nervous system into pairs the spleen divides the circulatory system into pairs. https://www.researchgate.net/figure/Embryology-of-the-gallbladder-A-In-the-early-embryo-liver-specification-occurs-in-the_fig1_303959093 https://embryology.med.unsw.edu.au/embryology/index.php?title=Cardiovascular_System_-_Spleen_Development https://embryology.med.unsw.edu.au/embryology/index.php/Gastrointestinal_Tract_Development#Germ_Layer_Contributions | {
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100,960 | mRNA vaccines instruct cells to produce spike protein that will trigger an immune response. But which types of cells will it work on? and which cells will it not work on? | Your organs can be grouped into two categories. The digestive tract organs, which are singular. These form from the endoderm. The liver and pancreases are all direct outgrowths from the digestive tract which is again singular. Everything else which comes in pairs. These form from the mesoderm or ectoderm. Even the brain and heart are paired organs, the heart starts as two organs and fused during embryonic development. The whole circulatory system starts perfectly paired, (embryonically and evolutionarily) but then specific parts close off to create the complex circulatory system of "higher" animals so we can have a high pressure section and low pressure section. The spine is also sort of singular but is basically the the line splitting the left from right half of the body. Everything that branches off the spine does so in pairs. The real questions is why you have two lungs and one spleen . They are the only organs that breaks the rules. The lungs are an outgrowth of the digestive tract and the endoderm, but is paired. The spleen is part of the circulatory system, but singular. Now the most primitive lungs are singular, it split later likely as animals got larger and needed more lung capacity and also needed a tight connection with circulatory system (paired). The spleen is the weird one, and likely harkens all the way back to before vertebrates existed, it predates the closed circulatory system, and develops on the midline of the body just like the spine and digestive organs. Just like how the spine is the midline dividing the nervous system into pairs the spleen divides the circulatory system into pairs. https://www.researchgate.net/figure/Embryology-of-the-gallbladder-A-In-the-early-embryo-liver-specification-occurs-in-the_fig1_303959093 https://embryology.med.unsw.edu.au/embryology/index.php?title=Cardiovascular_System_-_Spleen_Development https://embryology.med.unsw.edu.au/embryology/index.php/Gastrointestinal_Tract_Development#Germ_Layer_Contributions | {
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101,696 | I know that proteins perform a lot of functions and as a result there are a lot of different types of proteins in our bodies. When I eat food that has x grams of 'protein', what is this? A homogenous mix of proteins? A heterogenous one? Is it specific set of them that are general enough to be used by my body despite coming from a different organism? How can it be sure that my body can use the kind of protein in the food? | When we say "protein" with respect to food , what is generally meant is material that contains amino acids. Every protein is, at its heart, a long string of amino acids, which then gets processed through some combination of folding, cutting, and bonding together with other molecules. Much of our food is made out of cells, whether animal (e.g., meat), plant (e.g., vegetables, fruits, grains), fungal (e.g., mushrooms), or bacterial (e.g., yogurt). Every cell has a widely heterogeneous mix of proteins, comprised in turn of a widely heterogeneous mix of amino acids. Milk-based foods aren't cellular, but also have a wide range of amino acid content, because mammals produce milk as a complete food source for their babies. Inside your body, digestion breaks the proteins, whatever they might have been originally, down into amino acids, and that's what you really need to pay attention to in terms of nutrition. The human body can synthesize the majority of amino acids out of other molecules, but there are nine essential animo acids that we have to get from our food. Any diet that provides a sufficiency of those amino acids, no matter what sort of proteins they may be originally bound up in, will provide what you body needs in terms of protein. | {
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101,824 | This question has a specific context, a religious one, and so I'm not sure this is the right place to ask, but I can't think of a better place. I would like as objective and unbiased an answer as possible. I hope the religious context doesn't make this an unsuitable question. I'll explain the religious context: There is a religion that believes that a small number of Jews left Israel circa 600BC and sailed to the Americas, where they multiplied and built their own new civilization(s). This religious organization also has a history of teaching Native Americans that they are the descendants of this population, so therefore that their ancestors are Jews from 600BC. But we're quite lucky in the modern age that we can do genetic testing! And they have done, and of course they've found no signs of a genetic relationship between any Native American tribes and any known Israeli or Jewish populations. The organizations response to this is that, after 2600 years, you wouldn't expect any genetic similarities between the two populations - if they've been physically separated for so long, all genetic markers of a relationship would have disappeared. Is that correct? Would 2600 years be enough time to erase all genetic evidence that this population originated from Israel Jewish people? | If we assume a population of 100 individuals migrated from the Middle East to Central America 2600 years ago and, even if they underwent admixture from the local population, then there would be extremely clear genetic signal that those individuals were from the Middle East and not 'native' to Central America. Native Americans and individuals from the Middle East are sufficiently diverged that they are easily distinguished from one another. For example, you could plot all the populations on a Principle Component Analysis and the migrants from the Middle East would cluster with other Middle East populations and not Native Americans. The fact that 2600 years had passed since the migration event doesn't change this. In the context of distinguishing between populations, that amount of time doesn't erase genetic differences. A very similar event to what you mention has been shown to have occured when migrants from Persia moved to India with their Zoroastrian religion, forming the Parsee community in India. Clearly Middle East and Native Americans are much less genetically similar to one another than Indians and Iranians, so it would be similarly much easier to disinguish them genetically. | {
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103,027 | Given that each trophic level of the food chain has a decrease of 90% of available energy, would it be fair to say that 1kg of lettuce has more energy than 1kg of beef? If it's not true, can you explain the reason? | 1kg of beef has more energy than 1kg of lettuce but it isn't directly related to the trophic level energy loss. Given that each level of the food chain has a decrease of 10% of available energy You're all mixed up here. What the rule is saying is that if you start out with n units of solar energy, you lose 90% of it for every trophic level it passes through; Only 10% passes through as stuff that "stays around" materially (i.e. used to build the structure of the organism rather than being burned away as fuel to keep it alive). That means that it takes about 10x more energy to produce the same amount of edible calories in beef than it does in vegetables and grains, if they are separated by one trophic level. It's not talking strictly talking about the energy density in food, but instead about how wasteful it is to produce the food containing those edible calories from the point of view of the total solar energy invested. For the same solar energy, you can feed a lot more people calorie-wise with vegetables and grains than beef. It's kind of like thinking how many vegetables a rabbit eats over the couple years of its life from birth to when the rabbit becomes food for you. How long could you feed yourself on those same vegetables? Weeks maybe? How long could you feed yourself, if you ate the rabbit? A few days at most. You can imagine all those vegetables weigh more than the rabbit, but supply more energy than the rabbit meat, while the same mass of rabbit flesh has more calories than the same mass of vegetable. The rule isn't talking about calorie density of food. Obviously, there are complicating factors, such as the actual composition of the food, since that determines calories and nutrition (which isn't related to solar energy). The reason the same mass of beef has more energy is that 10% that sticks around keeps on accumulating. This is also the reason toxins accumulate in animals higher up the food chain. A little plankton might have a tiny bit of mercury in it, but a small fish might eat a billions of plankton. And, then a large fish might eat a thousand small fish. And, you might eat one large fish. If that mercury stuck around in everything that ate it, all that accumulated mercury ends up in you. | {
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104,444 | Heavy water (D 2 O) is known to be lethal to humans and other life in large quantities. All I've been able to find on the toxicity is that it's similar to chemotherapy chemistry. I'd like to know precisely how having a single neutron in two atoms of an otherwise non-toxic molecule can cause the body to degrade. What's the root cause here? | The question is already answered by Armand . I am just going to elaborate on that by referencing the paper. Different isotopes of chemical elements have slightly different chemical behaviors, but for most elements the differences are far too small to have a biological effect. In the case of hydrogen, differences in chemical properties among protium (light hydrogen), deuterium , and tritium occur, in part because chemical bond energy (the strength of a bond) changes with changed mass of the nucleus–electron system . The isotope effects are especially relevant in biological systems because of the prevalence of hydrogen atoms in biological molecules (even deuterated water can have significant effects in the human body). Note that enzymes have a finely-tuned network of hydrogen bonds, both in the active center with their substrates, and outside the active center, to stabilize their tertiary structures. In a deuterated environment, some hydrogen bonds will be replaced with deuterium bonds which have different strength ( Ref. 3 ), so normal reactions in cells can be disrupted. Studies and experiments* show that heavy water affects cell division(mitosis), cell membrane changes and cellular heat stability, possibly as a result of inhibition of chaperonin formation. Also noted among the presumably wide-ranging cellular effects was the display of an altered glucose metabolism under deuterated condition in cells. $D_2O$ is more toxic towards at least some malignant cells, but the difference in sensitivity vs. normal cells does not seem high enough for therapeutic use. In ref. 2, you will find a paper which shows the biochemical and pharmacological effects of heavy water on humans. Basically, to study the effects of heavy water on the metabolism humans, $D_2O$ and deuterated drugs were used and various changes were noted. Have a look for more details. References Effect on biological systems (Wikipedia) Kushner DJ, Baker A, Dunstall TG. Pharmacological uses and perspectives of heavy water and deuterated compounds. Can J Physiol Pharmacol. 1999 Feb;77(2):79-88. PMID: 10535697 . Steve Scheiner and Martin Čuma. Relative Stability of Hydrogen and Deuterium Bonds. J. Am. Chem. Soc. 1996 118, 6, 1511–1521 DOI: 10.1021/ja9530376 *Experiments with mice, rats, and dogs have shown that a degree of 25% deuteration causes (sometimes irreversible) sterility, because neither gametes nor zygotes can develop. Mammals (e.g. rats) were given heavy water to drink die after a week, at a time when their body water approaches about 50% deuteration. The mode of death appears to be the same as that in cytotoxic poisoning or in acute radiation syndrome , and is due to deuterium's action in generally inhibiting cell division. | {
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105,239 | A simple mental model of a viral infection is that an infected cell emits a lot of virions and eventually dies. The emitted virions have a chance of infecting other cells. Nearby cells are at a higher risk of infection. Based on this model, if one cell in my nose gets infected, I would expect a large part of my nose to be destroyed, as the infection spreads and destroys more and more cells in the same area. This does not happen! I survived a number of infections and still have my nose. Why? I know there are "flesh eating" bacteria. Why isn't this the norm for infections? Does a common cold virus or SARS-CoV-2 not infect a lot of cells within the same area? | A virus does not destroy that many cells before it is exterminated by the immune system or before the host dies. Perhaps even more crucially, viruses typically target a very specific type of cell — those on the inner mucal surface of the nose in the case of cold or flu, those of the gastrointestinal tract in the case of stomach viruses, CD4 immune cells in the case of HIV, etc. Update As an example of how much time it takes for a virus to eat a noticeable wound, one could take the extermination of the immune cells by HIV - although it does not look as a physical wound, it is one, in the sense that enough of the specific tissue is destroyed to cause a life-threatening condition. It takes about a decade(!) - from the initial infection to the immune system failure. On the other hand, the lethal effect of typical respiratory viruses is typically via obstructions of the respiratory ways due to inflammation or secretions resulting from the immune response, or via creating suitable conditions for a more serious bacterial infection. | {
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105,271 | I read the generalization that life originates from a cell, and from my understanding animals, they originate from a single cell, produced as a result of sexual reproduction. And then life begins to develop from there on. But when it comes to botany, I stumble upon this doubt because of plant seed varieties. During any stage of seed production, can the seed be designated as having come from a single cell. Can i use the following generalization and correct me wherever i am wrong. every life is made of cells, and every life comes from a single cell | A virus does not destroy that many cells before it is exterminated by the immune system or before the host dies. Perhaps even more crucially, viruses typically target a very specific type of cell — those on the inner mucal surface of the nose in the case of cold or flu, those of the gastrointestinal tract in the case of stomach viruses, CD4 immune cells in the case of HIV, etc. Update As an example of how much time it takes for a virus to eat a noticeable wound, one could take the extermination of the immune cells by HIV - although it does not look as a physical wound, it is one, in the sense that enough of the specific tissue is destroyed to cause a life-threatening condition. It takes about a decade(!) - from the initial infection to the immune system failure. On the other hand, the lethal effect of typical respiratory viruses is typically via obstructions of the respiratory ways due to inflammation or secretions resulting from the immune response, or via creating suitable conditions for a more serious bacterial infection. | {
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105,362 | I would like to understand the effect of an mRNA vaccine on more complex processes in the human body. To what extent does this "artificial", external addition of mRNA interfere with the body's processes? It seems naïve to me to think that it cannot set processes in motion that can be passed on - positively or negatively - to future generations. Do I have a wrong idea about "artificiality" or the processes in the body? As far as I know, there are (permanent) processes going on in the human body to modify the genetic information that will be passed on to future generations. I also wonder to what extent this "reprogramming" of the immune system places a (too) strong focus on COVID-19 and whether this can weaken the immune response to other diseases. I have a naive idea of a "point system" where only a certain number of resources are available for different disease control. | I can address some of the points made in the post. One point about the "artificiality": I think there's one fact that's often overlooked in the discussion of mRNA vaccines. SARS‑CoV‑2 , for example, is a positive-sense single-stranded RNA (+ssRNA) virus. That means, the information that the virus uses to replicate itself and which describes the "blueprint" of its components, is stored as a single RNA. This RNA can more or less directly be translated into corresponding proteins by the ribosomes outside the nucleus, just like the mRNA used by mRNA vaccines. So, during a "natural" infection with such a virus, the virus's RNA also gets inside the cells and is translated into proteins, just like with the "artificial" mRNAs by vaccines! But the way this RNA enters the cell is somewhat different. With viruses, they dock onto the cell and release their RNA into the cell. With mRNA vaccines like the one by BioNTech/Pfizer and by Moderna , this RNA is packaged into lipids (the stuff cell membranes are made of), which integrate more or less directly into the cell membrane and release the RNA. With vector vaccines like the Sputnik V or the Oxford–AstraZeneca vaccine, a different virus is used to carry the RNA load and infect cells (in the case of AstraZeneca, an adenovirus is used which usually infects chimpanzees and is normally harmless to humans). RNA in any case is degraded by the cells within a short time and leaves no traces. Regarding the permanent modification of genetic information in humans: the genetic information in humans is stored as genomic DNA in the cell nucleus. DNA has a structure similar to RNA, but they do not work together, so RNA can't be simply integrated into the DNA. For DNA to form proteins, which make up most of the parts of a cell, it needs to be transcribed into RNA, which then is further processed into mRNA. This mRNA is tagged with a molecular export factor, which it needs to pass through the nuclear pore complexes, which are the highly specific transporters between the nucleus and the cytosol . After an mRNA has been exported from the nucleus, this tag is cleaved, so it can't return to the nucleus. Additionally, only if genetic information of egg or sperm cells is altered, this change is actually passed to the next generation. So in summary: mRNA from vaccines behaves pretty much like the RNA inserted by RNA viruses into cells. And it can't find its way into the nucleus, where the genetic information is stored. And even if that happens by some way, it would first need to get "reversely transcribed" into DNA to be integrated. Some viruses can in fact do that, like HIV , which can also break into the nucleus in some instances (or wait for a cell division). Simple, "naked" mRNA of a vaccine however can't do that, only in extremely rare circumstances where the cell is already infected by another virus like HIV, I suppose. But maybe you were talking about what is called " epigenetic modification", which is the molecular modification of the genomic DNA, where the actual stored sequence information is not altered, but the way it is read is modified. This process however is mediated for example by methylation of parts of the genome, for example, and does not intrinsically have anything to do with mRNAs in the cytosol. It should be noted that epigenetic modification is usually also reversible, not permanent, but it can be passed to the next generation, just like the genome itself. What you said concerning the immune system focussing too much on another disease: I don't know a lot of immunology, but usually, building an immune protection against one pathogen also strengthens resistance against others. However, problems concerning the immune system most often arise when the immune system "overreacts" to an antigen and starts attacking parts of its own organism (autoimmune reaction). This can in fact be triggered by vaccines, even by only mRNA (and its protein products), as well as "natural infections", of course. Clinical studies are in place to analyze these occurrences. | {
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105,460 | If we can make RNA vaccines against COVID-19 and we know which errors in our DNA leads to different kinds of cancer, can we make a vaccine that will teach our immune system to detect and destroy cancer cells? | It is not only possible, these vaccines are in active development. Biontech (the company which developed the Comirnaty Corona vaccine) was founded to develop vaccines against cancer, Moderna is developing similar approaches. It was the research on the cancer vaccines and the development of the mRNA vaccine approach in general made the fast vaccine development for the SARS-CoV-2 vaccine possible. Biontech has published results of a mRNA based cancer vaccine against melanomna in the summer of 2020 (reference 1) which shows promising results, Moderna has shown data from a phase I study on head and neck squamous cell carcinoma (reference 2). See references 3 and 4 for an overview over the topic. References: An RNA vaccine drives immunity in checkpoint-inhibitor-treated
melanoma Moderna Announces Clinical Updates on Personalized Cancer Vaccine
Program mRNA vaccine for cancer immunotherapy mRNA vaccines — a new era in vaccinology | {
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105,552 | I was watching Vox’s video, Big questions about the Covid booster shot, answered , which references the New York Times article Omicron Prompts Swift Reconsideration of Boosters Among Scientists . In these sources, it is mentioned that the scientific community used to be mostly against giving a booster shot to the less vulnerable. With the emergence of the Omicron variant, the same scientists who were opposed to booster shots have now changed their minds. However, no complete explanation was given for this, and my further research led to nothing concrete. As per my understanding, vaccinations provide protection both by increasing antibodies in the blood (which provides protection for about 2 weeks), or by increasing B cells which would be able to identify the spike protein of the virus and help create antibodies (which provides more long-term protection). With the Omicron variant, my understanding is that there are several mutations in the spike protein, which means that B cells may not recognize it or the antibodies might not bind to its receptors. If this is the concern, then how is the Omicron variant a reason for extra doses of the preexisting vaccines? | (note: I'm simplifying things a bit here by only talking about antibodies; I don't mean to downplay other aspects of the immune response, just to keep it focused for a lay audience) Natural antibody responses by the immune system are polyclonal - there isn't just one antibody to meet one antigen, but numerous different antibodies that may each recognize a slightly different part of the antigen. Antibody binding (or ligand binding more generally) is also not "all-or-none". We usually describe ligand binding in biology by "affinity" . When a receptor has a lower affinity for some ligand, you need higher concentrations of the ligand to saturate the same fraction of receptors (or vice-versa). You can expect that antibodies raised against a coronavirus spike protein may have lower affinity for spike proteins altered by mutations in a viral lineage. It's also reasonable to expect that the more changes (mutations) there are, the more the affinity will change and the more antibody clones will be affected. It's still unlikely that every different antibody in a polyclonal response will stop binding completely, but the reduced affinity is likely to equate to a reduced immunity. It's not easy to quantify this at the level of the whole organism, but it's normal to do in vitro binding experiments where you mix a mutated viral protein with some antibodies raised to a previous version. The extent of binding is a good qualitative approximation for how well immune responses will transfer. Probably the best approach would be to give boosters with a spike closer to the new dominant variant at any point. However, that requires testing and manufacturing and simply isn't going to happen in time to be useful. In the meantime, the best alternative is to be prepared against the next-closest thing. As an approximation, you might say that if binding affinities are reduced by 50%, then if you can double your antibody response you've got about the same immunity. Previous experience with the delta variant showed that antibodies raised in response to vaccination with the original spike protein still bound, even if they didn't bind as strongly. It seems like vaccinated people had good protection against delta even if it wasn't as good as their protection against the original strains. We can expect the same trend for the new variant, though we'll need further data to understand quantitatively where that protection level is at. | {
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108,084 | I don't know, if it's a physics question, biology or chemistry question but anyways here it is: I have been taught that to produce one molecule of glucose in photosynthesis, 18 ATP molecules are used up, but that in respiration, oxidation of the same glucose molecule releases 38 ATP molecules. I just can't seem to wrap my head around it. Where are these extra 20 ATP molecules coming from (or in other words extra 20 units of energy)? I know there's a whole lot of reactions occurring in the cell that utilize energy, but the reactions of photosynthesis and respiration are reversible and I don't think the path to make or break glucose actually matters with respect to the amount of energy used or released in the processes. Glucose always remains glucose so of course writing the same reactions in reverse orders shouldn't change the energy used/given out in the reaction. I really can't understand why it should it depend on the path by which glucose is used or made as many people have told me. So in my opinion these two processes do seem to violate the law of conservation of energy, so please help! | With slight adjustments to the scientific wording, what the poster states is in effect: “…to produce one molecule of glucose in photosynthesis, 18 ATP molecules are used up hydrolysed” and “…oxidation of the same a glucose molecule releases phosphoryates 38 ADP molecules to ATP” These statements are both correct … …but the logical fallacy arises because the first one is incomplete . In the context of energy production and utilization, it is essential to add: …and 12 molecules of NADPH are used (i.e. oxidized to NADP) This is because 1 molecule of NADPH is energetically equivalent to 3 molecules of ATP. (Oxidative phosphorylation will convert NADPH + 3ADP to NADP + + 3ATP). Hence it takes 54 ATP equivalents to synthesize a molecule of glucose, but one only gets (approx) 38 molecules of ATP from oxidizing glucose. If you think right back to the light reactions of photosynthesis, the photons of light energy are used to do two things — phosphorylate ADP to ATP, and to reduce NADP + to NADPH. | {
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108,091 | When our teacher was talking about the gas exchange inside the alveoli, he mentioned the flow of air and the flow of blood was going in opposite directions so that there always would be a concentration difference. Because of this the gas exchange between the alveolar space and capillary continues and reaches ~99%. I could not understand how the air would always go in the same direction so I researched about the topic. All resources I found state that when the air enters the alveolus there is a pressure gradient for both oxygen and carbon dioxide between the capillary and the alveolar space. But I found nothing mentioning the opposite direction of flow for air/blood. So does that mean gas exchange for oxygen and carbon dioxide stop when diffusion equilibrium is reached? (I'm not a native English speaker so I hope this question makes sense.) | With slight adjustments to the scientific wording, what the poster states is in effect: “…to produce one molecule of glucose in photosynthesis, 18 ATP molecules are used up hydrolysed” and “…oxidation of the same a glucose molecule releases phosphoryates 38 ADP molecules to ATP” These statements are both correct … …but the logical fallacy arises because the first one is incomplete . In the context of energy production and utilization, it is essential to add: …and 12 molecules of NADPH are used (i.e. oxidized to NADP) This is because 1 molecule of NADPH is energetically equivalent to 3 molecules of ATP. (Oxidative phosphorylation will convert NADPH + 3ADP to NADP + + 3ATP). Hence it takes 54 ATP equivalents to synthesize a molecule of glucose, but one only gets (approx) 38 molecules of ATP from oxidizing glucose. If you think right back to the light reactions of photosynthesis, the photons of light energy are used to do two things — phosphorylate ADP to ATP, and to reduce NADP + to NADPH. | {
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108,749 | If, as a physicist, I were to be told that quarks have never been isolated, and so they are not actually real particles, it would take some effort to respond. I'd have to talk about the Standard Model and Asymptotic Freedom, and thus admit that they do have some properties that are not like other particles. If faced with insistance that this proves the case, that they are actually some sort of epiphenomenon of particle accelerators, I might have some difficulty knowing how to proceed. It's true that they manifest an as yet new characteristic, and so perhaps we have to expand our conceptualizaiton of what a particle is. That may not be a perfect analogy for my question, but I have a medical friend who would like to tell me that no virus has ever been isolated, and that as opposed to some kind of transmissible, infectious organism, they are actually some kind of waste product of cells. I am told that any attempt to satisfy Koch's postulates involves the injection of materials in addition to the viruses at issue, and the claim is that it's these combination of materials that is making the animal sick. I see a lot of varied "viruses don't exist" claims around the web, focused on HIV, measles, and CV19, and associated with names like Drs. Stefan Lanka, Andrew Kaufman, Tom Cowan, etc. Associated claims are that in any context that involves supposed exposure to a virus, less than 100% of the animals get sick, and so whatever may be going on, it's the animal itself at issue. In some quarters this is called "Terrain Theory." I would like to not have to dig too far into this. How can I respond in a coherent way that doesn't require becoming a virologist? | It is very easy to disprove their claims, but the burden of proof doesn't lie with you, it lies with the person making the claim. If they want to claim that there is a "cell waste product" that causes the widely varying symptoms and viral effects (in cells, model organisms etc) we see with different viruses (compare say chickenpox with SARS-CoV-2), then they need to prove that this is the case. They need to do the science and have it passed through peer review etc. Also remember that extraordinary claims require extraordinary proof - they need to prove the whole scientific consensus wrong in this case! At its most simple, you can purify viruses via a range of methods (e.g. ultrafiltration , ultracentrifugation , chromatography etc) and resuspend in a simple salt solution of varying compositions (e.g. phosphate buffered saline , ringer's solution , tris buffered saline ) and use that purified virus to infect. I would hope that even the most science-denying person would see that these solutions are very simple and don't contain anything special that could be "cell waste" or "its the fetal bovine serum" (another virus-denier claim). I would note that most of these denier people wouldn't understand the principles behind the above methods, but using them you can get pure preparations of viruses and other materials, down to separating out single molecule types from a crude solution. You also run controls of the solution alone and easily see that the animals/cells don't infect at all with these controls, but do infect with the virus containing material. You can also run controls on your sample prep - for example, treat uninfected cells to the same virus preparative procedures as you did for the virus and show that this also doesn't result in infection. If it were a product of cell waste you would expect to see these effects from all cells, not just virus infected ones. For a cell waste you should also see some sort of dilution effect that is non-propagable (i.e. can't be passed on) - take your purified virus and dilute it in your solution of choice and it will still infect, but "purified" material from un-infected cells won't. An additional note: You can also take the genetic material of the virus and use that to produce more virus. In some cases (as with positive sense RNA viruses and DNA viruses) you can use the genetic material directly and produce more viruses with the same characteristics as the source of the genetic material. Now, it doesn't work for some viruses - some genomes are too big, need special conditions, etc., but it does surpass some of Koch's postulates, as in you can synthesize this genetic material in the lab and using that material along with cells to produce a virus with exactly the characteristics of the original source of the genetic material. | {
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110,819 | It is my (very basic) understanding that neither plants nor animals utilize the nitrogen in the atmosphere. Humans do not make use of atmospheric nitrogen through respiration and plants do not extract nitrogen from the air, but rather from the soil. First of all, am I correct in this understanding? If I'm right so far, then what role (if any) does the nitrogen in our atmosphere play, biochemically speaking? I understand that it plays a significant physical role, contributing to air pressure, allowing light to permeate, allowing liquids to exist on the surface, burning up incoming meteors thus protecting life, and basically being a physical gas that is not oxygen or carbon dioxide thus keeping the concentration of those gasses low. But I'm interested in the biochemical use of atmospheric nitrogen if any. So, is nitrogen a necessary atmospheric component for life, in terms of its chemical reactions with living things? Or is the atmospheric nitrogen essentially unused in the chemistry of life? | To get soil nitrogen in the first place, nitrogen fixation is necessary which takes atmospheric N 2 and converts it into biologically useful forms. Nitrogen fixation is performed by bacteria and archaea. You may occasionally hear about nitrogen fixing plants, especially peas and beans in an agricultural context, but these involve symbiotic relationships with bacteria that do the actual work. | {
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111,146 | The majority of western nations have lifted most if not all COVID restrictions, however we are not seeing a massive rise in serious cases of COVID-19. Why is it different in China? Do they have a different strain? | There are a number of different reasons, all adding up to the current situation. The strain: There is not a special strain going on in China, according to different references it is mostly the Omicron BF.7 substrain. This strain is highly transmissible (with reported $R_0$ over 10, meaning each infected person infects on average another 10; the Delta strain (which was also already seen as highly infectious) "only" came to an $R_0$ of 5-6). Additionally this strain has accumulated mutations which allow immune escape, a shorter incubation time. Covid politics: China went from a very strict zero Covid politics to no restrictions at all in the matter of days. Additionally, testing almost completely stopped. This happened with the rise of the highly contagious variant. People started getting together and spread the virus very fast, leading to the current problems. Vaccinations: In China only the relatively inefficient Sinovac vaccine has been used, as far as I know only two vaccinations are common, with no preference for the older part of the society. How this vaccination (which happened some time ago mostly) will be able to prevent severe disease and death remains to be seen. However, the vaccination status could be better. Immune status: Curiously, this point is connected to the zero Covid policy. This lead to many people in the Chinese society having never had contact to SARS-COV2. Without this contact, immunity cannot be built (besides vaccinating), this may be an advantage for other societies which had more contact with the virus, although immunity wanes over time. Population: All the areas where Covid surges now are urban centers with a really high population density. Additionally public transport leads to a lot of potential contacts. Every of this point attributes a bit to the current problem, but only the combination made it so severe. References WHO concerned over increasing reports of severe COVID-19 cases in China COVID spreading faster than ever in China. 800 million could be
infected this winter China’s COVID Wave Is Coming Omicron BF.7, major strain causing latest outbreak in Beijing, has
strong infectious ability: medical expert | {
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111,169 | I was reading the paper "A survey of methods and tools to detect recent and strong positive selection" (2017) and came across this: Upon fixation of the beneficial mutation, elevated levels of LD emerge
on each side of the selected site, whereas a decreased LD level is
observed between sites found on different sides of the selected site.
The high LD levels on the different sides of the selected locus are
due to the fact that a single recombination event allows existing
polymorphisms on the same side of the sweep to escape the sweep. On
the other hand, polymorphisms that reside on different sides of the
selected locus need a minimum of two recombination events in order to
escape the sweep. Given that recombination events are independent, the
level of LD between SNPs that are located on different sides of the
positively selected mutation decreases. I am having trouble understanding how this works. If I am understanding this correctly, if you took two sites on the left side of the beneficial mutation during a selective sweep, you would see high LD between them. The same goes for taking two sites on the right side of the beneficial mutation. (Provided they are close enough to the mutation site of course.) However, if you took one site 300 bp to the left of the mutation, and another 300 bp to the right of it, you may not see the same rise in LD. I am not sure why this would be the case: wouldn't the entire region linked to the beneficial mutation, regardless of which side of the mutation it occurs to, be co-inherited and thus display similar high LD across the board, provided it is overall close enough to the site of beneficial mutation? | There are a number of different reasons, all adding up to the current situation. The strain: There is not a special strain going on in China, according to different references it is mostly the Omicron BF.7 substrain. This strain is highly transmissible (with reported $R_0$ over 10, meaning each infected person infects on average another 10; the Delta strain (which was also already seen as highly infectious) "only" came to an $R_0$ of 5-6). Additionally this strain has accumulated mutations which allow immune escape, a shorter incubation time. Covid politics: China went from a very strict zero Covid politics to no restrictions at all in the matter of days. Additionally, testing almost completely stopped. This happened with the rise of the highly contagious variant. People started getting together and spread the virus very fast, leading to the current problems. Vaccinations: In China only the relatively inefficient Sinovac vaccine has been used, as far as I know only two vaccinations are common, with no preference for the older part of the society. How this vaccination (which happened some time ago mostly) will be able to prevent severe disease and death remains to be seen. However, the vaccination status could be better. Immune status: Curiously, this point is connected to the zero Covid policy. This lead to many people in the Chinese society having never had contact to SARS-COV2. Without this contact, immunity cannot be built (besides vaccinating), this may be an advantage for other societies which had more contact with the virus, although immunity wanes over time. Population: All the areas where Covid surges now are urban centers with a really high population density. Additionally public transport leads to a lot of potential contacts. Every of this point attributes a bit to the current problem, but only the combination made it so severe. References WHO concerned over increasing reports of severe COVID-19 cases in China COVID spreading faster than ever in China. 800 million could be
infected this winter China’s COVID Wave Is Coming Omicron BF.7, major strain causing latest outbreak in Beijing, has
strong infectious ability: medical expert | {
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111,196 | In the answer(source - Campbell Essential Biology with Physiology, self-quiz question), it's given that "if the change doesn't affect the protein's shape in any way then it's possible to do so". But practically, is it possible to amend a protein without changing its shape? | There are a number of different reasons, all adding up to the current situation. The strain: There is not a special strain going on in China, according to different references it is mostly the Omicron BF.7 substrain. This strain is highly transmissible (with reported $R_0$ over 10, meaning each infected person infects on average another 10; the Delta strain (which was also already seen as highly infectious) "only" came to an $R_0$ of 5-6). Additionally this strain has accumulated mutations which allow immune escape, a shorter incubation time. Covid politics: China went from a very strict zero Covid politics to no restrictions at all in the matter of days. Additionally, testing almost completely stopped. This happened with the rise of the highly contagious variant. People started getting together and spread the virus very fast, leading to the current problems. Vaccinations: In China only the relatively inefficient Sinovac vaccine has been used, as far as I know only two vaccinations are common, with no preference for the older part of the society. How this vaccination (which happened some time ago mostly) will be able to prevent severe disease and death remains to be seen. However, the vaccination status could be better. Immune status: Curiously, this point is connected to the zero Covid policy. This lead to many people in the Chinese society having never had contact to SARS-COV2. Without this contact, immunity cannot be built (besides vaccinating), this may be an advantage for other societies which had more contact with the virus, although immunity wanes over time. Population: All the areas where Covid surges now are urban centers with a really high population density. Additionally public transport leads to a lot of potential contacts. Every of this point attributes a bit to the current problem, but only the combination made it so severe. References WHO concerned over increasing reports of severe COVID-19 cases in China COVID spreading faster than ever in China. 800 million could be
infected this winter China’s COVID Wave Is Coming Omicron BF.7, major strain causing latest outbreak in Beijing, has
strong infectious ability: medical expert | {
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111,543 | I was a molecular biology major a while ago, but I never think I really understood cladistics TBH. Now reading about paraphyly , it shows this: In this phylogenetic tree [second image], the green group is paraphyletic; it is composed of a common ancestor (the lowest green vertical stem) and some of its descendants, but it excludes the blue group (a monophyletic group) which diverged from the green group. Looking at the "simiiformes", I can understand why you would call that "monophyly", because everything is connected to a common ancestor. But why not just make the blue area a full blue triangle to make the prosimii and simiiformes one triangle/group? In the end, we all share the same ancestor, so I don't see why they are disconnected. TBH I'm not sure how to read this at all, and am not following the Wiki description. Can you explain how the 3 terms work for a child or layperson with a better concrete example? We are all composed of atoms, so we are all made of matter. Matter is made of particles, so we are all made of particles. But light is a particle and we are not made of light, even though in some way "we share the same common ancestor" of the quantum field. But light is still called a particle, so the triangle is the group of all particles. I'm not sure I'm getting on the right track. A paraphyletic group is a monophyletic group from which one or more subsidiary clades (monophyletic groups) are excluded to form a separate group. Why would they do that? | These are terms to describe names we give things that don't really follow phylogeny accurately. Fish, for example - a monophyletic group involving fish would include humans, too, yet there are many cases where it's useful to talk about fish without meaning every land vertebrate, too. From the page you link to : The term was coined by Willi Hennig to apply to well-known taxa like Reptilia (reptiles) which, as commonly named and traditionally defined, is paraphyletic with respect to mammals and birds. Reptilia contains the last common ancestor of reptiles and all descendants of that ancestor, including all extant reptiles as well as the extinct synapsids, except for mammals and birds. Other commonly recognized paraphyletic groups include fish, monkeys, and lizards. If you want to use any of these labels: fish, monkeys, lizards, reptiles, it's useful to have a term to describe how those labels relate to phylogeny, hence the term paraphyletic. | {
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86 | This FAQ explains and gives examples how to typeset chemical equations, quantities and units, and mathematical expressions on Chemistry Stack Exchange (rather than posting pictures, which you can't edit or search). Refer to the table of contents below to find topics you need to format questions and answers. The technology used for typesetting is called MathJax. MathJax's syntax is very similar to LaTeX, so if you have written mathematical expressios with LaTeX before, almost everything you are used to will work. Chemical equations can be typeset with the mhchem package for MathJax, which largely behaves identically to the mhchem LaTeX package. Units and scientific notation are also formatted using mhchem. Table of contents Getting started Basic MathJax Superscripts and subscripts Fractions and square roots Greek letters and other symbols Other commands Basic mhchem Chemical formulae Chemical reactions Quantities with units Learning by example Further reading | (1) Getting started There are three different types of markup (formatting commands) that we can differentiate between. Markdown Markdown is a simple markup language that is widely used on the Internet, and is built into all Stack Exchange websites. It allows you to (for example) write bold text, italicised text, and create hyperlinks. When writing a question or answer, there are a number of buttons in the editing box that can help you with this. For more information, please see the editing help . A limited subset of raw HTML tags are allowed on Stack Exchange, but these should generally not be required to write an answer. MathJax MathJax is a library which allows your web browser to display expressions written in $\LaTeX$ syntax. Expressions that are enclosed within single ( $...$ ) or double ( $$...$$ ) dollar signs are interpreted using MathJax. Where possible, all mathematical expressions, except those in titles, should be typed using MathJax. $...$ - A pair of single dollar signs specify an inline equation . This means you can use it seamlessly inside a sentence. Type this: Let $V$ denote the volume of a gas. to get this: Let $V$ denote the volume of a gas. $$...$$ - A pair of double dollar signs specify a display equation . It gets its own line, is generally slightly larger, and is centred on the page. Type this: The ideal gas law is written as:
$$ pV = nRT $$ to get this: The ideal gas law is written as: $$ pV = nRT $$ mhchem The mhchem package for MathJax adds extra functionality for chemical equations, as well as quantities with units, in MathJax. It provides two main commands: \ce{...} is used for typesetting chemical formulae and equations; \pu{...} is used for typesetting numbers with units / dimensions. These two commands must appear within a MathJax expression: that means it must itself be enclosed either with $...$ or $$...$$ . Whatever is placed within the braces will be automatically passed to the mhchem package for rendering. Note that the use of plain MathJax, i.e. $H_2O$ , leads to italicised chemical symbols like $H_2O$ which are not correct. Therefore, chemical equations should always be typeset using mhchem, and not simply in plain MathJax. Type this: The chemical formula of water is $\ce{H2O}$.
The freezing point of water is $\pu{273.15 K}$. to get this: The chemical formula of water is $\ce{H2O}$ . The freezing point of water is $\pu{273.15 K}$ . ( Back to index ) Next section: (2.1) Basic MathJax: Superscripts and subscripts | {
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3,044 | Making a good edit is hard. On Chem.SE, we (would/should/could) care about the finest points of formatting . There are basic points of editing many editors know about: Put some fancy MathJax/ $\mathrm\LaTeX$ -syntax in, some paragraphing, bullet points for "points", embolden instead of capitalize, etc. However, there are certain features only the best editors know. This post is a collection of those finer points, which may give a better push to the learning curve of the newer editors and people who want to try editing on chemistry.SE. This post is a community effort, hence it is community wiki. That means, that everybody who has more than 100 reputation points can freely edit it. If you see that anything is missing in this list, please add a new answer and also link to it in the Overview . For basic editing for beginners please see: How can I format math/chemistry expressions here? | Overview and Quicklinks (ordered chronologically, oldest entry first) Units formatting Use mhchem for MathJax to format chemical expressions Sizing for images Grammar, spelling, and style Compose good titles and headings Be judicious when editing questions that are [on hold] or [closed]. Don't let the broad tag be Text and spaces in MathJax Use display style maths wherever possible Comprehensive editing Add relevant keywords to images Use environments to cluster mathematical expressions Remove salutations, stick to the point Edit in new tab/window Above and below in mathematical (or chemical) expressions Write short \newcommand s|| \def ine short acronyms for complex terms Different font sizes in MathJax Write special characters with ease Add color to track/emphasize terms Hide text in posts | {
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3,066 | A small but significant fraction of the questions consists of nomenclature questions. In principle, virtually all nomenclature questions resemble one another, but they are quite different from other chemistry questions. Therefore, we gathered some guidelines about best practices for asking and answering nomenclature questions. These guidelines are meant to be recommendations, not absolute rules. The verbal forms “should” and “should not” are used to indicate that among several possibilities one is recommended as particularly suitable, without mentioning or excluding others, or that a certain course of action is preferred, but not necessarily required, or that (in the negative form) a certain possibility or course of action is deprecated but not prohibited. This specifically excludes changing a question after it was answered. Chameleon questions will be rolled back to the last edit, where the answer still made sense. The recommendations for questions and answers belong together, since usually the best way to answer depends on the actual question and the best way to ask a question depends on the expected answer. We decided to give an overview first, while extending the specific points in separate answers. You may discuss the recommendations in comments below each post. These guidelines have been established through general agreement based on the SE voting system. If you think something is missing or there is a mistake you can edit the post itself. However, it might be a better course of action to discuss drastic changes first. If you would like to propose an alternative strategy, or your comment is too long, you can add another answer for discussion, which may later be incorporated into the existing ones. Note that virtually all nomenclature questions ask for the name for a given chemical structure (convert structure to name) . Although the opposite direction (convert name to structure) may occur in nomenclature questions; the present recommendations are focused on the most frequent case. | Asking nomenclature questions Many nomenclature questions may be considered homework-like questions, even if they are not actual homework assignments. (For more details see the homework policy .) For most compounds, a thorough derivation of the complete name would involve many nomenclature rules, and therefore would be too long for this format. The correct answer to your question may depend on the particular case, and thus it may not be generally applicable to all cases. Complicated chemical structures depend on structural representations exhibiting the atom–atom connectivity, the order of the bonds, and the stereochemistry. Any edits to the question must not invalidate answers that have already been given. Changes that invalidate answers will be rolled back. The title of the question shall be as descriptive as possible. Tags are a means of finding experts who are able to answer by sorting questions into specific, well-defined categories. See below for a more detailed explanation of asking nomenclature questions. Answering nomenclature questions Since many compounds can have two or more names in accordance with several methods recommended by IUPAC, a compound may be named correctly in more ways than one. The rules for systematic nomenclature have changed several times. Furthermore, various drafts, corrections, extensions, modifications, and revisions have been issued. We are looking for long answers that provide some explanation and context. Names are written in accordance with a symbolism specific to the nomenclature in order to avoid ambiguity and to establish an unequivocal relationship between a name and the corresponding structure. See below for a more detailed explanation of answering nomenclature questions. | {
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3,222 | This site periodically attracts questions that essentially ask for a way to utilize the amassed synthetic knowledge and wisdom of the chemical profession without either 1) doing the hard work to get there, or (more commonly) 2) understanding that the question itself represents something akin to the total sum of all knowledge in the field. Here are some examples: https://chemistry.stackexchange.com/questions/50645/predicting-the-products-of-any-chemical-reaction How to predict the products of a organic chemical reaction Why is predicting products of chemical reactions difficult? Chemical software for solving reactions synthesizable functional groups These questions get closed as too broad which is probably the correct response. However, there can be a definitive correct answer to questions like this. Proposal: Let's have one definitive question and answer about this topic. Then we close the new questions as duplicates. The answers to this meta question are: Yes, this is a great idea! It is so great, I want to go back into the past and do it three years ago! Anyway, let's do it now. No, this is not a good idea. Let's just keep closing these questions as too broad . Vote! | Yes, this is a great idea! It is so great, I want to go back into the past and do it three years ago! Anyway, let's do it now. An example of such a definitive answer might be: $${\Large\text{Can I predict the products of any chemical reaction?}}$$ In theory, yes! Every substance has characteristic reactivity behavior. Likewise pairs and sets of substances have characteristic behavior. For example, the following combinations of substances only have one likely outcome each: $$
\ce{HCl + NaOH -> NaCl + H2O} \\
\ce{CH3CH2CH2OH->[1.\ \ce{(COCl)2,\ (CH3)2SO}][2.\ \ce{Et3N}] CH3CH2CHO}$$ However, it is a not suited to brute force or exhaustive approaches There are millions or perhaps billions of known or possible substances. Let's take the lower estimate of 1 million substances. There are $999,999,000,000$ possible pairwise combinations. Any brute force method (in other words a database that has an answer for all possible combinations) would be large and potentially resource intensive. Likewise you would not want to memorize the nearly 1 trillion combinations. If more substances are given, the combination space gets bigger. In the second example reaction above, there are four substances combined: $\ce{CH3CH2CH2OH,\ (COCl)2,\ (CH3)2SO,\ \& \ Et3N}$. Pulling four substances at random from the substance space generates a reaction space on the order of $1\times 10^{24}$ possible combinations. And that does not factor in order of addition. In the second reaction above, there is an implied order of addtion: $$\begin{align}
&1.\ \ce{CH3CH2CH2OH}\\
&2.\ \ce{(COCl)2,\ (CH3)2SO}\\
&3.\ \ce{Et3N}
\end{align}$$ However, there are $4!=24$ different orders of addition for four substances, some of which might not generate the same result. Our reaction space is up to $24\times 10^{24}$, a bewildering number of combinations. And this space does not include other variables, like time, temperature, irradiation, agitation, concentration, pressure, control of environment, etc. In practice, in can be manageable! Even though the reaction space is bewilderingly huge, chemistry is an orderly predictable business. Folks in the natural product total synthesis world do not resort to random combinations and alchemical mumbo jumbo. They can predict with some certainty what type of reactions do what to which substances and then act on that prediction. When we learn chemistry, we are taught to recognize if a molecule belongs to a certain class with characteristic behavior. In the first example above, we can identify $\ce{HCl}$ as an acid and $\ce{NaOH}$ as a base, and then predict an outcome that is common to all acid-base reactions. In the second example above, we are taught to recognize $\ce{CH3CH2CH2OH}$ as a primary alcohol and the reagents given as an oxidant. The outcome is an aldehyde. These examples are simple ones in which the molecules easily fit into one class predominantly. More complex molecules may belong to may categories. Organic chemistry calls these categories Functional Groups . The ability to predict synthetic outcomes then begins and ends with identifying functional groups within a compound's structure. For example, even though the following compound has a more complex structure, it contains a primary alcohol, which will be oxidized to an aldehyde using the same reagents presented above. We can also be reasonably confident that no unpleasant side reactions will occur. There are too many classes of compounds to list here. Likewise even one class, like primary alcohols (an OH group at the end of a hydrocarbon chain) has too many characteristic reactions to list here. Folks who learn how to analyze combinations of compounds spend years taking courses and reading books and research articles to accumulate the knowledge and wisdom necessary. It can be done. Computer programs can be (and have been) designed to do the same analysis, but they were designed by people who learned all of the characteristic combinations. There is no shortcut. | {
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3,467 | The question and its edit war So this edit war happened. Here's a quick recap: A poster asked a very clear question, two different ways. A user edited the question to eliminate the second phrasing. The OP added the second phrasing back in. A user who was subsequently elected to a moderator position after the edit in question deleted the second phrasing of the question. The original poster restored the second phrasing of the question. A moderator deleted the alternate phrasing again. The OP restored the alternate phrasing and posted a comment to the effect that he thought the alternate wording provided additional clarity into what he was was asking. A moderator deleted the alternate phrasing and locked the question to prevent any more revisions or comments. What message might users discern from this edit pattern? The first deletion by the moderator-to-be does seem like a legitimate attempt at improving the question. Everything should be as simple as possible, but not any simpler. I think we all agree with that. However, the original poster apparently felt that the revisions made the question "too simple", i.e. that clarity was lost. The question I ask here is, what message might question-askers take away from not being able to ask questions the way they want? Am I alone in thinking that question-askers might be irritated by repeated "revisions"? Perhaps the only thing OPs will be able to take away from situations like this is that they aren't in control of their own questions? Perhaps they may feel that this is a site where others presume to know their own question better than they do? I don't think any of the moderators wanted to send messages like these, but I'm confident that these are the messages that are coming across. If this is what moderation looks like, I want to hear more about why its a useful strategy. Three lines of redundant content (note: whether the content is redundant is certainly arguable) don't seem worth worth fighting over to me. Wouldn't it make sense to either let the (arguably too verbose) original question stand, or at least to propose a "third-way" edit that provides a new possibility, instead of just repeatedly rolling back the OP's own question? Why focus on the moderator behavior here? Comments and answers to date have brought up the valid point that my summary mentions only the actions of moderators (or future moderators), not of all the question editors. I apologize for not making this clear in my initial post. Let me explain why I wrote this question here. First, I wrote this question when the post was locked. The link on the lock notice specifically recommends that people raise issues with a locked question here on Meta. Second, a very large number of the rollbacks were made by moderators or moderators-to-be. I recognize that editing questions is not specifically a duty of moderators, but of all high-rep users. However, I do believe that moderators are (and should be) held to the highest standards and in general should serve as exemplars to the community. This question was in my mind a rare example of (some of) the moderators not meeting this admittedly lofty standard. I do think it is worth examining how we can avoid situations like this in the future. | I was involved in an edit war at EE.SE earlier this year, over this answer . The following meta discussion is here . Based on this experience, IMO if a particular edit is rolled back once by the OP, no further edits in that vein should be made, ever , except by the OP him/herself (or by someone who has their unambiguous blessing). The spurned editor then has three paths forward: Downvote Vote to close, if appropriate Invite OP to chat If OP's are okay with the general thrust of other people's edits, they have the option of tweaking those edits by making further edits of their own. If an OP objects so strongly to the change made by an edit that they desire to rescind it wholesale, then courtesy dictates that one should not try to force that change into their post. As an additional recommendation: Whenever I make what feels like a substantial revision to someone's post, whether excising a large portion or undertaking a major rewrite or whatever, I usually post a comment after I make the edit inviting the OP to review my edit and change anything they don't like, or roll back the entire thing if they wish. I do this to let them know that I know I've majorly changed their post, and that if they're not happy with what I've done, I won't be upset if they change/undo it. | {
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3,601 | I am officially changing the post to a tag-blacklist-request . I think, and so far there was no objection, that it is a meta-tag , and that it is not helpful. Unlike homework or reference-request it basically only serves as a placeholder. I would say it is on par (maybe a tiny bit better) with chemistry , which has been blacklisted for quite some time. What does blacklisting mean? First, it means the tag will be mass-removed from all questions. This is preferable to removing it in a mass retagging from about 900(+) question while flooding the homepage. Second, it will be banned from being reapplied. Why blacklist? I believe the tag will reappear, and once it is there it will again spread uncontrollably. When the tag cannot be reentered again, we don't have to worry about it. If it would have been applied to only a few questions, I would not bother to involve the developers, but it is on almost 5% of the questions. What needs to happen? $\color{green}{\textbf{(Done)}}$ We need to clean up the cases where reaction is the sole tag. That means manual retagging, editing, etc. This is necessary either way. After the delete all those questions would be untagged . We should avoid that. I am monitoring if this tag appears, it can due to migration, but it is better to have precautions in place. If you want to help out, you can use this SEDE query to find questions, which only have this tag. $\color{green}{\textbf{(Done)}}$ Wait for this post to gain enough votes to consider it a consensus. (I'd say we should see a double digit with at least a two in front.) $\color{green}{\textbf{(Done)}}$ Once consensus is reached, we need to contact the developers and let them go about their business. They will help us to silently remove the remaining uses of the tag ("burnination") and also prevent future uses of the tag ("blacklisting"). If you agree with the proposal, please upvote Klaus' answer . (You may upvote the question, but the answer is more important.) If you disagree, please leave a new answer outlining why. If there is already an answer disagreeing with the proposal, please vote on it instead. As usual we will disregard any down-votes to exclude double counting. If you think there is something left unsaid, you can of course always comment or add another answer. We've all seen it, we've probably all applied it at least once: reaction . Yes, sometimes desperate times need desperate measures, and I admit I have used this one. And if I recall correctly, I even wrote the description: This general tag should be used if the question is about a specific (set of) reaction(s). It should be specified with other tags like stoichiometry, inorganic-chemistry, organic-chemistry, acid-base, ... . For what it's worth, I (now) think it is an empty tag, with no value whatsoever. Maybe one of the most worthless meta-tags there is. On par with chemistry . It has incredible 930 (!!!) uses, of which there are 54 questions where it is the only tag. Recently I have seen it used as a placeholder from new users, because you have to specify a tag. Well, that specific one kind of hurtz™ my eyes and mind. What shall be done? If you consider leaving a comment, consider leaving an answer instead so that others can vote on it and we reach a conclusion faster. | You are right: it seems to spread like the plague. I agree that reaction is pointless and I think that it should be removed and blacklisted till the end of days.* At least ;-) (*Editorial remark: If you agree with the proposal please upvote this answer.) Currently, there are 93 questions with reaction and reaction-mechanism . Here, reaction can be removed immediately without causing harm. Solving all the other cases, particularly when the crap tag is the only one, means work . I've been on a retagging spree before and I know that this takes a considerable amount of time. From a brief overview, there seem to be quite some questions that would better be tagged with acid-base redox stoichiometry nomenclature to name just a few, but all this has to be decided individually. | {
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1 | It seems to me that the addition of electrons and protons as you move across a period would cause an atom to become larger. However, I'm told it gets smaller. Why is this? | As you move from left to right across a period, the number of protons in the nucleus increases. The electrons are thus attracted to the nucleus more strongly, and the atomic radius is smaller (this attraction is much stronger than the relatively weak repulsion between electrons). As you move down a column, there are more protons, but there are also more complete energy levels below the valence electrons. These lower energy levels shield the valence electrons from the attractive effects of the atom's nucleus, so the atomic radius gets larger. | {
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2 | My understanding is that $\mathrm{NaCl}$ is an ionic compound, in which $\mathrm{Cl}$ becomes (effectively) $\mathrm{Cl^-}$ and $\mathrm{Na}$ becomes $\mathrm{Na^+}$. So I understand why I would get a "sea" of particles that would stick together. But why does the above mean that it will have a face centered cubic structure with the ions held in place so rigidly? | Crystals have inspired a great many chemists because they are fascinating for a good reason . Not only are they aesthetically pleasing, but they serve as an excellent subject to tour a variety of theoretical subjects important for understanding high-level chemistry. Crystalline materials are made up of periodic structures. We’re only going to primarily focus on binary compounds where there is not a high degree of covalency. There are several ways to think about this problem, but let’s start with the melting of a crystal. We say that at some definite temperature a highly ordered crystal will melt into a liquid. Those of us familiar with the language of equilibrium thermodynamics might recognize that the change in free energy for this phase change can be written, at constant temperature, as, $$ G_\text{liquid} - G_\text{crystal} = H_\text{liquid} - H_\text{crystal} - T ( S_\text{liquid} - S_\text{crystal} ) $$ $$ \Delta G = \Delta H - T \Delta S $$ If we suppose that this process is spontaneous then we would say that the change in Gibbs’ free energy is negative, i.e. $\Delta G < 0$. This is true if and only if, $$\Delta H < T \Delta S$$ Traditionally we interpret this as saying that there is a thermally-driven increase in entropy when we melt a highly ordered crystal into a liquid which more than offsets the energy cost associated with the enthalpies of the interactions holding that crystal together. A chemist tends to learn early on that the reverse is not necessarily true: at some definite temperature a perfect crystal rarely forms from the liquid. This inability to just heat up any substance and always produce a perfect crystal by cooling illustrates how crystal formation is a case of kinetic- rather than thermodynamic- control . So the process by which you form your crystal could possibly result in a different crystal structure. Sometimes crystal structures change just by altering the temperature of the chamber you’re measuring the crystal structure in! Now neither of these cases apply to sodium chloride to the best of my knowledge. The formation of an ionic crystal such as sodium chloride is a delicate balance between electrostatic attraction and Pauli repulsion. Electrostatic attraction says that between two different charges, $q_+$ and $q_-$, there is a Coulomb force given by, $$F= \frac{k q_+ q_-}{r^2}$$ where $r$ is the distance between the two charges. If one plays with the numbers then it’s easy to see that at short distances the force is strongest, but there is a limit to how close they may come together. Eventually a repulsive force due to a quantum mechanical principle called the Pauli Exclusion Principle overpowers the attraction. An equilibrium results in which the atoms sit a certain distance from one another so that, if you will humor me, the “forces” between them balance out. This is why we traditionally represent crystal packing using marbles with a unique radii. The radii of the hard marble represents where the Pauli repulsion overpowers the attraction. You might say, “Sure, we have these kinetic, electrostatic and quantum mechanical factors to consider, but how do these help with the final crystal structure?” Hold your horses, we’re getting there. A famous mathematician and scientist thought about the most efficient ways to pack spheres of the same size together. By most efficient I mean this in terms of what FedEx considers efficient, fitting things together into the smallest possible volume. This is also what electrostatics want. Kepler suggested that the best way to pack spheres with this in mind can be maximized in two ways: fcc and hcp . This conjecture, however, rests on all the spheres being uniform. We can’t assume this is the same for the atoms in table salt because the cation, sodium, is said to be smaller than the chloride anion. A tool that is useful as a guide for helping predict the structure is based off of the relative size of the cation, $r_\text C$, to the anion, $r_\text A$. This radius ratio, $r_\text C / r_\text A$, is mostly only useful for simple binary species. These $r_\text C$ and $r_\text A$ are tabulated as ionic radii in many chemistry books; they are contrived by various rules proposed by researchers, such as Linus Pauling , applied to the experimentally determined interionic distances. In this system we find it useful to discuss how many neighbors an anion or a cation has of the opposite charge. The coordination number ($\mathrm{CN}$) tells us how many neighbors a type of atom has around it. A certain $r_\text C/r_\text A$ gives us a feel for the probable CN. From one source I was able to calculate the ratio for $\ce{NaCl}$ as $r_{\ce{Na+}}/r_{\ce{Cl-}} = 0.564$. Most textbooks will say that if your ratio is $0.414{–}0.732$, then you have $\mathrm{CN}=6$. I’ll show you how to calculate the minimum value for $\mathrm{CN}=6$. The easiest way to obtain the maximum is to obtain the minimum for $\mathrm{CN}=8$. Briefly, if we put a small cation on a $XY$ plane and surround it in the manner shown below then we could also place two circles in the $Z$-axis above and below the central cation for $\mathrm{CN}=6$. (I won’t show those two in the $Z$-axis for clarity.) We would say that a given $\mathrm{CN}$ is stable only if the spheres are all touching each other. We would say that for the ratios drawn that a $\mathrm{CN}=8$ is not stable because our cation’s sphere would be too small and wouldn’t touch all eight of its neighbors. A higher density is always preferred, so $\mathrm{CN}=4$ is not preferred when $\mathrm{CN}=6$ is stable. Clearly, $\angle \mathrm{DAC} = 45^{\circ}$. Moreover, we can say that $\overline{\mathrm{DC}} = r_\text A$ and $\overline{\mathrm{AC}} = r_\text A + r_\text C$. Trigonometry will tells us that $$\sin 45^{\circ} = \frac{\overline{\mathrm{DC}}}{\overline{\mathrm{AC}}}$$ Substituting in those values just determined,
$$\frac{\sqrt{2}}{2} = \frac{r_\text A}{\overline{r_\text A + r_\text C}}$$ Solving for $r_\text C/r_\text A$ gives, $$r_\text C/r_\text A=\frac{2}{\sqrt{2}} -1 = 0.414$$ which is the lower bound desired. So we can say that the $\mathrm{CN}=6$ for the cation. Similarly you can figure out that $\mathrm{CN}=6$ for the anion. This is why we say it has a 6:6 coordination pattern, which is indicative of a sodium chloride type structure. Cesium chloride, on the other hand, is 8:8 and indicative of its structure type. We tend to say that these patterns are consistent with a certain crystal structure because all the pieces fit together consistently. This geometric concept is based purely on sphere packing and is not without its limitations. A more quantitative way to figure out which geometry is preferred is to calculate the electrostatic energies for the different geometries. A Russian by the name of Kapustinskii derived a formula to do this, $$E_\text{lattice} (\mathrm{kJ/mol}) = \frac{\alpha}{r_\text C + r_\text A} $$ From here you need to put it in terms of the radius ratio with a constant $r_\text A$, (I should note that this is evil algebra: $ \frac{a/b}{d/b + 1}= \frac{a}{b+d} $ where $a=\alpha$, $b=r_\text A$, $d=r_\text C$.) $$E_\text{lattice} = \frac{\alpha/r_\text A}{\frac{r_\text C}{r_\text A} + 1} $$ Basically $\alpha$ is different for a change in the crystal structure type and from there you compare which has the preferred energy. You can reproduce the geometric trends using this more quantitative model. There are problems with this approach too, such as the neglected dipole and quadrupole and covalency. Yes, even in $\ce{NaCl}$ there is some covalent character. I think we say that $\ce{NaCl}$ $67\ \%$ ionic character. These become important when two different crystal structures are close in energy or when more exact calculations are required. | {
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4 | A reaction proceeds towards the direction of lesser Gibbs free energy (at constant $T$ (temperature) and $P$ (pressure)). So, we could say that Gibbs free energy at equilibrium is minimum . On the other hand, we have $$\Delta G=\Delta G^\circ + RT\ln Q$$, where $Q$ is the reaction quotient. At equilibrium, $Q=K_\text{eq}$, and we already know that $\Delta G^\circ =-RT\ln K_\text{eq}$. Substituting, we get $\Delta G=0$ at equilibrium. But, we know that $G$ minimized itself—thus there was a change in $G$ and $\Delta G < 0$. What am I missing here? | I think your question really arises from some confusion about what $\Delta G$ represents. In general, $\Delta X$ for a thermodynamic quantity $X$ is the change of $X$ along some process. You could make it clear by actually writing $\Delta G(\text{A}\rightarrow\text{B})$ where A and B are before and after states. (We'll note that, in the general case, $\Delta X$ depends on the path take from A to B, making this notation improper. If $X$ is a function of state, though, you're good to go.) However, in the equation you quote: $$\Delta G = \Delta G^0 + RT \ln Q$$ the $\Delta G$ is a free energy of reaction and should thus be denoted $\Delta_\mathrm r G$ , with the correct equation being: $$\Delta_\mathrm r G = \Delta_\mathrm r G^0 + RT \ln Q$$ The free energy of reaction is defined as $\Delta_\mathrm r G = G_{\text{products}} - G_{\text{reactants}}$ . Thus, this $\Delta_\mathrm r G$ is not the variation of $G$ over the entire reaction, which would be the $\Delta G$ of the system between the start of the reaction and the equilibrium. PS: I think this link is the online resource I found with the clearer use and explanation of notations. Notations are important in thermodynamics! | {
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7 | The nitration of N , N -dimethylaniline with $\ce{H2SO4}$ and $\ce{HNO3}$ gives mainly the meta product, even though $\ce{-NMe2}$ is an ortho , para -directing group. Why is this so? | In the presence of these strong acids the $\ce{-NMe2}$ group is protonated, and the protonated form is electron-withdrawing via the inductive effect . This discourages attack at the electron-poor ortho position. Under the conditions I know for that experiment, you get a mixture of para - and meta -product, but no ortho-product due to steric hindrance. | {
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18 | Organic compounds are typically defined as “molecules containing carbon”. Wikipedia states that there for some historical (read: non-logical) reasons, a few types of carbon-containing compounds such as carbides, carbonates, simple oxides of carbon, and cyanides, as well as the allotropes of carbon such as diamond and graphite, are considered inorganic. I thus wonder: is activated charcoal (also known as activated carbon) typically classified as an organic or inorganic material? If I follow the list of exceptions given by Wikipedia, it should be organic (it's not an allotrope of carbon, in particular), but I get the feeling that most people in the field of porous materials would classify it as inorganic. So, I'm looking for an authoritative reference on this question. | While nomenclature is of particular interest to organic chemists to specify an exact compound, the classification of X into broad category Y or Z isn't a precise science, and not really of practical use. The article cites a textbook by Seager to this effect, stating The distinction between "organic" and "inorganic" carbon compounds, while "useful in organizing the vast subject of chemistry... is somewhat arbitrary" Even if you find a source that says "charcoal is (in)organic", you may just as well find one stating the opposite. Just like the coal from which it may have been produced, it was once biomass and decidedly organic, but so was graphite and diamond, or CO 2 and CO 3 2− . I think it's overly pedantic and unproductive to try to come up with definitive judgements for these decidedly edge case scenarios. After all, it's just a chemical on the shelf, what one does with it is far more relevant. I don't use it on a daily basis, but it seems more like a tool than a reagent. The fact it contains carbon seems beside the point; it's value isn't in the chemical composition but rather its extraordinary adsorptive properties. | {
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30 | It is known that impurities in a desired isolated product lower the melting point of the mixture, even if the impurities' melting point is much higher than the desired product. Why is that so? | It's a very general statement, but it's not always true. I'll explain why it's often true, and give a counter-example at the end. Your majority component B and the impurity (let's call it A) form a binary system. In most cases, such binary mixtures exhibit a solid–liquid phase diagram as follows: (image taken from these lecture notes ). This binary phase diagram has pure A on the left, pure B on the right. A and B form, somewhere, a eutectic. It is the point here at concentration e and temperature y . Because the existence of a eutectic point is guaranteed for any A/B binary system, and because the eutectic corresponds to a lower temperature, your liquidus curve decreases with increasing impurity concentration, and the impurity thus lowers the melting point. However, not all binary mixtures form a eutectic. In the words of Wikipedia : Not all binary alloys have a eutectic point; for example, in the silver-gold system the melt temperature (liquidus) and freeze temperature (solidus) both increase monotonically as the mix changes from pure silver to pure gold. The corresponding phase diagram is as follows: | {
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33 | What conditions promote a nucleophile to undergo the Michael reaction over the nucleophilic attack at the alpha carbon of the carbonyl group in an alpha-beta-unsaturated ketone? I'm looking for an answer that considers organic and inorganic nucleophiles (like organocuprates/organolithium compounds). | An $\alpha,\beta$-unsaturated ketone is electrodeficient at the $\beta$ position. This can be seen if you draw the resonance structures of such a molecule. The $\beta$ carbon is thus a good site for nucleophilic attack. But, as you know, carbonyls are also prone to nucleophilic attack. To discriminate between the two, you need to look at how the reaction is controlled , either thermodynamically or kinetically . In a kinetically controlled reaction, the product that is formed fastest predominates. In a thermodynamically controlled reaction, the predominant product is the energetically favored one. A Michael addition is a 1-4 addition, where a nucleophile attacks the $\beta$ carbon, and produces the thermodynamically favored product. On the other hand, a 1-2 reaction (on the carbonyl) gives the kinetic product, and is obtained at low temperatures. Why is the 1-4 product thermodynamically more stable? Because the resulting product benefits from keto-enol tautomerism, which results in lowering the energy of the system. Usually, the more resonance forms a compound has, the more its electrons are delocalized, the more stable it is. Draw the resonance forms of the 1-4 and 1-2 products, and see. You asked for specific affinities of different organometallics in 1-4/1-2 additions. My knowledge is that organocuprates ($\mathrm{R-CuLi}$) will perform Michael additions, and that organolithians seem to prefer 1-2 addition. Also, according to this source , Grignard reagents do not seem to have a preference. My take on this is that the cuprate is less reactive, and therefore can form the thermodynamic product, whereas the lithium reagent is so destabilized that it reacts right away. | {
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63 | The most notable characteristic of polytetrafluoroethylene (PTFE, DuPont's Teflon) is that nothing sticks to it. This complete inertness is attributed to the fluorine atoms completely shielding the carbon backbone of the polymer. If nothing indeed sticks to Teflon, how might one coat an object (say, a frying pan) with PTFE? | It has to be so common a question that the answer is actually given in various places on Dupont's own website (Dupont are the makers of Teflon): “If nothing sticks to Teflon®, then how does Teflon® stick to a pan?" Nonstick coatings are applied in layers, just like paint. The first layer is the primer—and it's the special chemistry in the primer that makes it adhere to the metal surface of a pan. And from this other webpage of theirs: The primer (or primers, if you include the “mid coat” in the picture above) adheres to the roughened surface, often obtained by sandblasting, very strongly: it's chemisorption, and the primer chemical nature is chosen as to obtain strong bonding to both the metal surface. Then, the PTFE chain extremities create bonds with the primer. And thus, it stays put. | {
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69 | I'm currently taking VCE (Victorian Certificate of Education) Chemistry classes, and we're currently studying the interpretation of spectra produced by Hydrogen NMR (Nuclear Magnetic Resonance) spectroscopy. When studying the spectra of High Resolution 1 H NMR, the peaks representing the different Hydrogen environments are split into multiplets based on the protons surrounding these environments. There has been a considerable amount of confusion in my classes over the actual principles / rules of thumb on how to calculate the multiplets for a particular environment of a known chemical (i.e.; known structue), based off the 'n + 1' rule. (i.e.; an environment with n neighbours will be split into n+1 multiplets). We are absolute on the principles that; Peaks of a particular Hydrogen environment are not split by neighbouring protons in equivalent environments. OH does not, and is not split by, it's neighbouring environments. However, immense confusion arised over whether the following principle was correct. Peaks of a particular Hydrogen environment will only be split by the protons in neighbouring environments once for each type of neighbouring environment. e.g. The middle "CH 2 " environment in "CH 3 –CH 2 –CH 3 " will only have 4 peaks; Although it has 6 neighbouring protons, they are two lots of the same environment (CH 3 ). As a class, we found numerous examples from different text books and sources that provide examples of ¹H NMR spectra which did not clarify the matter; Some considered all neighbouring protons as neighbours, others discriminated on the repeated neighbouring environments. For example, the CH 2 in CH 3 –CH 2 –CH 3 was sometimes split into 4 peaks or 7 peaks, depending on the source. Many Chemistry teachers contradicted each other on the matter. There was repeated self corrections made by the teachers, such that now nobody really knows whether this principle is correct or not. So, is there anybody that has the correct information on the matter? Is there a reasonable explanation behind this strange lack of correlation, or is there a common misconception about multiplet splitting? Ultimately; How many multiplets should the CH 2 in CH 3 –CH 2 –CH 3 have? (Note that if there is a complicated explanation that I am currently only at Year 12 VCE level, so links to resources I can pursue would be extremely helpful! It's been established that VCAA (an authority for the education system in Australia) ensures that the chemicals featured in the exams for NMR analysis will not be of a structure so as to allow the ambiguity above.) | Which nuclei you should consider as neighboring atoms for the multiplet splitting depends on the size of the coupling constant. The coupling constant are usually named after the number of bonds between the coupling nuclei, so a coupling between two hydrogens that are three bonds apart from each other would be a $\mathrm{^3J_{HH}}$-coupling. In an alkyl chain like CH 3 CH 2 the coupling between the CH2 and the CH3 hydrogens would be a $\mathrm{^3J}$-coupling that is about 7 Hz large. Couplings over more than three bonds are usually not observed, because they are smaller than the linewidth of the signals in your NMR spectrum. The exception to that you're likely to encounter are couplings along C=C double bonds, where you can even see $\mathrm{^4J}$-couplings or more. So the simplified rule would be that couplings along three bonds are visible, couplings along more than three bonds are only visible when there is at least one C=C double bond along the way. The concepts of chemical and magnetic equivalence are essential to understanding how different multiplicities arise. Chemical equivalence means there exists a symmetry operation that exchanges those nuclei. Magnetically equivalent nuclei additionally need to have identical couplings to all other spins in the molecule. Magnetically equivalent nuclei don't couple to each other. In propane the hydrogens of both CH 3 groups are three bonds away from the hydrogens of the CH 2 group, so the coupling between those is visible in the NMR spectrum. The hydrogens of each CH 3 group are magnetically equivalent, due to the fast rotation along the C–C bond, and the two CH 3 groups should also be magnetically equivalant. So you have 6 magnetically equivalent hydrogens that couple to your CH 2 hydrogens. The result of that is a splitting into a septet (7). The OH-group is an interesting exception, as you would expect it to lead to a visible coupling on hydrogens connected to the same carbon, but you don't observe that under most conditions. The reason is that the OH is acidic enough that the hydrogen exchanges quickly with the solvent, so the hydrogen dissasociates and associates quickly. This happens too fast for NMR, so the other nuclei only see the average OH-hydrogen. This eliminates the coupling to the OH, and it is also the reason why the OH-signal is often very broad or even completely gone in NMR spectra. | {
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141 | I'm looking at the melting temperature of metallic elements, and notice that the metals with high melting temperature are all grouped in some lower-left corner of the $\mathrm{d}$ -block. If I take for example the periodic table with physical state indicated at $\pu{2165 K}$ : I see that (apart from boron and carbon) the only elements still solid at that temperature form a rather well-defined block around tungsten (which melts at $\pu{3695 K}$ ). So what makes this group of metals melt at such high temperature? | Some factors were hinted, but let me put them in an order of importance and mention some more: metals generally have a high melting point, because metallic interatomic bonding by delocalized electrons ( $\ce{Li}$ having only a few electrons for this "electron sea") between core atoms is pretty effective in those pure element solids compared to alternative bonding types (ionic $\pu{6-20 eV/atom}$ bond energy, covalent 1-7, metallic 1-5, van-der-Waals much lower). Also, ionic lattices like $\ce{NaCl}$ have a higher lattice and bonding energy, they have weak interatomic long-range bonding, unlike most metals. They break apart or are easily solvable, metals are malleable but don't break, the electron sea is the reason for their welding ability. the crystal structure and mass play an inferior role among your filtered elements (just look up the crystal structure of those elements), as metallic bonding is not directional unlike covalent bonding (orbital symmetry). Metals often have half filled $\mathrm{s}$ and $\mathrm{p}$ bands (stronger delocalized than $\mathrm{d}$ and $\mathrm{f}$ ) at the Fermi-edge (meaning high conductivity) and therefore many delocalised electrons which can move into unoccupied energy states yielding the biggest electron sea with half or less fill bands. noble metals like $\ce{Au,Ag}$ have a full $\mathrm{d}$ orbital, therefore low reactivity/electronegativity and are often used as contact materials (high conductivity because of "very fluid" electron sea consisting only of $\mathrm{s}$ -orbital electrons. Unlike tungsten with half or less occupied $\mathrm{d}$ -orbitals they show no interatomic $\mathrm{d-d}$ bonding by delocalized $\mathrm{d}$ -electrons, and more importantly, a half filled $\mathrm{d}$ -orbital contributes 5 electrons to the energy band, while a $\mathrm{s}$ only 1, $\mathrm{p}$ only 3, the electron sea is bigger among the $\mathrm{d}$ -group. The "packaging" of core atoms in the lattice (interatomic distance) among the high $Z$ atoms (compared to e.g. $\ce{Li}$ ) is denser (more protons, stronger attraction of shell electrons, smaller interatomic radius), means stronger interatomic bonding transmitted by the electron sea: You can see here that in each series ( $\ce{Li,\ Na,\ K}$ ) the melting points rise to a maximum and then decrease with increasing atomic number (lacking unoccupied energy states for delocalized $\mathrm{d}$ -electrons), bigger electron sea being here a stronger factor than a bit more dense packaging. Boron as a semi-metal shows metallic and covalent bonding, Carbon strong directional covalent bonding and is able to build a network of bonds unlike other non-metal elements showing covalent intramolecular bonding, e.g. , in diatomic molecules but not strong intermolecular bonding in macromolecules because of lacking unpaired electrons. So there are some bigger trends for melting points explaining the high melting points of $\mathrm{d}$ -metals, but also some minor exceptions to the rule like $\ce{Mn}$ . | {
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152 | My chemistry book explains that even though electrons in the $\mathrm{2p}$ orbital are closer to the nucleus on average, electrons from the $\mathrm{2s}$ orbital spend a very short time very close to the nucleus (penetration), so it has a lower energy. Why does this tiny amount of time spent close to the nucleus make such a big difference? It seems like it should be the average distance that matters, not the smallest distance achieved at any one point, in determining stability. What makes that momentary drop in energy so important that it is outweighs all the time spent farther away from the nucleus with a higher energy? | I think your question implicates another question (which is also mentioned in some comments here), namely: Why are all energy eigenvalues of states with a different angular momentum quantum number $\ell$ but with the same principal quantum number $n$ ( e.g. , $\mathrm{3s}$ , $\mathrm{3p}$ , $\mathrm{3d}$ ) degenerate in the hydrogen atom but non-degenerate in multi-electron atoms?
Although AcidFlask already gave a good answer (mostly on the non-degeneracy part) I will try to eleborate on it from my point of view and give some additional information.
I will split my answer in three parts: The first will address the $\ell$ -degeneracy in the hydrogen atom, in the second I will try to explain why this degeneracy is lifted, and in the third I will try to reason why $\mathrm{3s}$ states are lower in energy than $\mathrm{3p}$ states (which are in turn lower in energy than $\mathrm{3d}$ states). $\ell$ -degeneracy of the hydrogen atoms energy eigenvalues The non-relativistic electron in a hydrogen atom experiences a potential that is analogous to the Kepler problem known from classical mechanics.
This potential (aka Kepler potential) has the form $\frac{\kappa}{r}$ , where $r$ is the distance between the nucleus and the electron, and $\kappa$ is a proportionality constant.
Now, it is known from physics that symmetries of a system lead to conserved quantities ( Noether Theorem ).
For example from the rotational symmetry of the Kepler potential follows the conservation of the angular momentum, which is characterized by $\ell$ . But while the length of the angular momentum vector is fixed by $\ell$ there are still different possibilities for the orientation of its $z$ -component, characterized by the magnetic quantum number $m$ , which are all energetically equivalent as long as the system maintains its rotational symmetry.
So, the rotational symmetry leads to the $m$ -degeneracy of the energy eigenvalues for the hydrogen atom.
Analogously, the $\ell$ -degeneracy of the hydrogen atoms energy eigenvalues can also be traced back to a symmetry, the $SO(4)$ symmetry.
The system's $SO(4)$ symmetry is not a geometric symmetry like the one explored before but a so called dynamical symmetry which follows from the form of the Schroedinger equation for the Kepler potential.
(It corresponds to rotations in a four-dimensional cartesian space. Note that these rotations do not operate in some physical space.)
This dynamical symmetry conserves the Laplace-Runge-Lenz vector $\hat{\vec{M}}$ and it can be shown that this conserved quantity leads to the $\ell$ -independent energy spectrum with $E \propto \frac{1}{n^2}$ . (A detailed derivation, though in German, can be found here .) Why is the $\ell$ -degeneracy of the energy eigenvalues lifted in multi-electron atoms? As the $m$ -degeneracy of the hydrogen atom's energy eigenvalues can be broken by destroying the system's spherical symmetry, e.g. , by applying a magnetic field, the $\ell$ degeneracy is lifted as soon as the potential appearing in the Hamilton operator deviates from the pure $\frac{\kappa}{r}$ form.
This is certainly the case for multielectron atoms since the outer electrons are screened from the nuclear Coulomb attraction by the inner electrons and the strength of the screening depends on their distance from the nucleus.
(Other factors, like spin and relativistic effects, also lead to a lifting of the $\ell$ -degeneracy even in the hydrogen atom.) Why do states with the same $n$ but lower $\ell$ values have lower energy eigenvalues? Two effects are important here: The centrifugal force puts an "energy penalty" onto states with higher angular momentum. ${}^{1}$ So, a higher $\ell$ value implies a stronger centrifugal force, that pushes electrons away from the nucleus. The concept of centrifugal force can be seen in the radial Schroedinger equation for the radial part $R(r)$ of the wave function $\Psi(r, \theta, \varphi) = R(r) Y_{\ell,m} (\theta, \varphi )$ \begin{equation}
\bigg( \frac{ - \hbar^{2} }{ 2 m_{\mathrm{e}} } \frac{ \mathrm{d}^{2} }{ \mathrm{d} r^{2} } + \underbrace{ \frac{ \hbar^{2} }{ 2 m_{\mathrm{e}} } \frac{ \ell (\ell + 1) }{ r^{2} } } - \frac{ Z e^{2} }{ 2 m_{\mathrm{e}} r } - E \bigg) r R(r) = 0
\end{equation} \begin{equation}
{}^{= ~ V^{\ell}_{\mathrm{cf}} (r)} \qquad \qquad
\end{equation} The radial part experiences an additional $\ell$ -dependent potential $V^{\ell}_{\mathrm{cf}} (r)$ that pushes the electrons away from the nucleus. Core repulsion (Pauli repulsion), on the other hand, puts an "energy penalty" on states with a lower angular momentum. That is because the core repulsion acts only between electrons with the same angular momentum ${}^{1}$ . So it acts stronger on the low-angular momentum states since there are more core shells with lower angular momentum. Core repulsion is due to the condition that the wave functions must be orthogonal which in turn is a consequence of the Pauli principle. Because states with different $\ell$ values are already orthogonal by their angular motion, there is no Pauli repulsion between those states. However, states with the same $\ell$ value feel an additional effect from core orthogonalization. The "accidental" $\ell$ -degeneracy of the hydrogen atom can be described as a balance
between centrifugal force and core repulsion, that both act against the nuclear Coulomb
attraction.
In the real atom the balance between centrifugal force and core repulsion is broken,
The core electrons are contracted compared to the outer electrons because there are less inner electron-shells screening the nuclear attraction from the core shells than from the valence electrons.
Since the inner electron shells are more contracted than the outer ones, the core repulsion is weakened whereas the effects due to the centrifugal force remain unchanged. The reduced core repulsion in turn stabilizes the states with lower angular momenta, i.e. lower $\ell$ values. So, $\mathrm{3s}$ states are lower in energy than $\mathrm{3p}$ states which are in turn lower in energy than $\mathrm{3d}$ states. Of course, one has to be careful when using results of the hydrogen atom to describe effects in multielectron atoms as AcidFlask mentioned. But since only a qualitative description is needed this might be justifiable. I hope this somewhat lengthy answer is helpful. If something is wrong with my arguments I'm happy to discuss those points. | {
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180 | For example, why does for example oxygen turn into gas at a much lower temperature than water? Does it have anything to do with the molecular structure? A water molecule does have a more complex structure than oxygen, though the R-410A (a mixture of two gases commonly used in heating pumps) is much more complex than water, and it boils at -48.5 degrees Celsius. | The boiling point of a liquid depends on the intermolecular forces present between the atoms or molecules in the liquid since you must disrupt those forces to change from a liquid to a gas. The stronger the intermolecular forces, the higher the boiling point. Two oxygen molecules are attracted to each other through London dispersion forces (induced temporary dipoles between the molecules) while water molecules are attracted to each other by hydrogen bonding (attraction of the + dipole on H in one molecule to the – dipole on an oxygen in an adjacent molecule) that is relatively strong. (Hydrogen bonding is an important intermolecular force for molecules where H is directly covalently bonded to F, O or N, which are quite electronegative and thus form bond with H with a relatively strong dipole.) London dispersion forces become more important for atoms and molecules with more electrons. Dipole–dipole attractions are also important in some molecules. | {
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189 | Over the course of my studies, I have switched largely from using Z-matrix representations of molecular geometries in calculations to Cartesian representations. The software that I use now makes it easy to add the sorts of constraints/restraints/transits that I would have previously used Z-matrices for, and I know that Z-matrix geometries can be problematic in large molecules * where minute changes in a bond angle or dihedral (due, for instance, to rounding errors/low-quality gradients) can result in large movements in peripheral atoms. What pros or cons exist for either geometry definition that I don't know about? What circumstances recommend one representation over another? *Or small molecules with silly Z-matrices. | Cartesian Space In Cartesian space, three variables (XYZ) are used to describe the position of a point in space, typically an atomic nucleus or a basis function. To describe the locations of two atomic nuclei, a total of 6 variables must be written down and kept track of. The general ruling is that for Cartesian space, 3N variables must be accounted for (where N is the number of points in space you wish to index). Internal Coordinates Z-matrices use a different approach. When dealing with Z-matrices, we keep track of the relative positions of points in space. Cartesian space is 'absolute' so to speak. A point located at (0,0,1) is an absolute location for a coordinate space that extends to infinity. However, consider a two atom system. The translation of the molecule through space (assuming a vacuum) will have no affect on the properties of the molecule. An H2 molecule centered around the origin (0,0,0) is no different from the same H2 molecule being centered around (1,1,1). However, say we increase the distance between the hydrogen atoms. We now have altered the molecule in such a way that the properties of that molecule has changed. What did we change? We simply changed the bond length, one variable. We increased the distance between the two atoms by some length R. With Z-matrices, we keep tabs on internal coordinates: bond length (R), bond angle (A), and torsional/dihedral angle (T/D). Using internal coordinates reduces our 3N requirement set by the Cartesian space down to a 3N-6 requirement (for non-linear molecules). For linear molecules we keep tabs on 3N-5 coordinates. When performing complex computations, the less you have to keep track of, the less expensive the computation. Symmetry Consider the following molecule, H2O. We know from experience that this molecule has C2V symmetry. The OH bond lengths should be equivalent. When using some sort of optimizing routine, you may want to specify symmetry in your system. With a Z-matrix, the process is very straightforward. You would construct your Z-matrix to define the OH(1) bond as being equivalent to the OH(2) bond. Whatever program you use should automatically recognize the constraint and will optimize your molecule accordingly giving you an answer based off a structure that is constrained to C2v symmetry. With Cartesian space this is not guaranteed. Rounding errors can cause your program to break symmetry, or your program may not be very good at guessing the point group of your molecule based on the Cartesian coordinates alone. Picking the Right One As a preface, programs like Gaussian convert your Cartesian coordinate space (or your pre-defined Z-matrix) into redundant internal coordinates before proceeding with an optimization routine unless you specify it to stick with Cartesians or your Z-matrix. I warn you that specifying your program to optimize using Cartesian coordinates makes your calculation much more expensive. I find that I will explicitly specify 'Z-matrix' when I know I'm dealing with high symmetry and when I know my Z-matrix is perfect. You will want to use Z-matrices on systems that are rather small. If dealing with systems with high symmetry, Z-matrices are almost essential. They can be rather tricky to implement and you will likely spend some time figuring out the proper form of your Z-matrix through trial-and-error. If you wish to scan a particular coordinate, Z-matrices are also very helpful as you can tell a program to scan across a bond length, angle or torsion with ease (as long as you've properly defined that coordinate in your Z-matrix). I use Cartesian coordinates for large systems, systems with very little or no symmetry, or when I'm in a hurry. | {
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216 | You can buy NMR tubes in a huge variety of qualities, with an equally huge difference in price between the cheapest and the most expensive NMR tubes. They are usually rated for a specific spectrometer frequency, e.g. 300 MHz+ or 600 MHz+. What is the difference between these different grades of NMR tubes? And how large is the effect on the quality of the spectra if a lower-grade tube is used? | A general rule is: crap goes in, crap comes out. A large-sample low-field 1D NMR at room temperature is usually only minimally affected by using a cheap NMR tube. There are important differences though and I’ll highlight a few. The first distinction between prices is what the tube is constructed from: quartz obviously costs more than borosilicate. Why would a chemist ever use the more expensive quartz? You can heat/cool quartz faster (nice for thermal studies), the UV cutoff is lower (think 190 nm opposed to 320 nm) which is important for photolysis, you can work with quartz at higher temperatures (around 1300 °C instead of 250 °C), and the purity of quartz is better controlled than your typical Pyrex. There are different grades of quartz, fused and synthetic, and there are different grades of borosilicate, such as the high-quality Pyrex or the lower-quality Class B, each comes with its own limitations as far as purities are concerned and so forth. Three more important parameters have to do with the manufacturing of your tube are: concentricity, camber and wall thickness. Lower quality tubes will tend to have less precision and accuracy over each of these parameters and as a result your sample may wobble while spinning (introducing problems such as modulation sidebands). A particularly bad tube can hit your RF coils and cause damage to your probe over time slowly or quickly if it is ignoring any reasonable standard – even more apparent for a tube at this level of “quality” is that it may be easier to break while acquiring your sample and we all should be aware of how much fun that is for everybody involved. Shimming can deal with impurities present in the glass (such as ferric oxide) and increased impurities in the glass/inhomogeneities will result in taking longer to get a good shim. Time is money. A lot of these things have lower tolerances in more complex experiments and at higher fields. It really does depend on your particular experiment and what you’re hoping to get out of it. | {
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228 | Diborane has the interesting property of having two 3-centered bonds that are each held together by only 2 electrons (see the diagram below, from Wikipedia ). These are known as "banana bonds." I'm assuming there is some sort of bond hybridization transpiring, but the geometry doesn't seem like it is similar to anything I'm familiar with Carbon doing. What sort of hybridization is it, and why don't we see many (any?) other molecules with this bond structure? | Look carefully, it's (distorted) tetrahedral--four groups at nearly symmetrically positions in 3D space{*}. So the hybridization is $sp^3$. As you can see, the shape is distorted, but it's tetrahedral. Technically, the banana bonds can be said to be made up of orbitals similar to $sp^3$ but not exactly (like two $sp^{3.1}$ and two $sp^{2.9}$ orbitals--since hybridization is just addition of wavefunctions, we can always change the coefficients to give proper geometry). I'm not too sure of this though. $\ce{B}$ has an $2s^22p^1$ valence shell, so three covalent bonds gives it an incomplete octet. $\ce{BH3}$ has an empty $2p$ orbital. This orbital overlaps the existing $\ce{B-H}$ $\sigma$ bond cloud (in a nearby $\ce{BH3}$), and forms a 3c2e bond. It seems that there are a lot more compounds with 3c2e geometry . I'd completely forgotten that there were entire homologous series' under 'boranes' which all have 3c2e bonds (though not the same structure) And there are Indium and Gallium compounds as well. Still group IIIA, though these are metals. I guess they, like $\ce{Al}$, still form covalent bonds. So the basic reason for this happening is due to an incomplete octet wanting to fill itself. Note that "banana" is not necessarily only for 3c2e bonds. Any bent bond is called a "banana" bond. Regarding similar structures, $\ce{BeCl2}$ and $\ce{AlCl3}$ come to mind, but both of them have the structure via dative(coordinate) bonds. Additionally, $\ce{BeCl2}$ is planar. Sneaks off and checks Wikipedia. Wikipedia says $\ce{Al2(CH3)6}$ is similar in structure and bond type. I guess we have less such compounds because there are comparatively few elements ($\ce{B}$ group pretty much) with $\leq3$ valence electrons which form covalent bonds(criteria for the empty orbital). Additionally, $\ce{Al}$ is an iffy case--it like both covalent and ionic bonds. Also, for this geometry (either by banana bonds or by dative bonds), I suppose the relative sizes matter as well--since $\ce{BCl3}$ is a monomer even though $\ce{Cl}$ has a lone pair and can form a dative bond. *Maybe you're used to the view of tetrahedral structure with an atom at the top? Mentally tilt the boron atom till a hydrogen is up top. You should realize that this is tetrahedral as well. | {
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316 | In Density Functional Theory courses, one is often reminded that Kohn-Sham orbitals are often said to bear no any physical meaning. They only represent a noninteracting reference system which has the same electron density as the real interacting system. That being said, there are plenty of studies in that field’s literature that given KS orbitals a physical interpretation, often after a disclaimer similar to what I said above. To give only two examples, KS orbitals of H 2 O [1] and CO 2 closely resemble the well-known molecular orbitals. Thus, I wonder: What good (by virtue of being intuitive, striking or famous) examples can one give as a warning of interpreting the KS orbitals resulting from a DFT calculation? [1] “What Do the Kohn-Sham Orbitals and Eigenvalues Mean?”, R. Stowasser and R. Hoffmann, J. Am. Chem. Soc. 1999 , 121 , 3414–3420. | When people say that Kohn-Sham orbitals bear no physical meaning, they mean it in the sense that nobody has proved mathematically that they mean anything. However, it has been empirically observed that many times, Kohn-Sham orbitals often do look very much like Hartree-Fock orbitals, which do have accepted physical interpretations in molecular orbital theory. In fact, the reference in the OP lends evidence to precisely this latter viewpoint. To say that orbitals are "good" or "bad" is not really that meaningful in the first place. A basic fact that can be found in any electronic structure textbook is that in theories that use determinantal wavefunctions such as Hartree-Fock theory or Kohn-Sham DFT, the occupied orbitals form an invariant subspace in that any (unitary) rotation can be applied to the collection of occupied orbitals while leaving the overall density matrix unchanged. Since any observable you would care to construct is a functional of the density matrix in SCF theories, this means that individuals orbitals themselves aren't physical observables, and therefore interpretations of any orbitals should always be undertaken with caution. Even the premise of this question is not quite true. The energies of Kohn-Sham orbitals are known to correspond to ionization energies and electron affinities of the true electronic system due to Janak's theorem, which is the DFT analogue of Koopmans' theorem. It would be exceedingly strange if the eigenvalues were meaningful while their corresponding eigenvectors were completely meaningless. | {
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374 | In the standard brown ring test for the nitrate ion, the brown ring complex is:
$$\ce{[Fe(H2O)5(NO)]^{2+}}$$ In this compound, the nitrosyl ligand is positively charged, and iron is in a $+1$ oxidation state. Now, iron has stable oxidation states +2 and +3. Nitrosyl, as a ligand, comes in many flavours, of which a negatively charged nitrosyl is one. I see no reason why the iron doesn't spontaneously oxidise to +3 and reduce the $\ce{NO}$ to −1 to gain stability. But I don't know how to analyse this situation anyway. I think that there may be some nifty backbonding increasing the stability, but I'm not sure. So, why is iron in +1 here when we can have a seemingly stable situation with iron in +3? | Your basic assumption is incorrect: the iron in $\ce{[Fe(H2O)5NO]^{2+}}$ is Fe(III) , and the ligand is $\ce{NO-}$ . | {
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410 | Related: Reaction between silver nitrate and aluminum chloride Experimentally, $\ce{AgCl}$ is insoluble in water, but $\ce{AgNO3}$ is soluble. They're pretty common in a lab (well, $\ce{AgCl}$ is a common precipitate)--so I think most of us know this. By Fajan's rules , on the other hand, larger anion $\implies$ more polarization/covalent character $\implies$ less solubility. But, $\ce{NO3-}$ is the larger anion, yet $\ce{AgNO3}$ is more soluble. Is there any theoretical reason for this? | In the comment to my previous answer, you asked for a theoretical reason for the solubilities, not considering energy data. Since I know from energy considerations that the issue is not the solvation of the anions, I can present a reason based on the strength of the ionic bond in the two compounds. This reference (as well as others) states the bonding in $\ce{AgCl}$ has an unusually high covalent character which makes it a tighter bond. The $\ce{Ag+}$ ion and the $\ce{Cl-}$ ion are close to the same size (with the silver ion being smaller), so they can approach each other quite closely. In silver nitrate, the $\ce{NO3-}$ ion is larger and does not allow as close an approach as the chloride ion, so the bond is weaker, easier to break up, and the salt is more soluble. | {
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444 | According to some chemistry textbooks, the maximum number of valence electrons for an atom is 8, but the reason for this is not explained. So, can an atom have more than 8 valence electrons? If this is not possible, why can't an atom have more than 8 valence electrons? | Yes, it can. We have molecules which contain "superoctet atoms". Examples: $\ce{PBr5, XeF6, SF6, HClO4, Cl2O7, I3- , K4[Fe(CN)6], O=PPh3 }$ Almost all coordination compounds have a superoctet central atom. Non-metals from Period 3 onwards are prone to this as well. The halogens, sulfur, and phosphorus are repeat offenders, while all noble gas compounds are superoctet. Thus sulfur can have a valency of +6, phosphorus +5, and the halogens +1, +3, +5, and +7. Note that these are still covalent compounds -valency applies to covalent bonds as well. The reason why this isn't usually seen is as follows. We basically deduce it from the properties of atomic orbitals . By the aufbau principle , electrons fill up in these orbitals for period $n$: $n\mathrm{s}, (n-2)\mathrm{f},(n-1)\mathrm{d},n\mathrm{p}$ (theoretically, you'd have $(n-3)\mathrm{g}$ before the $\mathrm{f}$, and so on. But we don't have atoms with those orbitals, yet) Now, the outermost shell is $n$. In each period, there are only eight slots to fill in this shell by the Aufbau principle - 2 in $n\mathrm{s}$, and 6 in $n\mathrm{p}$. Since our periodic table pretty much follows this principle, we don't see any superoctet atoms usually. But, the $\mathrm{d,f}$ orbitals for that shell still exist (as empty orbitals) and can be filled if the need arises. By "exist", I mean that they are low enough in energy to be easily filled. The examples above consist of a central atom, that has taken these empty orbitals into its hybridisation, giving rise to a superoctet species(since the covalent bonds add an electron each) I cooked up a periodic table with the shells marked. I've used the shell letters instead of numbers to avoid confusion. $K,L,M,N$ refer to shell 1,2,3,4 etc. When a slice of the table is marked "M9-M18", this means that the first element of that block "fills" the ninth electron in the M(third) shell, and the last element fills the eighteenth. Click to enlarge: (Derivative of this image ) Note that there are a few irregularities, with $\ce{Cu}$, $\ce{Cr}$, $\ce{Ag}$, and a whole bunch of others which I've not specially marked in the table. | {
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537 | Inspired by this question , I'm wondering why arsenous acid is frequently denoted $\ce{H3AsO3}$ , as opposed to $\ce{As(OH)3}$ , which would appear to more accurately reflect its connectivity? [edit] I feel like such a doofus, forgetting about sulfuric acid ( $\ce{H2SO4}$ ), phosphoric acid ( $\ce{H3PO4}$ ), and boric acid ( $\ce{B(OH)3}$ ), etc. Great discussion, people! | All quoted stuff copied from IUPAC Red Book , IR-4 unless otherwise specified It's not only $\ce{H3AsO3}$ . What about $\ce{H3BO3,H3PO4,H2SO4,HClO4}$? Or indeed, any other oxyacid? Basically, we have multiple ways of writing inline formulae of covalent compounds . One is the boring way ( molecular formula ), and one is the fun way ( structural formula ) where the formula reveals a bit of the structure. $\ce{As(OH)3}$ reveals the structure, $\ce{H3AsO3}$ doesn't. For compounds consisting of discrete molecules, the molecular formula, as opposed to the
empirical formula, may be used to indicate the actual composition of the molecules. For the
order of citation of symbols in molecular formulae, see Section IR-4.4. A structural formula gives partial or complete information about the way in which the atoms
in a molecule are connected and arranged in space. In simple cases, a line formula that is just
a sequence of atomic symbols gives structural information provided the reader knows that
the formula represents the order of the atoms in the linear structure. So, what are the rules for writing the molecular formula? Well, initially these rules were basically that we just follow electronegativity--the most electropositive element is listed first and so on. Looks like they slightly changed it . For one, there are actually two ordering standards--one is the extremely boring alphabetical one, which I've never seen used (except in emperical formulae), and one is via electronegativity. Now, instead of following the absolute electronegativities, the IUPAC has assigned a "pseudo-electronegativity" order (my terminology). The rules are as follows (source) : for two elements in different groups - then the element in the higher numbered group has higher "electronegativity" for two elements within the same group the element with the lower the atomic number has the higher "electronegativity" Hydrogen is fitted in to be less electronegative than polonium and more electronegative than nitrogen. Hence the formulae of water and ammonia can be written H2O and NH3 respectively. This leads to the following "pseudo-electronegativity" order of elements: (click to enlarge) The motivation behind this must probably be the erratic and hard-to-quantify nature of "real" enectronegativity. Now, we can apply these rules in the following way: If the compound is a binary compound (only two elements, not two atoms), then we just follow the pseudo-electronegativity thingy. In accordance with established practice, the electronegativity criterion (Section IR-4.4.2.1)
is most often used in binary species. If the compound is a coordination compound, we order central atoms by pseudo-electronegativity, and ligands by alphabetical order, as written (eg $\ce{(en)}$ before $\ce{(dmg)}$, but $\ce{C2H4(NH2)2}$ after $\ce{(dmg)}$, even though $\ce{(en)}$ and $\ce{C2H4(NH2)2}$ are the same). The order of citation of central atoms is based on electronegativity as described in
Section IR-4.4.2.1. Ligands are cited alphabetically (Section IR-4.4.2.2) according to the
first symbol of the ligand formula or ligand abbreviation (see Section IR-4.4.4) as written.
Where possible, the ligand formula should be written in such a way that a/the donor atom
symbol is closest to the symbol of the central atom to which it is attached. Finally (barring annoying extra rules for isotopes and hydration), we have what are called "generalized salts" . This is for compounds which can be treated as being made up of ions. The ions are ordered by electronegativity, and the elements within each ion are ordered alphabetically{*}. If the formula of a compound containing three or more elements is not naturally assigned
using the preceding two sections, the compound can be treated as a generalized salt. This
term is taken to mean any compound in which it is possible to identify at least one
constituent which is a positive ion or can be classified as electropositive or more
electropositive than the other constituents, and at least one constituent which is a negative
ion or can be classified as electronegative or more electronegative than the rest of the
constitutents. The ordering principle is then: (i) all electropositive constituents precede all electronegative constituents; (ii) within each of the two groups of constituents, alphabetical order is used. This is the rule we need to write the formula for $\ce{H3AsO3}$. First, we need to clear up what is meant by " treated as being made up of ions". Well, for this, as @Terry noted above, we look for the weaker bond. In $\ce{NaOH}$, we have relative bond strengths $\ce{Na...O-H}$, whereas $\ce{H3AsO3}$ is $\ce{As-(O...H)3}$. Thus, in $\ce{NaOH}$, the "ion" breakup is $\ce{Na+, OH-}$, while in $\ce{H3AsO3}$, the ions are $\ce{H+,AsO3-}$. So, arsenous acid is broken up into ions, of which $\ce{H+}$ is written first. Within each ion, we order alphabetically, so we get $\ce{AsO3}$, not $\ce{O3As}$. Putting them together, we get $\ce{H3AsO3}$. *Despite being the IUPAC rule, it seems that, within ions, most people just follow the electronegativity rules again. Selenous acid seems to be commonly named $\ce{H2SeO3}$, when it should be $\ce{H2O3Se}$. But this seems to be a minor offence: Deviation from alphabetical order of constituents in the same class is allowed to
emphasize similarities between compounds. | {
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539 | I am currently reading the CRC Handbook of Phosphorus-31 Nuclear Magnetic Resonance Data by John C. Tebby (CRC Press, 1991) and on several figures (ex. pages 9 to 14) there is a caption that reads along these lines $\ce{^{31}P}$ NMR chemical shifts of three coordinate (λ3 σ3) phosphorus compounds. (Tables B to E.) What does the (λ3 σ3) signify? I've not seen that notation before, and it is on the captions of some of the charts I need. | The notation refers to the valency (number of valence electrons involved in bonds, i.e., either 3 or 5) and coordination number (number of substituents attached) in organophosphorus compounds. For example, it could refer to the tautomeric forms of phosphonate esters: 1 So the λ 3 σ 3 refers to a P with 3 bonding valence electrons (the lone pair doesn't count) and 3 substituents attached while λ 5 σ 4 refers to a P with all five of its valence electrons involved in bonds and 4 substituents attached. Reference Kraszewski, A.; Stawinski, J. H-Phosphonates: Versatile synthetic precursors to biologically active phosphorus compounds. Pure Appl. Chem. 2009, 79 (12), 2217–2227. DOI: 10.1351/pac200779122217 . | {
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554 | Most of the existing software I know (like VMD or Pymol) say that they can be used to create PDF files with 3D representations of molecules: actual 3D models, which you can rotate inside the Adobe Acrobat viewer. However, they all require the use of “Adobe Acrobat Pro 9 Extended” for its 3D capture feature. From what I can read , this feature does not exist any more in Acrobat X and was transferred to a separate product, Tetra4D , which doesn't work on Mac OS. So, how can I produce PDF files including 3D molecular models using free (or better, open source) tools? | Disclaimer This is not for the faint-hearted. If you are not interested in using LaTeX , stop reading now, as this uses the media15 or movie9 packages to embed U3D in a pdfLaTeX generated PDF. This answer assumes basic familiarity with LaTeX. I have tested this with pdfLaTeX and it should work fine in XeLaTeX. One of the tools I have used (DAZ Studio) is apparently 'free for a limited time'. It is also not available on Linux. FOSS replacement suggestions are welcome. I'm of the personal opinion that 3D in PDF is not as good as it sounds. What doesn't work VMD offers the ability to output as OBJ, which can then be processed with FOSS MeshLab into a U3D file that can be embedded into a PDF. This is sub-optimal for two reasons: There is no way to tell MeshLab that the VMD-generated mesh is supposed to be Gouraud-shaded. This means that the hard facets of the mesh will be glaringly obvious in the pdf, even if you use an unwieldy degree of subdivision. Colours are not preserved. Your model will appear in the PDF with a uniform grey texture. As such, MeshLab is not suitable at this stage . Preparing a model VMD offers a number of decent export options to get our geometry out of .PDB or what have you and into a mesh format. I opted to use the VRML format to output a mesh of a ribbon representation of PDB entry 4DM9 . I then imported this into Blender . Blender has no reliable U3D export capabilities, however I can use it to assign Gouraud shading to all of the shapes and assign colours to them. I then use the blender export function to export the scene as a Wavefront .OBJ file, with attendant .MTL file. Processing with DAZ Studio I am indebted to the author of this article (John Nyquist), which indicated that DAZ Studio can convert Wavefront to U3D just fine, with preservation of textures. DAZ is a very specific program that seems to be heavily geared towards posing, clothing and rendering humanoid figures in the spirit of programs like Poser. However all we really need is the U3D export function and we can read in the structure just fine. Sometimes, this is how I see myself: Okay in all seriousness, don't put a human figure in or on your molecule without good reason. Export as U3D and then we can embed in pdfLaTeX. pdfLaTeX and movie9 As a proof of concept, I just followed the minimal example given in the media9 manual for getting a 3D model into a pdfLaTeX-generated PDF. Here it is, being viewed in Adobe Reader X (I know, I know!). Bear in mind that very few readers can actually display 3D PDF, which is one of the reasons why I feel that it is not such a good idea for chemical visualisation. It starts off zoomed way too far in because I did not set up any options for the import (however you can find out all about that in the media9 or movie15 package manuals) and is a bit laggy on account of having over 1 million faces (I went way overboard with subdivision), however the important thing is that it works . Improvements welcome! Obviously, this is a pretty Rube Goldbergesque route to getting a molecule into a PDF. There probably exist easier ways which should definitely be suggested. | {
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594 | Carbon is well known to form single, double, and triple $\ce{C-C}$ bonds in compounds. There is a recent report (2012) that carbon forms a quadruple bond in diatomic carbon, $\ce{C2}$. The excerpt below is taken from that report. The fourth bond seems pretty odd to me. $\ce{C2}$ and its isoelectronic molecules $\ce{CN+}$, BN and $\ce{CB-}$ (each having eight valence electrons) are bound by a quadruple bond. The bonding comprises not only one σ- and two π-bonds, but also one weak ‘inverted’ bond, which can be characterized by the interaction of electrons in two outwardly pointing sp hybrid orbitals. According to Shaik, the existence of the fourth bond in $\ce{C2}$ suggests that it is not really diradical... If $\ce{C2}$ were a diradical it would immediately form higher clusters. I think the fact that you can isolate $\ce{C2}$ tells you it has a barrier, small as it may be, to prevent that. Molecular orbital theory for dicarbon , on the other hand, predicts a C-C double bond in $\ce{C2}$ with 2 pairs of electrons in $\pi$ bonding orbitals and a bond order of two. "The bond dissociation energies (BDE) of $\ce{B2, C2}$, and $\ce{N2}$ show increasing BDE consistent with single, double, and triple bonds." ( Ref ) So this model of the $\ce{C2}$ molecule seems quite reasonable. My questions, since this is most definitely not my area of expertise: Is dicarbon found naturally in any quantity and how stable is it? Is it easy to make in the lab? (The Wikipedia article reports it in stellar atmospheres, electric arcs, etc.) Is there good evidence for the presence of a quadruple bond in $\ce{C2}$ that wouldn't be equally well explained by double bonding? | Okay, this is not so much of an answer as it is a summary of my own progress on this topic after giving it some thought. I don't think it's a settled debate in the community yet, so I don't feel so much ashamed about it :) A few of the things worthy of note are: The bond energy found by the authors for this fourth bond is $\pu{13.2 kcal/mol}$ , i.e. about $\pu{55 kJ/mol}$ . This is very weak for a covalent bond. You can compare it to other values here , or to the energies of the first three bonds in triple-bonded carbon, which are respectively $348, 266$ , and $\pu{225 kJ/mol}$ . This fourth bond is actually even weaker than the strongest of hydrogen bonds ( $\ce{F\bond{...}H–F}$ , at $\pu{160 kJ/mol}$ ). Another point of view on this article could thus be: “valence bond necessarily predicts a quadruple bond, and it was now precisely calculated and found to be quite weak.” The findings of this article are consistent with earlier calculations using other quantum chemistry methods (e.g. the DFT calculations in ref. 48 of the Nature Chemistry paper) which have found a bond order between 3 and 4 for molecular dicarbon. However, the existence of this quadruple bonds is somewhat at odds with the cohesive energy of gas-phase dicarbon, which according to Wikipedia is $\pu{6.32 eV}$ , i.e. $\pu{609 kJ/mol}$ . This latter value is much more in line with typical double bonds, reported at an average of $\pu{614 kJ/mol}$ . This is still a bit of a misery to me… | {
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608 | What are the advantages and disadvantages of the various types of condensers commonly found in the laboratory? Obviously more intricate pieces of glassware are more costly but assuming they are all available why would one use a Dimroth condenser vs. a Friedrichs when refluxing something? I've heard that Graham condensers are to be avoided when refluxing due to the possibility of clogging, and yet it is still very common - when is it appropriate to use one? Illustration made with ChemDraw. Feel free to reference other designs but please attach a schematic for clarity. Edit : This question was motivated by an organic preparation which involved the bromination of an alkene in boiling water. Bromine has a boiling point of 58.8 °C and on top of that the reaction was exothermic. It was difficult to avoid the loss of Br 2 gas with your typical Allihn condenser, but the increased cooling capacity provided by a Friedrichs returned Br 2 back to the flask as it was produced. Also, while the Friedrichs forces vapors up a spiral path, the path itself is wide, and in my condenser at least, there was a bit of leeway for liquid to drop down the sides, helping to prevent blockages. I didn't try a Graham condenser but I imagine a much slower rate of addition would be supported by this condenser. | @Mart 's comment impelled me to return to this question and correct my answer. I've deleted incorrect material and expanded the discussion to, hopefully, provide correct information. There is a good discussion (better than the reference previously cited) of the issue here . Reflux is the process of boiling reactants while continually cooling the vapor returning it back to the flask as a liquid. It is used to heat a mixture for extended periods and at certain temperatures...A condenser is attached to the boiling flask, and cooling water is circulated to condense escaping vapors. If you are refluxing a mixture, as you might in organic synthesis to increase the speed of the reaction by doing it at a higher temperature (i.e., the boiling point of the solvent), then any of the condensers that worked well enough to avoid the loss of solvent and avoid "flooding" would work equally well. When you're refluxing, you want the "reflux ring", the place where the vapor is visibly condensing into a liquid, to be no more than 1/3 of the way up the reflux column. You have two different basic types of condensers shown, Graham-type condensers (the first 3) and coil condensers (the last two). In the coil condensers (the left condenser in the picture below), the water flows through the coil and the vapor moves up in the larger, outside area of the condenser, condenses onto the cooled coils, then drips back into the pot. In a Graham-type condenser (the right condenser in the picture below), the water flows around a tube (whether straight or coiled) that contains the vapor/condensed liquid.( picture source ) The Graham-type condensers clog (or flood) more easily since they have a more restricted path for the liquid to return to the pot. Graham-type condensers: The Liebig condenser is simple, but has low cooling capacity and can be fairly easily clogged as the condensed liquid flows back into the flask and blocks the vapor that is trying to escape. The Allihn improves on this design by having a wider bore at the bottom and condensing the liquid on the "bubbles" where it can run down the sides and avoid blocking the vapor. (I've used this to good effect in refluxing many reactions.) The Graham condenser is the same basic design as the other two, but the condensation tube is coiled which provides more surface area for cooling...but also tends to send the condensed liquid right into the path of the vapor trying to move up. It is particularly prone to flooding. Coil condensers , such as the Dimroth and Freidrichs, have high capacity for cooling with fewer problems from flooding since the vapor condenses on the coils and drips back from the little prominence at the bottom of the coils into the center of the pot. The vapor has an easy time getting past the drops falling into the pot. If you can afford it, this seems like a good choice for most applications. The Freidrichs condensers, which incorporate a cold-finger with the spiral, are higher capacity, quite bulky and heavy. I have seen them used with rotovaps where you are taking a lot of solvent off quickly, but not with an ordinary reflux apparatus. This would be over-kill for a simple reflux reaction situation. Sorry for the incorrect information (for those of you who looked at this before) and hope this is helpful. | {
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652 | Was there any false chemical element introduced in history of chemistry? I mean a substance that after a while proved that it was not an element. | The example that comes to mind is didymium , which turned out to be a mixture of praesodymium and neodymium. The term is still used, as far as I know, to refer to glass doped with a mixture of these lanthanides. This is discussed in one of the 'Chemistry in its element' podcast episodes . As it turns out, wikipedia has a category called 'Misidentified Chemical Elements' . Especially notable are illmenium, dianium and pelopium, which were all likely mixtures of niobium and tantalum, two rather similar elements. | {
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710 | I understand that covalent bonding is an equilibrium state between attractive and repulsive forces, but which one of fundamental forces actually causes atoms to attract each other? Also, am I right to think that "repulsion occurs when atoms are too close together" comes from electrostatic interaction? | I understand that covalent bonding is an equilibrium state between attractive and repulsive forces, but which one of fundamental forces actually causes atoms to attract each other? The role of Pauli Exclusion in bonding It is an unfortunate accident of history that because chemistry has a very convenient and predictive set of approximations for understanding bonding, some of the details of why those bonds exist can become a bit hard to discern. It's not that they aren't there -- they most emphatically are! -- but you often have to dig a bit deeper to find them. They are found in physics, in particular in the concept of Pauli exclusion . Chemistry as avoiding black holes Let's take your attraction question first. What causes that? Well, in one sense that question is easy: it's electrostatic attraction, the interplay of pulls between positively charged nuclei and negatively charged electrons. But even in saying that, something is wrong. Here's the question that points that out: If nothing else was involved except electrostatic attraction, what would be the most stable configuration of two or more atoms with a mix of positive and negative charges? The answer to that is a bit surprising. If the charges are balanced, the only stable, non-decaying answer for conventional (classical) particles is always the same: "a very, very small black hole." Of course you could modify that a bit by assuming that the strong force is for some reason stable, in which case the answer becomes "a bigger atomic nucleus," one with no electrons around it. Or maybe atoms as Get Fuzzy? At this point some of you reading this should be thinking loudly "Now wait a minute! Electrons don't behave like point particles in atoms, because quantum uncertainty makes them 'fuzz out' as they get close to the nucleus." And that is exactly correct -- I'm fond of quoting that point myself in other contexts! However, the issue here is a bit different, since even "fuzzed out" electrons provide a poor barrier for keeping other electrons away by electrostatic repulsion alone, precisely because their charge is so diffuse. The case of electrons that lack Pauli exclusion is nicely captured by Richard Feynman in his Lectures on Physics , in Volume III, Chapter 4, page 4-13, Figure 4-11 at the top of the page. The outcome Feynman describes is pretty boring, since atoms would remain simple, smoothly spherical, and about the same size as more and more protons and electrons get added in. While Feynman does not get into how such atoms would interact, there's a problem there too. Because the electron charges would be so diffuse in comparison to the nuclei, the atoms would pose no real barrier to each other until the nuclei themselves begin to repel each other. The result would be a very dense material that would have more in common with neutronium than with conventional matter. For now I'll just forge ahead with a more classical description, and capture the idea of the electron cloud simply by asserting that each electron is selfish and likes to capture as much "address space" (see below) as possible. Charge-only is boring! So, while you can finagle with funny configurations of charges that might prevent the inevitable for a while by pitting positive against positive and negative against negative, positively charged nuclei and negatively charged electrons with nothing much else in play will always wind up in the same bad spot: either as very puny black holes, or as tiny boring atoms that lack anything resembling chemistry. A universe full of nothing but various sizes of black holes or simple homogenous neutronium is not very interesting! Preventing the collapse So, to understand atomic electrostatic attraction properly, you must start with the inverse issue: What in the world is keeping these things from simply collapsing down to zero size -- that is, where is the repulsion coming from? And that is your next question: Also, am I right to think that "repulsion occurs when atoms are too close together" comes from electrostatic interaction? No; that is simply wrong. In the absence of "something else," the charges will wiggle about and radiate until any temporary barrier posed by identical charges simply becomes irrelevant... meaning that once again you will wind up with those puny black holes. What keeps atoms, bonds, and molecules stable is always something else entirely, a "force" that is not traditionally thought of as being a force at all, even though it is unbelievably powerful and can prevent even two nearby opposite electrical charges from merging. The electrostatic force is enormously powerful at the tiny separation distances within atoms, so anything that can stop charged particles from merging is impressive! The "repulsive force that is not a force" is the Pauli exclusion I mentioned earlier. A simple way to think of Pauli exclusion is that identical material particles (electrons, protons, and neutrons in particular) all insist on having completely unique "addresses" to tell them apart from other particles of the same type. For an electron this address includes: where the electron is located in space, how fast and in what direction it is moving (momentum), and one last item called spin, which can only have on of two values that are usually called "up" or "down." You can force such material particles (called fermions ) into nearby addresses, but with the exception of that up-down spin part of the address, doing so always increases the energy of at least one of the electrons. That required increase in energy is a nutshell is why material objects push back when you try to squeeze them . Squeezing them requires minutely reducing the available space of many of the electrons in the object, and those electrons respond by capturing the energy of the squeeze and using it to push right back at you. Now, take that thought and bring it back to the question about where repulsion comes from when to atoms bond at a certain distance, but no closer . They are the same mechanism! That is, two atoms can "touch" (move so close, but no closer) only because they both have a lot of electrons that require separate space, velocity, and spin addresses. Push them together and they start hissing like cats from two households who have suddenly been forced to share the same house. (If you own multiple cats, you'll know exactly what I mean by that.) So, what happens is that the overall set of plus-and-minus forces of the two atoms is trying really hard to crush all of the charges down into a single very tiny black hole -- not into some stable state! It is only the hissing and spitting of the overcrowded and very unhappy electrons that keeps this event from happening. Orbitals as juggling acts But just how does that work? It's sort of a juggling act, frankly. Electrons are allowed to "sort of" occupy many different spots, speeds, and spins (mnemonic $s^3$ , and no , that is not standard, I'm just using it for convenience in this answer only) at the same time, due to quantum uncertainty . However, it's not necessary to get into that here beyond recognizing that every electron tries to occupy as much of its local $s^3$ address space as possible. Juggling between spots and speeds requires energy. So, since only so much energy is available, this is the part of the juggling act that gives atoms size and shapes. When all the jockeying around wraps up, the lowest energy situations keep the electrons stationed in various ways around the nucleus, not quite touching each other. We call those special solutions to the crowding problem orbitals , and they are very convenient for understanding and estimating how atoms and molecules will combine. Orbitals as specialized solutions However, it's still a good idea to keep in mind that orbitals are not exactly fundamental concepts, but rather outcomes of the much deeper interplay of Pauli exclusion with the unique masses, charges, and configurations of nuclei and electrons. So, if you toss in some weird electron-like particle such as a muon or positron , standard orbital models have to be modified significantly and applied only with great care. Standard orbitals can also get pretty weird just from having unusual geometries of fully conventional atomic nuclei, with the unusual dual hydrogen bonding found in boron hydrides such as diborane probably being the best example. Such bonding is odd if viewed in terms of conventional hydrogen bonds, but less so if viewed simply as the best possible "electron juggle" for these compact cases. "Jake! The bond!" Now on to the part that I find delightful, something that underlies the whole concept of chemical bonding. Recall that it takes energy to squeeze electrons together in terms of the main two parts of their "addresses," the spots (locations) and speeds (momenta)? I also mentioned that spin is different in this way: the only energy cost for adding two electrons with different spin addresses is that of conventional electrostatic repulsion. That is, there is no "forcing them closer" Pauli exclusion cost like you get for locations and velocities. Now you might think "but electrostatic repulsion is huge!", and you would be exactly correct. However, compared to the Pauli exclusion "non-force force" cost, the energy cost of this electrostatic repulsion is actually quite small -- so small that it can usually be ignored for small atoms. So when I say that Pauli exclusion is powerful, I mean it, since it even makes the enormous repulsion of two electrons stuck inside the same tiny sector of a single atom look so insignificant that you can usually ignore its impact! But that's secondary, because the real point is this: When two atoms approach each other closely, the electrons start fighting fierce energy-escalation battles that keep both atoms from collapsing all the way down into a black hole. But there is one exception to that energetic infighting: spin! For spin and spin alone, it become possible to get significantly closer to that final point-like collapse that all the charges want to do. Spin thus becomes a major "hole" -- the only such major hole -- in the ferocious armor of repulsion produced by Pauli exclusion. If you interpret atomic repulsion due to Pauli exclusion as the norm, then spin-pairing two electrons becomes another example of a "force that is not a force," or a pseudo force. In this case, however, the result is a net attraction . That is, spin-pairing allows two atoms (or an atom and an electron) to approach each other more closely that Pauli exclusion would otherwise permit. The result is a significant release of electrostatic attraction energy. That release of energy in turn creates a stable bond, since it cannot be broken unless that same energy is returned. Sharing (and stealing) is cheaper So, if two atoms (e.g. two hydrogen atoms) each have an outer orbital that contains only one electron, those two electrons can sort of look each other over and say, "you know, if you spin downwards and I spin upwards, we could both share this space for almost no energy cost at all!" And so they do, with a net release of energy, producing a covalent bond if the resulting spin-pair cancels out positive nuclear charges equally on both atoms. However, in some cases the "attractive force" of spin-pairing is so overwhelming greater for one of the two atoms that it can pretty much fully overcome (!) the powerful electrostatic attraction of the other atom for its own electron. When that happens, the electron is simply ripped away from the other atom. We call that an ionic bond, and we act as it if it's no big deal. But it is truly an amazing thing, one that is possible only because the pseudo force of spin-pairing. Bottom line: Pseudo forces are important! My apologies for having given such a long answer, but you happened to ask a question that cannot be answered correctly without adding in some version of Pauli "repulsion" and spin-pair "attraction." For that matter, the size of an atom, the shape of its orbitals, and its ability to form bonds similarly all depend on pseudo forces. | {
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893 | From school, I remember a very important rule: first you need to pour the water and then the acid (when you need to mix them) not vice-versa. This is because otherwise the aсid becomes very hot and splashing may happen. So, why does it get hotter when water is poured into it? What reaction takes place? | This is mostly the case for sulfuric acid. Commercially available sulfuric acid is dense (~1.8 g/ml) and when water is added, it may not mix. In this case a layer of hot weak acid solution is formed, which boils and sprays around. When acid is poured into water, it flows down the flask and mixes much better, so no boiling occurs. The reason this occurs is due to the large amount of energy released in the hydration reaction of sulfuric acid ions. Do not believe that heat comes from dissociation, as the dissociation of acids, bases, and salts always consumes energy. The energy is released from subsequent hydration, and the release may be high, especially if $\ce{H+}$ or $\ce{OH-}$ ions are hydrated. | {
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915 | How can $\ce{CO2}$ be converted into carbon and oxygen? $$\ce{CO2 -> C + O2}$$ Alternatively: $$\ce{CO2 + ? -> C + O2}$$ I'm aware that plants are capable of transforming $\ce{CO2 + H2O}$ to glucose and oxygen via photosynthesis, but I'm interested in chemical or physical means rather than biological. | In my opinion, the catalytic, solar-driven conversion of carbon dioxide to methanol, formic acid, etc. is much more interesting and promising, but since Enrico asked for the conversion of carbon dioxide to carbon itself: The group around Yutaka Tamaura was/is active in this field. In one of their earlier publications, [1] they heated magnetite ($\ce{Fe3O4}$) at 290 °C for 4 hours in a stream of hydrogen to yield a material which turned out to be stable at room temperature under nitrogen . This material, $\ce{Fe_{3+\delta}O4}$ $(\delta=0.127)$, i.e. the metastable cation-excess magnetite is able to incorporate oxygen in the form of $\ce{O^2-}$. Under a $\ce{CO2}$ atmosphere, the oxygen-deficient material converted to "ordinary" $\ce{Fe3O4}$ with carbon deposited on the surface . This remarkable reaction however is not catalytic , but a short recherche showed that the authors have published a tad more in this field. Maybe somebody else finds a a report on a catalytic conversion among their publications. Tamaura, Y.; Tahata, M. Complete reduction of carbon dioxide to carbon using cation-excess magnetite. Nature 1990, 346 (6281), 255–256. DOI: 10.1038/346255a0 . | {
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922 | Consider a chemical reaction where two different particles form another one $$\ce{O + O_2 -> O_3}$$ I find it confusing how this can be an exothermic process. How to picture the release of $+\Delta H$ to the surroundings. And am I right in viewing this energy value only as the net energy coming from an integration of the particle potentials as they get closer along the reaction coordinate? | In my opinion, the catalytic, solar-driven conversion of carbon dioxide to methanol, formic acid, etc. is much more interesting and promising, but since Enrico asked for the conversion of carbon dioxide to carbon itself: The group around Yutaka Tamaura was/is active in this field. In one of their earlier publications, [1] they heated magnetite ($\ce{Fe3O4}$) at 290 °C for 4 hours in a stream of hydrogen to yield a material which turned out to be stable at room temperature under nitrogen . This material, $\ce{Fe_{3+\delta}O4}$ $(\delta=0.127)$, i.e. the metastable cation-excess magnetite is able to incorporate oxygen in the form of $\ce{O^2-}$. Under a $\ce{CO2}$ atmosphere, the oxygen-deficient material converted to "ordinary" $\ce{Fe3O4}$ with carbon deposited on the surface . This remarkable reaction however is not catalytic , but a short recherche showed that the authors have published a tad more in this field. Maybe somebody else finds a a report on a catalytic conversion among their publications. Tamaura, Y.; Tahata, M. Complete reduction of carbon dioxide to carbon using cation-excess magnetite. Nature 1990, 346 (6281), 255–256. DOI: 10.1038/346255a0 . | {
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949 | As I was doing my Ap Chem homework, sometimes the question would use Iron(III) and sometimes it would use Ferric. What's the difference in usage? Also, what's the difference between Iron(II) and Ferrous? | In my opinion, the catalytic, solar-driven conversion of carbon dioxide to methanol, formic acid, etc. is much more interesting and promising, but since Enrico asked for the conversion of carbon dioxide to carbon itself: The group around Yutaka Tamaura was/is active in this field. In one of their earlier publications, [1] they heated magnetite ($\ce{Fe3O4}$) at 290 °C for 4 hours in a stream of hydrogen to yield a material which turned out to be stable at room temperature under nitrogen . This material, $\ce{Fe_{3+\delta}O4}$ $(\delta=0.127)$, i.e. the metastable cation-excess magnetite is able to incorporate oxygen in the form of $\ce{O^2-}$. Under a $\ce{CO2}$ atmosphere, the oxygen-deficient material converted to "ordinary" $\ce{Fe3O4}$ with carbon deposited on the surface . This remarkable reaction however is not catalytic , but a short recherche showed that the authors have published a tad more in this field. Maybe somebody else finds a a report on a catalytic conversion among their publications. Tamaura, Y.; Tahata, M. Complete reduction of carbon dioxide to carbon using cation-excess magnetite. Nature 1990, 346 (6281), 255–256. DOI: 10.1038/346255a0 . | {
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