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1635_58 | Leadership tensions
On March 8, 2021, CBC News reported that following discontent about the travel controversy and government policies around pandemic measures and coal mining, several UCP constituency associations had discussed holding a leadership review at an upcoming convention, putting Kenney's leadership of the party to a vote. On March 13, the UCP announced a leadership review will be held at the party's annual general meeting in 2022, expected to be held in October, six months ahead of the fixed election date for the next Alberta general election. |
1635_59 | On April 7, 2021, 15 UCP MLAs, including former Minister of Municipal Affairs Tracy Allard and Speaker Nathan Cooper, signed a letter criticizing the Government's public health orders. Two other MLAs added their names to the letter after it had been released publicly. UCP MLA Dan Williams also released a video criticizing the closure of GraceLife Church by Alberta Health Services. Kenney stated that Government MLAs were permitted to dissent over COVID-19 health restrictions but breaking health rules or encouraging others to do so would result in their expulsion from the Government Caucus. This has been described as a "revolt" and an unprecedented level of opposition from within a government caucus. During a three hour caucus meeting following the release of the letter, Kenney reportedly threatened to ask the lieutenant governor to dissolve the legislature and call a snap election if dissidents did not support the government. |
1635_60 | On April 22, 2021, a letter calling for the resignation of Premier Kenney, started circulating within the UCP party's leadership boards. The letter gained 90 signatures composed of board presidents and board members of UCP riding associations. The letter states that the boards believed that they did not believe Kenney has the moral authority or trustworthiness to lead this party into the next election or to continue to deliver on important conservative priorities and that for the sake of a strong and free Alberta and for the well-being of the conservative movement in this province, the boards ask that Kenney do the proper thing and resign. The petitioners will bring up the letter during an upcoming board meeting.
On May 13, 2021, MLA Todd Loewen stepped down from his role as UCP caucus chair and called on Jason Kenney to resign, citing "persistent issues of dysfunction within the government" and claiming that "the Premier chooses not listen to caucus". |
1635_61 | On September 22, 2021, MLA RJ Sigurdson presented a motion of no-confidence at a UCP caucus meeting, after the government introduced new public health restrictions, including a vaccine passport, following a fourth wave of the COVID-19 pandemic in Alberta. The motion was withdrawn after it was agreed that the UCP would hold a leadership review in Spring 2022, rather than October 2022 as previously scheduled.
"Wuhan Bat Soup" controversy
On December 23, 2021, Kenney likened the origins of COVID-19 to a "bat soup thing out of Wuhan". Following criticism for his remarks, Kenney said, "...if anybody did take offence, that I apologize to them, if they took offence, certainly none was intended".
Policy positions
Kenney has been a social conservative in his political career, voting in favor of abortion restrictions and against same-sex marriage. |
1635_62 | Abortion
Kenney is an anti-abortion politician, voting in favour of abortion restrictions and receiving an endorsement from the socially conservative lobbyist group Campaign Life Coalition. In 2018, a bill to create "no-protest zones" around abortion clinics was introduced to the Alberta legislature, following similar legislation in place in Ontario, Quebec, British Columbia, and Newfoundland and Labrador. As leader of the United Conservative Party, Kenney refused to debate on the bill and led his caucus to walk out of the house 14 times over the course of two months when the bill was at issue. |
1635_63 | LGBTQ issues
Kenney voted against same-sex marriage as an MP, saying, "A majority of Canadians support the provision of benefits on grounds such as domestic partnership relationships, which are grounded on unions of economic dependency rather than relationships of a mere conjugal nature, and yet still two-thirds of Canadians, from every culture that exists in this country, from every corner of the globe who have come to this country to build a future for themselves and their families, recognize that marriage is, as the Supreme Court said the last time it spoke to this issue in the Egan case in 1995, 'by nature a heterosexual institution'."
In 2016, Kenney supported the removal of "traditional definition of marriage" from the conservative party policy book. |
1635_64 | Kenney was criticized by the provincial NDP, some LGBTQ activists, and some journalists for saying in a Postmedia interview that parents generally have a right to know if their child has joined a Gay-Straight Alliance, unless it would be contrary to the best interests of the child in the circumstances.
In November 2018, Kenney faced pressure to expel an outspoken member of the United Conservative Party who compared the gay pride flag to the flag of Nazi Germany. Although Kenney had previously directed the party to cancel the membership of another member, he said that the decision to expel members rested with the party's board. |
1635_65 | A two-decade-old audio recording surfaced in December 2018 of Kenney boasting about overturning a gay marriage law in 1989 in San Francisco. Kenney was referring to his role in organizing a petition to repeal the city ordinance that extended recognition rights of heterosexual couples to same-sex couples. This ordinance, originating during the 1980s AIDS epidemic, extended rights that were previously exclusive to heterosexual couples, such as hospital visitation, to same-sex couples. Kenney addressed the audio clip by stating that he regrets the comments he made and that, since then, his record shows he supports domestic partner arrangements and benefits for couples regardless of sexual orientation. The comments led to backlash from outside and within the United Conservative Party. One board member and campaign manager for the party resigned his positions and membership with the party, citing the audio recording of Kenney as his reason for departure.
Premiership of Jason Kenney |
1635_66 | Under Kenney's leadership, the United Conservative Party won a majority government in the 2019 Alberta general election, winning 63 seats and 54.88% of the popular vote. On April 30, 2019, Kenney was sworn in by Lieutenant Governor Lois Mitchell, becoming the 18th Premier of Alberta. |
1635_67 | During the first session of the 30th Alberta Legislature, the Kenney government passed several notable of pieces of legislation, including the Act to Repeal the Carbon Tax, the Alberta Corporate Tax Amendment, and the Public Sector Wage Arbitration Deferral Act. Premier Kenney established a one-year, $2.5 million Public Inquiry into Anti-Alberta Energy Campaigns and a Calgary-based $30 million 'war room' to "fight misinformation related to oil and gas". They announced their first provincial budget on October 24, 2019, which fulfilled their "promise of slight austerity" with "cuts to spending programs and the elimination of hundreds of bureaucracy jobs", according to The National Post. The Post said that these and the corporate tax cuts "were the key planks of a four-year plan to bring the budget into balance." The goal is to reduce government spending by $4-billion over four years.
Personal life
Kenney is bilingual. He has never been married and has no children. |
1635_68 | Awards and recognition
Kenney received the Queen Elizabeth II Golden Jubilee Medal in 2002, and the Queen Elizabeth II Diamond Jubilee Medal in 2012.
In 2004, Kenney was named one of Canada's "100 Leaders of the Future" by Maclean's magazine, "one of Canada's leading conservative activists" by The Globe and Mail, and one of "21 Canadians to watch in the 21st century" by the Financial Post.
On May 13, 2009, Maclean's, in association with the Dominion Institute, L'actualité, and presenting sponsor Enbridge, presented Kenney with the award for "Best Overall MP".
Maclean's named Kenney the "hardest working" MP of 2011, citing overwhelming support from all political parties who recognized Kenney's constant "20-hour work days" and "permanent 5 o'clock shadow".
On November 4, 2012, he received an honorary doctorate from the University of Haifa. |
1635_69 | In 2014, Kenney received the UN Watch Moral Courage Award for speaking out on behalf of those who had been victimized by international tyranny. At the ceremony in Geneva, representatives of the 14th Dalai Lama presented Kenney with a traditional Tibetan scarf. Also in 2014, Kenney was awarded the inaugural Benjamin Disraeli Prize by Policy Exchange, a centre-right UK think tank, in recognition of the successful outreach to Canada's ethnic and cultural communities. The award was presented by British Conservative cabinet minister Michael Gove.
In August 2016, President Petro Poroshenko of Ukraine awarded Jason Kenney with an Order of Merit, Third Class.
Electoral record
References
External links
Premier of Alberta Official website |
1635_70 | 1968 births
Athol Murray College of Notre Dame alumni
Canadian Alliance MPs
Canadian Roman Catholics
Canadian Zionists
Conservative Party of Canada MPs
Defence ministers of Canada
Living people
Members of the 28th Canadian Ministry
Members of the House of Commons of Canada from Alberta
Members of the Queen's Privy Council for Canada
People from Oakville, Ontario
Politicians from Calgary
Reform Party of Canada MPs
Leaders of the United Conservative Party
Leaders of the Progressive Conservative Association of Alberta
United Conservative Party MLAs
Recipients of the Order of Merit (Ukraine), 3rd class
Premiers of Alberta
21st-century Canadian politicians |
1636_0 | Phagocytes are cells that protect the body by ingesting harmful foreign particles, bacteria, and dead or dying cells. Their name comes from the Greek , "to eat" or "devour", and "-cyte", the suffix in biology denoting "cell", from the Greek kutos, "hollow vessel". They are essential for fighting infections and for subsequent immunity. Phagocytes are important throughout the animal kingdom and are highly developed within vertebrates. One litre of human blood contains about six billion phagocytes. They were discovered in 1882 by Ilya Ilyich Mechnikov while he was studying starfish larvae. Mechnikov was awarded the 1908 Nobel Prize in Physiology or Medicine for his discovery. Phagocytes occur in many species; some amoebae behave like macrophage phagocytes, which suggests that phagocytes appeared early in the evolution of life. |
1636_1 | Phagocytes of humans and other animals are called "professional" or "non-professional" depending on how effective they are at phagocytosis. The professional phagocytes include many types of white blood cells (such as neutrophils, monocytes, macrophages, mast cells, and dendritic cells). The main difference between professional and non-professional phagocytes is that the professional phagocytes have molecules called receptors on their surfaces that can detect harmful objects, such as bacteria, that are not normally found in the body. Phagocytes are crucial in fighting infections, as well as in maintaining healthy tissues by removing dead and dying cells that have reached the end of their lifespan. |
1636_2 | During an infection, chemical signals attract phagocytes to places where the pathogen has invaded the body. These chemicals may come from bacteria or from other phagocytes already present. The phagocytes move by a method called chemotaxis. When phagocytes come into contact with bacteria, the receptors on the phagocyte's surface will bind to them. This binding will lead to the engulfing of the bacteria by the phagocyte. Some phagocytes kill the ingested pathogen with oxidants and nitric oxide. After phagocytosis, macrophages and dendritic cells can also participate in antigen presentation, a process in which a phagocyte moves parts of the ingested material back to its surface. This material is then displayed to other cells of the immune system. Some phagocytes then travel to the body's lymph nodes and display the material to white blood cells called lymphocytes. This process is important in building immunity, and many pathogens have evolved methods to evade attacks by phagocytes. |
1636_3 | History
The Russian zoologist Ilya Ilyich Mechnikov (1845–1916) first recognized that specialized cells were involved in defense against microbial infections. In 1882, he studied motile (freely moving) cells in the larvae of starfishes, believing they were important to the animals' immune defenses. To test his idea, he inserted small thorns from a tangerine tree into the larvae. After a few hours he noticed that the motile cells had surrounded the thorns. Mechnikov traveled to Vienna and shared his ideas with Carl Friedrich Claus who suggested the name "phagocyte" (from the Greek words , meaning "to eat or devour", and , meaning "hollow vessel") for the cells that Mechnikov had observed. |
1636_4 | A year later, Mechnikov studied a fresh water crustacean called Daphnia, a tiny transparent animal that can be examined directly under a microscope. He discovered that fungal spores that attacked the animal were destroyed by phagocytes. He went on to extend his observations to the white blood cells of mammals and discovered that the bacterium Bacillus anthracis could be engulfed and killed by phagocytes, a process that he called phagocytosis. Mechnikov proposed that phagocytes were a primary defense against invading organisms.
In 1903, Almroth Wright discovered that phagocytosis was reinforced by specific antibodies that he called opsonins, from the Greek opson, "a dressing or relish". Mechnikov was awarded (jointly with Paul Ehrlich) the 1908 Nobel Prize in Physiology or Medicine for his work on phagocytes and phagocytosis. |
1636_5 | Although the importance of these discoveries slowly gained acceptance during the early twentieth century, the intricate relationships between phagocytes and all the other components of the immune system were not known until the 1980s.
Phagocytosis |
1636_6 | Phagocytosis is the process of taking in particles such as bacteria, parasites, dead host cells, and cellular and foreign debris by a cell. It involves a chain of molecular processes. Phagocytosis occurs after the foreign body, a bacterial cell, for example, has bound to molecules called "receptors" that are on the surface of the phagocyte. The phagocyte then stretches itself around the bacterium and engulfs it. Phagocytosis of bacteria by human neutrophils takes on average nine minutes. Once inside this phagocyte, the bacterium is trapped in a compartment called a phagosome. Within one minute the phagosome merges with either a lysosome or a granule to form a phagolysosome. The bacterium is then subjected to an overwhelming array of killing mechanisms and is dead a few minutes later. Dendritic cells and macrophages are not so fast, and phagocytosis can take many hours in these cells. Macrophages are slow and untidy eaters; they engulf huge quantities of material and frequently release |
1636_7 | some undigested back into the tissues. This debris serves as a signal to recruit more phagocytes from the blood. Phagocytes have voracious appetites; scientists have even fed macrophages with iron filings and then used a small magnet to separate them from other cells. |
1636_8 | A phagocyte has many types of receptors on its surface that are used to bind material. They include opsonin receptors, scavenger receptors, and Toll-like receptors. Opsonin receptors increase the phagocytosis of bacteria that have been coated with immunoglobulin G (IgG) antibodies or with complement. "Complement" is the name given to a complex series of protein molecules found in the blood that destroy cells or mark them for destruction. Scavenger receptors bind to a large range of molecules on the surface of bacterial cells, and Toll-like receptors—so called because of their similarity to well-studied receptors in fruit flies that are encoded by the Toll gene—bind to more specific molecules. Binding to Toll-like receptors increases phagocytosis and causes the phagocyte to release a group of hormones that cause inflammation.
Methods of killing |
1636_9 | The killing of microbes is a critical function of phagocytes that is performed either within the phagocyte (intracellular killing) or outside of the phagocyte (extracellular killing).
Oxygen-dependent intracellular
When a phagocyte ingests bacteria (or any material), its oxygen consumption increases. The increase in oxygen consumption, called a respiratory burst, produces reactive oxygen-containing molecules that are anti-microbial. The oxygen compounds are toxic to both the invader and the cell itself, so they are kept in compartments inside the cell. This method of killing invading microbes by using the reactive oxygen-containing molecules is referred to as oxygen-dependent intracellular killing, of which there are two types. |
1636_10 | The first type is the oxygen-dependent production of a superoxide, which is an oxygen-rich bacteria-killing substance. The superoxide is converted to hydrogen peroxide and singlet oxygen by an enzyme called superoxide dismutase. Superoxides also react with the hydrogen peroxide to produce hydroxyl radicals, which assist in killing the invading microbe.
The second type involves the use of the enzyme myeloperoxidase from neutrophil granules. When granules fuse with a phagosome, myeloperoxidase is released into the phagolysosome, and this enzyme uses hydrogen peroxide and chlorine to create hypochlorite, a substance used in domestic bleach. Hypochlorite is extremely toxic to bacteria. Myeloperoxidase contains a heme pigment, which accounts for the green color of secretions rich in neutrophils, such as pus and infected sputum.
Oxygen-independent intracellular |
1636_11 | Phagocytes can also kill microbes by oxygen-independent methods, but these are not as effective as the oxygen-dependent ones. There are four main types. The first uses electrically charged proteins that damage the bacterium's membrane. The second type uses lysozymes; these enzymes break down the bacterial cell wall. The third type uses lactoferrins, which are present in neutrophil granules and remove essential iron from bacteria. The fourth type uses proteases and hydrolytic enzymes; these enzymes are used to digest the proteins of destroyed bacteria. |
1636_12 | Extracellular
Interferon-gamma—which was once called macrophage activating factor—stimulates macrophages to produce nitric oxide. The source of interferon-gamma can be CD4+ T cells, CD8+ T cells, natural killer cells, B cells, natural killer T cells, monocytes, macrophages, or dendritic cells. Nitric oxide is then released from the macrophage and, because of its toxicity, kills microbes near the macrophage. Activated macrophages produce and secrete tumor necrosis factor. This cytokine—a class of signaling molecule—kills cancer cells and cells infected by viruses, and helps to activate the other cells of the immune system. |
1636_13 | In some diseases, e.g., the rare chronic granulomatous disease, the efficiency of phagocytes is impaired, and recurrent bacterial infections are a problem. In this disease there is an abnormality affecting different elements of oxygen-dependent killing. Other rare congenital abnormalities, such as Chédiak–Higashi syndrome, are also associated with defective killing of ingested microbes. |
1636_14 | Viruses
Viruses can reproduce only inside cells, and they gain entry by using many of the receptors involved in immunity. Once inside the cell, viruses use the cell's biological machinery to their own advantage, forcing the cell to make hundreds of identical copies of themselves. Although phagocytes and other components of the innate immune system can, to a limited extent, control viruses, once a virus is inside a cell the adaptive immune responses, particularly the lymphocytes, are more important for defense. At the sites of viral infections, lymphocytes often vastly outnumber all the other cells of the immune system; this is common in viral meningitis. Virus-infected cells that have been killed by lymphocytes are cleared from the body by phagocytes.
Role in apoptosis |
1636_15 | In an animal, cells are constantly dying. A balance between cell division and cell death keeps the number of cells relatively constant in adults. There are two different ways a cell can die: by necrosis or by apoptosis. In contrast to necrosis, which often results from disease or trauma, apoptosis—or programmed cell death—is a normal healthy function of cells. The body has to rid itself of millions of dead or dying cells every day, and phagocytes play a crucial role in this process. |
1636_16 | Dying cells that undergo the final stages of apoptosis display molecules, such as phosphatidylserine, on their cell surface to attract phagocytes. Phosphatidylserine is normally found on the cytosolic surface of the plasma membrane, but is redistributed during apoptosis to the extracellular surface by a protein known as scramblase. These molecules mark the cell for phagocytosis by cells that possess the appropriate receptors, such as macrophages. The removal of dying cells by phagocytes occurs in an orderly manner without eliciting an inflammatory response and is an important function of phagocytes. |
1636_17 | Interactions with other cells |
1636_18 | Phagocytes are usually not bound to any particular organ but move through the body interacting with the other phagocytic and non-phagocytic cells of the immune system. They can communicate with other cells by producing chemicals called cytokines, which recruit other phagocytes to the site of infections or stimulate dormant lymphocytes. Phagocytes form part of the innate immune system, which animals, including humans, are born with. Innate immunity is very effective but non-specific in that it does not discriminate between different sorts of invaders. On the other hand, the adaptive immune system of jawed vertebrates—the basis of acquired immunity—is highly specialized and can protect against almost any type of invader. The adaptive immune system is not dependent on phagocytes but lymphocytes, which produce protective proteins called antibodies, which tag invaders for destruction and prevent viruses from infecting cells. Phagocytes, in particular dendritic cells and macrophages, |
1636_19 | stimulate lymphocytes to produce antibodies by an important process called antigen presentation. |
1636_20 | Antigen presentation |
1636_21 | Antigen presentation is a process in which some phagocytes move parts of engulfed materials back to the surface of their cells and "present" them to other cells of the immune system. There are two "professional" antigen-presenting cells: macrophages and dendritic cells. After engulfment, foreign proteins (the antigens) are broken down into peptides inside dendritic cells and macrophages. These peptides are then bound to the cell's major histocompatibility complex (MHC) glycoproteins, which carry the peptides back to the phagocyte's surface where they can be "presented" to lymphocytes. Mature macrophages do not travel far from the site of infection, but dendritic cells can reach the body's lymph nodes, where there are millions of lymphocytes. This enhances immunity because the lymphocytes respond to the antigens presented by the dendritic cells just as they would at the site of the original infection. But dendritic cells can also destroy or pacify lymphocytes if they recognize |
1636_22 | components of the host body; this is necessary to prevent autoimmune reactions. This process is called tolerance. |
1636_23 | Immunological tolerance
Dendritic cells also promote immunological tolerance, which stops the body from attacking itself. The first type of tolerance is central tolerance, that occurs in the thymus. T cells that bind (via their T cell receptor) to self antigen (presented by dendritic cells on MHC molecules) too strongly are induced to die. The second type of immunological tolerance is peripheral tolerance.
Some self reactive T cells escape the thymus for a number of reasons, mainly due to the lack of expression of some self antigens in the thymus. Another type of T cell; T regulatory cells can down regulate self reactive T cells in the periphery. When immunological tolerance fails, autoimmune diseases can follow.
Professional phagocytes |
1636_24 | Phagocytes of humans and other jawed vertebrates are divided into "professional" and "non-professional" groups based on the efficiency with which they participate in phagocytosis. The professional phagocytes are the monocytes, macrophages, neutrophils, tissue dendritic cells and mast cells. One litre of human blood contains about six billion phagocytes. |
1636_25 | Activation
All phagocytes, and especially macrophages, exist in degrees of readiness. Macrophages are usually relatively dormant in the tissues and proliferate slowly. In this semi-resting state, they clear away dead host cells and other non-infectious debris and rarely take part in antigen presentation. But, during an infection, they receive chemical signals—usually interferon gamma—which increases their production of MHC II molecules and which prepares them for presenting antigens. In this state, macrophages are good antigen presenters and killers. If they receive a signal directly from an invader, they become "hyperactivated", stop proliferating, and concentrate on killing. Their size and rate of phagocytosis increases—some become large enough to engulf invading protozoa. |
1636_26 | In the blood, neutrophils are inactive but are swept along at high speed. When they receive signals from macrophages at the sites of inflammation, they slow down and leave the blood. In the tissues, they are activated by cytokines and arrive at the battle scene ready to kill.
Migration
When an infection occurs, a chemical "SOS" signal is given off to attract phagocytes to the site. These chemical signals may include proteins from invading bacteria, clotting system peptides, complement products, and cytokines that have been given off by macrophages located in the tissue near the infection site. Another group of chemical attractants are cytokines that recruit neutrophils and monocytes from the blood. |
1636_27 | To reach the site of infection, phagocytes leave the bloodstream and enter the affected tissues. Signals from the infection cause the endothelial cells that line the blood vessels to make a protein called selectin, which neutrophils stick to on passing by. Other signals called vasodilators loosen the junctions connecting endothelial cells, allowing the phagocytes to pass through the wall. Chemotaxis is the process by which phagocytes follow the cytokine "scent" to the infected spot. Neutrophils travel across epithelial cell-lined organs to sites of infection, and although this is an important component of fighting infection, the migration itself can result in disease-like symptoms. During an infection, millions of neutrophils are recruited from the blood, but they die after a few days.
Monocytes |
1636_28 | Monocytes develop in the bone marrow and reach maturity in the blood. Mature monocytes have large, smooth, lobed nuclei and abundant cytoplasm that contains granules. Monocytes ingest foreign or dangerous substances and present antigens to other cells of the immune system. Monocytes form two groups: a circulating group and a marginal group that remain in other tissues (approximately 70% are in the marginal group). Most monocytes leave the blood stream after 20–40 hours to travel to tissues and organs and in doing so transform into macrophages or dendritic cells depending on the signals they receive. There are about 500 million monocytes in one litre of human blood.
Macrophages |
1636_29 | Mature macrophages do not travel far but stand guard over those areas of the body that are exposed to the outside world. There they act as garbage collectors, antigen presenting cells, or ferocious killers, depending on the signals they receive. They derive from monocytes, granulocyte stem cells, or the cell division of pre-existing macrophages. Human macrophages are about 21 micrometers in diameter. |
1636_30 | This type of phagocyte does not have granules but contains many lysosomes. Macrophages are found throughout the body in almost all tissues and organs (e.g., microglial cells in the brain and alveolar macrophages in the lungs), where they silently lie in wait. A macrophage's location can determine its size and appearance. Macrophages cause inflammation through the production of interleukin-1, interleukin-6, and TNF-alpha. Macrophages are usually only found in tissue and are rarely seen in blood circulation. The life-span of tissue macrophages has been estimated to range from four to fifteen days. |
1636_31 | Macrophages can be activated to perform functions that a resting monocyte cannot. T helper cells (also known as effector T cells or Th cells), a sub-group of lymphocytes, are responsible for the activation of macrophages. Th1 cells activate macrophages by signaling with IFN-gamma and displaying the protein CD40 ligand. Other signals include TNF-alpha and lipopolysaccharides from bacteria. Th1 cells can recruit other phagocytes to the site of the infection in several ways. They secrete cytokines that act on the bone marrow to stimulate the production of monocytes and neutrophils, and they secrete some of the cytokines that are responsible for the migration of monocytes and neutrophils out of the bloodstream. Th1 cells come from the differentiation of CD4+ T cells once they have responded to antigen in the secondary lymphoid tissues. Activated macrophages play a potent role in tumor destruction by producing TNF-alpha, IFN-gamma, nitric oxide, reactive oxygen compounds, cationic |
1636_32 | proteins, and hydrolytic enzymes. |
1636_33 | Neutrophils |
1636_34 | Neutrophils are normally found in the bloodstream and are the most abundant type of phagocyte, constituting 50% to 60% of the total circulating white blood cells. One litre of human blood contains about five billion neutrophils, which are about 10 micrometers in diameter and live for only about five days. Once they have received the appropriate signals, it takes them about thirty minutes to leave the blood and reach the site of an infection. They are ferocious eaters and rapidly engulf invaders coated with antibodies and complement, and damaged cells or cellular debris. Neutrophils do not return to the blood; they turn into pus cells and die. Mature neutrophils are smaller than monocytes and have a segmented nucleus with several sections; each section is connected by chromatin filaments—neutrophils can have 2–5 segments. Neutrophils do not normally exit the bone marrow until maturity but during an infection neutrophil precursors called metamyelocytes, myelocytes and promyelocytes are |
1636_35 | released. |
1636_36 | The intra-cellular granules of the human neutrophil have long been recognized for their protein-destroying and bactericidal properties. Neutrophils can secrete products that stimulate monocytes and macrophages. Neutrophil secretions increase phagocytosis and the formation of reactive oxygen compounds involved in intracellular killing. Secretions from the primary granules of neutrophils stimulate the phagocytosis of IgG-antibody-coated bacteria. When encountering bacteria, fungi or activated platelets they produce web-like chromatin structures known as neutrophil extracellular traps (NETs). Composed mainly of DNA, NETs cause death by a process called netosis – after the pathogens are trapped in NETs they are killed by oxidative and non-oxidative mechanisms.
Dendritic cells |
1636_37 | Dendritic cells are specialized antigen-presenting cells that have long outgrowths called dendrites, that help to engulf microbes and other invaders. Dendritic cells are present in the tissues that are in contact with the external environment, mainly the skin, the inner lining of the nose, the lungs, the stomach, and the intestines. Once activated, they mature and migrate to the lymphoid tissues where they interact with T cells and B cells to initiate and orchestrate the adaptive immune response.
Mature dendritic cells activate T helper cells and cytotoxic T cells. The activated helper T cells interact with macrophages and B cells to activate them in turn. In addition, dendritic cells can influence the type of immune response produced; when they travel to the lymphoid areas where T cells are held they can activate T cells, which then differentiate into cytotoxic T cells or helper T cells.
Mast cells |
1636_38 | Mast cells have Toll-like receptors and interact with dendritic cells, B cells, and T cells to help mediate adaptive immune functions. Mast cells express MHC class II molecules and can participate in antigen presentation; however, the mast cell's role in antigen presentation is not very well understood. Mast cells can consume and kill gram-negative bacteria (e.g., salmonella), and process their antigens. They specialize in processing the fimbrial proteins on the surface of bacteria, which are involved in adhesion to tissues. In addition to these functions, mast cells produce cytokines that induce an inflammatory response. This is a vital part of the destruction of microbes because the cytokines attract more phagocytes to the site of infection. |
1636_39 | Non-professional phagocytes
Dying cells and foreign organisms are consumed by cells other than the "professional" phagocytes. These cells include epithelial cells, endothelial cells, fibroblasts, and mesenchymal cells. They are called non-professional phagocytes, to emphasize that, in contrast to professional phagocytes, phagocytosis is not their principal function. Fibroblasts, for example, which can phagocytose collagen in the process of remolding scars, will also make some attempt to ingest foreign particles.
Non-professional phagocytes are more limited than professional phagocytes in the type of particles they can take up. This is due to their lack of efficient phagocytic receptors, in particular opsonins—which are antibodies and complement attached to invaders by the immune system. Additionally, most non-professional phagocytes do not produce reactive oxygen-containing molecules in response to phagocytosis.
Pathogen evasion and resistance |
1636_40 | A pathogen is only successful in infecting an organism if it can get past its defenses. Pathogenic bacteria and protozoa have developed a variety of methods to resist attacks by phagocytes, and many actually survive and replicate within phagocytic cells. |
1636_41 | Avoiding contact
There are several ways bacteria avoid contact with phagocytes. First, they can grow in sites that phagocytes are not capable of traveling to (e.g., the surface of unbroken skin). Second, bacteria can suppress the inflammatory response; without this response to infection phagocytes cannot respond adequately. Third, some species of bacteria can inhibit the ability of phagocytes to travel to the site of infection by interfering with chemotaxis. Fourth, some bacteria can avoid contact with phagocytes by tricking the immune system into "thinking" that the bacteria are "self". Treponema pallidum—the bacterium that causes syphilis—hides from phagocytes by coating its surface with fibronectin, which is produced naturally by the body and plays a crucial role in wound healing. |
1636_42 | Avoiding engulfment
Bacteria often produce capsules made of proteins or sugars that coat their cells and interfere with phagocytosis. Some examples are the K5 capsule and O75 O antigen found on the surface of Escherichia coli, and the exopolysaccharide capsules of Staphylococcus epidermidis. Streptococcus pneumoniae produces several types of capsule that provide different levels of protection, and group A streptococci produce proteins such as M protein and fimbrial proteins to block engulfment. Some proteins hinder opsonin-related ingestion; Staphylococcus aureus produces Protein A to block antibody receptors, which decreases the effectiveness of opsonins. Enteropathogenic species of the genus Yersinia bind with the use of the virulence factor YopH to receptors of phagocytes from which they influence the cells capability to exert phagocytosis.
Survival inside the phagocyte |
1636_43 | Bacteria have developed ways to survive inside phagocytes, where they continue to evade the immune system. To get safely inside the phagocyte they express proteins called invasins. When inside the cell they remain in the cytoplasm and avoid toxic chemicals contained in the phagolysosomes. Some bacteria prevent the fusion of a phagosome and lysosome, to form the phagolysosome. Other pathogens, such as Leishmania, create a highly modified vacuole inside the phagocyte, which helps them persist and replicate. Some bacteria are capable of living inside of the phagolysosome. Staphylococcus aureus, for example, produces the enzymes catalase and superoxide dismutase, which break down chemicals—such as hydrogen peroxide—produced by phagocytes to kill bacteria. Bacteria may escape from the phagosome before the formation of the phagolysosome: Listeria monocytogenes can make a hole in the phagosome wall using enzymes called listeriolysin O and phospholipase C. |
1636_44 | Killing
Bacteria have developed several ways of killing phagocytes. These include cytolysins, which form pores in the phagocyte's cell membranes, streptolysins and leukocidins, which cause neutrophils' granules to rupture and release toxic substances, and exotoxins that reduce the supply of a phagocyte's ATP, needed for phagocytosis. After a bacterium is ingested, it may kill the phagocyte by releasing toxins that travel through the phagosome or phagolysosome membrane to target other parts of the cell.
Disruption of cell signaling |
1636_45 | Some survival strategies often involve disrupting cytokines and other methods of cell signaling to prevent the phagocyte's responding to invasion. The protozoan parasites Toxoplasma gondii, Trypanosoma cruzi, and Leishmania infect macrophages, and each has a unique way of taming them. Some species of Leishmania alter the infected macrophage's signalling, repress the production of cytokines and microbicidal molecules—nitric oxide and reactive oxygen species—and compromise antigen presentation. |
1636_46 | Host damage by phagocytes
Macrophages and neutrophils, in particular, play a central role in the inflammatory process by releasing proteins and small-molecule inflammatory mediators that control infection but can damage host tissue. In general, phagocytes aim to destroy pathogens by engulfing them and subjecting them to a battery of toxic chemicals inside a phagolysosome. If a phagocyte fails to engulf its target, these toxic agents can be released into the environment (an action referred to as "frustrated phagocytosis"). As these agents are also toxic to host cells, they can cause extensive damage to healthy cells and tissues. |
1636_47 | When neutrophils release their granule contents in the kidney, the contents of the granule (reactive oxygen compounds and proteases) degrade the extracellular matrix of host cells and can cause damage to glomerular cells, affecting their ability to filter blood and causing changes in shape. In addition, phospholipase products (e.g., leukotrienes) intensify the damage. This release of substances promotes chemotaxis of more neutrophils to the site of infection, and glomerular cells can be damaged further by the adhesion molecules during the migration of neutrophils. The injury done to the glomerular cells can cause kidney failure. |
1636_48 | Neutrophils also play a key role in the development of most forms of acute lung injury. Here, activated neutrophils release the contents of their toxic granules into the lung environment. Experiments have shown that a reduction in the number of neutrophils lessens the effects of acute lung injury, but treatment by inhibiting neutrophils is not clinically realistic, as it would leave the host vulnerable to infection. In the liver, damage by neutrophils can contribute to dysfunction and injury in response to the release of endotoxins produced by bacteria, sepsis, trauma, alcoholic hepatitis, ischemia, and hypovolemic shock resulting from acute hemorrhage. |
1636_49 | Chemicals released by macrophages can also damage host tissue. TNF-α is an important chemical that is released by macrophages that causes the blood in small vessels to clot to prevent an infection from spreading. If a bacterial infection spreads to the blood, TNF-α is released into vital organs, which can cause vasodilation and a decrease in plasma volume; these in turn can be followed by septic shock. During septic shock, TNF-α release causes a blockage of the small vessels that supply blood to the vital organs, and the organs may fail. Septic shock can lead to death. |
1636_50 | Evolutionary origins |
1636_51 | Phagocytosis is common and probably appeared early in evolution, evolving first in unicellular eukaryotes. Amoebae are unicellular protists that separated from the tree leading to metazoa shortly after the divergence of plants, and they share many specific functions with mammalian phagocytic cells. Dictyostelium discoideum, for example, is an amoeba that lives in the soil and feeds on bacteria. Like animal phagocytes, it engulfs bacteria by phagocytosis mainly through Toll-like receptors, and it has other biological functions in common with macrophages. Dictyostelium discoideum is social; it aggregates when starved to form a migrating pseudoplasmodium or slug. This multicellular organism eventually will produce a fruiting body with spores that are resistant to environmental dangers. Before the formation of fruiting bodies, the cells will migrate as a slug-like organism for several days. During this time, exposure to toxins or bacterial pathogens has the potential to compromise |
1636_52 | survival of the species by limiting spore production. Some of the amoebae engulf bacteria and absorb toxins while circulating within the slug, and these amoebae eventually die. They are genetically identical to the other amoebae in the slug; their self-sacrifice to protect the other amoebae from bacteria is similar to the self-sacrifice of phagocytes seen in the immune system of higher vertebrates. This ancient immune function in social amoebae suggests an evolutionarily conserved cellular foraging mechanism that might have been adapted to defense functions well before the diversification of amoebae into higher forms. Phagocytes occur throughout the animal kingdom, from marine sponges to insects and lower and higher vertebrates. The ability of amoebae to distinguish between self and non-self is a pivotal one, and is the root of the immune system of many species of amoeba. |
1636_53 | References
Bibliography
Website
External links
White blood cell engulfing bacteria
Immune system
Leukocytes |
1637_0 | Booster Gold (Michael Jon Carter) is a superhero appearing in American comic books published by DC Comics. Created by Dan Jurgens, the character first appeared in Booster Gold #1 (February 1986) and has been a member of the Justice League.
He is initially depicted as a glory-seeking showboat from the future, staging high-publicity heroics through his knowledge of historical events and futuristic technology. Carter develops over the course of his publication history and through personal tragedies to become a hero weighed down by his reputation.
Publication history |
1637_1 | Booster Gold first appeared in Booster Gold #1 (February 1986), being the first significant new character introduced into DC Universe continuity after Crisis on Infinite Earths. The next year, he began to appear regularly in the Justice League series remaining a team member until the group disbanded in 1996. He and his former Leaguers subsequently appeared as the "Superbuddies" in the Formerly Known as the Justice League miniseries and its JLA: Classified sequel "I Can't Believe It's Not the Justice League". |
1637_2 | At Wizard World Los Angeles in March 2007, Dan DiDio announced a new ongoing series titled All-New Booster Gold, which was later published as simply Booster Gold. The series follows the events of 52 and was initially co-written by Geoff Johns and Jeff Katz, with art by creator Jurgens and Norm Rapmund. The series focuses primarily on Booster Gold's clandestine time travel within the DC Universe. The series also features Rip Hunter, Skeets, and Booster's ancestors Daniel Carter and Rose Levin as supporting characters. The tagline of the series is: "The greatest hero you've never heard of!" Katz and Johns left the book after 12 issues (#1-10, #0, and a One Million issue). Jurgens and Rapmund stayed. Jurgens assumed writing duties following four issues by guests Chuck Dixon and Rick Remender. |
1637_3 | In May 2010, Keith Giffen took over the Booster Gold title, linking it with the 26-week miniseries Justice League: Generation Lost, in which Booster united with Fire, Ice and Captain Atom to defeat the resurrected Maxwell Lord. From July 2010 through February 2011, Booster starred alongside Rip Hunter, Green Lantern, and Superman in the six-issue miniseries Time Masters: Vanishing Point, part of the "Return of Bruce Wayne" arc, which also reintroduced the Reverse-Flash and established the background for the 2011 DC crossover event Flashpoint. Jurgens returned to the main Booster Gold title with issue #44.
Fictional character biography |
1637_4 | From the future
Michael Jon Carter was born poor in 25th-century Gotham City. He and younger twin sister Michelle never knew their father because he left after gambling away all their money. Michael was a gifted athlete, attending Gotham University on a football scholarship. At Gotham U., Michael was a star quarterback until his father reentered his life and convinced him to deliberately lose games for gambling purposes. He was exposed, disgraced and expelled. Later he was able to secure a job as a night watchman at the Metropolis Space Museum, where he studied displays about superheroes and villains from the past, particularly the 20th century. |
1637_5 | Michael's sidekick is a robot named Skeets. Skeets is a 25th-century security robot (sometimes "valet unit") with artificial intelligence. He is capable of flight, cognition, and voice projection, which are all considered highly advanced for 21st century Earth. He also has historical records which give him a vast knowledge of what will happen between the 21st and 25th centuries, though its reliability has become questionable. He possesses numerous miniature tools and weapons kept within his shell, and is also equipped with a powerful energy blaster. He is apparently immune to reality and temporal manipulation. |
1637_6 | With the help of Skeets, Michael stole devices from the museum displays, including a Legion of Super-Heroes flight ring and Brainiac 5's force field belt. He used Rip Hunter's Time Sphere, also on display in the museum, to travel to the 20th century, intent on becoming a superhero and forming a corporation based around himself to make a comfortable living. He is a shameless self-promoter whose obsession with fame and wealth irritates other heroes.
Carter's nickname as a football player was "Booster", but his chosen 20th century superhero name was "Goldstar". After saving the president, Carter mangled the two names, causing US President Ronald Reagan to introduce him as "Booster Gold". The name stuck. In a running joke throughout the DC Universe, people erroneously call him "Buster" to his chagrin. |
1637_7 | Celebrity
Booster is originally based in Superman's home city, Metropolis. He starts his hero career by preventing the shapeshifting assassin Chiller, an operative of The 1000, from killing the President of the United States and replacing him. With the subsequent public exposure, Booster signs a multitude of commercial and movie deals. During his career, his sister Michelle Carter, powered by a magnetic suit, follows in his footsteps as the superheroine Goldstar. Booster is devastated when she dies battling creatures from another dimension. Amassing a small fortune, Booster founds Goldstar, Inc. (later Booster Gold International) as a holding company and hires Dirk Davis to act as his agent. During the Millennium event, Davis reveals that he is a Manhunter in disguise and that he siphoned money from Booster's accounts in hopes of leaving him no choice but to do the Manhunters' bidding. Although the Manhunters are ultimately defeated, Booster is left bankrupt. |
1637_8 | Justice League
Booster Gold is a key character in the late 1980s/early 1990s Justice League revamp by writers Keith Giffen and J. M. DeMatteis. Booster Gold is frequently partnered with fellow Justice League member Blue Beetle, and the two quickly become best friends. The duo's notable appearances include a stint as superhero repo men, and as the minds behind the construction of a gaming resort, Club JLI, on the living island Kooey Kooey Kooey.
After one too many embarrassments and longing for his old reputation, Booster quits the League to found The Conglomerate, a superhero team whose funding is derived from corporate sponsors. Booster and his team are determined to behave as legitimate heroes, but find that their sponsors compromise them far too often. The Conglomerate reforms several times after Booster rejoins the League, though without much success. |
1637_9 | When an alien comes to Earth on a rampage, Booster coins the name Doomsday for it. While battling the entity, Booster's costume is destroyed. Blue Beetle is able to design a new, bulkier costume to replace it, although this costume often malfunctions. During a later battle with Devastator, a servant of the Overmaster, Booster is nearly killed and loses an arm. Again, Blue Beetle comes to his aid, designing a suit that acts as a life support system in addition to replicating the powers of Booster's previous costumes. This suit also includes a cybernetic prosthetic for his lost arm. |
1637_10 | Extreme Justice
After the Justice League falls apart, Booster Gold joins Extreme Justice, a team led by Captain Atom. While a member of this team, Booster makes a deal with the supervillain Monarch, who fully heals Booster's wounds so that he can once again remove his battle suit. Booster dons a new costume created by Blue Beetle. Skeets acts as its systems controller, who aids Booster and is able to take control of the costume if Booster is rendered unconscious.Pig
Following the disbanding of Extreme Justice, this suit is destroyed. A new costume is created by Professor Hamilton, based on the designs of both the original 25th century costume and the energy containment suit Superman was wearing at this time. This costume is apparently later tweaked to resemble Booster's original costume more closely. |
1637_11 | Countdown to Infinite Crisis: The OMAC Project
After the events depicted in the limited series Identity Crisis, in which Sue Dibny is murdered, Gold retires briefly, but then helps Blue Beetle discover who is manipulating KORD Industries. Booster is badly injured in an explosion at Kord's home, and it is revealed that his companion Skeets has been dismantled for its 25th century technology by the Checkmate organization. |
1637_12 | In The OMAC Project limited series, Booster Gold gathers the old Justice League International heroes to investigate Blue Beetle's disappearance. At the series' end, he is ruined physically and emotionally, having destroyed much of his gear in the fight against the OMACs. He has seen his friend Rocket Red die in battle. He discovered that another friend, Maxwell Lord, is responsible for killing Blue Beetle and that in fact, Lord always hated metahumans and superheroes. In a moment of self-reflection, he realizes that if only he had bothered to recall more of what was history in his native era, he might have been able to warn his friends. Giving a farewell kiss to the forehead of his wounded teammate Fire as she lay in a hospital bed, he drops his trademark goggles on the floor and leaves, saying only that he has decided to "go home", implying a return to the 25th century. |
1637_13 | Infinite Crisis
In Infinite Crisis, Gold resurfaces in the ruins of the Justice League Watchtower on the moon, along with Skeets, again branded as a criminal in his time for "hijacking historical records". When Skeets fails to locate the absent Martian Manhunter, Booster searches for Jaime Reyes, the new Blue Beetle, whom he promptly takes to the Batcave. Booster tells Batman the subject of the stolen records: Batman never finds Brother Eye, but Booster implies that, with Jaime's aid, they can succeed. The mission is successful and Booster plays a pivotal role in the destruction of the satellite.
52 and Supernova |
1637_14 | In the aftermath of Infinite Crisis, Superman, Batman, and Wonder Woman temporarily retire their costumed identities, and the remaining heroes attend a memorial for Superboy in Metropolis. Booster attends the memorial, but when Superman, Batman, and Wonder Woman do not arrive as he expects, he suspects his robot sidekick Skeets is malfunctioning and becomes hysterical. After Skeets reports other incorrect historical data, Booster searches fellow time traveler Rip Hunter's desert bunker for answers, finding it littered with enigmatic scrawled notes. Booster finds photos of himself and Skeets surrounded by the words "his fault" with arrows pointing toward them. |
1637_15 | Booster is seemingly angered when a mysterious new superhero named Supernova appears. His reputation ruined, Booster tries to regain the spotlight by containing an explosion, but appears to be killed in the attempt. Skeets uses Booster's ancestor, Daniel Carter, to regain access to Hunter's lab, where he sees the photos and arrows pointing at him. Skeets traps Carter in a time loop in the bunker and sets out to locate Hunter himself.
Supernova meets with Rip Hunter in the Bottle City of Kandor, and Hunter examines a number of high-tech items Supernova has brought him. When Skeets discovers them, Supernova reveals himself to be Booster Gold and fights him, revealing how he and Rip Hunter used time travel to fake his death and create a rivalry between Booster and himself as Supernova. Hunter and Booster attempt to trap Skeets in the Phantom Zone, but Skeets appears to eat the subdimension and pursues his two adversaries through time. |
1637_16 | He appears in World War III. He tries to steal a missile, but leaves after realizing that he appeared before it was launched. Booster later appears before Steel and Natasha Irons, stealing the nanobot missile they were about to use on Black Adam, saying he needs it more than they and that it would not have worked for its original purpose anyway; Booster promptly disappears. During his time-hopping mission, he briefly stops in the far future, robbing the Dominators of an experimental weapon designed to deal with time travelers. Trying to explain his situation to the alien warlords, he makes them suspicious as they mistake his rant of "having to save 52 worlds" as a warning that the Earth and 52 unnamed worlds are going to invade them after Booster's raid. |
1637_17 | Booster returns to the present, using T. O. Morrow as bait to draw out Skeets. Skeets reveals itself to be Mister Mind in disguise, having used Skeets' shell as a cocoon to evolve into a being capable of devouring the Multiverse. Booster and Rip flee into the timestream with Skeets' remains and return to the end of the Infinite Crisis. Rip and Booster witness the birth of the new Multiverse, made up of 52 parallel universes. Mister Mind attempts to trap Booster and Rip in the Phantom Zone which he devoured when it was turned on him, but he is stopped by Supernova (now Daniel Carter, who was saved from the time loop he was trapped in by Rip and given Michael's outfit), who restores the Phantom Zone to its original place. Mister Mind then devours years and events of each of the 52 worlds, altering their history in the process. The real Skeets gives Booster a pep talk which inspires him to stop Mister Mind. |
1637_18 | Booster travels to the day after the end of Crisis on Infinite Earths on New Earth, where he retrieves the Blue Beetle scarab from Ted Kord. Using the scarab — along with Suspendium stolen by Rip Hunter, Skeets' mangled shell, and Supernova's powers — Rip, Booster, and Daniel trap Mister Mind inside Skeets and hurl it into the timestream, trapping Mister Mind within a repeating time loop of 52 seconds where he is captured by Doctor Sivana. As a reward for helping save the Multiverse, Rip downloads Skeets' programming into a spare Responsometer. Rip, Booster, and Daniel decide to keep the existence of the new Multiverse a secret.
Will Magnus then repairs Skeets using the Responsometer, although Skeets has no memory of the last year. Meanwhile, Daniel Carter decides to keep the Supernova costume and begin his own superhero career. His resolution weakening with time, he starts using the suit to play video games instead, because he does not need to eat, drink, or sleep while wearing it. |
1637_19 | One Year Later
Following the events of 52, Booster Gold returns in his second solo series with the first story arc "52 Pick-Up". Booster puts in a request to the Justice League that they admit him and the group begrudgingly decide to monitor him over the following week. However, Rip Hunter informs Booster that history has become malleable after Mister Mind's rampage and earlier damage to the timeline. |
1637_20 | A new villainous Supernova arises after stealing Daniel's costume, and, aided by evil time traveler Rex Hunter, intends to exploit weaknesses in history to rewrite it and destroy the League (they are later revealed to in fact be working under the orders of the Ultra-Humanite, Despero, and Per Degaton). Since Booster is thought of as a buffoon, he is not suspected to be capable of thwarting them, but Booster must maintain his poor reputation to protect himself. Booster's condition for following Rip's orders is that he must travel back in time to avert the death of his best friend, Ted Kord. |
1637_21 | Despite Rip's objections, Booster and three Blue Beetles team up to rescue Kord moments before his death. They succeed, and the restored Blue/Gold duo deserts Rip Hunter to side with the Blue Beetles group. Rip retaliates by presenting Michael's ancestors Daniel Carter and Rose Levin with replicas of the Supernova and Booster Gold suits, stating that the Carter family's heroic legacy starts "right freakin' now". When time "solidifies" following Kord's rescue, and the other three Beetles return to their own times, Ted and Michael find that the world has now become overrun by Maxwell Lord's OMACs.
During a final battle between the remade JLI and the OMACs, the Time Stealers return and are defeated. However, Booster suffers a tragedy when he is unable to stop Ted from entering a time sphere with the Black Beetle to change the past one final time, resetting history and sacrificing himself. |
1637_22 | He is later transported to the 853rd century, where he faces off against Peter Platinum, a con artist who is attempting to outdo Booster at making money off of heroic acts. When returned to the present, he is enraged by Rip's unsympathetic responses to his ordeal and quits. Batman tells Booster that he knew about Booster's attempts to prevent the crippling of Barbara Gordon and has long realized that Booster is not the fool he appears to be, offering his friendship. Booster resolves to continue working with Rip, even if it will not be "fun". Rip reveals that he is able to save Booster's sister Michelle from moments before she died, claiming there is a loophole due to Michelle being from the future. It is also revealed to the audience that Hunter is Booster's son: as Michelle and Michael go out to eat, Rip says "Keep it up, dad".
Booster has shown his dedication, now calling himself a "Time Master" (with Hunter), and trains his sister.
Blackest Night |
1637_23 | In a tie-in to the Blackest Night event, Booster faces Ted Kord, reanimated as a Black Lantern. At first unavailable due to reliving Ted's funeral in the past, he returns to meet his ancestor Daniel Carter, only to find the crashed, derelict Bug at his house. Then, he finds the Black Lantern pummeling Jaime Reyes, Daniel, and Skeets. Attacked by him, he removes Daniel and Rose from the scene and heads to Kord Industries to arm himself. He uses a special light gun designed by Ted to blast the corpse and separate the ring with light, simulating the emotional spectrum. |
1637_24 | Upon separating the corpse from the ring, he collects Ted's remains before the ring can reanimate them and takes them into the Time Sphere to Vanishing Point Fortress to secure them. He is somewhat relieved when Skeets uses the Fortress's special chronal surveillance equipment to display images of the days of Team Blue and Gold. Jaime promises to live up to Kord's legacy and eventually form a new Blue and Gold team. They find evidence at the warehouse of someone else entering, even though the doors were genetically coded, with only two people cleared for access: Ted and Booster.
Brightest Day |
1637_25 | Booster next finds his sister living in Coast City mere hours before its destruction. Though unable to save her boyfriend, Booster and Michelle patch up their relationship, with her agreeing not to leave him. This arc introduces an older Booster Gold, the man that trained Rip Hunter and was the master of both Time, the Multiverse, and Hypertime. Rip reveals that this Booster is not only his father, but also has been watching Rip training the young Booster Gold, aiding him when needed. Older Booster also reveals that he is still married to Rip's mother, and that Michelle is with them in some unknown time. |
1637_26 | In Justice League: Generation Lost, Booster is part of the manhunt to bring the resurrected Maxwell Lord to justice. He finds Max but is beaten badly. Fire, Ice, and Captain Atom find him just as Lord uses his psychic powers to the utmost to erase all memory of himself from the minds of the entire world. For some reason, Booster, Fire, Ice, and Atom are the only ones who remember Lord and see him in recorded images. Trying to convince Batman (Dick Grayson), Booster is horrified to learn that, thanks to Max, the world believes Ted Kord committed suicide. Fire, Ice, and Captain Atom are soon set up by Max to cut them off from allies, but, ironically, Booster is left alone because his reputation is already poor. |
1637_27 | Return of the JLI
The remnants of the JLI are, seemingly by chance, joined by the successors of Blue Beetle (Jaime Reyes) and Rocket Red. Rocket Red declares the newly formed team as the new Justice League International, prompting Booster to figure out that Max Lord manipulated them to be together. Later, during the assault on Checkmate, Fire and Ice discuss how Booster has become the leader of the team. |
1637_28 | When his team member, Jaime, is kidnapped and tortured by Max, Jaime signals the rest of the JLI to lead them to Max's headquarters. The JLI arrives too late, and Jaime is shot in the head by Max, killing him in the same manner as his predecessor, Ted Kord. Booster Gold is enraged and his team tries to take down Max, but Max escapes from the JLI using one of his headquarters' escape pods. The JLI carries Jaime to the land surface, where paramedics try to resuscitate him. However, their efforts fail as Jaime had already died. As the team deals with the loss of Jaime, Booster Gold blames himself for leading the team into so much danger, and wants to abdicate as leader. The rest of the team overhear his ranting and convince him that they believe in him. Gold is still upset, saying they cannot win against Max, when Blue Beetle suddenly sits up, his wound healed, declaring he knows Max's ultimate plans and that they can stop him. |
1637_29 | While the JLI learn that Jaime is alive, Batman and Power Girl join the team. Meanwhile, Max sends the OMACs to attack the JLI. While the JLI are battling against OMAC Prime, Booster locates Max's flying headquarters and attacks it to come face-to-face with Max. During the battle, Booster pulled Max out of the headquarters and ends up falling to the earth. Booster Gold saves Max at the last moment, but Max mind-controls him until he is confronted by Captain Atom. Captain Atom forces Max to undo the global mindwipe. Max then teleports to escape. Afterwards, Booster and Batman set out to re-form the JLI.
Flashpoint |
1637_30 | After the Time Masters: Vanishing Point event, Rip Hunter informed them that someone snuck into the JLI base, leaving messages on a chalkboard about the altered timeline. When Earth entered an alternate timeline due to the actions of the Flash, Booster and Skeets awaken and are the only ones who remember the original timeline (later, Booster realizes that the chronal protection in his suit saved him from being erased). Gold travels to Coast City, but US soldiers attack him mistaking him to be an Atlantean threat. Skeets is damaged when Gold is attacked by the military's Project Six, which is revealed to be Doomsday. |
1637_31 | During the battle in Coast City, he discovers that Doomsday is controlled by General Nathaniel Adam. He escapes from Doomsday and then saves a woman named Alexandra Gianopoulos from Doomsday's attack. He learns the timeline has been changed, suspecting Professor Zoom. Alexandra and Booster split up, but she secretly has powers allowing her to take others' powers and follows him. Later, he flies to Gotham City when Doomsday attacks him. General Adam's control link is destroyed by Alexandra in an attempt to rescue Booster. Doomsday's true personality comes to the surface and he attacks Booster. During the fight, Doomsday beats him nearly to death, but he is rescued by Alexandra. He tries to prevent Doomsday from killing innocent people, and manages to put Doomsday's helmet back on. Doomsday's control is restored to Adam, who grabs Booster, hoping to kill him. Fortunately, Adam takes him back to the base for interrogation, allowing him to escape when the sight of "Project Superman" |
1637_32 | causes Doomsday's true personality to resurface. Alexandra defeats Doomsday by using the control helmet to make Doomsday tear himself apart, subsequently asking Booster to take her with him when he restores history to normal. Alexandra subsequently sacrifices herself to save Booster from an Atlantean attack, leaving him to return to Vanishing Point as history resets without any clear memory of his time in the "Flashpoint" universe. Before the Time Masters: Vanishing Point event, Alexandra somehow appeared in the JLI base and left the messages regarding the altered timeline on the chalkboard before vanishing. |
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