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    vaccine-gentaur-bullet-blender-gold-kronos-dio-targattThe dream of many scientists to create a vaccine against AIDS has failed. National Institutes of Health in the U.S. announced that it attempts to immunize volunteers with an experimental vaccine known as HVTN 505 is officially terminated, since it is clear that it does not prevent infection.

    Clinical trial began in 2009 and since then, 1,250 voluntary participants received vaccine and 1244 others - control infusion of placebo, both groups over a period of 24 weeks. Among all the volunteers in total, so far has 41 infected with HIV than those who received the vaccine and 30 infected than those who received placebo. The study focused mainly people who have unprotected sex.

    Vaccine strategy using "double whammy" that aimed to strengthen the immune system. Three initial injections are placed initially, and after 16 weeks - another injection containing genetic material which creates a molecule of the type produced by HIV in order to induce a response in the immune system against viruses. Scientists say the vaccine itself did not cause infection. After presenting the matter collected data and results collected until mid-April at the National Institute of Allergy and Infectious Diseases, which sponsored the clinical trial recommended stopping the attempt to create the vaccine. Volunteers will be monitored for 5 years, and the data will be analyzed for further information.

    130422154756-largeCurrent techniques for turning patients' marrow cells into cells of some other desired type are relatively cumbersome, risky and effectively confined to the lab dish. The new finding points to the possibility of simpler and safer techniques. Cell therapies derived from patients' own cells are widely expected to be useful in treating spinal cord injuries, strokes and other conditions throughout the body, with little or no risk of immune rejection.
    "These results highlight the potential of antibodies as versatile manipulators of cellular functions," said Richard A. Lerner, the Lita Annenberg Hazen Professor of Immunochemistry and institute professor in the Department of Cell and Molecular Biology at TSRI, and principal investigator for the new study. "This is a far cry from the way antibodies used to be thought of -- as molecules that were selected simply for binding and not function."
    The researchers discovered the method, reported in the online Early Edition of the Proceedings of the National Academy of Sciences the week of April 22, 2013, while looking for lab-grown antibodies that can activate a growth-stimulating receptor on marrow cells. One antibody turned out to activate the receptor in a way that induces marrow stem cells -- which normally develop into white blood cells -- to become neural progenitor cells, a type of almost-mature brain cell.
    Nature's Toolkit
    Natural antibodies are large, Y-shaped proteins produced by immune cells. Collectively, they are diverse enough to recognize about 100 billion distinct shapes on viruses, bacteria and other targets. Since the 1980s, molecular biologists have known how to produce antibodies in cell cultures in the laboratory. That has allowed them to start using this vast, target-gripping toolkit to make scientific probes, as well as diagnostics and therapies for cancer, arthritis, transplant rejection, viral infections and other diseases.
    In the late 1980s, Lerner and his TSRI colleagues helped invent the first techniques for generating large "libraries" of distinct antibodies and swiftly determining which of these could bind to a desired target. The anti-inflammatory antibody Humira®, now one of the world's top-selling drugs, was discovered with the benefit of this technology.
    Last year, in a study spearheaded by TSRI Research Associate Hongkai Zhang, Lerner's laboratory devised a new antibody-discovery technique -- in which antibodies are produced in mammalian cells along with receptors or other target molecules of interest. The technique enables researchers to determine rapidly not just which antibodies in a library bind to a given receptor, for example, but also which ones activate the receptor and thereby alter cell function.
    Lab Dish in a Cell
    For the new study, Lerner laboratory Research Associate Jia Xie and colleagues modified the new technique so that antibody proteins produced in a given cell are physically anchored to the cell's outer membrane, near its target receptors. "Confining an antibody's activity to the cell in which it is produced effectively allows us to use larger antibody libraries and to screen these antibodies more quickly for a specific activity," said Xie. With the improved technique, scientists can sift through a library of tens of millions of antibodies in a few days.
    In an early test, Xie used the new method to screen for antibodies that could activate the GCSF receptor, a growth-factor receptor found on bone marrow cells and other cell types. GCSF-mimicking drugs were among the first biotech bestsellers because of their ability to stimulate white blood cell growth -- which counteracts the marrow-suppressing side effect of cancer chemotherapy.
    The team soon isolated one antibody type or "clone" that could activate the GCSF receptor and stimulate growth in test cells. The researchers then tested an unanchored, soluble version of this antibody on cultures of bone marrow stem cells from human volunteers. Whereas the GCSF protein, as expected, stimulated such stem cells to proliferate and start maturing towards adult white blood cells, the GCSF-mimicking antibody had a markedly different effect.
    "The cells proliferated, but also started becoming long and thin and attaching to the bottom of the dish," remembered Xie.
    To Lerner, the cells were reminiscent of neural progenitor cells -- which further tests for neural cell markers confirmed they were.
    A New Direction
    Changing cells of marrow lineage into cells of neural lineage -- a direct identity switch termed "transdifferentiation" -- just by activating a single receptor is a noteworthy achievement. Scientists do have methods for turning marrow stem cells into other adult cell types, but these methods typically require a radical and risky deprogramming of marrow cells to an embryonic-like stem-cell state, followed by a complex series of molecular nudges toward a given adult cell rate. Relatively few laboratories have reported direct transdifferentiation techniques.
    "As far as I know, no one has ever achieved transdifferentiation by using a single protein -- a protein that potentially could be used as a therapeutic," said Lerner.
    Current cell-therapy methods typically assume that a patient's cells will be harvested, then reprogrammed and multiplied in a lab dish before being re-introduced into the patient. In principle, according to Lerner, an antibody such as the one they have discovered could be injected directly into the bloodstream of a sick patient. From the bloodstream it would find its way to the marrow, and, for example, convert some marrow stem cells into neural progenitor cells. "Those neural progenitors would infiltrate the brain, find areas of damage and help repair them," he said.
    While the researchers still aren't sure why the new antibody has such an odd effect on the GCSF receptor, they suspect it binds the receptor for longer than the natural GCSF protein can achieve, and this lengthier interaction alters the receptor's signaling pattern. Drug-development researchers are increasingly recognizing that subtle differences in the way a cell-surface receptor is bound and activated can result in very different biological effects. That adds complexity to their task, but in principle expands the scope of what they can achieve. "If you can use the same receptor in different ways, then the potential of the genome is bigger," said Lerner.
    In addition to Lerner and Xie, contributors to the study, "Autocrine Signaling Based Selection of Combinatorial Antibodies That Transdifferentiate Human Stem Cells," were Hongkai Zhang of the Lerner Laboratory, and Kyungmoo Yea of The Scripps Korea Antibody Institute, Chuncheon-si, Korea.
    Funding for the study was provided by The Scripps Korea Antibody Institute and Hongye Innovative Antibody Technologies (HIAT).

    Red squirrel gentaur antibodiesAs parents, we set our children up for life’s challenges by feeding them, caring for their health, and sending them to school. Many animals also provide for their young, and some do it in inadvertent and surprising ways. Take the red squirrel. The first year of this cute creature’s life is marked by intense competition and imminent death. Its goal is simple: get a territory before winter sets in, or face death by starvation. That goal becomes tougher if there are lots of other competitors around, but a mother squirrel has ways of preparing her pups for these trials. If she hears the sounds of crowded forest, stress hormones surge through her body and begin affecting her pups even before they are born. When they finally pop into the world, they start growing faster. The hormones are a chemical message from mum: Live fast, so you don’t die young.

    Red squirrels have a diverse diet, but the seeds of the white spruce are among the most important items on their menu. These trees are “mast seeders” meaning that they all produce tons of seeds every 2 to 6 years and very few seeds in others. In the bonanza years, the squirrels have plenty of spruce seeds to bury in the autumn and snack on through the harsh winter. This means that a bumper autumn for spruce is always followed by a crowded spring for squirrels. That leads to conflict. Red squirrels defend large areas surrounding a central store of spruce cones. They’ll fight for this real estate, because if the youngsters don’t establish a territory before winter sets in, they’ll find themselves bereft of buried grains, and almost certainly die. A team of Canadian scientists has been studying the fates of red squirrels in the Yukon, Canada for the last 22 years. Back in 2006, they showed that the squirrels can actually anticipate gluts of spruce seeds, and produce more young in anticipation. Now, the same team have found that females can also adjust how quickly their young grow up depending on how much competition they will face.

    The team, led by Ben Dantzer, now at the University of Cambridge, found that in competitive years following a spruce bonanza, the fastest-growing squirrels fare best and are more likely to survive their first winter. In normal years, these fast-growers have no advantage. This explains why the mothers don’t always give birth to fast-growing young. It comes at a price—squirrels tend to have shorter lifespans if they are born in crowded years, so their early spurt seems to cost them later on in life. It’s a cost that’s only worth paying if there’s some advantage to be gained. To test this link between density and growth, Dantzer’s team carried out a wonderfully simple but beautiful experiment where they simulated the sounds of a crowd. They recorded the loud “rattles” that squirrels make to defend their territories, and played them back to the creatures at two levels—one representing six times more squirrels than the other. If the females heard what sounded like squirrel-infested woods, they gave birth to pups that grew much faster.

    How? The answer lies in the mothers’ hormones. The more crowded an area is, the higher the levels of cortisol - a stress hormone - in the squirrels’ bodies. Indeed, if Dantzer’s team created more crowded forests - either genuinely so by feeding the squirrels and boosting their numbers, or dishonestly so by playing the rattle recordings - the females’ cortisol levels went up. Mums with higher cortisol levels gave birth to pups that grew faster. This wasn’t just a correlation. The team also injected some females with extra cortisol, and saw that their offspring grew up 41 percent faster.

    Why? This part of the story is less clear. We know from other studies that and early dose of stress hormones can steer the development of young animals, affecting their ability to learn or handle stressful situations. Think of the hormones as an fortune-telling system, plugged into the mother’s senses. It provides the young squirrel with omens of the conditions it will face in the outside world, and prepares its brain and body to deal with those challenges.


    Friday, 19 April 2013 10:28

    The Human Papillomavirus

    The 3D model of HPVPapillomaviruses are a very diverse group of viruses that infect human skin and mucosal cells, which serve as a barrier between the environment and a human being. Most representatives of this group do not cause any symptoms, but highly pathogenic types may cause cancer. Ancient literature contains the first known mention of skin warts. The first classification of warts was introduced by Roman physician Aulus Cornelius Celsus in 25 AD, and the assumption that warts may be transmitted via infection originated even earlier. However, the viral nature of papillomas was not demonstrated until the beginning of the twentieth century (reviewed in 4). The first papillomavirus was isolated in 1933 by the American virologist Richard Shope, who also isolated an influenza virus.

    The evolutionary history of papillomaviruses seems to coincide with the origin of higher-order vertebrates, amniotes (including reptiles, birds, and mammals). Mammalian skin structure appears to make them the most suitable hosts for the papillomaviruses, and — today — papillomaviruses are widespread in mammals and rarely found in birds. The relationship between papillomaviruses and similar groups of DNA-viruses, such as polyomaviruses, is not well-demonstrated at the present time. There are more than a hundred types of papillomaviruseshigh-risk that can infect humans. These are collectively referred to as human papilloma viruses or HPV and are divided into (HR) and low-risk (LR) types by their carcinogenic properties. HPV are transmitted through direct skin-to-skin contact, and approximately 30 types are transmitted sexually. LR HPV are much more common than HR HPV among humans and often do not cause any symptoms. In fact, only 18 types of HPV pose a cancer risk, mostly for anogenital cancers.

    Current research suggests that LR HPVs produce more virions and infect more human hosts whereas HR types are less virulent but more difficult for the immune system to neutralize. The most dangerous HR HPV types are also the most widespread, HPV16 (reference strain) and HPV18, and the main cause of skin warts (especially in the anogenital zone) are HPV types 6 and 11. These and several other types of HPV attract serious attention.

    Human papilloma virus particles lack a lipid envelope and are relatively small, with a diameter of only about 30 nm. In comparison, the human immunodeficiency virus (HIV) and influenza virus virions are enveloped by a lipid bilayer derived from the host cell and are approximately four times larger. The papillomavirus genome consists of double-stranded DNA decorated and packed by histones of the host cell. It encodes two types of proteins, early (E) proteins and late (L) proteins: early HPV proteins maintain regulatory functions (and are responsible for oncotransformation of the host cell in the case of HR types), and late proteins form the capsid of the virion. The life cycle of HPV is bound to the life cycle of its host cells, keratinocytes, and HPV can only be cultivated in special organotypic raft cultures containing a population of cells at different developmental stages — similar to the skin of a living organism. Keratinocytes are the main cells of epidermis, the outermost layer of the skin. Actively dividing young keratinocytes are found near the basal membrane that separates the epidermis from other layers of the skin and move towards the skin surface during maturation. Viral particles infect non-differentiated cells, and new virions are produced inside the keratinocytes during the terminal stage of differentiation.

    The HPV early proteins are responsible for maintaining a proper amount of viral DNA inside the host cell nucleus. However, they also coordinate the expression of viral genes. Proteins E1 and E2 form a complex with viral DNA, which recruits the cell replication systems. Proteins E6 and E7 are responsible for the carcinogenic effect in HR HPV types. E6 is able to bind to the tumor suppressor p53 and promote its ubiquitination and degradation. Protein E7 binds several cell proteins and tumor suppressors, including theretinoblastoma protein. The activity of the E6 and E7 proteins leads to uncontrolled cell division.

    Late proteins of HPV form the viral capsid and mediate packaging of DNA into the virion. The pentamer-forming L1 protein is the major component of the HPV capsid, and the L2 protein is a minor constituent. The HPV capsid looks roughly spherical, but, in fact, it has a icosahedral symmetry with the triangulation number that equals 7. Rather than a structure based on pentamers mixed with hexamers (like that of the soccer ball), the HPV capsid is composed of 72 L1 pentamers of two different types — 60 hexavalent pentamers and 12 pentavalent pentamers (reviewed in 2, chapter 3). Remarkably, the fold of HPV L1 proteins is similar to that of human nucleoplasmins, the proteins that regulate the assembly of nucleosomes. Whether they share a common ancestor or whether their similarity is the result of convergent evolution is not yet clear. Perhaps the interaction between L1 and nucleosomes on viral DNA is crucial for the encapsidation of the HPV genetic material.

    One monomer of L2 is associated with each L1 pentamer of the HPV virion, and current research suggests that L2 is crucial for DNA recruitment to the viral particle. Some hypothesize that L2 — as well as L1 — may interact not with viral DNA but rather with its histones. To date, however, much of the process through which HPV DNA is packed inside the virion remains unknown. One facet of the process that is known may make HPV an important tool in human gene therapy: any segment of DNA less than 8 kb long may be packed inside the capsid [link], which enables the development and use of HPV-based transformation vectors. Interestingly, human cyclophilin participates in HPV capsid unpacking, a mechanism that has also been demonstrated for HIV.

    A growing interest in HPV research can be partially — if not wholly — attributed to discovery of the relationship between HPV and cancer and the subsequent Nobel Prize in Physiology or Medicine (2008) awarded for this work. German scientist Harald zur Hausen has shown that nearly all cases of cervical cancer are the result of HPV infection. Vaccines against HPV are currently being actively developed and introduced, and the main targets for such vaccines include the most dangerous and common HPV types: HPV6, HPV11, HPV16, HPV18.

    Dr. Christopher Buck from the U.S. National Cancer Institute: Current vaccines against human papillomaviruses (HPVs) are a triumph of applied structural virology. However, the current vaccines, which use recombinant virus-like particles composed of the L1 major capsid protein, do not protect against all disease-causing HPV types. Fortunately, a new generation of HPV vaccines targeting conserved „Achilles’ heel“ epitopes present in the L2 minor capsid protein promise to offer broad protection against all HPVs, including all types that cause cancer, as well as types that cause benign skin warts (for which the papillomavirus family is named). Current knowledge about the structure, dynamics, and function of L2 during the infectious entry process is very limited. This structural information is desperately needed to inform the development of pan-protective HPV vaccines.

    two-faced-cat-antibodiesFrank and Louie the cat, 12, was born with two faces, two mouths, two noses, three eyes , setting the world record for the Oldest living two-faced cat, according to World Record Academy

    The Guinness world record for the Longest surviving Janus cat was also set by Frank and Louie, from Millbury, Ohio, USA, which had reached six years of age, thereby outliving all other recorded specimens.

    Guinness World Records also recognized the world record for the oldest cat living, set by Pinky, who was born on 31 October 1989 and lives with her owner, Linda Anno (USA), Hoyt, Kansas, USA.

    Now, 12 years after Marty Stevens rescued him from being euthanized because of his condition, the exotic blue-eyed rag doll cat is not only thriving, but has also made it into the 2012 edition of Guinness World Records as the longest-surviving member of a group known as Janus cats, named for a Roman god with two faces. 
    "Every day is kind of a blessing; being 12 and normal life expectancy when they have this condition is one to four days," Stevens said, stroking Frank and Louie's soft fur as he sat on her lap purring. 

    "So, he's ahead of the game; every day I just thank God I still have him."

    "The condition itself is very rare, and I think that the fact that this cat became an adult, a healthy adult, is remarkable," said Dr. Armelle deLaforcade, an associate professor at Cummings and head of the emergency services section.

    Frank and Louie's two faces have a complicated relationship. Both noses work, but one mouth does not have a lower jaw and isn't connected to his one esophagus, so he can't eat with it. Stevens discovered that only after the cat got an MRI later in life.

    The animal can see out of only two of his three eyes. The middle one can't even blink and makes Frank and Louie appear to be staring even when his other eyes are closed. 

    Frank and Louie does not seem to be bothered by his condition and has developed a friendly personality. The breed is known for its soft and silky fur, docile temperament and penchant for relaxing in a person's arms like a rag doll. 

    He is "very, very laid back, not afraid of people, very friendly and he's actually more of a dog than a cat," Stevens said. "He walks on a leash, he goes right in the car; he loves car rides."


    evolution hedgehog gentaurThe original hedgehog gene was discovered using fruit flies. Rather than the usual smooth cuticle they should have had, the fruit fly embryos defective for hedgehog had spiky bristles - earning the gene its name. The search for corresponding genes (or homologues) in vertebrates revealed 3: Indian Hedgehog (IHH), Desert Hedgehog (DHH) and Sonic Hedgehog (SHH), named for the Sega character. These genes all encode signalling proteins, which bear the same names, and of these 3 sonic hedgehog is the most researched and best understood. 

    So what does SHH do? It has key roles in embryonic development, affecting limb and organ creation. The shh protein guides cell growth, cell differentiation and the "patterning" of the embryo. It is also extremely important in creating the facial geometry. Different concentrations of shh in different parts of the embryo guide formation of different cells.

    Sometimes the best way to understand what something does is to look at what happens when it's not working. Many defects are associated with mutations to SHH: we've already discussed how it can cause a type of holoprosencephaly (where the forebrain does not split into two hemispheres). Cyclopia accompanies severe holoprosencephaly: like the forebrain, the eyes start out as one and are split into two by shh. Some mutations leave one large eye; others create the two eyes but leave them together in a single middle socket.

    The effects on organ development can be seen in mice with both copies of SHH disabled (see image). Their hearts, lungs, kidneys and guts are malformed. The face does not have its usual shape and instead forms a strange trunk, absent of eyes, ears or mouth. They have no paws and are always stillborn.

    As hinted at with eye development, shh is key in creating the symmetry of the face. It controls the growth of the what will become the jaws and features. Shh has a lot of control over the width of the face; creatures with too much shh develop very wide faces. Increase the amount of shh even more and the face starts doubling, resulting in a condition known as diprosopus - "two faced". The organism can have two distorted faces, typically united by an eye in the middle.

    Read more of the pathogenesis of holoprosencephaly 

    cyclop GENTAUR antibodiesIn this world of Photoshop and online scams, it pays to have a hearty dose of skepticism at reports of something strange — including an albino fetal shark with one eye smack in the middle of its nose like a Cyclops.

    But the Cyclops shark, sliced from the belly of a pregnant mama dusky shark caught by a commercial fisherman in the Gulf of California earlier this summer, is by all reports the real thing. Shark researchers have examined the preserved creature and found that its single eye is made of functional optical tissue, they said last week. It's unlikely, however, that the malformed creature would have survived outside the womb.

    "This is extremely rare," shark expert Felipe Galvan Magana of Mexico's Centro Interdisciplinario de Ciencias del Mar told the Pisces Fleet Sportfishing blog in July. "As far as I know, less than 50 examples of an abnormality like this have been recorded." 

    Pisces Fleet, a sportfishing company, rocketed the Cyclops shark to viral status online this summer with their photos of the creepy-cute creature. But this isn't the first time that reports of a mythical-seeming creature have spurred media sensations — last week alone, Russian officials announced "proof" of a Yeti, and paleontologists spun a theory about an ancient Kraken-like squid. Few reports of mythical beasts, however, come with proof.

    Cyclops shark

    Cyclops shark is an exception. While rare, "cyclopia" is a real developmental anomaly in which only one eye develops. Human fetuses are sometimes affected, as in a 1982 case in Israel reported in 1985 in the British Journal of Ophthalmology. In that case, a baby girl was born seven weeks early with no nose and only one eye in the center of her face. The infant, who lived only 30 minutes after birth, also had severe brain abnormalities.

    In 2006, a kitten born with one eye and no nose (a rare condition called holoprosencephaly), created a stir online as news organizations and bloggers tried to determine if the bizarre photos of the animal were real. A veterinarian confirmed the kitten's condition; "Cy," as the cat was known, lived only a day. The remains were sold to the creationist Lost World Museum.

    The fisherman who discovered the Cyclops shark is reportedly hanging on to the preserved remains, news outlets reported. But scientists have recently examined and X-rayed the fish, authenticating the catch. According to Seth Romans, a spokesman for Pisces Fleet, Galvan Magana and his colleagues will publish a scientific paper about the find within the next several weeks.

    Romans told LiveScience that the fisherman who caught the strange shark is "amazed and fascinated" by the attention his catch has drawn.

    It's not the first strange shark fetus Galvan Magana has found; he and his colleagues discovered two-headed shark embryos in two different female blue sharks. It's possible that one embryo started to split into twins, but failed to completely separate because of crowding in the womb, the researchers reported in January 2011 in the journal Marine Biodiversity Records.



    dna structure gentaurDNA is known to scientists for more than one hundred years. Swiss biologist Friedrich Miescher and chemist (doctor of education) identify it first in 1868 in the blood-soaked bandages and swabs of bandages for wounded soldiers in Tübingen, and later, after 1870 in Basel - the sperm of salmon of which the first isolate pure DNA. He called the discovery of the substance nuklein and in 1874 managed to break nucleic of protein and acid acid in 1889 was named by his student Richard Altman "nucleic". DNA is recognized as the only carrier of heredity in 1944 as a result of an experiment made ​​by Oswald Avery and his colleagues Colin McCarthy MakLoyd and MacLynn. The structure of the DNA double helix was discovered in 1953 by James Watson and Francis Crick at Cambridge University. For this discovery they received the Nobel Prize in Physiology or Medicine with Maurice Wilkins in whose lab made ​​X-ray crystallographic analysis of DNA, suggested to Watson and Crick's idea of ​​its structure.


    rna-dna-monoclonal-cytokes-anti-mouse-rat-knockViruses are not cells and cell structure, unlike bacteria, parasites, people and anything that is sure to take live. Note that life is first and viruses - the other. In fact, the majority of scientists consider viruses as a matter of the boundary between the living and the undead.

    How is this possible? Is not that a mistake?
    As is well known, living matter has the following immutable characteristics - ability to self-organize and self-reproduction. For this purpose, each living cell and in every living organism vital processes occur - feeding, respiration, excretion, etc., so to speak, keep cells and organisms alive. In viruses, however, things are very different.

    Generally, viruses are particles (but not cells!), Representing a small amount of DNA or RNA wrapped in a protein, fewer carbohydrates and / or lipids (fatty substances). Proteins on the surface of the viral envelope, which can have various forms, recognize and provide host cell of virus in it. When the virus enters the cell, its DNA is integrated in this cell that it "forces" to form virus particles assemble spontaneously and leave the cell.

    Viral just like living organisms, there are self-organization processes and reproduction. They, however, they are performed only in the host cell, and all other vital processes are absent altogether. By entering into the cell, viruses (which, incidentally, outside the cell are called virions) are completely dead particles. Only when entering it, they show some properties of living matter - samoorganizarane and reproduction. However, these qualities are not considered sufficient virus to be identified as living matter. For life is inherently inherent nutrition, respiration, excretion, etc. or summary speaking to a constant metabolism. Indeed, some organisms may greatly slow it down, but no body can stop it completely, and so called life.

    Viruses do not have their own structures to carry out metabolism, and harness resources and structures of the host cell to carry out its goals. Therefore, they can not be called living. Apparently, however, they are not dead matter, since if it gets into the cell organization and show a high capacity for self-reproduction - something completely alien to the undead.
    An interesting question is how the virus originated. It is believed that early in the evolution of the first primitive cells, viruses were parts of cells that are separate and distinct self-replicating particles. This theory is supported by the astonishing ease with which viruses penetrate into the cell and then subject yourself - it is placed entirely at their disposal, accepting them as part of ourselves.

    cellsThe biggest breakthrough in understanding the genetics of cancer before. So Iyls Ross, professor of cancer genetics at the Institute of Cancer Research in London, described the results of an international effort of more than 1,000 scientists, presented in late Wednesday.

    Their study - the largest ever study of "faults" of DNA that promote the development of cancer - revealed a series of genetic markers with which can identify people most likely to develop these conditions. In this case for three of the most encountered its forms - prostate, breast and ovarian.

    According to London's "Guardian" doctors have said that they can in five years with a simple saliva test based markers make for each risk profile and create a foundation for individual monitoring. For people with an increased risk of developing cancer would go more often reviewing and possibly developing cancer will be detected at an early stage, when there is a much greater chance of prolonging life.

    Test based on genetic markers can identify men who are 50% likely to become ill from prostate cancer. This would not only allow the UK have called for a national program. screening of men, it will stop the practice because of inaccurate blood tests a quarter of people with this diagnosis are treated, there was no need.

    To identify genetic markers for prostate cancer, the researchers compared the DNA data of 25,000 patients with the disease with the same number of healthy men. So were discovered 23 new "defect" in the DNA, increasing the risk of disease, 16 were identified as "culprits" to reach the most aggressive form. In practice, few men wear markers for prostate cancer, but 1% of them have DNA "defects" that increase the risk of developing it 5 times.

    The same procedure has found 49 new DNA "defect" associated with the risk of developing breast cancer.

    The third part of the project included the 130 institutes worldwide to compare DNA profiles of women with ovarian cancer with this healthy. This established eight new sections of DNA associated with increased risk of disease.

    Professor Iyls believe that a simple test in the GP's office soon enough every patient to have a personal account of the risk of these diseases. Physicians can improve performance by adding factors of lifestyle specific person - the risk of breast cancer, for example, alcohol increases and decreases from birth and breastfeeding.

    The big problem started after that - experts disagree on what age should these tests, complement it with ultrasound, magnetic rezonas and biopsies and what kind therapy to apply.

    The result of the research was published in Nature Genetics and several other scientific journals.