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    News

    virus-primary-cells-mef cells-rat-knock-out-stem-cell-characterization-teratoma-formation

    Researchers have discovered a tube-shaped structure that forms temporarily in a certain type of virus to deliver its DNA during the infection process and then dissolves after its job is completed.
    The researchers discovered the mechanism in the phiX174 virus, which attacks E. coli bacteria. The virus, called a bacteriophage because it infects bacteria, is in a class of viruses that do not contain an obvious tail section for the transfer of its DNA into host cells.
    "But, lo and behold, it appears to make its own tail," said Michael Rossmann, Purdue University's Hanley Distinguished Professor of Biological Sciences. "It doesn't carry its tail around with it, but when it is about to infect the host it makes a tail."
    Researchers were surprised to discover the short-lived tail.
    "This structure was completely unexpected," said Bentley A. Fane, a professor in the BIO5 Institute at the University of Arizona. "No one had seen it before because it quickly emerges and then disappears afterward, so it's very ephemeral."
    Although this behavior had not been seen before, another phage called T7 has a short tail that becomes longer when it is time to infect the host, said Purdue postdoctoral research associate Lei Sun, lead author of a research paper to appear in the journal Nature on Dec. 15.
    The paper's other authors are University of Arizona research technician Lindsey N. Young; Purdue postdoctoral research associate Xinzheng Zhang and former Purdue research associate Sergei P. Boudko; Purdue assistant research scientist Andrei Fokine; Purdue graduate student Erica Zbornik; Aaron P. Roznowski, a University of Arizona graduate student; Ian Molineux, a professor of molecular genetics and microbiology at the University of Texas at Austin; Rossmann; and Fane.
    Researchers at the BIO5 institute mutated the virus so that it could not form the tube. The mutated viruses were unable to infect host cells, Fane said.
    The virus's outer shell, or capsid, is made of four proteins, labeled H, J, F and G. The structures of all but the H protein had been determined previously. The new findings show that the H protein assembles into a tube-shaped structure. The E. coli cells have a double membrane, and the researchers discovered that the two ends of the virus's H-protein tube attach to the host cell's inner and outer membranes.
    Images created with a technique called cryoelectron tomography show this attachment. The H-protein tube was shown to consist of 10 "alpha-helical" molecules coiled around each other. Findings also showed that the inside of the tube contains a lining of amino acids that could be ideal for the transfer of DNA into the host.
    "This may be a general property found in viral-DNA conduits and could be critical for efficient genome translocation into the host," Rossmann said.
    Like many other viruses, the shape of the phiX174 capsid has icosahedral symmetry, a roughly spherical shape containing 20 triangular faces.

    vascular dementia topThe progress of many serious health conditions can be suppressed by drugs that "chase" metabolism. The findings may lead to a new kind of treatment of cancer, inflammatory diseases, and as macular degeneration. The study was conducted by experts from the University of Leuven, Belgium.

    For some time doctors try to stop the progression of the condition to develop resistance to drugs, such as stopping the process of formation of new cells, associated with the pathological growth.

    Ineffectiveness of the drugs and the frequent occurrence of relapse, however, make these attempts failed. The new study, which is published in the journal Cell Metabolism, describes a completely new approach that can solve the problem.

    While the efforts of previous research and treatments aimed at limiting formation in blood vessels, thus targeting the so-called endothelial growth factor, the new method "attack" glycolysis. This is the process in which cells of Alzheimer generate the necessary energy.

    In other words, instead of suppressing growth itself, the new method stops "power" to which the cell count. According to researchers, the new findings could inspire scientists to develop new treatments for many diseases.

    They could also be useful in tumors, vision loss, chronic inflammation and the like.

    thema-rosa26-feeder-cells-human-primary-cells-mef cellsAmerican and Canadian researchers have identified a biomarker which predict which patients are at risk of developing cancer of the prostate or relapsed disease , reported UPI . Andris Zeylstra Medical Center at the University Vanderbilt and John Lewis from the University of Alberta said that some cases of prostate cancer are spread slowly and are not associated with severe symptoms , while others patients experience metastatic disease , often have fatal . Oncologists have long sought biomarkers that identify which patients must pass intensive care

    Zeylstra and colleagues examined the protein CD151, which facilitates the migration of cancer cells in the body. Researchers found that when affected by prostate cancer patients CD151 is "free", ie is not bound by his partner, integrin protein, which allows cells to adhere to the surrounding tissue. It turns out that this form of CD151 is important functions in cancer.

    "I was surprised we observed that some proteins are CD151 released by the presence of your partner and that it happens when there is a cancer, "said Zeylstra." New in is that it is not about traditional no change the expression of a protein in a protein that modifies molecular state. Namely, it is an indicator of the development of disease. "

    The researchers studied tissue samples from 137 patients undergoing to treat a cancer of the prostate in Canada for the past 12 years. The results showed that if patients have "FREE" CD151, the risk of prostate cancer is greater, than for those without detectable "free" CD151.

    o 855039-cells-rat-knock-out-stem-cell-characterization-teratoma-formation-embryoidResearchers at the Massachusetts Institute of Technology (MIT) and the University of Hanyang (Hanyang University) created a "synthetic antibodies". As a basis chemists have used carbon nanotubes, which fluoresce under laser irradiation.

    Previously, this phenomenon has been used by other investigators, the carbon nanotubes are coated with the natural antibodies. When meeting with certain molecules such structures either light or dimmed, so you can use them as a sort of sensors. However, such sensors are destroyed in the living cell, which significantly limits their period of operation.

    To solve this problem MIT chemists replaced by antibodies specifically synthesized amphiphilic polymers. These macromolecules contain regions that interact with water (hydrophilic) or push it (hydrophobic).

    Polymers synthesized so that their hydrophobic portions fixed firmly on the surface nanotubok as armature, and constitute a hydrophilic "loops", which form a kind of crown around the particle. Loops arranged strictly along the tube, and the distance between anchors determines which target molecule can hook into the loop and change the nanotube fluorescence.

    The uniqueness of this new approach is that before the polymer is attached to the nanotube is impossible to predict the possibility of molecular recognition, looking at the structure of the target and the polymer. That is, the polymer itself can not selectively detect a particular molecule.

    o 855037-cells-rat-knock-out-stem-cell-characterization-teratoma-formation-embryoid

    In his article, published in the journal Nature Nanotechnology, researchers publish a description of molecular sensors, specific for riboflavin (vitamin B2), estradiol (female sex hormone) and L-thyroxine (thyroid hormone).

    Currently, scientists are actively developing on certain neurotransmitters, carbohydrates and proteins. Another important challenge for the research team is to understand exactly what is happening with the polymer and nanoparticle throughout the whole capture specific target molecule.

    The researchers believe that their current and future developments in the field of molecular recognition will open huge opportunities for monitoring of diseases such as cancer, multiple inflammations, diabetes and many others in any living organism.

    ImmunodeficiencySevere autoimmunity in childhood can be an indication of a primary immunodeficiency (PID) -- this has now been demonstrated in a 13-year-old patient by a research group from the MedUni Vienna belonging to the CeMM Research Center for Molecular Medicine of the AAS and the St. Anna paediatric hospital. A previously unknown B-cell defect was identified in the teenager with the aid of so-called "next generation sequencing," with which genetic mutations in the genetic material can be detected within a few days. The study has been published in the leading journal Blood.

    "Our discovery created a sense of relief in the family as they now know at last what is wrong with the boy," says Kaan Boztug, who works routinely as a doctor at the University Department of Paediatrics and Adolescent Medicine treating seriously ill children, and as a researcher at CeMM, searching for the molecular causes of diseases of the immune system using the most modern genetic technologies. In this specific case a defect in the PRKCD gene was discovered. This causes a malfunction in the regulation of the B lymphocytes which are regarded as "antibody factories." Severe autoimmunity develops as a consequence.

    According to Boztug and Elisabeth Förster-Waldl, paediatrician and immunologist at the University Department of Paediatrics and Adolescent Medicine of the MedUni Vienna, not only diagnostic, but also therapeutic, consequences can be derived from the recently successful molecular identification of the deficiency. From early childhood the patient had suffered periodically from severe autoimmunity of the kidneys, lymph nodes and connective tissues. The now 13-year-old had previously been globally immunosuppressed with cortisone for long periods but now the target of the therapy can be precisely isolated. Says Förster-Waldl: "Only when you know the mechanism, an individually-tailored therapy can be appropriately used or developed."

    Data from the Anglo-American world assume that the prevalence of a clinically relevant immunodeficiency that can sometimes involve life-threatening consequences for those affected lies at between 1:1200 and 1:2000. Such figures can only be estimated for Austria as the systematic collection of data has only been taking place for the last two years.

    At present around 30 to 40 percent of these deficiencies remain without a precise diagnosis according to Förster-Waldl. This could now change with the aid of the latest diagnostic processes including "next generation sequencing." Most immunodeficiencies are classified as so-called "rare diseases." Kaan Boztug: "However, the sum total of all these defects cannot be categorised as rare."

     

    ucsbteamdisc

    Cells almost don't change their type,just with a few exceptions, once they have become specialized - a heart cell, for example, won't suddenly become a brain cell. However, new findings by researchers at UC Santa Barbara have identified a method for changing one cell type into another in a process called forced transdifferentiation.

    With C. elegans as the animal model, lead author Misty Riddle, a Ph.D. student in the Rothman Lab, used transcription factor ELT-7 to change the roundworm's pharynx cells into intestine cells in a single-step process. Every cell has the genetic potential to become any kind of cell. However, the cell's history and the signals it receives changes the transcription factors it contains and thus determines what kind of cell it will become. A transcription factor is a protein that causes genes to turn on.

    "This discovery is quite surprising because it was previously thought that only early embryonic cells could be coaxed into changing their identity this readily," Riddle said. "The committed cells that we switched are completely remodeled and reprogrammed in every way that we tested."

    Switching one cell type into another to replace lost or damaged tissue is a major focus of regenerative medicine. The stumbling block is that cells are very resistant to changing their identity once they've committed to a specific kind.

    "Our discovery means it may become possible to create a tissue or organ of one type directly out of one of another type," says Joel Rothman, professor in UCSB's Department of Molecular, Cellular and Developmental Biology, who heads the lab.

    1-ucsbteamdisc

    Riddle and her colleagues challenged all C. elegans cells to make the switch to intestine, but only the pharynx cells were able to do this. "We asked skin cells, muscles, neurons to modify but found that only the cells in the pharynx were able to transform," Riddle explained. "So this brings up some big questions. Why aren't other cells changing their identities? What is so special about the cells in the pharynx that allows them to change their identity into intestine?

    "Since C. elegans is such an incredible model system we can really tackle these questions," she continued. "By knocking down certain genes and manipulating the animal, we can begin to better understand the conditions under which skin cells and muscles cells might change their identities. That will help us understand what is special about the cells in the pharynx."

    Previous studies in the Rothman lab revealed the cascade of transcription factors required for the proper development of the C. elegans intestine. Used in the later stage of intestine development, ELT-7 continues to be expressed for the life of the animal and has important functions not only in gut development but also in gut function.

    This study is revolutionary in that researchers have clearly demonstrated that cells are not limited to their original identities. "Think of them as different rooms in a house," Riddle said.

    "Like cells, different rooms in your house have different structures and functions. Changing the function of a room is likely to be easier if the structures are similar, say, turning a bedroom into a living room or vice versa. But changing the bathroom into a living room presents a bigger challenge," Riddle explained. "Just as some rooms in a house are more easily converted to others, some cell types may be more easily coaxed into changing their identity to another specific type. This doesn't seem to depend on the relatedness of the cells in terms of when they were born or how closely related they are in their lineage."

    Maybe the heart cell can become a brain cell after all.

    As demonstrated by another important discovery in the UCSB study, the cells reshaped themselves in a continuous process; there were stages in the remodeling process during which the identity of the cell was mixed. "Going back to the home remodeling example," Riddle said, "the couch and television were added to the bedroom before the bed and dresser were removed."

    "The important key of our discovery is that we have observed cells undergoing a process of morphing in which one specialized cell type is converted into another of an entirely different type," Rothman said. "This means that it may be possible to turn any cell into any other cell in a direct conversion. In terms of our understanding of biological constraints over cell identity, we've shown a barrier that we believed absolutely prevents cells from switching their identity does not exist. It may one day be possible to switch an entire organ from one kind to another."

    Wednesday, 04 December 2013 11:16

    6 Simple ways to decrease your risk of cancer

    Pharma would make tens of thousands of dollars off of your cancer diagnosis. They wouldn’t really solve your prolem, but would merely prolong your illness so you can continue to spend your savings (and beyond) on their toxic cancer drugs. What the medical industry doesn’t seem to want to discuss (in addition to a cure) is how to prevent cancer. The fact is: cancer can be prevented.
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    Cancer rates have climbed significantly over the past 100 years and that’s due, in part, to our diets and lifestyle choices. Fortunately, we can take this knowledge and take big steps towards cancer prevention. Best of all, we can start now.
    In addition to eating these cancer-fighting foods, here are 6 simple ways to prevent cancer:

    1. Do Exercises - As Dr. Mercola reports, exercise can reduce your risk of cancer and improve cancer treatment outcomes. Go outside and walk in the sun, do some strength training, and improve balance and flexibility with yoga. Exercising outside can be especially beneficial.

    2. Remove Processed Foods - Processed carbohydrates and sugars are cancer fuel. They feed cancer cells and essentially help them grow. Eliminating these foods ensures you don’t have a cancer-friendly environment waiting for the cancerous cells to arrive. At the very least, avoid all processed sugars and foods, instead getting any sugar from natural fruits.

    3. Increase Vitamin D - While you are outside exercising in the sunshine, you’ll already be ahead of the game, creating natural vitamin D for immune function and immediately reducing your cancer risk. Don’t underestimate the connection between vitamin D and cancer reduced cancer risk.

    4. Minimize Radiation Exposure - You can minimize your risk of radiation exposure simply by using your phone less. Use speakerphone when you can to avoid holding the cell phone to your head. Never sleep with your phone next to you on your pillow. (Don’t laugh, you would be surprised at how many people do this). Also, reduce your exposure to medical scans including x-rays and CT scans.

    5. Optimize Essential Fat Consumption - The modern western diet is laden with omega-6 fats and deficient in omega-3s. Normalize your ratio of omega 3 and omega 6 fats by reducing your consumption of omega-6 by limiting the use of processed vegetable oils.

    6. Sleep Plenty and Decrease Stress - Cancer thrives in bodies that are imbalanced or otherwise unhealthy. A stress-free and well-rested person is naturally a healthier person. Make sure you are getting plenty of sleep and doing everything you can do eliminate what has been called the mother of all disease – stress.

    Tuesday, 03 December 2013 12:33

    Guam tests toxic mice to kill invasive snakes

    11-cf-1-gene-knock-in-technology-ipsc-generation-cell-lineBiologists on Guam are trying to find out if mildly toxic dead mice can help eradicate an invasive species of snake that has caused millions of dollars in damages by creating power outages on the island.

    Crews on Monday distributed mice packed with 80 milligrams of acetaminophen on two plots in a test to kill brown tree snakes, which were accidentally introduced to the island about 60 years ago.

    Representatives from several federal agencies watched the aerial bait drop, Pacific Daily News reported.

    The mice should not affect other species, said U.S. Department of Agriculture wildlife services biologist Dan Vice, who has worked on snake eradication for more than a decade.

    "The risk to nontargets is slight," Vice said. "It would take 500 baits to kill a pig (or dog and) 15 baits to kill a cat."

    A pilot project with 280 mice in 2010 led to more aerial bait drops that began in September. Research and the drops have cost $8 million annually with funding from the Interior and Defense departments.

    An estimated 1 to 2 million snakes live on the island. Aerial bait drops might be the most efficient way to control the population without affecting deer or pigs, Vice said.

    "If it proves to be successful, then we may potentially start ramping up the efforts and doing this on a larger basis across more of Guam," Vice said.

    Mice were dropped Monday on two 136-acre plots, a combined area about the size of 210 football fields. Some mice were implanted with tiny radios to allow the USDA to determine whether mice were eaten.

    Biologists are also tracking populations of small animals, which will increase with fewer snakes.

    The mice drops are only for area where humans don't live, Vice said.

    No deaths from the venomous bite of a brown tree snake have been recorded, Vice said. Most bites cause no more damage to an adult than a bee sting, he said. But Brown tree snakes cause problems by creating outages on the Guam Power Authority power grid with damage reaching $1 million to $4 million annually, according USDA documents.

    Major substations use special fences to keep snakes out. Traps on fences catch about 8,000 snakes per year, Vice said.

    A stable population of brown tree snakes could be disastrous to Hawaii, Vice said, and the threat of them spreading is real. Guam ports use snake-sniffing dogs to detect invasive species.

    Friday, 29 November 2013 10:44

    New species of wild cat identified in Brazil

     71349713-knock-out-stem-cell-characterization-teratoma-formation-embryoid-body

    By comparing DNA sequences, the team revealed that two populations of tigrina in Brazil do not interbreed and are evolutionarily distinct.

    Results also show the two populations have contrasting interactions with the closely related pampas cat and Geoffroy's cat.

    There are at least seven species of small wild cat in the genus Leopardus in Central and South America, which are thought to have first colonised the region during the late Pliocene (2.5 - 3.5 million years ago).

    A team of researchers led by Dr Eduardo Eizirik from the Pontifical Catholic University of Rio Grande do Sul, Porto Alegre, Brazil collected samples of DNA from pampas cats (Leopardus colocolo) in the north of the country, Geoffroy's cats (L. geoffroyi) from the south and two separate populations - north eastern and southern - of tigrina (L. tigrinus).

    "We used several different types of molecular markers to investigate the evolutionary history of these species," explained Dr Eizirik.

    "These [molecular markers] evolve at different rates, which helps in the sense that they provide information on different time frames," he said.

    By comparing these different chromosomal and mitochondrial DNA marker sequences the scientists could track patterns of interbreeding - or hybridisation - between the cat species and populations.

    The markers revealed that the southern population of tigrina were actively breeding with Geoffroy's cat in areas where the two species came into contact. In contrast, they found evidence for ancient hybridisation between the north eastern tigrina and the pampas cat.

    But what surprised Dr Eizirik and his colleagues most was the lack of evidence for recent mating between the north eastern and southern tigrinas.

    "This observation implies that these tigrina populations are not interbreeding, which led us to recognise them as distinct species," Dr Eizirik told BBC Nature.

    "This species-level distinction between the tigrina populations we really did not expect to find," he said.

     71351087-primary-cells-mef cells-rat-knock-out-stem-cell

    The rules of zoological nomenclature mean the north eastern tigrinas (pictured) remain Leopardus tigrinus

    It is the rarer north eastern populations that will keep the original scientific name of Leopardus tigrinus because they live geographically closer to the type locality and the more common southern form that will acquire the newly recognised scientific name of Leopardus guttulus.

    "Recognising a distinct tigrina species in Brazil highlights the need for urgent assessment of its conservation status...and it may be found to be threatened," Dr Eizirik told BBC Nature.

    "[These results] illustrate how much is still unknown about the natural world, even in groups that are supposed to be well-characterised, such as cats," he explained.

    "In fact there are many basic aspects that we still don't know about wild cats, from their precise geographic distribution and their diets to even species-level delimitation, as in this case."

    131108124848-largeViral infections are the primary cause of liver inflammation or hepatitis, affecting hundreds of millions of people all over the world, and they represent a public health problem worldwide. The acute condition can cause irreversible damage to the liver, and if not cured can become chronic, leading to serious diseases such as cirrhosis or cancer.

    A study published today in the online edition of The Journal of Clinical Investigation, and carried out by Erwin Wagner's team, Director of the BBVA Foundation-CNIO Cancer Cell Biology Programme and holder of an ERC Advanced Grant, shows how the immune system 'attacks' liver cells during hepatitis by using the AP-1 gene JunB.

    Latifa Bakiri, one of the study's authors and a researcher in Wagner's laboratory details: "The activation of the JunB/AP-1 gene in a subset of immune cells, called NK cells, increases the production of interferon-gamma that attacks liver cells while the organ is suffering from hepatitis."

    With this discovery, the study's authors propose a new mechanism by which AP-1 acts as a double-edged sword in the liver: it's a first line of defence against viruses that cause the disease, but also encourages liver damage depending on the diet or genetics of the patient.

    "The balance of these signals is fundamental to the understanding of the pathogenesis of inflammatory liver disease and to design new therapeutic approaches to reverse this disease," says Wagner.

    NK-type immune cells are also part of the micro-environment surrounding tumours. Researchers point out in the discussion of the article that a better knowledge of these cells may be vital for designing immune-therapies that specifically target tumour cells.