Researchers work to save endangered New England cottontail

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Scientists with the NH Agricultural Experiment Station are working to restore New Hampshire and Maine’s only native rabbit after new research based on genetic monitoring has found that in the last decade, cottontail populations in northern New England have become more isolated and seen a 50 percent contraction of their range.The endangered New England cottontail is now is at risk of becoming extinct in the region, according to NH Agricultural Experiment Station researchers at the University of New Hampshire College of Life Sciences and Agriculture who believe that restoring habitats is the key to saving the species.”The New England cottontail is a species of great conservation concern in the Northeast. This is our only native rabbit and is an integral component of the native New England wildlife. Maintaining biodiversity gives resilience to our landscape and ecosystems,” said NHAES researcher Adrienne Kovach, research associate professor of natural resources at UNH.New England cottontails have been declining for decades. However, NHAES researchers have found that in the last decade, the New England cottontail population in New Hampshire and Maine has contracted by 50 percent; a decade ago, cottontails were found as far north as Cumberland, Maine.The majority of research on New England cottontails has come out of UNH, much of it under the leadership of John Litvaitis, professor of wildlife ecology, who has studied the New England cottontail for three decades. Kovach’s research expands on this knowledge by using DNA analysis to provide new information on the cottontail’s status, distribution, genetic diversity, and dispersal ecology.The greatest threat and cause of the decline of the New England cottontail is the reduction and fragmentation of their habitat, Kovach said. Fragmentation of habitats occurs when the cottontail’s habitat is reduced or eliminated due to the maturing of forests or land development. Habitats also can become fragmented by roads or natural landscape features, such as bodies of water.”Cottontails require thicketed habitats, which progress from old fields to young forests. Once you have a more mature forest, the cottontail habitat is reduced. A lot of other species rely on these thicket habitats, including bobcats, birds, and reptiles. Many thicket-dependent species are on decline, and the New England cottontail is a representative species for this kind of habitat and its conservation,” Kovach said.Kovach explained that for cottontail and most animal populations to be healthy and grow, it is important for adult animals to leave the place where they were born and relocate to a new habitat, which is known as dispersal. …


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#Agriculture, #Alzheimer, #Dna, #Ecology, #England, #Gene, #Professor, #Region, #Research, #Species, #Unh

Epigenetic changes can drive cancer, study shows

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Cancer has long been thought to be primarily a genetic disease, but in recent decades scientists have come to believe that epigenetic changes — which don’t change the DNA sequence but how it is ‘read’ — also play a role in cancer. In particular DNA methylation, the addition of a methyl group (or molecule), is an epigenetic switch that can stably turn off genes, suggesting the potential to cause cancer just as a genetic mutation can. Until now, however, direct evidence that DNA methylation drives cancer formation was lacking.Researchers at the USDA/ARS Children’s Nutrition Research Center at Baylor College of Medicine and Texas Children’s Hospital have now created a mouse model providing the first in vivo evidence that epigenetic alterations alone can cause cancer. Their report appears in the Journal of Clinical Investigation.”We knew that epigenetic changes are associated with cancer, but didn’t know whether these were a cause or consequence of cancer. Developing this new approach for ‘epigenetic engineering’ allowed us to test whether DNA methylation changes alone can drive cancer,” said Dr. Lanlan Shen, associate professor of pediatrics at Baylor and senior author of the study.Shen and colleagues focused on p16, a gene that normally functions to prevent cancer but is commonly methylated in a broad spectrum of human cancers. They devised an approach to engineer DNA methylation specifically to the mouse p16 regulatory region (promoter). As intended, the engineered p16 promoter acted as a ‘methylation magnet’. As the mice reached adulthood, gradually increasing p16 methylation led to a higher incidence of spontaneous cancers, and reduced survival.”This is not only the first in vivo evidence that epigenetic alteration alone can cause cancer,” said Shen. “This also has profound implications for future studies, because epigenetic changes are potentially reversible. …


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Whole genome analysis speeds up: 240 full genomes in 50 hours

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Although the time and cost of sequencing an entire human genome has plummeted, analyzing the resulting three billion base pairs of genetic information from a single genome can take many months.In the journal Bioinformatics, however, a University of Chicago-based team — working with Beagle, one of the world’s fastest supercomputers devoted to life sciences — reports that genome analysis can be radically accelerated. This computer, based at Argonne National Laboratory, is able to analyze 240 full genomes in about two days.”This is a resource that can change patient management and, over time, add depth to our understanding of the genetic causes of risk and disease,” said study author Elizabeth McNally, MD, PhD, the A. J. Carlson Professor of Medicine and Human Genetics and director of the Cardiovascular Genetics Clinic at the University of Chicago Medicine.”The supercomputer can process many genomes simultaneously rather than one at a time,” said first author Megan Puckelwartz, a graduate student in McNally’s laboratory. “It converts whole genome sequencing, which has primarily been used as a research tool, into something that is immediately valuable for patient care.”Because the genome is so vast, those involved in clinical genetics have turned to exome sequencing, which focuses on the two percent or less of the genome that codes for proteins. This approach is often useful. An estimated 85 percent of disease-causing mutations are located in coding regions. But the rest, about 15 percent of clinically significant mutations, come from non-coding regions, once referred to as “junk DNA” but now known to serve important functions. If not for the tremendous data-processing challenges of analysis, whole genome sequencing would be the method of choice.To test the system, McNally’s team used raw sequencing data from 61 human genomes and analyzed that data on Beagle. They used publicly available software packages and one quarter of the computer’s total capacity. …


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#Alzheimer, #Beagle, #Cancer, #Chicago, #Computing, #Gene, #Human, #Medicine, #Washington

Regenerating orthopedic tissues within the human body

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By combining a synthetic scaffolding material with gene delivery techniques, researchers at Duke University are getting closer to being able to generate replacement cartilage where it’s needed in the body.Performing tissue repair with stem cells typically requires applying copious amounts of growth factor proteins — a task that is very expensive and becomes challenging once the developing material is implanted within a body. In a new study, however, Duke researchers found a way around this limitation by genetically altering the stem cells to make the necessary growth factors all on their own.They incorporated viruses used to deliver gene therapy to the stem cells into a synthetic material that serves as a template for tissue growth. The resulting material is like a computer; the scaffold provides the hardware and the virus provides the software that programs the stem cells to produce the desired tissue.The study appears online the week of Feb. 17 in the Proceedings of the National Academy of Sciences.Farshid Guilak, director of orthopaedic research at Duke University Medical Center, has spent years developing biodegradable synthetic scaffolding that mimics the mechanical properties of cartilage. One challenge he and all biomedical researchers face is getting stem cells to form cartilage within and around the scaffolding, especially after it is implanted into a living being.The traditional approach has been to introduce growth factor proteins, which signal the stem cells to differentiate into cartilage. Once the process is under way, the growing cartilage can be implanted where needed.”But a major limitation in engineering tissue replacements has been the difficulty in delivering growth factors to the stem cells once they are implanted in the body,” said Guilak, who is also a professor in Duke’s Department of Biomedical Engineering. “There’s a limited amount of growth factor that you can put into the scaffolding, and once it’s released, it’s all gone. We need a method for long-term delivery of growth factors, and that’s where the gene therapy comes in.”For ideas on how to solve this problem, Guilak turned to his colleague Charles Gersbach, an assistant professor of biomedical engineering and an expert in gene therapy. Gersbach proposed introducing new genes into the stem cells so that they produce the necessary growth factors themselves.But the conventional methods for gene therapy are complex and difficult to translate into a strategy that would be feasible as a commercial product.This type of gene therapy generally requires gathering stem cells, modifying them with a virus that transfers the new genes, culturing the resulting genetically altered stem cells until they reach a critical mass, applying them to the synthetic cartilage scaffolding and, finally, implanting it into the body.”There are a few challenges with that process, one of them being that there are way too many extra steps,” said Gersbach. “So we turned to a technique I had previously developed that affixes the viruses that deliver the new genes onto a material’s surface.”The new study uses Gersbach’s technique — dubbed biomaterial-mediated gene delivery — to induce the stem cells placed on Guilak’s synthetic cartilage scaffolding to produce growth factor proteins. …


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#Academy, #Agriculture, #Delivery, #Gene, #Pregnancy, #Proteins, #Repair, #Stem, #Study, #Tissue, #Virus

Water samples taken from the Upper Ganges River shed light on the spread of potential "superbugs"

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Experts from Newcastle University, UK, and the Indian Institute of Technology in Delhi (IIT-Delhi), reveal the spread of antibiotic-resistance to one of the most pristine locations in Asia is linked to the annual human pilgrimages to the region. The research team are now calling on governments around the world to recognise the importance of clean drinking water in our fight against antibiotic resistance.The spread of antibiotic-resistance to one of the most pristine locations in Asia is linked to the annual human pilgrimages to the region, new research has shown.Experts from Newcastle University, UK, and the Indian Institute of Technology in Delhi (IIT-Delhi), sampled water and sediments at seven sites along the Upper Ganges River, in the foothills of the Himalayas.They found that in May and June, when hundreds of thousands of visitors travel to Rishikesh and Haridwar to visit sacred sites, levels of resistance genes that lead to “superbugs” were found to be about 60 times greater than other times of the year.Publishing their findings today in the journal Environmental Science and Technology, the team say it is important to protect people visiting and living at these sites while also making sure nothing interferes with these important religious practices.They argue that preventing the spread of resistance genes that promote life-threating bacteria could be achieved by improving waste management at key pilgrimage sites.”This isn’t a local problem — it’s a global one,” explains Professor David Graham, an environmental engineer based at Newcastle University who has spent over ten years studying the environmental transmission of antibiotic resistance around the world.”We studied pilgrimage areas because we suspected such locations would provide new information about resistance transmission via the environment. And it has — temporary visitors from outside the region overload local waste handling systems, which seasonally reduces water quality at the normally pristine sites.”The specific resistance gene we studied, called blaNDM-1, causes extreme multi-resistance in many bacteria, therefore we must understand how this gene spreads in the environment.”If we can stem the spread of such antibiotic resistant genes locally — possibly through improved sanitation and waste treatment — we have a better chance of limiting their spread on larger scales, creating global solutions by solving local problems.”Funded by the Engineering and Physical Sciences Research Council (EPSRC), the aim of the research was to understand how antibiotic resistance was transmitted due to a specific human activity. Local “hot-spots” of antibiotic resistance exist around the world, particularly densely-populated regions with inconsistent sanitation and poor water quality.By comparing water quality of the Upper Ganges in February and again in June, the team showed that levels of blaNDM-1 were 20 times higher per capita during the pilgrimage season than at other times.Monitoring levels of other contaminants in the water, the team showed that overloading of waste treatment facilities was likely to blame and that in many cases, untreated sewage was going straight into the river where the pilgrims bathe.”The bugs and their genes are carried in people’s guts,” explains Professor Graham. “If untreated wastes get into the water supply, resistance potential in the wastes can pass to the next person and spiralling increases in resistance can occur.”Worldwide, concern is growing over the threat from bacteria that are resistant to the so-called “last resort” class of antibiotics known as Carbapenems, especially if resistance is acquired by aggressive pathogens.Of particular concern is NDM-1, which is a protein that confers resistance in a range of bacteria. NDM-1 was first identified in New Delhi and coded by the resistant gene blaNDM-1.Until recently, strains that carry blaNDM-1 were only found in clinical settings, but in 2008, blaNDM-1 positive strains were found in surface waters in Delhi. Since then, blaNDM-1 has been found elsewhere in the world, including new variants.There are currently few antibiotics to combat bacteria that are resistant to Carbapenems and worldwide spread of blaNDM-1 is a growing concern.Professor Graham, who is based in the School of Civil Engineering and Geosciences at Newcastle University, UK, said the team had planned to repeat their experiments last year, but the region was hit by massive floods in June and the experiments were abandoned.The team has since returned to Rishikesh and Haridwar and hope their work will prompt public action to improve local sanitation, protecting these socially important sites. On a global scale, they want policymakers to recognise the importance of clean drinking water in our fight against antibiotic resistance.”What humans have done by excess use of antibiotics is accelerate the rate of evolution, creating a world of resistant strains that never existed before” explains Graham.”Through the overuse of antibiotics, contamination of drinking water and other factors, we have exponentially speeded-up the rate at which superbugs might develop.”For example, when a new drug is developed, natural bacteria can rapidly adapt and become resistant; therefore very few new drugs are in the pipeline because it simply isn’t cost-effective to make them.”The only way we are going to win this fight is to understand all of the pathways that lead to antibiotic resistance. Clearly, improved antibiotic stewardship in medicine and agriculture is crucial, but understanding how resistance transmission occurs through our water supplies is also critical. We contend that improved waste management and water quality on a global scale is a key step.”


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Scientists chip away at mystery of what lives in our mouths

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Scientists have pieced together sections of DNA from 12 individual cells to sequence the genome of a bacterium known to live in healthy human mouths.With this new data about a part of the body considered “biological dark matter,” the researchers were able to reinforce a theory that genes in a closely related bacterium could be culprits in its ability to cause severe gum disease.Why the dark matter reference? More than 60 percent of bacteria in the human mouth refuse to grow in a laboratory dish, meaning they have never been classified, named or studied. The newly sequenced bacterium, Tannerella BU063, is among those that to date have not successfully been grown in culture — and its genome is identified as “most wanted” by the Human Microbiome Project.The federal Human Microbiome Project aims to improve research about the microbes that play a role in health and disease. Those 12 cells of BU063 are a good example of the complexity of life in the mouth: They came from a single healthy person but represented eight different strains of the bacterium.BU063 is closely related to the pathogen Tannerella forsythia, a bacterium linked to the gum disease periodontitis. Despite being “cousins,” this research revealed that they have clear differences in their genetic makeup.Those genes lacking in BU063 but present in forsythia — meaning they are a likely secret behind forsythia’s virulence — are now identified as good targets for further study, researchers say.”One of the tantalizing things about this study was the ability to do random searches of other bacteria whose levels are higher in periodontitis,” said Clifford Beall, research assistant professor of oral biology at The Ohio State University and lead author of the study. “We looked for genes that were present in these bacteria and forsythia and not in BU063. There is one particular gene complex in a whole list of these periodontitis-related bacteria that could be involved with virulence.”The research is published in the journal PLOS ONE.Periodontitis results when extensive inflammation or infection of the gums spreads beyond the gums to damage structures that support the teeth, including bone. Pockets that form between the gums and teeth are filled with different kinds of bacteria. Treatment typically involves deep cleaning or surgery to remove these infected pockets. Because multiple bacteria are associated with the disease, antibiotics have not been considered effective for treatment.And though many bacteria in these pockets have been collected and at least partially identified, their characteristics remain a mystery.”We think some of the gene differences we’ve found in this study are important, but it’s still not clear what all these genes do, meaning we still don’t know why certain bacteria in periodontitis are pathogenic in the first place. …


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#Body, #Dna, #Federal, #Gene, #Health, #State, #Study, #University

Better broccoli, enhanced anti-cancer benefits with longer shelf life

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While researching methods to increase the already well-recognized anti-cancer properties of broccoli, researchers at the University of Illinois also found a way to prolong the vegetable’s shelf life.And, according to the recently published study, the method is a natural and inexpensive way to produce broccoli that has even more health benefits and won’t spoil so quickly on your refrigerator shelf.Jack Juvik, a U of I crop sciences researcher, explained that the combined application of two compounds, both are natural products extracted from plants, increased the presence of cancer-fighting agents in broccoli while prolonging the post-harvest storage period.”We had figured out ways to increase the anti-cancer activity in broccoli, but the way we figured it out created a situation that would cause the product to deteriorate more rapidly after application,” Juvik said. “For fresh-market broccoli that you harvest, it’s not too big a deal, but many of these products have to be shipped, frozen, cut up, and put into other products. Usually the idea is to get it from the farm to at least the distributor (grocery store) within two to three days.”If we could figure out a way to prolong the appearance, taste, and flavor long after harvest and maintain the improved health-promoting properties, that’s always of great interest to growers,” he added.The researchers first used methyl jasmonate (MeJA), a non-toxic plant-signal compound (produced naturally in plants) to increase the broccoli’s anti-cancer potential, which they sprayed on the broccoli about four days before harvest. When applied, MeJA initiates a process of gene activity affiliated with the biosynthesis of glucosinolates (GS), which are compounds found in the tissue of broccoli and other brassica vegetables (such as cauliflower, cabbage, and kale).Glucosinolates have been identified as potent cancer-preventative agents because of their ability to induce detoxification enzymes, such as quinone reductase (QR), that detoxify and eliminate carcinogens from the human body.However, during this process, MeJA also signals a network of genes that lead to plant decay by inducing the release of ethylene, Juvik explained. “While we can use MeJA to turn on phytochemicals like the glucosinolates and dramatically increase the abundance of those helpful anti-cancer compounds, MeJA also reduces the shelf life after harvest,” he said.So the researchers tried using the recently developed compound 1-methylcyclopropene (1-MCP), which has been shown to interfere with receptor proteins in the plant that are receptor-sensitive to ethylene. They applied the compound after harvesting the same broccoli that had already been treated with MeJA before harvest.”Ethylene will move and bind to ethylene receptors and that binding process initiates decay. What this compound does is that it more competitively lands on the protein and binds to or pushes out ethylene,” Juvik explained. “It basically stops or dramatically slows down the decay associated with ethylene.”The combination is good,” he said.Like MeJA, 1-MCP is also a non-toxic compound naturally produced in plants, although Juvik said synthetic forms can be produced. He stressed that both the MeJA and 1-MCP treatments required very small amounts of the compounds.”It’s very cheap, and it’s about as toxic as salt. It takes very little to elevate all the desirable aspects. …


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Prostate cancer advance could improve treatment options

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Findings published today in the British Journal of Cancer, and funded by the Association for International Cancer Research (AICR), show how a genetic mutation in untreated patients is linked to aggressive cancer later in life. It was previously thought that the mutation only occurred in response to therapy.The research highlights why relapses could occur in some men following hormone therapy. And it could help identify those patients that will develop fatal prostate cancer much earlier for life-extending therapy.Prostate cancer is the most common cancer in men in the UK, with more than 40,000 new cases diagnosed every year. Treatment options for patients diagnosed with early stage prostate cancer vary from “watchful waiting” to hormone-withdrawal therapy, radiotherapy or surgery.Additional tests for indicators of aggressive cancer are necessary to help categorise patients so that those with a low-risk of the disease spreading can avoid unnecessary treatment, and those diagnosed with a high-risk can be targeted for more aggressive first line therapy.Hormone-withdrawal therapy often results in a dramatic remission, however the disease invariably relapses with a resistant form of the cancer. A third of these are due to an increase in copy number of a particular gene called the ‘androgen receptor’. The gene is on the X-Chromosome and so there is normally only one copy of this gene present in men. Prostate cancer thrives on male hormones, and one way that they develop to grow better is to increase the number of copies of the androgen receptor gene. This also enables the cancer to resist therapy.Lead researchers Dr Jeremy Clark and Prof Colin Cooper from UEA’s school of Biological Sciences carried out the research at the Institute of Cancer Research, London, and at UEA.Dr Clark said: “By the age of 60, the majority of men will have signs of prostate cancer. However, only a small proportion of men will die of the disease. The question is — which of these cancers are dangerous and which are not? …


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#Agriculture, #Alzheimer, #Association, #British, #Discovery, #Gene, #Number, #Prostate, #Research

Investigating the fiber of our being: How our gut bacteria metabolizes complex carbohydrates from fruits, vegetables

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We are all aware of the health benefits of dietary fiber. But what is dietary fiber and how do we metabolize it?Research at the University of Michigan Medical School, the University of York’s Structural Biology Laboratory, and institutions in Canada and Sweden, has begun to uncover how our gut bacteria metabolize the complex dietary carbohydrates found in fruits and vegetables.Trillions of bacteria live in human intestines — there are about ten times more bacterial cells in the average person’s body than human ones. Known as “microbiota,” these bacteria have a vital role to play in human health: they are central to our metabolism and well-being.The research team has uncovered how one group of gut bacteria, known as Bacteroidetes, digest complex sugars known as xyloglucans. These make up to 25 per cent of the dry weight of dietary fruit and vegetables including lettuce, onion, eggplant and tomatoes.In a recent issue of Nature, the researchers reported on a particular gene sequence that allows Bacteroidetes to carry out this function. They show that about 92 per cent of the population harbors bacteria with a variant of the gene sequence, according to a survey of public genome data from 250 adult humans.Understanding how these bacteria digest complex carbohydrates informs studies on a wide range of nutritional issues. These include probiotics (the consumption of ‘beneficial’ micro-organisms as a food supplement) and prebiotics (the consumption of foods or supplements intended to stimulate the production of healthy bacteria in the gut).”Its been appreciated for a long time that our symbiotic gut bacteria provide us with greatly expanded abilities to digest dietary fiber. However, the precise details of how this happens remain largely unexplored,” says co-corresponding author Eric Martens, Ph.D., an assistant professor in the Department of Microbiology & Immunology at the U-M Medical School. Martens is participating in the Host Microbiome Initiative, part of the U-M Medical School’s Strategic Research Initiative.Large-scale genome sequencing efforts, like the Human Microbiome Project, have focused on the community of microorganisms that live in the human gut. But these approaches can only uncover functions that have already been experimentally described, and much of what is sequenced is still unknown.”In this study, we took an empirical approach to decipher how one model gut bacterium digests one type of fiber that is abundant in the foods we eat. We were subsequently able to fit our findings into a much larger picture because of the existing data that the Human Microbiome Project has already gathered. …


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#Alzheimer, #Bacteroidetes, #Biology, #Cancer, #Gene, #Initiative, #Michigan, #Professor, #Project, #Research, #Science

Revolutionary new view on heritability in plants: Complex heritable traits not only determined by changes in DNA sequence

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Complex heritable traits are not only determined by changes in the DNA sequence. Scientists from the University of Groningen Bioinformatics Centre, together with their French colleagues, have shown that epigenetic marks can affect traits such as flowering time and architecture in plants. Furthermore, these marks are passed on for many generations in a stable manner. Their results were published in Science on the 6th of February 2014. It seems that a revision of genetics textbooks is now in order.We’ve all been taught that DNA is the physical foundation of heredity. Our genes are spelled out in the four famous letters A, T, C and G, which together form the genetic code. A single letter change in this code can lead to a gene ceasing to function or failing to work properly.The fact that the functioning of our genes is also affected by epigenetic marks has been known for decades. For example, the nucleotide cytosine (the C in the genetic code) can be changed into a methylcytosine. This cytosine methylation, which is one type of epigenetic mark, is typically associated with repression of gene activity.Epigenetic inheritance’While in mammals epigenetic marks are typically reset every generation, in plants no such dramatic resetting takes place. This opens the door to epigenetic inheritance in plants: epigenetic changes that are acquired in one generation tend to be stably passed on to the next generation’, explains Frank Johannes, assistant professor at the GBIC and co-lead scientist for the Science study.Johannes’s French colleagues have produced inbred strains of the model plant Arabidopsis, in which the epigenetic marks vary between strains although the DNA sequence is almost identical. …


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