New hope for powdery mildew resistant barley

New research at the University of Adelaide has opened the way for the development of new lines of barley with resistance to powdery mildew.In Australia, annual barley production is second only to wheat with 7-8 million tonnes a year. Powdery mildew is one of the most important diseases of barley.Senior Research Scientist Dr Alan Little and team have discovered the composition of special growths on the cell walls of barley plants that block the penetration of the fungus into the leaf.The research, by the ARC Centre of Excellence in Plant Cell Walls in the University’s School of Agriculture, Food and Wine in collaboration with the Leibniz Institute of Plant Genetics and Crop Plant Research in Germany, will be presented at the upcoming 5th International Conference on Plant Cell Wall Biology and published in the journal New Phytologist.”Powdery mildew is a significant problem wherever barley is grown around the world,” says Dr Little. “Growers with infected crops can expect up to 25% reductions in yield and the barley may also be downgraded from high quality malting barley to that of feed quality, with an associated loss in market value.”In recent times we’ve seen resistance in powdery mildew to the class of fungicide most commonly used to control the disease in Australia. Developing barley with improved resistance to the disease is therefore even more important.”The discovery means researchers have new targets for breeding powdery mildew resistant barley lines.”Powdery mildew feeds on the living plant,” says Dr Little. “The fungus spore lands on the leaf and sends out a tube-like structure which punches its way through cell walls, penetrating the cells and taking the nutrients from the plant. The plant tries to stop this penetration by building a plug of cell wall material — a papillae — around the infection site. Effective papillae can block the penetration by the fungus.”It has long been thought that callose is the main polysaccharide component of papilla. But using new techniques, we’ve been able to show that in the papillae that block fungal penetration, two other polysaccharides are present in significant concentrations and play a key role.”It appears that callose acts like an initial plug in the wall but arabinoxylan and cellulose fill the gaps in the wall and make it much stronger.”In his PhD project, Jamil Chowdhury showed that effective papillae contained up to four times the concentration of callose, arabinoxylan and cellulose as cell wall plugs which didn’t block penetration.”We can now use this knowledge find ways of increasing these polysaccharides in barley plants to produce more resistant lines available for growers,” says Dr Little.Story Source:The above story is based on materials provided by University of Adelaide. Note: Materials may be edited for content and length.

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Novel drug cocktail may improve clinical treatment for pancreatic cancer

Pancreatic cancer is the fourth leading cause of cancer deaths in the U.S. and has the lowest overall survival rate of all major cancers (~6%). With current treatment options being met with limited success it is anticipated that pancreatic cancer will move up to the second leading cause of cancer deaths by as early as 2015. Surgical removal of the tumor presents the best chance of survival, however only 15% of patients are eligible due to the late stage of diagnosis common with this disease. With very limited improvements in patient outcome over the last two decades there remains an enormous need for new therapies and treatment options.David Durrant, a Ph.D. student in the laboratory of Dr. Rakesh Kukreja from the Pauley Heart Center at Virginia Commonwealth University’s School of Medicine, is studying a novel combination therapy for the treatment of pancreatic cancer. The traditional chemotherapy drug, doxorubicin (DOX), has long been used in the treatment of several cancers. However, patients commonly acquire resistance to DOX because of increased activation of specific survival proteins or through increased expression of drug transporters which reduce cellular levels of the drug. This is especially true for pancreatic cancer, which does not respond to multiple treatment strategies, including those that contain DOX. …

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Protein researchers closing in on the mystery of schizophrenia

Schizophrenia is a severe disease for which there is still no effective medical treatment. In an attempt to understand exactly what happens in the brain of schizophrenic people, researchers from the University of Southern Denmark have analysed proteins in the brains of rats that have been given hallucinogenic drugs. This may pave the way for new and better medicines.Seven per cent of the adult population suffer from schizophrenia, and although scientists have tried for centuries to understand the disease, they still do not know what causes the disease or which physiological changes it causes in the body. Doctors cannot make the diagnosis by looking for specific physiological changes in the patient’s blood or tissue, but have to diagnose from behavioral symptoms.In an attempt to find the physiological signature of schizophrenia, researchers from the University of Southern Denmark have conducted tests on rats, and they now believe that the signature lies in some specific, measurable proteins. Knowing these proteins and comparing their behavior to proteins in the brains of not-schizophrenic people may make it possible to develop more effective drugs.It is extremely difficult to study brain activity in schizophrenic people, which is why researchers often use animal models in their strive to understand the mysteries of the schizophrenic brain. Rat brains resemble human brains in so many ways that studying them makes sense if one wants to learn more about the human brain.Schizophrenic symptoms in ratsThe strong hallucinogenic drug phenocyclidine (PCP), also known as “angel’s dust,” provides a range of symptoms in people which are very similar to schizophrenia.”When we give PCP to rats, the rats become valuable study objects for schizophrenia researchers,” explains Ole Nrregaard Jensen, professor and head of the Department of Biochemistry and Molecular Biology.Along with Pawel Palmowski, Adelina Rogowska-Wrzesinska and others, he is the author of a scientific paper about the discovery, published in the international Journal of Proteome Research.Among the symptoms and reactions that can be observed in both humans and rats are changes in movement and reduced cognitive functions such as impaired memory, attention and learning ability.”Scientists have studied PCP rats for decades, but until now no one really knew what was going on in the rat brains at the molecular level. We now present what we believe to be the largest proteomics data set to date,” says Ole Nrregaard Jensen.PCP is absorbed very quickly by the brain, and it only stays in the brain for a few hours. Therefore, it was important for researchers to examine the rats’ brain cells soon after the rats were injected with the hallucinogenic drug.”We could see changes in the proteins in the brain already after 15 minutes. And after 240 minutes, it was almost over,” says Ole Nrregaard Jensen.The University of Southern Denmark holds some of the world’s most advanced equipment for studying proteins, and Ole Nrregaard Jensen and his colleagues used the university’s so-called mass spectrometres for their protein studies.352 proteins cause brain changes”We found 2604 proteins, and in 352 of them, we saw changes that can be associated with the PCP injections. These 352 proteins will be extremely interesting to study in closer detail to see if they also alter in people with schizophrenia — and if that’s the case, it will of course be interesting to try to develop a drug that can prevent the protein changes that lead to schizophrenia,” says Ole Nrregaard Jensen about the discovery and the work that now lies ahead.The 352 proteins in rat brains responded immediately when the animals were exposed to PCP. …

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Deforestation of sandy soils a greater climate threat

Deforestation may have far greater consequences for climate change in some soils than in others, according to new research led by Yale University scientists — a finding that could provide critical insights into which ecosystems must be managed with extra care because they are vulnerable to biodiversity loss and which ecosystems are more resilient to widespread tree removal.In a comprehensive analysis of soil collected from 11 distinct U.S. regions, from Hawaii to northern Alaska, researchers found that the extent to which deforestation disturbs underground microbial communities that regulate the loss of carbon into the atmosphere depends almost exclusively on the texture of the soil. The results were published in the journal Global Change Biology.”We were astonished that biodiversity changes were so strongly affected by soil texture and that it was such an overriding factor,” said Thomas Crowther, a postdoctoral fellow at the Yale School of Forestry & Environmental Studies and lead author of the study. “Texture overrode the effects of all the other variables that we thought might be important, including temperature, moisture, nutrient concentrations, and soil pH.”The study is a collaboration among Yale researchers and colleagues at the University of Boulder, Colorado and the University of Kentucky.A serious consequence of deforestation is extensive loss of carbon from the soil, a process regulated by subterranean microbial diversity. Drastic changes to the microbial community are expected to allow more CO2 to escape into the atmosphere, with the potential to exaggerate global warming.Specifically, the researchers found that deforestation dramatically alters microbial communities in sandy soils, but has minimal effects in muddy, clay-like soils, even after extensive tree removal.According to the researchers, particles in fine, clay-like soil seem to have a larger surface area to bind nutrients and water. This capacity might buffer soil microbes against the disturbance of forest removal, they said. In contrast, sandy soils have larger particles with less surface area, retaining fewer nutrients and less organic matter.”If you disrupt the community in a sandy soil, all of the nutrients the microbes rely on for food are leached away: they’re lost into the atmosphere, lost into rivers, lost through rain,” Crowther said. “But in clay-like soil, you can cut down the forest and the nutrients remain trapped tightly in the muddy clay.”The researchers also examined how the effects of deforestation on microbial biodiversity change over time. Contrary to their expectations, they found no correlation, even over the course of 200 years.”The effects are consistent, no matter how long ago deforestation happened,” Crowther said. “In a clay soil, you cut down the forest and the nutrients are retained for long periods of time and the community doesn’t change. …

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Tumor suppressor gene linked to stem cells, cancer biologists report

Just as archeologists try to decipher ancient tablets to discern their meaning, UT Southwestern Medical Center cancer biologists are working to decode the purpose of an ancient gene considered one of the most important in cancer research.The p53 gene appears to be involved in signaling other cells instrumental in stopping tumor development. But the p53 gene predates cancer, so scientists are uncertain what its original function is.In trying to unravel the mystery, Dr. John Abrams, Professor of Cell Biology at UT Southwestern, and his team made a crucial new discovery — tying the p53 gene to stem cells. Specifically, his lab found that when cellular damage is present, the gene is hyperactive in stem cells, but not in other cells. The findings suggest p53’s tumor suppression ability may have evolved from its more ancient ability to regulate stem cell growth.”The discovery was that only the stem cells light up. None of the others do. The exciting implication is that we are able to understand the function of p53 in stem cells,” said Dr. Abrams, Chair of the Genetics and Development program in UT Southwestern’s Graduate School of Biomedical Sciences. “We may, in fact, have some important answers for how p53 suppresses tumors.”The findings appear online in the journal eLife, a joint initiative of the Howard Hughes Medical Institute, the Max Planck Society, and the Wellcome Trust.p53 is one of the hardest working and most effective allies in the fight against cancer, said Dr. Abrams. …

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Salamanders shrinking as their mountain havens heat up

Wild salamanders living in some of North America’s best salamander habitat are getting smaller as their surroundings get warmer and drier, forcing them to burn more energy in a changing climate.That’s the key finding of a new study, published March 25 in the journal Global Change Biology, that examined museum specimens caught in the Appalachian Mountains from 1957 to 2007 and wild salamanders measured at the same sites in 2011-2012. The salamanders studied from 1980 onward were, on average, 8% smaller than their counterparts from earlier decades. The changes were most marked in the Southern Appalachians and at low elevations — settings where detailed weather records showed the climate has warmed and dried out most.Scientists have predicted that some animals will get smaller in response to climate change, and this is strongest confirmation of that prediction.”This is one of the largest and fastest rates of change ever recorded in any animal,” said Karen R. Lips, an associate professor of biology at the University of Maryland and the study’s senior author. “We don’t know exactly how or why it’s happening, but our data show it is clearly correlated with climate change.” And it’s happening at a time when salamanders and other amphibians are in distress, with some species going extinct and others dwindling in number.”We don’t know if this is a genetic change or a sign that the animals are flexible enough to adjust to new conditions,” Lips said. “If these animals are adjusting, it gives us hope that some species are going to be able to keep up with climate change.”The study was prompted by the work of University of Maryland Prof. Emeritus Richard Highton, who began collecting salamanders in the Appalachian Mountains in 1957. The geologically ancient mountain range’s moist forests and long evolutionary history make it a global hot spot for a variety of salamander species. Highton collected hundreds of thousands of salamanders, now preserved in jars at the Smithsonian Institution’s Museum Service Center in Suitland, MD.But Highton’s records show a mysterious decline in the region’s salamander populations beginning in the 1980s. Lips, an amphibian expert, saw a similar decline in the frogs she studied in Central America, and tracked it to a lethal fungal disease. …

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Serious side effect: Several FDA-approved anti-cancer drugs induce stem cell tumors

Using a new approach to systematically test chemotherapy drugs in an unusual animal model, a research team led by University of Massachusetts Amherst molecular biologist Michele Markstein, with Norbert Perrimon at Harvard Medical School, report that several have a serious side effect: Inducing hyper proliferation in stem cells that could lead to tumor recurrence.Markstein says, “We discovered that several chemotherapeutics that stop fast growing tumors have the opposite effect on stem cells in the same animal, causing them to divide too rapidly. This was a surprise, because it showed that the same drug could have opposite actions on cells in the same animal: Suppressing tumor growth on one cell population while initiating growth in another. Not only is the finding of clinical interest, but with this study we used an emerging new non-traditional tool for assessing drugs using stem cells in the fruit fly gut.”She adds, “We did these experiments in the fly because Drosophila stem cells, in the intestine, are very much like the stem cells in our intestine, and it’s a lot easier to do experiments in flies than humans or even mice.”Further, Markstein explains, “When it comes to stem cells, it is important to conduct studies in living animals because stem cells are acutely attuned to the other cells in their microenvironment. Indeed the side effect that we observed is caused by damage that the chemotherapy drugs to cells in the stem cell microenvironment. The stem cells respond to this damage by hyper proliferating.”Markstein and Samantha Dettorre at UMass, with Perrimon and colleagues at Harvard Medical School, pioneered large-scale chemical screening in adult fruit flies that they feel will be useful for testing other chemicals. Conventional in vitro cell screens can identify drugs that act directly on stem cells, the authors note, but they cannot test and identify drugs that act on the all-important microenvironment, which provides cues for stem cell division, differentiation, and death.The flies provide “ready-made stem cell microenvironments” that are “difficult-to-impossible” to create in petri dishes, Markstein notes. Specifically, she and her colleagues inserted a human cancer-causing gene in the fly genome, turned on that gene in its intestinal stem cells, and found that it did form fast-growing tumors.To take full advantage of Drosophila’s ready-made microenvironments, they developed new technology to determine the size of tumors inside each fly gut. The previous standard in the field was to dissect flies to visualize tumors, which are typically labeled green with green fluorescent protein. In the new method, the researchers decided to use a different label, an enzyme from fireflies called luciferase. This allows them to measure tumor size simply by crushing the flies en masse, rather than dissecting them one-by-one.They asked the National Cancer Institute for chemotherapy drug samples and received a library of 88 currently in clinical use. …

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Warmer temperatures push malaria to higher elevations

Researchers have debated for more than two decades the likely impacts, if any, of global warming on the worldwide incidence of malaria, a mosquito-borne disease that infects more than 300 million people each year.Now, University of Michigan ecologists and their colleagues are reporting the first hard evidence that malaria does — as had long been predicted — creep to higher elevations during warmer years and back down to lower altitudes when temperatures cool.The study, based on an analysis of records from highland regions of Ethiopia and Colombia, suggests that future climate warming will result in a significant increase in malaria cases in densely populated regions of Africa and South America, unless disease monitoring and control efforts are boosted and sustained.”We saw an upward expansion of malaria cases to higher altitudes in warmer years, which is a clear signal of a response by highland malaria to changes in climate,” said U-M theoretical ecologist Mercedes Pascual, senior author of a paper scheduled for online publication in Science on March 6.”This is indisputable evidence of a climate effect,” said Pascual, the Rosemary Grant Collegiate Professor of Ecology and Evolutionary Biology and a Howard Hughes Medical Institute Investigator. “The main implication is that with warmer temperatures, we expect to see a higher number of people exposed to the risk of malaria in tropical highland areas like these.”More than 20 years ago, malaria was identified as a disease expected to be especially sensitive to climate change, because both the Plasmodium parasites that cause it and the Anopheles mosquitoes that spread it thrive as temperatures warm.Some early studies concluded that climate change would lead to a big increase in malaria cases as the disease expanded its range into higher elevations, but some of the assumptions behind those predictions were later criticized. More recently, some researchers have argued that improved socioeconomic conditions and more aggressive mosquito-control efforts will likely exert a far greater influence over the extent and intensity of malaria worldwide than climatic factors.What’s been missing in this debate has been an analysis of regional records with sufficient resolution to determine how the spatial distribution of malaria cases has changed in response to year-to-year temperature variations, especially in countries of East Africa and South America with densely populated highlands that have historically provided havens from the disease.Pascual and her colleagues looked for evidence of a changing spatial distribution of malaria with varying temperature in the highlands of Ethiopia and Colombia. They examined malaria case records from the Antioquia region of western Colombia from 1990 to 2005 and from the Debre Zeit area of central Ethiopia from 1993 to 2005.By focusing solely on the altitudinal response to year-to-year temperature changes, they were able to exclude other variables that can influence malaria case numbers, such as mosquito-control programs, resistance to anti-malarial drugs and fluctuations in rainfall amounts.They found that the median altitude of malaria cases shifted to higher elevations in warmer years and back to lower elevations in cooler years. The relatively simple analysis yielded a clear, unambiguous signal that can only be explained by temperature changes, they said.”Our latest research suggests that with progressive global warming, malaria will creep up the mountains and spread to new high-altitude areas. And because these populations lack protective immunity, they will be particularly vulnerable to severe morbidity and mortality,” said co-author Menno Bouma, honorary senior clinical lecturer at the London School of Hygiene & Tropical Medicine.In addition, the study results suggest that climate change can explain malaria trends in both the highland regions in recent decades.In the Debre Zeit region of Ethiopia, at an elevation range of between 5,280 feet and 7,920 feet, about 37 million people (roughly 43 percent of the country’s population) live in rural areas at risk of higher malaria exposure under a warming climate.In a previous study, the researchers estimated that a 1 degree Celsius temperature increase could result in an additional 3 million malaria cases annually in Ethiopia in the under-15 population, unless control efforts are strengthened.”Our findings here underscore the size of the problem and emphasize the need for sustained intervention efforts in these regions, especially in Africa,” Pascual said.

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3-D imaging sheds light on Apert syndrome development

Three dimensional imaging of two different mouse models of Apert Syndrome shows that cranial deformation begins before birth and continues, worsening with time, according to a team of researchers who studied mice to better understand and treat the disorder in humans.Apert Syndrome is caused by mutations in FGFR2 — fibroblast growth factor receptor 2 — a gene, which usually produces a protein that functions in cell division, regulation of cell growth and maturation, formation of blood vessels, wound healing, and embryonic development. With certain mutations, this gene causes the bones in the skull to fuse together early, beginning in the fetus. These mutations also cause mid-facial deformation, a variety of neural, limb and tissue malformations and may lead to cognitive impairment.Understanding the growth pattern of the head in an individual, the ability to anticipate where the bones will fuse and grow next, and using simulations “could contribute to improved patient-centered outcomes either through changes in surgical approach, or through more realistic modeling and expectation of surgical outcome,” the researchers said in today’s (Feb. 28) issue of BMC Developmental Biology.Joan T. Richtsmeier, Distinguished Professor of Anthropology, Penn State, and her team looked at two sets of mice, each having a different mutation that causes Apert Syndrome in humans and causes similar cranial problems in the mice. They checked bone formation and the fusing of sutures, soft tissue that usually exists between bones n the skull, in the mice at 17.5 days after conception and at birth — 19 to 21 days after conception.”It would be difficult, actually impossible, to observe and score the exact processes and timing of abnormal suture closure in humans as the disease is usually diagnosed after suture closure has occurred,” said Richtsmeier. “With these mice, we can do this at the anatomical level by visualizing the sutures prenatally using micro-computed tomography — 3-D X-rays — or at the mechanistic level by using immunohistochemistry, or other approaches to see what the cells are doing as the sutures close.”The researchers found that both sets of mice differed in cranial formation from their littermates that were not carrying the mutation and that they differed from each other. They also found that the changes in suture closure in the head progressed from 17.5 days to birth, so that the heads of newborn mice looked very different at birth than they did when first imaged prenatally.Apert syndrome also causes early closure of the sutures between bones in the face. Early fusion of bones of the skull and of the face makes it impossible for the head to grow in the typical fashion. The researchers found that the changed growth pattern contributes significantly to continuing skull deformation and facial deformation that is initiated prenatally and increases over time.”Currently, the only option for people with Apert syndrome is rather significant reconstructive surgery, sometimes successive planned surgeries that occur throughout infancy and childhood and into adulthood,” said Richtsmeier. …

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Zebrafish neurons may lead to understanding of birth defects like spina bifida

The zebrafish, a tropical freshwater fish similar to a minnow and native to the southeastern Himalayan region, is well established as a key tool for researchers studying human diseases, including brain disorders. Using zebrafish, scientists can determine how individual neurons develop, mature and support basic functions like breathing, swallowing and jaw movement. Researchers at the University of Missouri say that learning about neuronal development and maturation in zebrafish could lead to a better understanding of birth defects such as spina bifida in humans.”We are studying how neurons move to their final destinations,” said Anand Chandrasekhar, professor of biological sciences and a researcher in the Bond Life Sciences Center at MU. “It’s especially critical in the nervous system because these neurons are generating circuits similar to what you might see in computers. If those circuits don’t form properly, and if different types of neurons don’t end up in the right locations, the behavior and survival of the animal will be compromised.”The scientists studied zebrafish embryos, which are nearly transparent, making internal processes easy to observe. Using modified zebrafish expressing green fluorescent jellyfish protein, Chandrasekhar and his team were able to track neuronal migration.”This approach is used extensively to visualize a group of cells,” Chandrasekhar said. “In our study, clusters of green cells glowed and indicated where motor neurons were located in the brain. Some groupings are shaped like sausages while others are round, but each cluster of 50 to150 cells sends out signals to different groups of jaw muscles.”These motor neurons that Chandrasekhar studied are located in the hindbrain, which corresponds to the human brainstem and controls gill and jaw movement in these tiny fish. Genes controlling the development and organization of these neurons in zebrafish are functionally similar to genes in higher vertebrates including mammals.Chandrasekhar’s work contributes to a better understanding of how neuronal networks are organized and “wired” during development. These studies also may provide insight into birth defects like spina bifida, which affects 1 in every 2,000 births, according to the National Institutes of Health.”One of the hallmarks of spina bifida is an open neural tube in the spinal cord,” Chandrasekhar said. …

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Beauty and bacteria: Slim, attractive men have less nasal bacteria than heavy men

Do attractive traits tell us anything about a person’s reproductive health? New research in the American Journal of Human Biology reveals a link between Body Mass Index (BMI) and the amount of bacteria colonizing noses. The results show that heavier men harbor more potentially pathogenic species of bacteria in their nose, compared with slimmer, more traditionally attractive men.”According to an evolutionary point of view, traits related to attractiveness are supposed to be honest signals of biological quality,” said Dr. Boguslaw Pawlowski. “We analyzed whether nasal and throat colonization with potentially pathogenic bacteria is related to body height and BMI in both sexes.”103 healthy females and 90 healthy males participated in the study. Heights and weights were self-reported, while waist and hip circumferences were measured. Six potentially pathogenic bacteria were isolated and identified from nasal and throat swabs. The results showed that ‘colonized’ men were found to have a higher BMI than non-colonized males, although no differences were found in females.”To our knowledge, this is the first attempt to study body morphology traits related to physical attractiveness in relation to bacterial colonization in young people,” said Pawlowski. “The results confirmed our hypothesis, but only for BMI in males.”Story Source:The above story is based on materials provided by Wiley. Note: Materials may be edited for content and length.

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Better batters from brain-training research: Baseball player study significantly improves vision, reduces strikeouts

Four words no baseball player wants to hear: Strike three. You’re out.The University of California, Riverside’s baseball team heard those words less frequently in the 2013 season after participating in novel brain-training research that significantly improved the vision of individual players and may have added up to four or five games to the win column.The results of that study appear in a paper, “Improved vision and on-field performance in baseball through perceptual learning,” published in the Feb. 17 issue of the peer-reviewed Current Biology.Most studies of visual abilities focus on mechanisms that might be used to improve sight, such as exercising the ocular muscles. Improvements in vision resulting from those experiments typically do not transfer to real-world tasks, however.A team of UCR psychologists — professors Aaron Seitz and Daniel Ozer and recent Ph.D. graduate Jenni Deveau — combined multiple perceptual-learning approaches to determine if improvements gained from an integrated, perceptual learning-based training program would transfer to real-world tasks.They did.Before the start of the 2013 NCAA Division 1 baseball season the UCR researchers assigned 19 baseball players to complete 30 25-minute sessions of a vision-training video game Seitz developed. Another 18 team members received no training. Players who participated in the training saw a 31 percent improvement in visual acuity — some gaining as much as two lines on the Snellen eye chart — and greater sensitivity to contrasts in light.”The vision tests demonstrate that training-based benefits transfer outside the context of the computerized training program to standard eye charts,” Seitz said. “Players reported seeing the ball better, greater peripheral vision and an ability to distinguish lower-contrast objects.”The researchers found that the trained players had 4.4 percent fewer strikeouts — a decrease not experienced in the rest of the Big West Conference. The UCR team also scored 41 more runs than projected after controlling for skills improvements players would be expected to gain over the course of a season. Ozer arrived at this number by using the runs-created formula developed by baseball historian and statistician Bill James.The longtime baseball fan then used the Pythagorean Winning Percentage formula, a statistical tool used by sabermetricians to compute a team’s wins and losses based upon their runs scored and runs allowed, to estimate that the training resulted in as many as four or five more wins.(The team had a season record of 22-32, but later was forced to vacate eight wins due to an ineligible player.)UCR’s year-over-year improvements were at least three times greater than the rest of the league in batting average, slugging percentage, on-base percentage, walks and strikeouts, the researchers determined.”Elite baseball batters use various kinds of sensory information to be successful batters, but most weight is given to visual feedback,” Seitz said. …

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Researchers rejuvenate stem cell population from elderly mice, enabling muscle recovery

Researchers at the Stanford University School of Medicine have pinpointed why normal aging is accompanied by a diminished ability to regain strength and mobility after muscle injury: Over time, stem cells within muscle tissues dedicated to repairing damage become less able to generate new muscle fibers and struggle to self-renew.”In the past, it’s been thought that muscle stem cells themselves don’t change with age, and that any loss of function is primarily due to external factors in the cells’ environment,” said Helen Blau, PhD, the Donald and Delia B. Baxter Foundation Professor. “However, when we isolated stem cells from older mice, we found that they exhibit profound changes with age. In fact, two-thirds of the cells are dysfunctional when compared to those from younger mice, and the defect persists even when transplanted into young muscles.”Blau and her colleagues also identified for the first time a process by which the older muscle stem cell populations can be rejuvenated to function like younger cells. “Our findings identify a defect inherent to old muscle stem cells,” she said. “Most exciting is that we also discovered a way to overcome the defect. As a result, we have a new therapeutic target that could one day be used to help elderly human patients repair muscle damage.”Blau, a professor of microbiology and immunology and director of Stanford’s Baxter Laboratory for Stem Cell Biology, is the senior author of a paper describing the research, which will be published online Feb. 16 in Nature Medicine. Postdoctoral scholar Benjamin Cosgrove, PhD, and former postdoctoral scholar Penney Gilbert, PhD, now an assistant professor at the University of Toronto, are the lead authors.The researchers found that many muscle stem cells isolated from mice that were 2 years old, equivalent to about 80 years of human life, exhibited elevated levels of activity in a biological cascade called the p38 MAP kinase pathway. This pathway impedes the proliferation of the stem cells and encourages them to instead become non-stem, muscle progenitor cells. …

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Fertilization destabilizes global grassland ecosystems

A new study led by University of Minnesota researchers demonstrates that fertilization of natural grasslands — either intentionally or unintentionally as a side effect of global farming and industry — is having a destabilizing effect on global grassland ecosystems. Using a network of natural grassland research sites around the world called the Nutrient Network, the study represents the first time such a large experiment has been conducted using naturally occurring sites.Led by Yann Hautier, a Marie Curie Fellow associated with both the Department of Ecology, Evolution, and Behavior at the University of Minnesota and the Institute of Evolutionary Biology and Environmental Studies at the University of Zurich, the research team included U of M associate professors Eric Seabloom and Elizabeth Borer, and research scientist Eric Lind, along with scientists from institutions around the world including Andy Hector at Oxford University’s Department of Plant Sciences. The findings were published on February 16 in the journal Nature.The researchers found that plant diversity in natural ecosystems creates more stable ecosystems over time because of less synchronized growth of plants. “This is sometimes called the portfolio effect,” says Seabloom. “If you have money in two investments and they’re both stocks, they’re going to track each other, but if one is a stock and one is a bond, they’re going to respond differently to the overall economy and are more likely to balance each other.”The researchers collected plants from each of the sites, then sorted, dried, and weighed them to monitor the number of species of plants and total amount of plants, or “biomass,” grown over time. They used this information to quantify species diversity and ecosystem stability. Says Hautier: “It was really striking to see the relationship between diversity and stability” and the similarities to data collected from artificial grasslands as part of a research effort called BioDepth, indicating that the results from natural grasslands of the Nutrient Network could be predicted from the results of artificial grasslands.”The results of our study emphasize that we need to consider not just how productive ecosystems are but also how stable they are in the long-term, and how biodiversity is related to both aspects of ecosystem functioning,” says Andy Hector.The researchers also found that grassland diversity and stability are reduced when fertilizer is added. Fertilizers are intentionally used in grassland to increase livestock fodder. Fertilizer addition is also occurring unintentionally in many places around the world because nitrogen, a common fertilizer, is released into the atmosphere from farming, industry, and burning fossil fuels. Rainfall brings nitrogen out of the atmosphere and on to grasslands, changing the growth and types of plant species. …

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New RNA interference technique finds seven genes for head and neck cancer

In the hunt for genetic mutations that cause cancer, there is a lot of white noise. So although genetic sequencing has identified hundreds of genetic alterations linked to tumors, it’s still an enormous challenge to figure out which ones are actually responsible for the growth and metastasis of cancer. Scientists in Rockefeller’s Laboratory of Mammalian Cell Biology and Development have created a new technique that can weed out that noise — eliminating the random bystander genes and identifying the ones that are critical for cancer. Applying their technique to head and neck cancers, they’ve discovered seven new tumor-suppressor genes whose role in cancer was previously unknown.The new technique, which the lab recently applied to a screen for skin tumor genes, is particularly useful because it takes a fraction of the resources and much less time than the traditional method for determining gene function — breeding genetically modified animals to study the impact of missing genes.”Using knockout mice, which are model organisms bred to have a particular gene missing, is not feasible when there are 800 potential head and neck cancer genes to sort through,” says Daniel Schramek, a postdoctoral fellow in the lab, which is headed by Rebecca C. Lancefield Professor Elaine Fuchs. “It can take about two years per gene. Our method can assess about 300 genes in a single mouse, in as little as five weeks.”The researchers made use of RNA interference, a natural process whereby RNA molecules inhibit gene expression. They took short pieces of RNA which are able to turn off the function of specific genes, attached them to highly concentrated viruses, and then, using ultrasound to guide the needle without damaging surrounding tissue, they injected the viruses into the sacs of mouse embryos.”The virus is absorbed and integrated into the chromosomes of the single layer of surface cells that cover the tiny embryo,” explains Fuchs. “As the embryo develops, this layer of cells becomes the skin, mammary glands and oral tissue, enabling us to efficiently, selectively and quickly eliminate the expression of any desired gene in these tissues. The non-invasive method avoids triggering a wound or inflammatory response that is typically associated with conventional methods to knockdown a gene in cultured cells and then engraft the cells onto a mouse.”When the mice grew, the researchers determined which genes, when turned off, were promoting tumor growth, and what they found was surprising.”Among the seven novel tumor suppressor genes we found, our strongest hit was Myh9, which codes for the protein myosin IIa, a motor protein with well-known function in cell structure and cell migration,” says Schramek. …

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Geographic variation of human gut microbes tied to obesity

People living in cold, northern latitudes have bacteria in their guts that may predispose them to obesity, according to a new study by researchers at the University of California, Berkeley, and the University of Arizona, Tucson.The researchers’ analysis of the gut microbes of more than a thousand people from around the world showed that those living in northern latitudes had more gut bacteria that have been linked to obesity than did people living farther south.The meta-analysis of six earlier studies was published this month in the online journal Biology Letters by UC Berkeley graduate student Taichi Suzuki and evolutionary biology professor Michael Worobey of the University of Arizona.”People think obesity is a bad thing, but maybe in the past getting more fat and more energy from the diet might have been important to survival in cold places. Our gut microbes today might be influenced by our ancestors,” said Suzuki, noting that one theory is that obesity-linked bacteria are better at extracting energy from food. “This suggests that what we call ‘healthy microbiota’ may differ in different geographic regions.””This observation is pretty cool, but it is not clear why we are seeing the relationship we do with latitude,” Worobey said. “There is something amazing and weird going on with microbiomes.”To Worobey, the results are fascinating from an evolutionary biology perspective. “Maybe changes to your gut community of bacteria are important for allowing populations to adapt to different environmental conditions in lots of animals, including humans,” he said.Body size increases with latitudeSuzuki proposed the study while rotating through Worobey’s lab during his first year as a graduate student at the University of Arizona. Studies of gut microbes have become a hot research area among scientists because the proportion of different types of bacteria and Archaea in the gut seems to be correlated with diseases ranging from diabetes and obesity to cancer. In particular, the group of bacteria called Firmicutes seems to dominate in the intestines of obese people — and obese mice — while a group called Bacteroidetes dominates in slimmer people and mice.Suzuki reasoned that, since animals and humans in the north tend to be larger in size — an observation called Bergmann’s rule — then perhaps their gut microbiota would contain a greater proportion of Firmicutes than Bacteriodetes. While at the University of Arizona, and since moving to UC Berkeley, Suzuki has been studying how rodents adapt to living at different latitudes.”It was almost as a lark,” Woroby said. “Taichi thought that if Firmicutes and Bacteroidetes are linked to obesity, why not look at large scale trends in humans. When he came back with results that really showed there was something to it, it was quite a surprise.”Suzuki used data published in six previous studies, totaling 1,020 people from 23 populations in Africa, Europe, North and South America and Asia. …

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Embryology: Scientists crack open ‘black box’ of development and see a ‘rosette’

We know much about how embryos develop, but one key stage — implantation — has remained a mystery. Now, scientists from Cambridge have discovered a way to study and film this ‘black box’ of development. Their results — which will lead to the rewriting of biology text books worldwide — are published in the journal Cell.Embryo development in mammals occurs in two phases. During the first phase, pre-implantation, the embryo is a small, free-floating ball of cells called a blastocyst. In the second, post-implantation, phase the blastocyst embeds itself in the mother’s uterus.While blastocysts can be grown and studied outside the body, the same has not been true from implantation. And because embryos are so closely connected to their mothers, implantation has also been difficult to study in the womb.According to study author Professor Magdalena Zernicka-Goetz of the University of Cambridge: “We know a lot about pre-implantation, but what happens after implantation — and particularly the moment of implantation — is an enigma.”Scientists are interested in studying implantation because the embryo undergoes huge changes in such a short space of time.”During these two days, it goes from a relatively simple ball to a much larger, more complex cup-like structure, but exactly how that happens was a mystery — a black box of development. That is why we needed to develop a method that would allow us to culture and study embryos during implantation,” she explained.Working with mouse cells, Professor Zernicka-Goetz and her colleague Dr Ivan Bedzhov succeeded in creating the right conditions outside the womb to study the implantation process.To be able to support development, they created a system comprising a gel and medium that, as well as having the right chemical and biological properties, was of similar elasticity to uterine tissue. Crucially, this gel was transparent to optical light, allowing then to film the embryo during implantation.This new method revealed that on its way from ball to cup, the blastocyst becomes a ‘rosette’ of wedge-shaped cells, a structure never before seen by scientists.”It’s a beautiful structure. This rosette is what a mouse looks like on the 4th day of its life, and most likely what we look like on the 7th day of ours, and it’s fascinating how beautiful we are then, and how these small cells organise so perfectly to allow us to develop.”As well as answering a fundamental question in developmental biology, the new method will allow scientists to study embryo growth and development at implantation for the first time, which could help improve the success of IVF, and extend our knowledge of stem cells, which could advance their use in regenerative medicine.The findings also mean developmental biology text books will need rewriting. “The text books make an educated guess of what happened during this part of development, but we now know that what I learned and what I teach my students about this was totally wrong,” said Professor Zernicka-Goetz.Story Source:The above story is based on materials provided by University of Cambridge. …

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

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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Birds of a different color: Three major genes set feather hue in pigeons

Scientists at the University of Utah identified mutations in three key genes that determine feather color in domestic rock pigeons. The same genes control pigmentation of human skin.”Mutations in these genes can be responsible for skin diseases and conditions such as melanoma and albinism,” says Michael Shapiro, associate professor of biology and senior author of the study published online Feb. 6 in the journal Current Biology.”In humans, mutations of these genes often are considered ‘bad’ because they can cause albinism or make cells more susceptible to UV (ultraviolet sunlight) damage and melanoma because the protective pigment is absent or low,” says Eric Domyan, a biology postdoctoral fellow and first author of the study. “In pigeons, mutations of these same genes cause different feather colors, and to pigeon hobbyists that is a very good thing.”Pigeon breeders have drawn on their centuries-long experience to produce about 350 distinct pigeon breeds, focusing particularly on beak shape, plumage color and feather ornaments on the head, feet, beaks and elsewhere. But until this study, the specific mutations that control color in rock pigeons (Columba livia) were unknown.”Across all pigeon breeds, mutations in three major genes explain a huge amount of color variation,” Shapiro says.Various forms of a gene named Tyrp1 make pigeons either blue-black (the grayish color of common city pigeons), red or brown. Mutations of a second gene, named Sox10, makes pigeons red no matter what the first gene does. And different forms of a third gene, named Slc45a2, make the pigeons’ colors either intense or washed out.The scientists discovered how pigeons’ feather color is determined by different versions of these three genes — known as variants or alleles — and by what are called “epistatic” interactions, in which one gene obscures the effects of other genes.”Our work provides new insights about how mutations in these genes affect their functions and how the genes work together,” Shapiro says. “Many traits in animals, including susceptibility to diseases such as cancer, are controlled by more than one gene. To understand how these genes work together to produce a trait, we often have to move beyond studies of humans. It’s difficult to study interactions among the genes in people.””Both Tyrp1 and Sox10 are potential targets for treatment of melanoma,” he adds. …

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Mood-stabilizing drug could treat inherited liver disease, study shows

Opening up a can of worms is a good way to start hunting for new drugs, recommend researchers from Children’s Hospital of Pittsburgh of UPMC and the University of Pittsburgh School of Medicine. In a study published today in the Public Library of Science One, they used a primitive worm model to show that a drug typically used to treat agitation in schizophrenia and dementia has potential as a treatment for ╬▒-1 antitrypsin (AT) deficiency, an inherited disease that causes severe liver scarring.In the classic form of AT deficiency, which affects 1 in 3,000 live births, a gene mutation leads to production of an abnormal protein, dubbed ATZ, that unlike its normal counterpart is prone to clumping, explained David H. Perlmutter, M.D., physician-in-chief and scientific director, Children’s Hospital, and Distinguished Professor and Vira I. Heinz Endowed Chair, Department of Pediatrics, Pitt School of Medicine.”These protein aggregates accumulate in liver cells and eventually lead to scarring of the organ or to tumor formation,” Dr. Perlmutter said. “If we could find a drug that slows or stops this process, we might be able to prevent the need for liver transplantation in these patients.”To find that drug, Dr. Perlmutter’s team worked with Pitt’s Stephen Pak, Ph.D., assistant professor of pediatrics, and Gary Silverman, M.D., Ph.D., Twenty-five Club Professor of Pediatrics, Cell Biology and Physiology, who developed a model of AT deficiency in Caenorhabditis elegans, or C. elegans, a harmless microscopic worm or nematode typically found in soil. Previous experiments conducted by Drs. Pak and Silverman, in which more than 2,000 compounds were screened, showed that fluphenazine, a drug approved for human use as a mood stabilizer, could reduce ATZ accumulation in the worm, so the team studied it further.Worms that produce ATZ die sooner than normal ones, which typically have a life span of fewer than 20 days. …

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