Genes increase the stress of social disadvantage for some children

Genes amplify the stress of harsh environments for some children, and magnify the advantage of supportive environments for other children, according to a study that’s one of the first to document how genes interacting with social environments affect biomarkers of stress.”Our findings suggest that an individual’s genetic architecture moderates the magnitude of the response to external stimuli — but it is the environment that determines the direction” says Colter Mitchell, lead author of the paper and a researcher at the University of Michigan Institute for Social Research (ISR).The study, published today in the Proceedings of the National Academy of Sciences, uses telomere length as a marker of stress. Found at the ends of chromosomes, telomeres generally shorten with age, and when individuals are exposed to disease and chronic stress, including the stress of living in a disadvantaged environment.For the study, Mitchell and colleagues used telomere samples from a group of 40 nine-year-old boys from two very different environments – one nurturing and the other harsh. Those in the nurturing environment came from stable families, with nurturing parenting, good maternal mental health, and positive socioeconomic conditions, while those in the harsh environment experienced high levels of poverty, harsh parenting, poor maternal mental health, and high family instability.For those children with heightened sensitivity in the serotonergic and dopaminergic genetic pathways compared to other children, telomere length was shortest in a disadvantaged environment, and longest in a supportive environment.Story Source:The above story is based on materials provided by University of Michigan. Note: Materials may be edited for content and length.

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First peanut genome sequenced

The International Peanut Genome Initiative — a group of multinational crop geneticists who have been working in tandem for the last several years — has successfully sequenced the peanut’s genome.Scott Jackson, director of the University of Georgia Center for Applied Genetic Technologies in the College of Agricultural and Environmental Sciences, serves as chair of the International Peanut Genome Initiative, or IPGI.The new peanut genome sequence will be available to researchers and plant breeders across the globe to aid in the breeding of more productive and more resilient peanut varieties.Peanut, known scientifically as Arachis hypogaea and also called groundnut, is important both commercially and nutritionally. While the oil- and protein-rich legume is seen as a cash crop in the developed world, it remains a valuable sustenance crop in developing nations.”The peanut crop is important in the United States, but it’s very important for developing nations as well,” Jackson said. “In many areas, it is a primary calorie source for families and a cash crop for farmers.”Globally, farmers tend about 24 million hectares of peanuts each year and produce about 40 million metric tons.”Improving peanut varieties to be more drought-, insect- and disease-resistant can help farmers in developed nations produce more peanuts with fewer pesticides and other chemicals and help farmers in developing nations feed their families and build more secure livelihoods,” said plant geneticist Rajeev Varshney of the International Crops Research Institute for Semi-Arid Tropics in India, who serves on the IPGI.The effort to sequence the peanut genome has been underway for several years. While peanuts were successfully bred for intensive cultivation for thousands of years, relatively little was known about the legume’s genetic structure because of its complexity, according to Peggy Ozias-Akins, a plant geneticist on the UGA Tifton campus who also works with the IPGI and is director of the UGA Institute of Plant Breeding, Genetics and Genomics.”Until now, we’ve bred peanuts relatively blindly, as compared to other crops,” said IPGI plant geneticist David Bertioli of the Universidade de Braslia. “We’ve had less information to work with than we do with many crops, which have been more thoroughly researched and understood.”The peanut in fields today is the result of a natural cross between two wild species, Arachis duranensis and Arachis ipaensis, which occurred in north Argentina between 4,000 and 6,000 years ago. Because its ancestors were two different species, today’s peanut is a polyploid, meaning the species can carry two separate genomes, designated A and B subgenomes.To map the peanut’s structure, researchers sequenced the genomes of the two ancestral parents because together they represent the cultivated peanut. The sequences provide researchers access to 96 percent of all peanut genes in their genomic context, providing the molecular map needed to more quickly breed drought- and disease-resistant, lower-input and higher-yielding varieties of peanuts.The two ancestor wild species had been collected in nature, conserved in germplasm banks and then used by the IPGI to better understand the peanut genome. The genomes of the two ancestor species provide excellent models for the genome of the cultivated peanut. A. duranenis serves as a model for the A subgenome of the cultivated peanut while A. …

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Reducing E. coli in cows, improving food safety

A new biological treatment could help dairy cattle stave off uterine diseases and eventually may help improve food safety for humans, a University of Florida study shows.Kwang Cheol Jeong, an assistant professor in animal sciences and UF’s Emerging Pathogens Institute, examined cattle uterine illnesses because they can make cows infertile, lower milk production and because those maladies are often linked to bacteria, he said. The UF researchers did their experiments in labs and at the Dairy Unit on the Gainesville campus.Jeong and his research team infused chitosan microparticles ─ an antimicrobial material derived from dissolved shrimp shells ─ into diseased cow uteri. When bought in stores, chitosan can be used to treat many ailments from obesity to anemia. On its own, chitosan only works at acidic pH levels, Jeong said. For cattle, Jeong’s team developed chitosan microparticles, which work in acidic and neutral pH, because cattle uteri have a neutral pH.The study’s findings suggest chitosan microparticles kill bacteria in the uteri, he said. Jeong said it may someday be possible for chitosan microparticles to be used to help humans who have become ill from consuming E. coli-contaminated food, but more research is needed.Developing a new antimicrobial agent is critical to human and animal health, said Jeong, a member of UF’s Institute of Food and Agricultural Sciences.”Dangerous infections are diminishing the role of some antibiotics, making them less able to treat infections, as pathogens are developing resistance to the drugs,” he said, adding that about 23,000 people die in the U.S. annually because of exposure to pathogens that don’t respond to antibiotics.Once bacteria become resistant, whether on farms, hospitals or in the environment, they can infect humans, through water, food or contact with contaminated feces, Jeong said.Further, some antibiotics used to treat humans and animals kill good and bad bacteria. Scientists can use the UF study’s findings to begin to develop better drugs that target bad pathogens but leave beneficial bacteria, Jeong said.E. coli are everywhere, including the human gut, but can contaminate beef, unpasteurized milk, soft cheeses made from raw milk and raw fruits and vegetables that haven’t been washed properly.The most recent outbreak of meat-traced E. …

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Gene family that suppresses prostate cancer discovered

Cornell researchers report they have discovered direct genetic evidence that a family of genes, called MicroRNA-34 (miR-34), are bona fide tumor suppressors.The study is published in the journal Cell Reports, March 13.Previous research at Cornell and elsewhere has shown that another gene, called p53, acts to positively regulate miR-34. Mutations of p53 have been implicated in half of all cancers. Interestingly, miR-34 is also frequently silenced by mechanisms other than p53 in many cancers, including those with p53 mutations.The researchers showed in mice how interplay between genes p53 and miR-34 jointly inhibits another cancer-causing gene called MET. In absence of p53 and miR-34, MET overexpresses a receptor protein and promotes unregulated cell growth and metastasis.This is the first time this mechanism has been demonstrated in a mouse model, said Alexander Nikitin, a professor of pathology in Cornell’s Department of Biomedical Sciences and the paper’s senior author. Chieh-Yang Cheng, a graduate student in Nikitin’s lab, is the paper’s first author.In a 2011 Proceedings of the National Academy of Sciences paper, Nikitin and colleagues showed that p53 and miR-34 jointly regulate MET in cell culture but it remained unknown if the same mechanism works in a mouse model of cancer (a special strain of mice used to study human disease).The findings suggest that drug therapies that target and suppress MET could be especially successful in cancers where both p53 and miR-34 are deficient.The researchers used mice bred to develop prostate cancer, then inactivated the p53 gene by itself, or miR-34 by itself, or both together, but only in epithelium tissue of the prostate, as global silencing of these genes may have produced misleading results.When miR-34 genes alone were silenced in the mice, the mice developed cancer free. When p53 was silenced by itself, there were signs of precancerous lesions early in development, but no cancer by 15 months of age. When miR-34 and p53 genes were both silenced together, the researchers observed full prostate cancer in the mice.The findings revealed that “miR-34 can be a tumor-suppressor gene, but it has to work together with p53,” Nikitin said.In mice that had both miR-34 and p53 silenced concurrently, cancerous lesions formed in a proximal part of the prostrate ducts, in a compartment known to contain prostate stem cells. The early lesions that developed when p53 was silenced alone occurred in a distal part of the ducts, away from the compartment where the stem cell pool is located. This suggested there was another mechanism involved when p53 and miR-34 were jointly silenced.Also, the number of stem cells in mice with both p53 and miR-34 silenced increased substantially compared with control mice or mice with only miR-34 or p53 independently silenced.”These results indicated that together [miR-34 and p53] regulate the prostate stem cell compartments,” said Nikitin.This is significant, as cancer frequently develops when stem cells become unregulated and grow uncontrollably, he said.Researchers further found that p53 and miR-34 affect stem cell growth by regulating MET expression. In absence of p53 and miR-34, MET is overexpressed, which leads to uncontrolled growth of prostate stem cells and high levels of cancer in these mice.Future work will further examine the role of p53/miR-34/MET genes in stem cell growth and cancer. …

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Farm salmon pose clear reproductive threat to wild gene pools, researchers say

Findings published today reveal that, while farmed salmon are genetically different to their wild counterparts, they are just as fertile. This is important information because millions of farmed salmon escape into the wild — posing threats to wild gene pools.Lead Researcher Prof Matt Gage from UEA’s school of Biological Sciences said: “Around 95 per cent of all salmon in existence are farmed, and domestication has made them very different to wild populations, each of which is locally adapted to its own river system.”Farmed salmon grow very fast, are aggressive, and not as clever as wild salmon when it comes to dealing with predators. These domestic traits are good for producing fish for the table, but not for the stability of wild populations.”The problem is that farmed salmon can escape each year in their millions, getting into wild spawning populations, where they can then reproduce and erode wild gene pools, introducing these negative traits.”We know that recently-escaped farmed salmon are inferior to wild fish in reproduction, but we do not have detailed information on sperm and egg performance, which could have been affected by domestication. Our work shows that farm fish are as potent at the gamete level as wild fish, and if farm escapes can revive their spawning behaviour by a period in the wild, clearly pose a significant threat of hybridisation with wild populations.”Researchers used a range of in vitro fertilization tests in conditions that mimicked spawning in the natural environment, including tests of sperm competitiveness and egg compatibility. All tests on sperm and egg form and function showed that farmed salmon are as fertile as wild salmon — identifying a clear threat of farmed salmon reproducing with wild fish.”Some Norwegian rivers have recorded big numbers of farmed fish present — as much as 50 per cent. Both anglers and conservationists are worried by farmed fish escapees which could disrupt locally adapted traits like timing of return, adult body size, and disease resistance.”Salmon farming is a huge business in the UK, Norway and beyond, and while it does reduce the pressure on wild fish stocks, it can also create its own environmental pressures through genetic disruption.”A viable solution is to induce ‘triploidy’ by pressure-treating salmon eggs just after fertilisation — where the fish grows as normal, but with both sex chromosomes; this is normal for farming rainbow trout. The resulting adult develops testes and ovaries but both are much reduced and most triploids are sterile. These triploid fish can’t reproduce if they escape, but the aquaculture industry has not embraced this technology yet because of fears that triploids don’t perform as well in farms as normal diploid fish, eroding profits.”Story Source:The above story is based on materials provided by University of East Anglia. Note: Materials may be edited for content and length.

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How gut bacteria communicate within our bodies, build special relationship

Communication is vital to any successful relationship. Researchers from the Institute of Food Research and the University of East Anglia have discovered how the beneficial bacteria in our guts communicate with our own cells.This is a key step in understanding how our bodies maintain a close relationship with the population of gut bacteria that plays crucial roles in maintaining our health, fighting infection and digesting our food.A study, published in the journal Cell Reports, shows that the gut bacteria produce an enzyme that modifies signalling in cells lining the gut. The enzyme also has another role in breaking down food components.”Our study provides a breakthrough in understanding how bacteria communicate across different kingdoms to influence our own cells’ behavior, as well as how we digest our food,” said Dr Regis Stentz from the IFR, which is strategically funded by the Biotechnology and Biological Sciences Research Council.We all rely on trillions of bacteria in our gut to break down certain components of our diet. One example is phytate, the form phosphorus takes in cereals and vegetables. Broken down phytate is a source of vital nutrients, but in its undigested form it has detrimental properties. It binds to important minerals preventing them being taken up by the body, causing conditions like anemia, especially in developing countries. Phytate also leads to excess phosphorus leaching into the soil from farm animal waste, and feed supplements are used to minimize this.But despite the importance of phytate, we know very little about how it is broken down in our gut. To address this Dr Stentz and colleagues screened the genomes of hundreds of different species of gut bacteria. They found, in one of the most prominent gut bacteria species, an enzyme able to break down phytate. In collaboration with Norwich Research Park colleagues at the University of East Anglia, they crystallized this enzyme and solved its 3D structure. …

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How evolution shapes the geometries of life

Why does a mouse’s heart beat about the same number of times in its lifetime as an elephant’s, although the mouse lives about a year, while an elephant sees 70 winters come and go? Why do small plants and animals mature faster than large ones? Why has nature chosen such radically different forms as the loose-limbed beauty of a flowering tree and the fearful symmetry of a tiger?These questions have puzzled life scientists since ancient times. Now an interdisciplinary team of researchers from the University of Maryland and the University of Padua in Italy propose a thought-provoking answer based on a famous mathematical formula that has been accepted as true for generations, but never fully understood. In a paper published the week of Feb. 17, 2014 in the Proceedings of the National Academy of Sciences, the team offers a re-thinking of the formula known as Kleiber’s Law. Seeing this formula as a mathematical expression of an evolutionary fact, the team suggests that plants’ and animals’ widely different forms evolved in parallel, as ideal ways to solve the problem of how to use energy efficiently.If you studied biology in high school or college, odds are you memorized Kleiber’s Law: metabolism equals mass to the three-quarter power. This formula, one of the few widely held tenets in biology, shows that as living things get larger, their metabolisms and their life spans increase at predictable rates. Named after the Swiss biologist Max Kleiber who formulated it in the 1930s, the law fits observations on everything from animals’ energy intake to the number of young they bear. It’s used to calculate the correct human dosage of a medicine tested on mice, among many other things.But why does Kleiber’s Law hold true? …

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Why white dots appear larger than equal size black dots: How Galileo’s visual illusion works in the mind’s eye

Scientists have studied a visual illusion first discovered by Galileo Galilei, and found that it occurs because of the surprising way our eyes see lightness and darkness in the world. Their results advance our understanding of how our brains are wired for seeing white versus black objects.The work was done by Jens Kremkow and collaborators in the laboratories of Jose Manuel Alonso and Qasim Zaidi at the State University of New York College of Optometry. It will be published on February 10 of 2014 in the Proceedings of the National Academy of Sciences.Galileo was puzzled by the fact that the appearance of the planets depended on whether one looked with the naked eye or with a telescope. Viewed directly, planets seemed “expanded” and had “a radiant crown,” which made Venus looked eight to ten times larger than Jupiter even though Jupiter was four times larger. Though Galileo realized this size illusion was not created by the object — but by his eyes — he did not understand why or how.He mused, “Either because their light is refracted in the moisture that covers the pupil, or because it is reflected from the edges of the eyelids and these reflected rays are diffused over the pupil, or for some other reason.” Generations of scientists following Galileo continued to assume the illusion was caused by blur or similar optical effects. However, though blur can distort size, it does not explain why Venus looks larger than Jupiter with the naked eye. Hermann von Helmholtz — the venerable 19th Century German physician-physicist — was the first to realize that something else was needed to explain the illusion, as he described in his Treatise on Physiological Optics.Only now, with Kremkow and colleagues’ new study, has science finally zoomed in and illuminated the scope of the problem. It’s a feature of how we see everything, no less. By examining the responses of neurons in the visual system of the brain — to both light stimuli and dark stimuli — the neuroscientists discovered that, whereas dark stimuli result in a faithful neural response that accurately represents their size, light stimuli on the contrary result in non-linear and exaggerated responses that make the stimulus look larger. So white spots on a black background look bigger than same-sized black spots on white background, and Galileo’s glowing stellar objects are not really as big as they might appear to the unaided eye.This effect is responsible for how we see everything from textures and faces — based on their dark parts in bright daylight — to why it is easier to read this very page with black-on-white lettering, rather than white-on-black (a well known, and until now, unexplained phenomenon). …

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New live-cell printing technology works like ancient Chinese woodblocking

HOUSTON — ( Feb. 6, 2014 ) — With a nod to 3rd century Chinese woodblock printing and children’s rubber stamp toys, researchers in Houston have developed a way to print living cells onto any surface, in virtually any shape. Unlike recent, similar work using inkjet printing approaches, almost all cells survive the process, scientists report in this week’s Proceedings of the National Academy of Sciences.The researchers, led by Houston Methodist Research Institute nanomedicine faculty member Lidong Qin, Ph.D., say their approach produces 2-D cell arrays in as little as half an hour, prints the cells as close together as 5 micrometers (most animal cells are 10 to 30 micrometers wide), and allows the use of many different cell types. They’ve named the technology Block-Cell-Printing, or BloC-Printing.”We feel the current technologies are inadequate,” Qin said. “Inkjet-based cell printing leaves many of the cells damaged or dead. We wanted to see if we could invent a tool that helps researchers obtain arrays of cells that are alive and still have full activity.”Recent work to print cells in two and three dimensions using electricity-gated inkjet technology have been largely successful, but sometimes only half of the printed cells survive the printing process — a source of frustration for many laboratory scientists.”Cell printing is used in so many different ways now — for drug development and in studies of tissue regeneration, cell function, and cell-cell communication,” Qin said. “Such things can only be done when cells are alive and active. A survival rate of 50 to 80 percent is typical as cells exit the inkjet nozzles. By comparison, we are seeing close to 100 percent of cells in BloC-Printing survive the printing process.”BloC-Printing manipulates microfluidic physics to guide living cells into hook-like traps in the silicone mold. Cells flow down a column in the mold, past trapped cells to the next available slot, eventually creating a line of cells (in a grid of such lines). …

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Peaches can be profitable in three years: Researcher to growers

Florida peach growers, some of whom are looking for an alternative to citrus as greening takes a toll on that crop, could see a small profit by their third year of operation, a UF researcher says.Greening, a disease first found in Florida in 2005, has led to $4 billion in lost revenue and industry-related jobs since 2006 for the $9 billion-a-year citrus industry.As some farmers turn to peaches, they want to know how long before they turn a profit and how long they can sustain that profit, said Mercy Olmstead, assistant professor in horticultural sciences at UF’s Institute of Food and Agricultural Sciences. Growers should see steady profit through years 10-12, when the tree starts to decline in the South.”This is good news,” she said. “It is typically seven years before you get a commercial crop on citrus and probably eight before you are profitable.”Olmstead co-wrote a paper that created four-year peach orchard budgets and growing operation plans with former UF doctoral student Kim Morgan, now an assistant professor in agriculture and applied economics at Virginia Tech.Florida peaches go to market earlier than others around the nation, giving growers here a leg up on national competition, Olmstead said.Growers invest about $11,600 in a peach orchard during the first two years before they see a profit, with a third-year income of about $10,150 per acre, with $8,342 in grower costs, for a profit of about $1,800, , she said.A 2011 Florida grower survey showed peaches grown on about 670 acres, according to the paper. Another 300 to 400 acres were added in 2012. Those acres are now producing about 4.5 million pounds per year, at an estimated value of $6 million, the paper says.While an assistant professor at Mississippi State University, Morgan interviewed 26 of the estimated 40 Florida peach growers and then created four-year budgets and operation plans for the growers. The growers had varying amounts of experience, from just having established an orchard to five or more years’ experience, Olmstead said.The budget plans included prices of pest sprays, tree costs, fuel, repairs and more. Morgan presented her paper last summer at the Proceedings of the Florida State Horticultural Society, and it is online at society’s website, http://www.fcla.edu/fshs.Story Source:The above story is based on materials provided by University of Florida Institute of Food and Agricultural Sciences. Note: Materials may be edited for content and length.

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Brain connections underlying accurate introspection revealed

Oct. 16, 2013 — The human mind is not only capable of cognition and registering experiences but also of being introspectively aware of these processes. Until now, scientists have not known if such introspection was a single skill or dependent on the object of reflection. Also unclear was whether the brain housed a single system for reflecting on experience or required multiple systems to support different types of introspection.A new study by UC Santa Barbara graduate student Benjamin Baird and colleagues suggest that the ability to accurately reflect on perceptual experience and the ability to accurately reflect on memories were uncorrelated, suggesting that they are distinct introspective skills. The findings appear in the Journal of Neuroscience.The researchers used classic perceptual decision and memory retrieval tasks in tandem with functional magnetic resonance imaging to determine connectivity to regions in the front tip of the brain, commonly referred to as the anterior prefrontal cortex. The study tested a person’s ability to reflect on his or her perception and memory and then examined how individual variation in each of these capacities was linked to the functional connections of the medial and lateral parts of the anterior prefrontal cortex.”Our results suggest that metacognitive or introspective ability may not be a single thing,” Baird said. “We actually find a behavioral dissociation between the two metacognitive abilities across people, which suggests that you can be good at reflecting on your memory but poor at reflecting on your perception, or vice versa.”The newly published research adds to the literature describing the role of the medial and lateral areas of the anterior prefrontal cortex in metacognition and suggests that specific subdivisions of this area may support specific types of introspection. The findings of Baird’s team demonstrate that the ability to accurately reflect on perception is associated with enhanced connectivity between the lateral region of the anterior prefrontal cortex and the anterior cingulate, a region involved in coding uncertainty and errors of performance.In contrast, the ability to accurately reflect on memory is linked to enhanced connectivity between the medial anterior prefrontal cortex and two areas of the brain: the precuneus and the lateral parietal cortex, regions prior work has shown to be involved in coding information pertaining to memories.The experiment assessed the metacognitive abilities of 60 participants at the Max Planck Institute for Human Cognitive and Brain Sciences in Leipzig, Germany, where Baird was a visiting researcher. The perceptual decision task consisted of visual displays with six circles of vertical alternating light and dark bars — called Gabor gratings — arranged around a focal point. Participants were asked to identify whether the first or second display featured one of the six areas with a slight tilt, not always an easy determination to make.A classic in psychology literature, the memory retrieval task consisted of two parts. …

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Hybrid cars are status symbol of sorts for seniors

Oct. 10, 2013 — Paying extra bucks to “go green” in a hybrid car may pay off in self-esteem and image for older drivers, as well as give a healthy boost to the environment, according to a Baylor University study.The finding is significant because some segments of the older-consumer population control a considerable share of the discretionary income in the United States, and the population size of the “mature market” is growing rapidly, researchers said.The study is published in the journal Human Factors and Ergonomics in Manufacturing and Service Industries.”If I want to pay $5 for a ‘green’ detergent or sponge, I’ll know that I’m helping the environment. But those things aren’t highly visible. Other people aren’t going to notice,” said Jay Yoo, Ph.D., an assistant professor of family and consumer sciences in Baylor’s College of Arts & Sciences.Researchers analyzed a national cross-sectional survey of 314 consumers age 60 and older who had bought hybrid cars. The study showed that their satisfaction was influenced by social values — including pride and prestige — as well as quality and price, not only in vehicle purchase but in future savings on gasoline expenses.Those three variables — social value, price and quality –are significant in enhancing senior citizens’ customer loyalty as shown by repurchase intention and positive word-of-mouth, Yoo said. Emotional values — such as excitement — did not significantly influence their purchase intention or satisfaction, according to the study.”The findings suggest that elderly consumers are concerned about how they appear to others when driving a hybrid car,” the researchers wrote. “They believe that driving a hybrid car builds a positive self-image of the people who drive them.””This knowledge can help as a marketing tool,” Yoo said. “Hybrid cars have increased in visibility because of their environmental consciousness. So people may be willing to pay an extra $5,000 or so in order to think, ‘I’m great, and this is good for the environment.'”Previous research has shown that older consumers are more inclined to behave in a pro-environment way than younger generations are, Yoo said.

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Molecular structure reveals how HIV infects cells

Sep. 12, 2013 — In a long-awaited finding, a team of Chinese and US scientists has determined the high-resolution atomic structure of a cell-surface receptor that most strains of HIV use to get into human immune cells. The researchers also showed where maraviroc, an HIV drug, attaches to cells and blocks HIV’s entry.”These structural details should help us understand more precisely how HIV infects cells, and how we can do better at blocking that process with next-generation drugs,” said Beili Wu, PhD, professor at the Shanghai Institute of Materia Medica (SIMM), Chinese Academy of Sciences. Wu was the senior investigator for the study, which was published in Science Express on September 12, 2013.The study, which focused on the CCR5 receptor, was supported by both US and Chinese research funding agencies. “International collaborations like this one are increasingly needed to solve big problems in science,” said study co-author Raymond C. Stevens, PhD, a professor at The Scripps Research Institute (TSRI) in California. “Now that we have both human CXCR4 and CCR5 HIV co-receptor three-dimensional structures, it is likely we will see the next generation of HIV therapeutics.”A Major TargetThe CCR5 receptor is one of the most sought-after targets for new anti-HIV drugs. Although the AIDS-causing virus was initially discovered to infect cells via another receptor, CD4, researchers found in 1996 that HIV infection also requires a co-receptor — usually CCR5, which sits alongside CD4 on a variety of immune cells.CCR5’s importance to HIV infection is underscored by the fact that certain genetic variants of it can dramatically raise or lower HIV infection risk, as well as the speed of the disease process after infection. One shortened CCR5 variant, found in about 10 percent of Europeans, is not expressed at all on immune cell surfaces — and people who produce only this variant are almost invulnerable to HIV infection.Scientists therefore have sought to develop anti-HIV drugs that block the virus from binding to CCR5 or otherwise render the receptor inactive. Yet only a handful of CCR5-inhibiting compounds have been developed so far — and no one knows exactly how they work. …

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Radiotherapy in girls and the risk of breast cancer later in life

Sep. 11, 2013 — Exposing young women and girls under the age of 20 to ionizing radiation can substantially raise the risk of their developing breast cancer later in life. Scientists may now know why. A collaborative study, in which Berkeley Lab researchers played a pivotal role, points to increased stem cell self-renewal and subsequent mammary stem cell enrichment as the culprits. Breasts enriched with mammary stem cells as a result of ionizing irradiation during puberty show a later-in-life propensity for developing ER negative tumors — cells that do not have the estrogen receptor. Estrogen receptors — proteins activated by the estrogen hormone — are critical to the normal development of the breast and other female sexual characteristics during puberty.”Our results are in agreement with epidemiology studies showing that radiation-induced human breast cancers are more likely to be ER negative than are spontaneous breast cancers,” says Sylvain Costes, a biophysicist with Berkeley Lab’s Life Sciences Division. “This is important because ER negative breast cancers are less differentiated, more aggressive, and often have a poor prognosis compared to the other breast cancer subtypes.”Costes and Jonathan Tang, also with Berkeley Lab’s Life Sciences Division, were part of a collaboration led by Mary Helen Barcellos-Hoff, formerly with Berkeley Lab and now at the New York University School of Medicine, that investigated the so-called “window of susceptibility” known to exist between radiation treatments at puberty and breast cancer risk in later adulthood. The key to their success were two mammary lineage agent-based models (ABMs) they developed in which a system is modeled as a collection of autonomous decision-making entities called agents. One ABM simulated the effects of radiation on the mammary gland during either the developmental stages or during adulthood. The other simulated the growth dynamics of human mammary epithelial cells in culture after irradiation.”Our mammary gland ABM consisted of millions of agents, with each agent representing either a mammary stem cell, a progenitor cell or a differentiated cell in the breast,” says Tang. …

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Telemedicine initiative allows remote hearing tests for newborns

Sep. 5, 2013 — A telemedicine initiative in Vanderbilt’s Department of Hearing and Speech Sciences is working to make follow-up hearing tests for newborns more accessible in rural areas of Tennessee, while teaching young pediatric audiology and pediatric speech language pathology students to treat patients remotely.Approximately 50 percent of children who do not pass hearing screenings at birth are later “lost to follow-up,” said Anne Marie Tharpe, Ph.D., professor and chair of Hearing and Speech Sciences and associate director of the Vanderbilt Bill Wilkerson Center.Through a telemedicine initiative, Vanderbilt audiologists are conducting follow-up hearing tests on newborns whose families live in rural areas of Tennessee.Tharpe’s group teamed with the Tennessee Department of Health for a pilot project to set up a remote site in Union City, Tenn., that provides follow-up testing for newborns, with a Vanderbilt audiologist in Nashville on the other end of the connection, acting as the hub site.The technology allows the audiologist to take control of a remote computer during the testing and also interact with the family and technician as if they were standing side-by-side.“This allows the clinician at Vanderbilt to control the system at the remote site using some simple secure software. Additionally, video-conferencing equipment with high definition cameras is used to provide clear real-time communication between the caregiver and the clinician,” said Devin McCaslin, Ph.D., associate professor of Hearing and Speech Sciences.”Tharpe said one of the reasons these patients have been lost to follow-up is because families who live in rural areas have to miss work and drive into a city with a major medical center to do their follow-up testing.“If we can provide this easily, and closer to their homes, then our hope is that once a baby’s hearing loss is confirmed through our follow-up testing those families will seek intervention services for their child,” she said.The initiative is made possible in part by two training grants totaling $2.5 million from the U.S. Department of Education and additional support from the Maternal Child Health Bureau’s Leadership Education in Neurodevelopmental Disabilities (LEND) grant to the Department of Pediatrics.The training grant awarded to Tharpe is focused on providing training to graduate students who will work with deaf and hard-of-hearing children.“Professionals are starting to investigate the use of telepractice, especially in rehab areas like ours, but to my knowledge no one is looking at how we train students to provide remote services, and I think that is an important component. What are the safety and ethical considerations and how do they differ from providing face-to-face care?” Tharpe said.“We have to make extra effort to notify the patient of who is present in the room, even those they may not be able to see outside of the camera’s range, and to assure the patient that his or her information is secure and confidential, in the same way it is if the visit was on Vanderbilt’s campus.”The second $1.25 million grant, received by Lynn Hayes, Ph.D., associate professor of Hearing and Speech Sciences, will be used to train deaf educators in the Mama Lere Hearing School, a preschool and kindergarten program for children with hearing loss, and also in working with deaf education graduate students to provide remote consultation to teachers in rural areas across Tennessee.The goal at the Mama Lere Hearing School is to prepare the children for integration into general education classrooms in their home communities, Tharpe said. “Many of these communities are rural and a lot of the teachers where these students will be going may not have ever had a child who has hearing loss before,” she said.“This grant will help our graduate students learn to consult with outlying, rural, general education teachers and provide guidance in educating these children with hearing loss in their classrooms with normal hearing children.“These children are mainstreamed but they may still need special services. In some cases, we will be able to provide direct services via telepractice,” Tharpe said.

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Scientists discover new bat species in West Africa

Sep. 3, 2013 — An international team of scientists, including biologists from, the University of York, has discovered five new species of bats in West Africa.The team, which also included researchers from the Czech University of Life Sciences and the Academy of Sciences, Charles University in the Czech Republic, discovered a wealth of unexpected diversity among Vesper bats in Senegal.During seven expeditions to the Niokolo-Koba National Park in south-eastern Senegal, and subsequent genetic analysis, the scientists discovered that five species of bats looked similar to other populations in Africa, but differed significantly genetically from them.Taxonomists are now working on describing formally these new species — Vesper bats (Vespertilionidae) are already the largest family of bats with more than 400 known species. The research is published in Frontiers in Zoology.The researchers studied 213 vespertilionid bats from Senegal and identified ten species, five of which were significantly genetically different from their nominate species — Pipistrellus hesperidus, Nycticeinops schlieffenii, Scotoecus hirundo, Neoromicia nana and Neoromicia somalica.One of the research team, Nancy Irwin, of the Department of Biology at York, says: “The fact that these Senegalese bats are unrelated and are different to their cousins in other parts of Africa, suggests that West Africa may have been isolated in the past and formed a refugium, where populations gradually diverged and even acquired new chromosomal configurations.”This exciting finding confirms that West Africa may represent an underestimated bio-geographic hotspot with many more species to discover.”

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‘Mini human brains’ created: Scientists grow human brain tissue in 3-D culture system

Aug. 29, 2013 — Complex human brain tissue has been successfully developed in a three-dimensional culture system established in an Austrian laboratory. The method described in the current issue of Nature allows pluripotent stem cells to develop into cerebral organoids — or “mini brains” — that consist of several discrete brain regions.Instead of using so-called patterning growth factors to achieve this, scientists at the Institute of Molecular Biotechnology (IMBA) of the Austrian Academy of Sciences (OeAW) fine-tuned growth conditions and provided a conducive environment. As a result, intrinsic cues from the stem cells guided the development towards different interdependent brain tissues. Using the “mini brains,” the scientists were also able to model the development of a human neuronal disorder and identify its origin — opening up routes to long hoped-for model systems of the human brain.The development of the human brain remains one of the greatest mysteries in biology. Derived from a simple tissue, it develops into the most complex natural structure known to man. Studies of the human brain’s development and associated human disorders are extremely difficult, as no scientist has thus far successfully established a three-dimensional culture model of the developing brain as a whole. Now, a research group lead by Dr. Jürgen Knoblich at the Institute of Molecular Biotechnology of the Austrian Academy of Sciences (IMBA) has just changed that.Brain Size MattersStarting with established human embryonic stem cell lines and induced pluripotent stem (iPS) cells, the group identified growth conditions that aided the differentiation of the stem cells into several brain tissues. While using media for neuronal induction and differentiation, the group was able to avoid the use of patterning growth factor conditions, which are usually applied in order to generate specific cell identities from stem cells. …

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How untying knots promotes cancer

Aug. 20, 2013 — Researchers have long known that high levels of a specific protein in human cells are linked to tumor growth — but no one has fully understood how.Now, a groundbreaking discovery by UC Davis graduate student Kateryna Feoktistova and Assistant Professor Christopher Fraser illuminates the way that the protein, eukaryotic initiation factor 4E (eIF4E), acts upon cancer-promoting messenger RNA molecules. When translated, this type of mRNA can trigger the runaway cell replication that results in malignancies.Published in the August 13 edition of the Proceedings of the National Academy of Sciences, the results solve a decades-long scientific mystery and may lead to new, highly specific cancer treatments that will act only on growth-promoting cells as opposed to all cells.”This protein is one the most important initiation factors in this cellular pathway, and there is a lot of energy in the cell that goes into regulating the level and availability of it,” Fraser said. “To suddenly find this function is quite a transformative idea in the field; people can now try and study this new activity and its relation to growth-promotion and cancer.”With elevated eIF4E levels found in 30 percent of all major cancers, the protein is already a target of pharmaceutical research. Clinical trials are currently underway for drugs that act upon eIF4E’s long-known function of binding the cap at the head of all mRNA.But the protein’s cap-binding activity doesn’t fully explain its relationship to cancer.Feoktistova and Fraser solved that mystery while studying a region at the head of mRNA strands, where many cancer-promoting mRNA are much more complex than typical mRNA. In the cancer-promoting variants, a highly knotted region at the start of the strand must be unwound before a ribosome can bind and begin translating the genetic code into the amino acids that build our cellular proteins.Usually that knotted region prevents most of the ribosomes from starting the process, so cancer-promoting mRNAs aren’t translated effectively. But when high levels of eIF4E are present the 4E binds to a complex that activates another protein, 4A, which then is able to unwind the knot and translate the genetic code into proteins that can trigger tumor growth.The man who originally discovered eIF4E in 1978, Professor Nahum Sonenberg of McGill University, expressed his enthusiasm for what he calls “logical, beautiful” research.”This is really a big discovery — it explains a lot of the biology that we have. At the beginning of my talks I used to emphasize that mRNAs are eIF4E-sensitive, but people would ask ‘how does it work?’ and I never had an answer,” Sonenberg said. “In the last month, I have been able to mention Chris Fraser’s paper and finally provide an explanation.”It has made my life much easier,” he joked.Feoktistova, a fifth-year Ph.D. student who also got her undergraduate degree at UC Davis, made the breakthrough when she purified the individual components of eIF4E’s larger protein complex and then observed the complex’s activity with individual parts missing. …

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Copper identified as culprit in Alzheimer’s disease

Aug. 19, 2013 — Copper appears to be one of the main environmental factors that trigger the onset and enhance the progression of Alzheimer’s disease by preventing the clearance and accelerating the accumulation of toxic proteins in the brain.That is the conclusion of a study appearing today in the journal Proceedings of the National Academy of Sciences.”It is clear that, over time, copper’s cumulative effect is to impair the systems by which amyloid beta is removed from the brain,” said Rashid Deane, Ph.D., a research professor in the University of Rochester Medical Center (URMC) Department of Neurosurgery, member of the Center for Translational Neuromedicine, and the lead author of the study. “This impairment is one of the key factors that cause the protein to accumulate in the brain and form the plaques that are the hallmark of Alzheimer’s disease.”Copper’s presence in the food supply is ubiquitous. It is found in drinking water carried by copper pipes, nutritional supplements, and in certain foods such as red meats, shellfish, nuts, and many fruits and vegetables. The mineral plays an important and beneficial role in nerve conduction, bone growth, the formation of connective tissue, and hormone secretion.However, the new study shows that copper can also accumulate in the brain and cause the blood brain barrier — the system that controls what enters and exits the brain — to break down, resulting in the toxic accumulation of the protein amyloid beta, a by-product of cellular activity. Using both mice and human brain cells Deane and his colleagues conducted a series of experiments that have pinpointed the molecular mechanisms by which copper accelerates the pathology of Alzheimer’s disease.Under normal circumstances, amyloid beta is removed from the brain by a protein called lipoprotein receptor-related protein 1 (LRP1). These proteins — which line the capillaries that supply the brain with blood — bind with the amyloid beta found in the brain tissue and escort them into the blood vessels where they are removed from the brain.The research team”dosed” normal mice with copper over a three month period. The exposure consisted of trace amounts of the metal in drinking water and was one-tenth of the water quality standards for copper established by the Environmental Protection Agency.”These are very low levels of copper, equivalent to what people would consume in a normal diet.” said Deane.The researchers found that the copper made its way into the blood system and accumulated in the vessels that feed blood to the brain, specifically in the cellular “walls” of the capillaries. These cells are a critical part of the brain’s defense system and help regulate the passage of molecules to and from brain tissue. In this instance, the capillary cells prevent the copper from entering the brain. …

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Breaking up the superbugs’ party

Aug. 13, 2013 — The fight against antibiotic-resistant superbugs has taken a step forward thanks to a new discovery by scientists at The University of Nottingham.A multi-disciplinary research team at the University’s Centre for Biomolecular Sciences has uncovered a new way of inhibiting the toxicity and virulence of the notorious superbug, Pseudomonas aeruginosa.This bacteria produces an armoury of virulence factors and is resistant to many conventional antibiotics. It is almost impossible to eradicate P. aeruginosa from the lungs of people with cystic fibrosis and is therefore a leading cause of death among sufferers. The bug also causes a wide range of infections particularly among hospital patients.The new discovery concerns the bacterial cells’ ability to ‘talk’ to each other by producing and sensing small chemical signal molecules. This is called ‘quorum sensing’ (QS) and enables a population of individual bacteria to act socially rather than as individuals. QS allows a population of bacteria to assess their numerical strength and make a decision only when the population is ‘quorate’.The mechanism through which QS signals work is by activating gene expression upon interaction of a QS signal molecule with a receptor protein. In many disease-causing bacteria, QS controls genes which are essential for infection. These genes code for virulence factors such as toxins which cause damage to host tissues and the immune system. Interfering with the QS signalling process blocks bacterial virulence and renders bacteria unable to cause infection. …

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