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Archive - May 2013

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May 20th

Scientists Chart Astounding Impact of Insulin on Cells

Australian scientists have charted the path of insulin action in cells in precise detail like never before. This provides a comprehensive blueprint for understanding what goes wrong in diabetes. The breakthrough study, conducted by Ph.D. student Sean Humphrey and Professor David James from Sydney’s Garvan Institute of Medical Research, was published online on May 16, 2013 in Cell Metabolism. First discovered in 1921, the insulin hormone plays a very important role in the body because it helps us lower blood sugar after a meal, by enabling the movement of sugar from the blood into cells. Until now, although scientists have understood the purpose of insulin at a broad level, they have struggled to understand exactly how it achieves its task. Sophisticted analytical devices called mass spectrometers now provide the tool that has been missing – the means of looking into the vastly complex molecular maze that exists in every single cell in the human body. These powerful devices have opened up a field known as ‘proteomics,’ the study of proteins on a very large scale. Proteins represent the working parts of cells, using energy to perform essential functions such as muscle contraction, heartbeat, or even memory. Each cell houses multiple copies of between 10,000 and 12,000 protein types, which communicate with each other using various methods, the most common of which is a process known as ‘phosphorylation.’ Phosphate molecules are deliberately added to proteins in order to convey information, or else change the protein’s function. Each of the protein types in a cell has up to 20 potential ‘phosphorylation sites,’ regions to which a phosphate molecule can be added. This pushes the total number of possible cell states from one moment to the next into the billions.

May 20th

Meat Adulteration Worldwide--"Zone in with Zon"

Dr. Gerald Zon’s latest blog post in “Zone in with Zon—What’s Trending in Nucleic Acid Research,” (http://zon.trilinkbiotech.com/) was posted on May 20, 2013. It features Dr. Zon’s analysis of meat and fish adulteration around the world, based on DNA analyses. Dr. Zon takes the reader on a sobering gastronomical journey from horsemeat to sushi to game meat to rats disguised as mutton in this DNA-based discussion. Dr. Zon is an eminent nucleic acid chemist and Director of Business Development at TriLink BioTechnologies in San Diego, California. [Zon blog post]

Apigenin in Mediterranean Diet Appears to Make Cancer Cells Mortal

New research suggests that a compound abundant in the Mediterranean diet takes away cancer cells' "superpower" to escape death. By altering a very specific step in gene regulation, this compound essentially re-educates cancer cells into normal cells that die as scheduled. One way that cancer cells thrive is by inhibiting a process that would cause them to die on a regular cycle that is subject to strict programming. This study in cells, led by Ohio State University researchers, found that a compound in certain plant-based foods, called apigenin, could stop breast cancer cells from inhibiting their own death. Much of what is known about the health benefits of nutrients is based on epidemiological studies that show strong positive relationships between eating specific foods and better health outcomes, especially reduced heart disease. But how the actual molecules within these healthful foods work in the body is still a mystery in many cases, and particularly with foods linked to lower risk for cancer. Parsley, celery, and chamomile tea are the most common sources of apigenin, but it is found in many fruits and vegetables. The researchers also showed in this work that apigenin binds with an estimated 160 proteins in the human body, suggesting that other nutrients linked to health benefits – called "nutraceuticals" – might have similar far-reaching effects. In contrast, most pharmaceutical drugs target a single molecule. "We know we need to eat healthfully, but in most cases we don't know the actual mechanistic reasons for why we need to do that," said Dr. Andrea Doseff, associate professor of internal medicine and molecular genetics at Ohio State and a co-lead author of the study. "We see here that the beneficial effect on health is attributed to this dietary nutrient affecting many proteins.

Gene Involved in Neurodegeneration Keeps Clock Running

Northwestern University scientists have shown that a gene involved in neurodegenerative disease also plays a critical role in the proper function of the circadian clock. In a study of the common fruit fly, the researchers found the gene, called Ataxin-2, keeps the clock responsible for sleeping and waking on a 24-hour rhythm. Without the gene, the rhythm of the fruit fly's sleep-wake cycle is disturbed, making waking up on a regular schedule difficult for the fly. The discovery is particularly interesting because mutations in the human Ataxin-2 gene are known to cause a rare disorder called spinocerebellar ataxia (SCA) and also contribute to amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig's disease. People with SCA suffer from sleep abnormalities before other symptoms of the disease appear. This study linking the Ataxin-2 gene with abnormalities in the sleep-wake cycle could help pinpoint what is causing these neurodegenerative diseases as well as provide a deeper understanding of the human sleep-wake cycle. The findings were published online on May 17. 2013 in Science. Ravi Allada, M.D., professor of neurobiology in Northwestern’s Weinberg College of Arts and Sciences, and Dr. Chunghun Lim, a postdoctoral fellow in his lab, are authors of the paper. Period (per) is a well-studied gene in fruit flies that encodes a protein, called PER, which regulates circadian rhythm. Drs. Allada and Lim discovered that Ataxin-2 helps activate translation of PER RNA into PER protein, a key step in making the circadian clock run properly. "It's possible that Ataxin-2's function as an activator of protein translation may be central to understanding how, when you mutate the gene and disrupt its function, it may be causing or contributing to diseases such as ALS or spinocerebellar ataxia," Dr. Allada said.

May 17th

Personalized Medicine Conference Will Focus on Next-Gen Sequencing for Targeted Therapeutics

The sixth annual Personalized Medicine Conference (6.0) organized by San Francisco State University will focus on the amazing technological challenges and advances of “next-generation sequencing,” examining the very latest approaches and how they are leading to profound changes in our understanding of basic biological questions and to more efficacious and cost-effective therapies. The conference is entitled, “Next-Generation Sequencing for Targeted Therapeutics.” Featured speakers include Kimberly J. Popovits, Chairman of the Board, Chief Executive Officer & President of Genomic Health; Dr. Mark Sliwkowski, Distinguished Staff Scientist at Genentech; Professor Atul Butte of Stanford University; and Dr. Carl Borrebaeck, Professor & Chair of Immunotechnology and Director of CREATE Health at Lund University in Sweden. The conference will take place at the South San Francisco Conference Center (http://www.ssfconf.com/directions-top) from 8:00 am to 5:30 pm on Thursday, May 30, 2013, with a reception to follow. Those wishing to attend are urged to register as soon as possible (http://personalizedmedicine.sfsu.edu/register.html). For additional information, to help sponsor the event, or to inquire about special academic rates, contact dnamed@sfsu.edu. The conference organizers, including Michael Goldman, Ph.D., Professor and Chair of San Francisco State’s Department of Biology, noted that with the price of sequencing a complete human genome falling into the $1,000 range, stunning advances are sure to come over the next few years. It is likely that a detailed genome sequence will soon be part of a routine medical history, allowing unprecedented precision in diagnosis and treatment. The DNA and RNA signatures of both complex, common diseases and rare, elusive conditions will yield their secrets.

May 17th

Genome of Tibetan Antelope Illuminates High-Altitude Adaptation

Why can Tibetan antelope live at elevations of 4,000-5,000m on the Qinghai-Tibetan Plateau? In a collaborative research effort published online in an open-access article on May 14, 2013 in Nature Communications, investigators from Qinghai University, BGI, and other institutes present the draft genome sequence of the Tibetan antelope and provide evidence that some genetic factors may be associated with the species' adaption to harsh highland environments. The data in this work will also provide implications for studying specific genetic mechanisms and the biology of other ruminant species. The Tibetan antelope (Pantholops hodgsonii) is a native of the high mountain steppes and semi-desert areas of the Tibetan plateau. Interestingly, it is the only member of the genus Pantholops. Tibetan antelope is a medium-sized antelope with unique adaptations to survive in the harsh high-altitude climate. For non-native mammals such as humans, they may experience life-threatening acute mountain sickness when visiting high-altitude regions. In this study, researchers suggest that Tibetan antelopes must have evolved exceptional mechanisms to adapt to this extremely inhospitable habitat. Using next-gen sequencing technology, they have decoded the genome of theTibetan antelope and studied the underlying genetic mechanism of high-altitude adaptations. Through the comparison between Tibetan antelope and other plain-dwelling mammals, researchers found the Tibetan antelope had the signals of adaptive evolution and gene-family expansion in genes associated with energy metabolism and oxygen transmission, indicating that gene categories involved in energy metabolism appear to have an important role for Tibetan antelope via efficiently providing energy in conditions of low partial pressure of oxygen (pO2).

May 15th

Brain Rewires Itself after Damage or Injury

When the brain's primary "learning center" is damaged, complex new neural circuits arise to compensate for the lost function, say life scientists from UCLA and Australia who have pinpointed the regions of the brain involved in creating those alternate pathways — often far from the damaged site. The research, conducted by UCLA's Dr. Michael Fanselow and Moriel Zelikowsky in collaboration with Dr. Bryce Vissel, a group leader of the neuroscience research program at Sydney's Garvan Institute of Medical Research, was published online on May 15, 2013 in PNAS. The researchers found that parts of the prefrontal cortex take over when the hippocampus, the brain's key center of learning and memory formation, is disabled. Their breakthrough discovery, the first demonstration of such neural-circuit plasticity, could potentially help scientists develop new treatments for Alzheimer's disease, stroke, and other conditions involving damage to the brain. For the study, Dr. Fanselow and Ms. Zelikowsky conducted laboratory experiments with rats showing that the rodents were able to learn new tasks even after damage to the hippocampus. While the rats needed more training than they would have normally, they nonetheless learned from their experiences — a surprising finding. "I expect that the brain probably has to be trained through experience," said Dr. Fanselow, a professor of psychology and member of the UCLA Brain Research Institute, who was the study's senior author. "In this case, we gave animals a problem to solve." After discovering the rats could, in fact, learn to solve problems, Zelikowsky, a graduate student in Fanselow's laboratory, traveled to Australia, where she worked with Dr. Vissel to analyze the anatomy of the changes that had taken place in the rats' brains.

Natural Selection Shapes Collective Behavior in Harvester Ants

In ancient Greece, the city-states that waited until their own harvest was in before attacking and destroying a rival community's crops often experienced better long-term success. It turns out that ant colonies that show similar selectivity when gathering food yield a similar result. The latest findings from Stanford biology ProfessorDeborah M. Gordon's long-term study of harvester ants reveal that the colonies that restrain their foraging except in prime conditions also experience improved rates of reproductive success. Importantly, the study provides the first evidence of natural selection shaping collective behavior, said Dr. Gordon, who is also a senior fellow at the Stanford Woods Institute for the Environment. A long-held belief in biology has posited that the amount of food an animal acquires can serve as a proxy for its reproductive success. The hummingbirds that drink the most nectar, for example, stand the best chance of surviving to reproduce. But the math isn't always so straightforward. The harvester ants that Gordon studies in the desert in southeast Arizona, for instance, have to spend water to obtain water: an ant loses water while foraging, and obtains water from the fats in the seeds it eats. The ants use simple positive feedback interactions to regulate foraging activity. Foragers wait near the opening of the nest, and bump antennae with ants returning with food. The faster outgoing foragers meet ants returning with seeds, the more ants go out to forage. (Last year, Dr. Gordon, Katie Dektar, an undergraduate, and Dr. Balaji Prabhakar, a professor of computer science and of electrical engineering at Stanford, showed that the ants' "Anternet" algorithm follows the same rules as the protocols that regulate data traffic congestion in the Internet).

Human Skin Cells Converted to Embryonic Stem Cells

Scientists at Oregon Health & Science University (OHSU) and the Oregon National Primate Research Center (ONPRC) have successfully reprogrammed human skin cells to become embryonic stem cells capable of transforming into any other cell type in the body. It is believed that stem cell therapies hold the promise of replacing cells damaged through injury or illness. Diseases or conditions that might be treated through stem cell therapy include Parkinson's disease, multiple sclerosis, cardiac disease, and spinal cord injuries. The research breakthrough, led by Shoukhrat Mitalipov, Ph.D., a senior scientist at ONPRC, follows previous success in transforming monkey skin cells into embryonic stem cells in 2007. This latest research was published online on May 15, 2013 in Cell. The technique used by Drs. Mitalipov, Paula Amato, M.D., and their colleagues in OHSU's Division of Reproductive Endocrinology and Infertility, Department of Obstetrics & Gynecology, is a variation of a commonly used method called somatic cell nuclear transfer, or SCNT. It involves transplanting the nucleus of one cell, containing an individual's DNA, into an egg cell that has had its genetic material removed. The unfertilized egg cell then develops and eventually produces stem cells. "A thorough examination of the stem cells derived through this technique demonstrated their ability to convert, just like normal embryonic stem cells, into several different cell types, including nerve cells, liver cells, and heart cells. Furthermore, because these reprogrammed cells can be generated with nuclear genetic material from a patient, there is no concern of transplant rejection," explained Dr. Mitalipov.

Malaria Parasites “Talk” to Each Other Via Exosome-Like Vesicles

Melbourne scientists have made the surprise discovery that malaria parasites can 'talk' to each other – a social behaviour to ensure the parasite's survival and improve its chances of being transmitted to other humans. The finding could provide a niche for developing antimalarial drugs and vaccines that prevent or treat the disease by cutting these communication networks. Professor Alan Cowman, Dr. Neta Regev-Rudzki, Dr. Danny Wilson, and colleagues from the Walter and Eliza Hall Institute, in collaboration with Professor Andrew Hill from the University of Melbourne's Bio21 Institute and Department of Biochemistry and Molecular Biology, showed that malaria parasites are able to send out messages in exosome-like vesicles to communicate with other malaria parasites in the body. The study was published on March 15, 2013 in Cell. Professor Cowman said the researchers were shocked to discover that malaria parasites work in unison to enhance 'activation' into sexually mature forms that can be picked up by mosquitoes, which are the carriers of this deadly disease. "When Neta showed me the data, I was absolutely amazed, I couldn't believe it," Professor Cowman said. "We repeated the experiments many times in many different ways before I really started to believe that these parasites were signalling to each other and communicating. But we came to appreciate why the malaria parasite really needs this mechanism – it needs to know how many other parasites are in the human to sense when is the right time to activate into sexual forms that give it the best chance of being transmitted back to the mosquito." Malaria kills about 700,000 people a year, mostly children aged under five and pregnant women. Every year, hundreds of millions of people are infected with the malaria parasite, Plasmodium, which is transmitted through mosquito bites.