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Scientists Generate Electricity from Viruses

Imagine charging your phone as you walk, thanks to a paper-thin generator embedded in the sole of your shoe. This futuristic scenario is now a little closer to reality. Scientists from the U.S. Department of Energy's Lawrence Berkeley National Laboratory (Berkeley Lab) have developed a way to generate power using harmless viruses that convert mechanical energy into electricity. The scientists tested their approach by creating a generator that produces enough current to operate a small liquid-crystal display. It works by tapping a finger on a postage stamp-sized electrode coated with specially engineered viruses. The viruses convert the force of the tap into an electric charge. This generator is the first to produce electricity by harnessing the piezoelectric properties of a biological material. Piezoelectricity is the accumulation of a charge in a solid in response to mechanical stress. The milestone could lead to tiny devices that harvest electrical energy from the vibrations of everyday tasks such as shutting a door or climbing stairs. It also points to a simpler way to make microelectronic devices. That's because the viruses arrange themselves into an orderly film that enables the generator to work. Self-assembly is a much-sought-after goal in the finicky world of nanotechnology. The scientists describe their work in an article published on May 13, 2012 in Nature Nanotechnology. "More research is needed, but our work is a promising first step toward the development of personal power generators, actuators for use in nano-devices, and other devices based on viral electronics," says Dr. Seung-Wuk Lee, a faculty scientist in Berkeley Lab's Physical Biosciences Division and a UC Berkeley associate professor of bioengineering. He conducted the research with a team that includes Dr.

Researchers Identify Key Genes and Prototype Predictive Test for Schizophrenia

An Indiana University (IU)-led research team, along with a group of national and international collaborators, has identified and prioritized a comprehensive group of genes most associated with schizophrenia that together can generate a score indicating whether an individual is at higher or lower risk of developing the disease. Using a convergent functional genomics approach that incorporates a variety of experimental techniques, the scientists were also able to apply a panel of their top genes to data from other studies of schizophrenia and successfully identify which patients had been diagnosed with schizophrenia and which had not, according to a report published online on May 15, 2012 by the journal Molecular Psychiatry. Evaluating the biological pathways in which the genes are active, the researchers also proposed a model of schizophrenia as a disease emerging from a mix of genetic variations affecting brain development and neuronal connections along with environmental factors, particularly stress. "At its core, schizophrenia is a disease of decreased cellular connectivity in the brain, precipitated by environmental stress during brain development, among those with genetic vulnerability," said principal investigator Alexander B. Niculescu III, M.D., Ph.D., associate professor of psychiatry and medical neuroscience at the IU School of Medicine and director of the Laboratory of Neurophenomics at the Institute of Psychiatric Research at the IU School of Medicine. "For first time we have a comprehensive list of the genes that have the best evidence for involvement in schizophrenia," said Dr. Niculescu, who is also staff psychiatrist and investigator at the Richard L. Roudebush Veterans Affairs Medical Center.

San Francisco Personalized Medicine Conference 5.0 Will Focus on Epigenetics

The fifth annual Personalized Medicine Conference (5.0) hosted by San Francisco State University, this year with a focus on epigenetics, will be held on Thursday, May 24, 2012 from 8:00 am to 7:30 pm at the South San Francisco Conference Center. To view the conference website and to register for the conference, please go to http://personalizedmedicine.sfsu.edu/. Scheduled speakers include Michael Snyder, M.D., Ph.D., Chair/Director, Department of Genetics & Stanford Center for Genomics and Personalized Medicine, Stanford University; Brian Kennedy, Ph.D., CEO, Buck Institute for Age Research; Cristina Gentilini, Ph.D., Commercial Research Scientist, Swedish Biomimetics 3000; Jorge A. Leon, President/CEO, Leomics Associates, Inc.; and Stephen M. Anderson, Ph.D., CSO of Oncology and Genetics, LabCorp. The organizers note that epigenetics, or genetic changes above and beyond the DNA sequence level, have profound implications for personalized medicine, pharmacogenomics, aging, and oncology. While personalized medicine is poised to transform healthcare over the next several decades, it has become abundantly clear that the DNA sequence itself is only part of the story. The regulation of gene expression, and how it changes in health and disease, and in response to therapy, are crucial. The organizers invite you to attend this conference and learn the latest information on how epigenetics is and will be impacting personalized medicine. The conference will also be an excellent networking opportunity for health and industry professionals, educators, and scientists. Seating is limited, so register soon. Sponsors of the conference include Genentech, Celgene, LabCorp, and BioMarin, among many others. To obtain additional information concerning the conference, you may email the organizers at dnamed@sfsu.edu or telephone Arlene Essex at 415-405-4107.

Long-Lived Naked Mole Rats Have Large Amounts of Key Brain Protein

The typical naked mole rat lives 25 to 30 years, during which time it shows little decline in activity, bone health, reproductive capacity, and cognitive ability. What is the secret to this East African rodent’s long, healthy life? Scientists from the United States and Israel have found a clue. From infancy to old age, naked mole rats are blessed with large amounts of a protein essential for normal brain function. “Naked mole rats have the highest level of a growth factor called NRG-1 (neuregulin 1) in the cerebellum. Its levels are sustained throughout their life, from development through adulthood,” said Yael Edrey, doctoral student at The University of Texas Health Science Center San Antonio’s Barshop Institute for Longevity and Aging Studies. The Barshop Institute has the largest colony of naked mole rats in the U.S. — 2,000 rodents scampering around a network of tubes and cages in humid conditions that mimic their natural underground habitat. Edrey is the lead author of research that compared lifelong NRG-1 levels across seven species of rodents, from mice and guinea pigs to blind mole rats and Damaraland mole rats. NRG-1 levels were monitored in naked mole rats at different ages ranging from 1 day to 26 years. The other six rodent species have maximum life spans of three to 19 years. The cerebellum coordinates movements and maintains bodily equilibrium. The research team hypothesized that long-lived species would maintain higher levels of NRG-1 in this region of the brain, with simultaneous healthy activity levels. Among each of the species, the longest-lived members exhibited the highest lifelong levels of NRG-1. The naked mole rat had the most robust and enduring supply. “In both mice and in humans, NRG-1 levels go down with age,” Edrey said.

Long-Lived Naked Mole Rats Have Unusual Proteasomes

The naked mole rat, a curiously strange, hairless rodent, lives many years longer than any other mouse or rat. Scientists at The University of Texas (UT) Health Science Center San Antonio’s Barshop Institute of Longevity and Aging Studies continue to explore this mystery. On May 2, 2012, a Barshop Institute team reported that the naked mole rat’s cellular machines for protein disposal — called proteasome assemblies — differ in composition from those of other short-lived rodents. The study appeared in the journal PLoS ONE. This is the first report of the molecular mechanisms that underlie the naked mole rat’s superior ability to maintain protein integrity. “More effective removal of damaged proteins within the cell would enable the animal to be able to maintain good function and is likely to contribute to its excellent maintenance of good health well into its third decade of life,” said Rochelle Buffenstein, Ph.D., of the Barshop Institute. Dr. Buffenstein is a professor of physiology and cellular and structural biology in the School of Medicine at the UT Health Science Center. Dr. Buffenstein and her research team reported in 2009 that the naked mole rat maintains exceptional protein integrity throughout its long and healthy life. In the new study, the team found a greater number of proteasomes and higher protein-disposal activity in naked mole rat liver cells. The Barshop Institute scientists, including lead author Karl Rodriguez, Ph.D., postdoctoral fellow, and Yael Edrey, a graduate student, also found large numbers of immunoproteasomes in the liver cells — a bit of a surprise because these protein disposers, which remove antigens after presentation in the immune system, are more commonly found in the spleen and thymus.

New Technique Captures MicroRNA Targets

Human cells are thought to produce thousands of different microRNAs (miRNAs)—small pieces of genetic material that help determine which genes are turned on or off at a given time. miRNAs are an important part of normal cellular function, but they can also contribute to human disease—some are elevated in certain tumors, for example, where they promote cell survival. But to better understand how miRNAs influence health and disease, researchers first need to know which miRNAs are acting upon which genes—a big challenge considering their sheer number and the fact that each single miRNA can regulate hundreds of target genes. Enter miR-TRAP, a new easy-to-use method to directly identify miRNA targets in cells. This technique, developed by Tariq Rana, Ph.D., professor and program director at Sanford-Burnham Medical Research Institute (Sanford-Burnham), and his team, was first revealed in a paper published May 8, 2012 by the journal Angewandte Chemie International Edition. "This method could be widely used to discover miRNA targets in any number of disease models, under physiological conditions," Dr. Rana said. "miR-TRAP will help bridge a gap in the RNA field, allowing researchers to better understand diseases like cancer and target their genetic underpinnings to develop new diagnostics and therapeutics. This will become especially important as new high-throughput RNA sequencing technologies increase the numbers of known miRNAs and their targets." miRNAs block gene expression not by attaching directly to the DNA itself, but by binding to messenger RNA (mRNA), the type that normally carries a DNA recipe out of the nucleus and into the cytoplasm, where the sequence is translated into protein. Next, these RNAs are bound by a group of proteins called the RNA-induced silencing complex, or RISC.

Next-Gen Sequencing Used at Duke to Aid Difficult Diagnoses

Advanced high-speed gene-sequencing has been used in the clinical setting to find diagnoses for seven children out of a dozen who were experiencing developmental delays and congenital abnormalities for mysterious reasons. "I thought if we could obtain even a couple of relatively secure diagnoses out of the 12 patients, that would prove the value of deploying sequencing approaches systematically in patients with unknown but apparently genetic conditions," said David Goldstein, Ph.D., director of the Duke Center for Human Genome Variation and professor of molecular genetics and microbiology. "Few sequencing studies have approached the problem as we did, taking a very heterogeneous group of patients," Dr. Goldstein said. "Getting a likely diagnosis about half of the time is quite stunning and strongly motivates next-generation sequencing for all patients who fail to get a genetic diagnosis through traditional testing." The research team used next-generation sequencing, a new technology that can rapidly read a person's entire genome or just their exome, the sections of DNA that make the proteins, which direct physiological activities. The cost of such sequencing is becoming lower, making it feasible to do the study in a clinical setting. The work was published online on May 8, 2012 in the Journal of Medical Genetics. "There are up to 50,000 live births in America each year with the children having features of developmental delays, intellectual disabilities, or congenital abnormalities similar to those we studied," said Vandana Shashi, M.D., co-author and associate professor of pediatrics in the Duke Center for Human Genetics.

Antisense Oligo Is Drug Candidate for Human Retinal Neovascular Diseases

Gene Signal, a Swiss company focused on developing innovative drugs to manage angiogenesis-based conditions, announced on May 8, 2012 that positive data from a study of aganirsen (GS-101, eye drops) in a nonhuman primate model of choroidal neovascularization has been presented at the 2012 ARVO Annual Meeting in Fort Lauderdale, Florida. Topical administration of aganirsen was found to inhibit neovascular growth and leakage in this model and strongly suggests a role for the drug candidate in human retinal neovascular diseases such as wet age-related macular degeneration (AMD) and ischemic retinopathy. Gene Signal's aganirsen is an antisense oligonucleotide that is expected to complete a phase III trial for the treatment of progressive neovascularization in the cornea in 2012. Clinical studies in retinal diseases are schedule to begin during the second quarter of 2012. "This study demonstrates the ability of aganirsen to address neovascularization formation in the retina by inhibiting the expression of the angiogenic protein IRS-1. Importantly, this is achieved without affecting normal vascularisation," noted Dr. Matthew Lawrence of RxGen, Inc, who presented the data. "With the demand for new, effective antiangiogenic agents that are easier to use in the treatment of several eye diseases growing, we believe these data strongly support a role for aganirsen." Aganirsen blocks pathological neovascularization by inhibiting IRS-1. Clinical studies to date have shown that aganirsen is able to safely and effectively inhibit the development of progressive corneal neovascularization secondary to infectious keratitis or chemical burns, both of which could lead to corneal graft replacement. "A topical agent for neovascular disease would revolutionize treatment.

Orangutans Host Ancient Jumping Genes

Louisiana State University’s Dr. Mark Batzer, along with research associate Dr. Jerilyn Walker and assistant professor Dr. Miriam Konkel, have published research determining that modern-day orangutans are host to ancient jumping genes called Alu, which are more than 16 million years old. The study was done in collaboration with the Zoological Society of San Diego and the Institute of Systems Biology in Seattle and was published online on April 30, 2012 in the new open access journal Mobile DNA. These tiny pieces of mobile DNA are able to copy themselves using a method similar to that of retroviruses. They can be thought of as molecular fossils, as a shared Alu element sequence and location within the genome indicates a common ancestor. But, because this is an inexact process, a segment of “host” DNA is duplicated at the Alu insertion sites and these footprints, known as target site duplications, can be used to identify Alu insertions. “However, it has long been recognized that only a small fraction of these elements retain the ability to mobilize new copies as ‘drivers,’ while most are inactive,” said Dr. Batzer, Boyd Professor and Dr. Mary Lou Applewhite Distinguished Professor of Biological Sciences. “In humans, telling the difference has proven quite difficult, mainly because the human genome is filled with plenty of relatively young Alu insertions, all with slight differences while at the same time lacking easily identifiable features characteristic for Alu propagation. This makes it hard to find their ‘parent’ or ‘source Alu’ from potentially hundreds of candidates that look similar.” In contrast to humans and other studied primates, recent activity of Alu elements in the orangutan has been very slow, with only a handful of recent events by comparison.

San Francisco Personalized Medicine Conference 5.0 Will Focus on Epigenetics

The fifth annual Personalized Medicine Conference (5.0) hosted by San Francisco State University, this year with a focus on epigenetics, will be held on Thursday, May 24, 2012 from 8:00 am to 7:30 pm at the South San Francisco Conference Center. To view the conference website and to register for the conference, please go to http://personalizedmedicine.sfsu.edu/. Scheduled speakers include Michael Snyder, M.D., Ph.D., Chair/Director, Department of Genetics & Stanford Center for Genomics and Personalized Medicine, Stanford University; Brian Kennedy, Ph.D., CEO, Buck Institute for Age Research; Cristina Gentilini, Ph.D., Commercial Research Scientist, Swedish Biomimetics 3000; Jorge A. Leon, President/CEO, Leomics Associates, Inc.; and Stephen M. Anderson, Ph.D., CSO of Oncology and Genetics, LabCorp. The organizers note that epigenetics, or genetic changes above and beyond the DNA sequence level, have profound implications for personalized medicine, pharmacogenomics, aging, and oncology. While personalized medicine is poised to transform healthcare over the next several decades, it has become abundantly clear that the DNA sequence itself is only part of the story. The regulation of gene expression, and how it changes in health and disease, and in response to therapy, are crucial. The organizers invite you to attend this conference and learn the latest information on how epigenetics is and will be impacting personalized medicine. The conference will also be an excellent networking opportunity for health and industry professionals, educators, and scientists. Seating is limited and if you register early, you can save $100 on the registration fee. Sponsors of the conference include Genentech, Celgene, LabCorp, and BioMarin, among many others.

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