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May 6th, 2011

Sequencing of Single-Cell Marine Organisms Offers Clues to How Cells Interact within the Environment

From a bucket of seawater, scientists have unlocked information that may lead to deeper understanding of organisms as different as coral reefs and those that cause human disease. By analyzing genomes of a tiny, single-celled marine animal, they have demonstrated a possible way to address diverse questions such as how diseased cells differ from neighboring healthy cells and what it is about some Antarctic algae that allows them to live in warming waters while other algae die out. Dr. Debashish Bhattacharya, professor of ecology, evolution and natural resources in Rutgers' School of Environmental and Biological Sciences, and Dr. Ramunas Stepanauskas and Dr. Hwan Su Yoon of the Bigelow Laboratory of Ocean Sciences, and colleagues, have published their results in the May 6, 2011 issue of Science. They used sophisticated new technologies to sequence the genomes of individual picobilophytes, tiny microbes first discovered in 2007. At less than 10 micrometers across, they are some of the tiniest marine animals known to science. "If we can peer inside the genome of a single cell and reconstruct its history, we can do that for many cells and figure out their interactions with other cells in the environment," Dr. Bhattacharya said. For example, why do different cancer cells from the same tumor grow at different rates? Their genomes might contain the answer, and the answer might lead to more effective treatment strategies. "Our results demonstrate how single cell genomics opens a window into the natural drama that constantly takes place in each drop of seawater – a drama featuring predation, viral infections, and the divergent fate of close relatives," Dr. Stepanauskas said. "The outcomes of this drama have profound effects on the lives of larger marine organisms, such as commercially valuable fish." Dr. Bhattacharya and Dr.

May 2nd

Antioxidant May Prevent Alcohol-Induced Liver Disease

An antioxidant may prevent damage to the liver caused by excessive alcohol, according to new research from the University of Alabama at Birmingham (UAB) and collaborating institutions. The findings, published in the May 2011 issue of the journal Hepatology, may point the way to treatments to reverse steatosis, or fatty deposits in the liver that can lead to cirrhosis and cancer. The research team, led by Dr. Victor Darley-Usmar, professor of pathology at UAB, introduced an antioxidant called mitochondria-targeted ubiquinone, or MitoQ, to the mitochondria of rats that were given alcohol every day for five to six weeks in an amount sufficient to mirror excessive intake in a human. Chronic alcoholics, those who drink to excess every day, experience a buildup of fat in the liver cells. When alcohol is metabolized in the liver, it creates free radicals that damage mitochondria in the liver cells and prevent them from using sufficient amounts of oxygen to produce energy. Moreover, the low-oxygen condition called hypoxia worsens mitochondrial damage and promotes the formation of the fatty deposits that can progress to cirrhosis. Dr. Darley-Usmar and his collaborators say that the antioxidant MitoQ is able to intercept and neutralize free radicals before they can damage the mitochondria, preventing the cascade of effects that ultimately leads to steatosis. "There has not been a promising pharmaceutical approach to preventing or reversing the long-term damage associated with fatty deposits in the liver that result from excessive consumption of alcohol," said Dr. Darley-Usmar. "Our findings suggest that MitoQ might be a useful agent for treating the liver damage caused by prolonged, habitual alcohol use." "Previous studies have shown that MitoQ can be safely administered long-term to humans," said Dr.

Scientists Track Evolution and Spread of Deadly Fungus

New research has shed light on the origins of a fungal infection which is one of the major causes of death from AIDS-related illnesses. The study, published on April 28, 2011, in the journal PLoS Pathogens, shows how the more virulent forms of Cryptococcus neoformans evolved and spread out of Africa and into Asia. Cryptococcus neoformans is a species of often highly aggressive fungi. One particular strain of the fungus – known as Cryptococcus neoformas varietygrubii (Cng) – causes meningitis amongst patients with compromised immune systems following HIV infection. There are believed to be up to a million cases of cryptococcal meningitis each year, resulting in over 600,000 deaths. Infection with the fungus, which invades the central nervous system, is treated with a life-long therapy of antifungal drugs, which can have highly unpleasant side effects. Sitali Simwami and Dr. Matthew Fisher from Imperial College London, together with colleagues from St Georges, University of London, Naresuan University, Thailand, and the CBS Fungal Biodiversity Centre, The Netherlands, used genetic sequencing techniques to compare the genetic diversity of Cng in 183 samples taken from the clinic and the environment in Thailand against the 77 samples from a global database. Thailand has an emerging HIV epidemic and nearly one in five HIV-infected patients is affected by cryptococcal infection. "Cryptococcal meningitis kills hundreds of thousands of people each year, almost as many as malaria, yet gets little attention," explains Dr. Fisher. "We know very little about where it originated from and how it evolved. If we can track its evolution and diversity, then we can begin to understand where the pathogen originates from, how it infects people, and how it adapts to become more – or less – virulent.

May 1st

DNA Reveals Convergent Evolution in Lichen

Lichen, those drab, fuzzy growths found on rocks and trees, aren't as cuddly and charismatic as kangaroos or intriguing as opossums, but they could be a fungal equivalent, at least evolutionarily. A Duke research team has found that lichen that seem identical in all outward appearances and produce the same internal chemicals are in fact two different species, one living in North America and one in Australia. They're an example of "convergent evolution," in which two species evolve separately but end up looking very similar, like the Tasmanian wolf and the American wolf. The lichens developed the same adaptations to survive and thrive in vastly different regions of the world. Because they show the same evolutionary patterns as marsupials and mammals, but are easier to study, they could become model organisms to further probe how mammals and other groups of organisms evolve, said Duke biologist Brendan Hodkinson. "Lichen can often seem dull and uncharismatic, but these two species turned out to be quite intriguing," said Hodkinson, a graduate student in the lab of Duke lichenologist Dr. François Lutzoni. "They're like sugar gliders and flying squirrels or wombats and groundhogs. They're fungal examples of convergent evolution." Scientists originally labeled specimens from both continents Xanthoparmelia tasmanica, which, like all lichen, is a type of fungus that "farms" algae. The lichen specimens were thought to be one species because they shared the same body plan and produced the same chemicals. But given the lichens' geography and the natural history of other species, some scientists still questioned whether the organisms were truly identical, even though previous tests showed that they were.

Protein Found in 70-Million-Year-Old Fossil

Fossil – just stone? No, a research team in Lund, Sweden, has discovered primary biological matter in a fossil of an extinct varanoid lizard (a mosasaur) that inhabited marine environments during Late Cretaceous times. Using state-of-the-art technology, the scientists have been able to link proteinaceous molecules to bone matrix fibers isolated from a 70-million-year-old fossil; i.e., they have found genuine remains of an extinct animal entombed in stone. With their discovery, the scientists Johan Lindgren, Per Uvdal, Anders Engdahl, and colleagues have demonstrated that remains of type I collagen, a structural protein, are retained in a mosasaur fossil. The scientists have used synchrotron radiation-based infrared microspectroscopy at the MAX-lab in Lund, southern Sweden, to show that amino-acid-containing matter remains in fibrous tissues obtained from a mosasaur bone. Previously, other research teams have identified collagen-derived peptides in dinosaur fossils based on, for example, mass spectrometric analyses of whole bone extracts. The present study provides compelling evidence to suggest that the biomolecules recovered are primary and not contaminants from recent bacterial biofilms or collagen-like proteins. Moreover, the discovery demonstrates that the preservation of primary soft tissues and endogenous biomolecules is not limited to large-sized bones buried in fluvial sandstone environments, but also occurs in relatively small-sized skeletal elements deposited in marine sediments. A paper reporting the discovery was published April 29, 2011, in PLoS ONE. [Press release] [PLoS ONE article]

April 30th

Possible Mechanism That Could Convert Cells to Pancreatic Beta Cells

Simply put, people develop diabetes because they don't have enough pancreatic beta cells to produce the insulin necessary to regulate their blood sugar levels. But what if other cells in the body could be coaxed into becoming pancreatic beta cells? Could we potentially cure diabetes? Researchers from UCLA's Larry L. Hillblom Islet Research Center have taken an important step in that direction. They report in the April 19, 2011 issue of the journal Developmental Cell that they may have discovered the underlying mechanism that could convert other cell types into pancreatic beta cells. While the current standard of treatment for diabetes — insulin therapy — helps patients maintain sugar levels, it isn't perfect, and many patients remain at high risk of developing a variety of medical complications. Replenishing lost beta cells could serve as a more permanent solution, both for those who have lost such cells due to an immune assault (Type 1 diabetes) and those who acquire diabetes later in life due to insulin resistance (Type 2). "Our work shows that beta cells and related endocrine cells can easily be converted into each other," said study co-author Dr. Anil Bhushan, an associate professor of medicine in the endocrinology division at the David Geffen School of Medicine at UCLA and in the UCLA Department of Molecular, Cell and Developmental Biology. It had long been assumed that the identity of cells was "locked" into place and that they could not be switched into other cell types. But recent studies have shown that some types of cells can be coaxed into changing into others — findings that have intensified interest in understanding the mechanisms that maintain beta cell identity.

April 29th

Gene Therapy Approach Shows Promise for Macular Degeneration

A gene therapy approach using a protein called CD59, or protectin, shows promise in slowing the signs of age-related macular degeneration (AMD), according to a new in vivo study by researchers at Tufts University School of Medicine. Led by senior author Dr. Rajendra Kumar-Singh, the researchers demonstrated for the first time that CD59 delivered by a gene therapy approach significantly reduced the uncontrolled blood vessel growth and cell death typical of AMD, the most common cause of blindness in the elderly. The study was published on April 28 in PLoS ONE. Activation of the complement system, a part of the immune system, is responsible for slowly killing cells in the back of the eye, leading to AMD. Activation of this system leads to the generation of pores or holes known as 'membrane attack complex' or MAC in cell membranes. CD59 is known to block the formation of MAC. "CD59 is unstable and hence previous studies using CD59 have had limited success. The gene therapy approach that we developed continuously produces CD59 in the eye and overcomes these barriers, giving us renewed hope that it can be used to fight the progression of AMD and potentially other diseases," said Dr. Kumar-Singh. Dr. Kumar-Singh is associate professor in the department of ophthalmology at Tufts University School of Medicine (TUSM) and member of the genetics; neuroscience; and cell, molecular, and developmental biology program faculties at the Sackler School of Graduate Biomedical Sciences at Tufts. Dr. Kumar-Singh and colleagues delivered CD59 to the eye using a deactivated virus similar to one previously shown to be safe in humans. Using an established mouse model of age-related macular degeneration, they found that eyes treated with CD59 had 62 percent less uncontrolled blood vessel growth and 52 percent less MAC than controls.

April 28th

New Technique Reveals Functional Gene Networks in C. elegans

An international team of scientists, led by researchers at the University of California, San Diego School of Medicine, has developed a new method for discerning the functions of previously uncharacterized genes and placing them in interactive, functional networks that reveal how gene products interact to bring about cellular events. The research is published in the April 29, 2011 issue of Cell. The effort was led by principal investigators Dr. Karen Oegema, professor of cellular and molecular medicine and head of the Laboratory of Mitotic Mechanisms in the Ludwig Institute for Cancer Research at UC San Diego, and Dr. Kristin C. Gunsalus, assistant professor in the Center for Genomics and Systems Biology in the Department of Biology at New York University. More than a decade of genome sequencing projects has generated a comprehensive "parts" list of the genes required to build an organism, an inventory of the necessary cellular building blocks. But the functions of many of these genes remain unknown, preventing researchers from fully deciphering their cellular pathways and how their interactions might shed light on human disease. One of the stars of this research is Caenorhabditis elegans, a tiny, much-studied worm that is an important model system for understanding processes in animal cells. In recent years, scientists have sought to create systemic catalogs of its gene functions, and those of other model organisms. These large-scale efforts place genes in interactive networks. Within these networks, proximity reflects similarity of function. In other words, genes with similar functions are directly linked and genes with dissimilar functions are further apart. The functions of uncharacterized genes are inferred based upon their proximity to genes whose functions are known.

Prairie Voles Used in Study of Autism Drug Treatment

Researchers at the Center for Translational Social Neuroscience (CTSN) at Emory University are focusing on prairie voles as a new model to screen the effectiveness of drugs to treat autism. They are starting with D-cycloserine, a drug Emory researchers have shown enhances behavioral therapy for phobias and also promotes pair bonding among prairie voles. Giving female voles D-cycloserine, which is thought to facilitate learning and memory, can encourage them to bond with a new male more quickly than usual. The results were published online on April 8, 2011, and will appear in a future issue of Biological Psychiatry. "The prairie vole model has enabled us to learn about complex neural pathways in social areas of the brain," says senior author Dr. Larry Young. “We believe these insights will be useful in identifying drugs that enhance social cognition and learning. Drugs with these properties, particularly when combined with behavioral therapies, may be beneficial in the treatment of autism spectrum disorders." Dr. Young is division chief of Behavioral Neuroscience and Psychiatric Disorders at the Yerkes National Primate Research Center, William P. Timmie professor of psychiatry and behavioral sciences at Emory University School of Medicine and director of the Emory CTSN. He and his colleagues have been studying the prairie vole for more than 15 years as a model to explore the neurobiology of prosocial behaviors, including cooperation, compassion, bonding, and social reciprocity. Now, they are hoping to identify drugs that can enhance social learning in individuals with autism spectrum disorders, and they think the process of pair bonding in the prairie vole may be a useful tool for identifying new therapies.

April 26th

Most Obese Adolescents Are Lacking Vitamin D

A new study from Hasbro Children's Hospital in Providence, Rhode Island, has found that most obese adolescents are lacking in vitamin D. The researchers call for increased surveillance of vitamin D levels in this population and for further studies to determine if normalizing vitamin D levels will help to lower the health risks associated with obesity. The study is published in the May edition of the Journal of Adolescent Health. Obesity in children and adolescents has reached epidemic proportions, with a prevalence of 16.4 percent among 10 to 17 year olds as of 2007. The increased prevalence of obesity may lead to increased risk of diabetes, hypertension, and cardiovascular disease, as well as to an increased risk of cancer. Some of these health consequences of obesity have also been associated with vitamin D deficiency or insufficiency. In addition, vitamin D status is significantly associated with muscle power/force, and therefore, a deficiency may interfere with the obese adolescent's ability to increase physical activity. Lead author Dr. Zeev Harel, a pediatrician specializing in adolescent medicine at Hasbro Children's Hospital, reports that screening obese adolescents for vitamin D status by measuring their blood 25 OH D level has become a routine protocol at the Adolescent Health Center of Hasbro Children's Hospital since 2007. For this retrospective study, Harel and his co-authors explored the prevalence of low vitamin D status among 68 obese adolescents, and examined the impact of treatment of low vitamin D status in these patients. The study found that low vitamin D status was present in all of the girls (72 percent deficient and 28 percent insufficient) and in 91 percent of the boys (69 percent deficient and 22 percent insufficient).