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Archive - Apr 2013

Date

April 9th

How Geckos Adhere to Surfaces Under Water—Clues to Future Synthetics That Will Retain Adhesion in Water

Geckos are known for their sticky adhesive toes that allow them to stick to, climb on, and run along surfaces in any orientation--even upside down! But until recently, it was not well understood how geckos kept their sticking ability even on wet surfaces, as are common in the tropical regions in which most geckos live. A 2012 study in which geckos slipped on wet glass perplexed scientists trying to unlock the key to gecko adhesion in climates with plentiful rain and moisture.A study supported by the National Science Foundation and published online on April 1, 2013 in PNAS solves the mystery, showing that wet, water-repellant surfaces, like those of leaves and tree trunks, actually secure a gecko's grip in a manner similar to dry surfaces. Researchers from the University of Akron, led by integrated bioscience doctoral candidate Alyssa Stark, tested geckos on four different surfaces. The surfaces ranged from hydrophilic--those that liquids spread across when wet, like glass--to hydrophobic--water-repellent surfaces on which liquids bead, like the natural leaves geckos walk on--and intermediate ones, like acrylic sheets. Geckos were tested on these surfaces both when the surfaces were dry and when they were submerged underwater, and water completely covered the gecko's feet. Fitting a small harness around the pelvis, geckos were gently pulled along the substrate until their feet began to slip. At this point the maximum force with which a gecko could stick was measured. On wet glass, geckos slipped and could not maintain adhesion. However when tested on more hydrophobic surfaces, geckos stuck just as well to the wet surface as they did to the dry ones. When tested, geckos stuck even better to wet Teflon than dry.

Use of Copper Surfaces Reduces Number of Healthcare-Acquired Infections

New research has revealed that the use of Antimicrobial Copper surfaces in hospital rooms can reduce the number of healthcare-acquired infections (HAIs) by 58% as compared to patients treated in intensive care units (ICUs) with non-copper touch surfaces. In the United States, 1 out of every 20 hospital patients develops an HAI, resulting in an estimated 100,000 deaths per year. Although numerous strategies have been developed to decrease these infections, Antimicrobial Copper is the only strategy that works continuously, has been scientifically proven to be effective and doesn't depend on human behavior, according to a recently study published in theMay 2013 issue of the SHEA Journal of Infection Control and Hospital Epidemiology. "The implications of this study are critical," said Dr. Harold Michels, Senior Vice President of the Copper Development Association (CDA). "Until now, the only attempts to reduce HAIs have required hand hygiene, increased cleaning, and patient screening, which don't necessarily stop the growth of these bacteria the way copper alloy surfaces do. We now know that copper is the game-changer: it has the potential to save lives." The study, funded by the U.S. Department of Defense, was conducted in the ICUs of three major hospitals: The Medical University of South Carolina, Memorial Sloan-Kettering Cancer Center in New York City, and the Ralph H. Johnson Veterans Affairs Medical Center in Charleston, South Carolina. To determine the impact of copper alloy surfaces on the rate of HAIs, copper-surfaced objects were placed in each ICU, where patients are at higher risk due to the severity of their illnesses, invasive procedures, and frequent interaction with healthcare workers.

“Amazing” Success Reported in Treating Major Depression with Brain-Implanted Pacemaker Electrodes

Researchers from the Bonn University Hospital implanted pacemaker electrodes into the medial forebrain bundle in the brains of patients suffering from major depression with amazing results. In six out of seven patients, symptoms improved both considerably and rapidly. The method of Deep Brain Stimulation had already been tested on various structures within the brain, but with clearly lesser effect. The results of this new study were published online on April 5, 2013 in the renowned international journal Biological Psychiatry. After months of deep sadness, a first smile appears on a patient's face. For many years, she had suffered from major depression and tried to end her life several times. She had spent the past years mostly in a passive state on her couch; even watching TV was too much effort for her. Now this young woman has found her joie de vivre again, enjoys laughing and travelling. She and an additional six patients with treatment-resistant depression participated in a study involving a novel method for addressing major depression at the Bonn University Hospital. Professor Dr. Volker Arnd Coenen, neurosurgeon in the Department of Neurosurgery (Klinik und Poliklinik für Neurochirurgie), implanted electrodes into the medial forebrain bundles in the brains of subjects suffering from major depression with the electrodes being connected to a brain pacemaker. The nerve cells were then stimulated by means of a weak electrical current, a method called Deep Brain Stimulation. In a matter of days, in six out of seven patients, symptoms such as anxiety, despondence, listlessness, and joylessness had improved considerably. "Such sensational success both in terms of the strength of the effects, as well as the speed of the response has so far not been achieved with any other method," says Professor Dr. Thomas E.

Gene Therapy Cures Inherited Vision Disorder in Dogs, Promises Hope for Humans

Researchers have discovered that using two kinds of therapy in tandem may be a knockout combination against inherited disorders that cause blindness. While their study focused on man's best friend, the treatment could help restore vision in people, too. Published online on April 9, 2013 in the journal Molecular Therapy, the study builds on earlier work by Michigan State University (MSU) veterinary ophthalmologist Dr. András Komáromy and colleagues. In 2010, the scientists restored day vision in dogs suffering from achromatopsia, an inherited form of total color blindness, by replacing the mutant gene associated with the condition. While that treatment was effective for most younger dogs, it didn't work for canines older than 1 year. Dr. Komáromy began to wonder if the older dogs' cones – the photoreceptor cells in the retina that process daylight and color – might be too worn out. "Gene therapy only works if the nonfunctional cell that is primarily affected by the disease is not too degenerated," he said. "That's how we came up with the idea for this new study. How about if we selectively destroy the light-sensitive part of the cones and let it grow back before performing gene therapy? Then you'd have a younger, less degenerated cell that may be more responsive to therapy." So, Dr. Komáromy and colleagues recruited more dogs with achromatopsia between 1 and 3 years old. To test their theory, they again performed gene therapy but first gave some of the dogs a dose of a protein called CNTF, which the central nervous system produces to keep cells healthy. At a high enough dose, CNTF’s effect on photoreceptors is a bit like pruning flowers: it partially destroys the receptors, but allows for new growth. "It was a long shot," said Dr. Komáromy, associate professor in MSU's Department of Small Animal Clinical Sciences. But it worked.

New Target and New Drug May Lead to Treatment for Melanoma

Collaborative research presented by the University of Colorado (CU) Cancer Center, the University of North Carolina at Chapel Hill, Harvard Medical School, and the University of Pittsburgh, at the American Association for Cancer Research (AACR) Annual Conference in Washington, D.C., shows that the protein receptor Mer is overexpressed in melanoma and that the investigational drug UNC1062 blocks Mer survival signaling in these cells, killing them. "It's exciting in that Mer receptor expression correlates so perfectly with disease progression. It's tiered – you see a bump in expression as you transition from nevus to melanoma and then again as you transition from melanoma to metastatic disease," says Doug Graham, M.D., Ph.D., investigator at the CU Cancer Center and associate professor of Pediatrics and Immunology at the CU School of Medicine, the paper's senior author. After proving the correlation between Mer receptor expression and disease stage in melanoma tissues from clinical patient samples, Dr. Graham and colleagues wondered what would happen if they interrupted this Mer signaling. Luckily, the University of North Carolina had recently developed a new compound that did just that – UNC1062. The results were dramatic. "We showed decreased survival signaling, increased apoptosis, and decreased growth of the melanoma cells in dishes and in mouse models," Dr. Graham says. It seems that Mer receptors are not only correlated with melanoma progression but are in fact driving the aggressiveness of the disease. "This is the first time there's been an association between Mer and melanoma and the first time to report about this new drug," Dr. Graham says. This news was reported on April 9, 2013. [Press release]

April 8th

MIT Scientists Develop Potent Antibody Against All Four Dengue Virus Serotypes

Nearly half of the world’s population is at risk of infection by the dengue virus, yet there is no specific treatment for the disease. Now a therapy to protect people from the virus could finally be a step closer, thanks to a team at MIT. In a paper published online on April 8, 2013 in PNAS, the researchers, from MIT’s Koch Institute of Integrative Cancer Research, present a novel approach to developing a dengue therapy using mutated antibodies. According to a study by the International Research Consortium on Dengue Risk Assessment, Management, and Surveillance, up to 390 million people are infected with the dengue virus each year. For most people the mosquito-borne virus causes flu-like symptoms, including fever, headache, and joint pain. But for some, particularly children, the virus can develop into the far more serious dengue hemorrhagic fever, causing severe blood loss and even death. Despite the threat posed by the disease, developing a vaccine against dengue has so far proven challenging, according to Dr. Ram Sasisekharan, the Alfred H. Caspary Professor of Biological Engineering at MIT. That’s because dengue is not one virus but four different viruses, or serotypes, each of which must be neutralized by the vaccine. Protecting people from only one or some of the four viruses could cause them to develop the more severe form of dengue if they later become infected with one of the other serotypes, in a process known as antibody-dependent enhancement, Dr. Sasisekharan says. “That was the motivation for carrying out our study, to generate a fully neutralizing antibody that works for all four serotypes.” Efforts to develop a therapeutic antibody for dengue are focused on a part of the virus called the envelope protein.

Hopkins Team Finds Genetic Cause of Some Gout, Suggests Possible Treatment

Johns Hopkins scientists have discovered how a gout-linked genetic mutation contributes to the disease: by causing a breakdown in a cellular pump that clears an acidic waste product from the bloodstream. By comparing this protein pump to a related protein involved in cystic fibrosis, the researchers also identified a compound that partially repairs the pump in laboratory tests. The mutation in question, known as Q141K, results from the simple exchange of one amino acid for another, but it prevents the protein ABCG2 from pumping uric acid waste out of the bloodstream and into urine. A buildup of uric acid in the blood can lead to its crystallization in joints, especially in the foot, causing excruciatingly painful gout. “The protein where the mutation occurs, ABCG2, is best known for its counterproductive activity in breast cancer patients, where it pumps anti-cancer drugs out of the tumor cells we are trying to kill,” says William Guggino, Ph.D., professor and director of the Department of Physiology at the Johns Hopkins University School of Medicine. “In kidney cells, though, ABCG2 is crucial for getting uric acid out of the body. What we figured out is exactly how a gout-causing genetic mutation inhibits ABCG2 function.” A description of the work with Q141K’s effects at the cellular level was published online on March 14, 2013 in PNAS. Gout affects 2 to 3 percent of Americans, approximately 6 million people. It usually involves sudden attacks of severe pain, often in the joint at the base of the big toe and frequently in the wee hours of the morning, when body temperature is lowest.

Fly Mutation Suggests New Approach to Treating ALS (Lou Gehrig's Disease)

A team of researchers, led by Marc Freeman, Ph.D., an early career scientist with the Howard Hughes Medical Institute and associate professor of neurobiology at the University of Massachusetts Medical School has discovered a gene in the fruit fly Drosophila melanogaster that, when mutant, blocks the self-destruction of damaged axons, which could hold clues to treating motor neuron diseases, such as amyotrophic lateral sclerosis (ALS), aslo known as Lou Gehrig’s disease. ALS also afflicts legendary physicist Dr. Stephen Hawking (photo). A neuron has a very distinctive form – a bush of dendrites that receive signals, an incredibly long axon, which is like a long tail, and "a little dot" between them that is the cell body, housing the genetic headquarters. Every part of the neuron is required for it to transmit messages. "If anything breaks along any part of the neuron, the cell unplugs from the circuit and no longer functions," explained Dr. Freeman, who presented this research at the Genetics Society of America's 54th Annual Drosophila Research Conference in Washington, D.C. The work was announced on April 8, 2013. Once the long tail-like axon is damaged, it shrivels away, basically self-destructing, and resulting in neurons that no longer operate. This catastrophic damage can happen in several ways: from inflammation, a neurodegenerative disease, a metabolic disorder such as diabetes, toxin exposure, or tumor growth. Such axon loss is thought to be a primary factor that leads to functional loss in patients with neurological disorders – it is equivalent to going into an electrical circuit and randomly cutting wires.

“Jumping Genes” May Contribute to Aging-Related Brain Defects

As the body ages, the physical effects are notable; wrinkles in the skin appear, physical exertion becomes harder. But there are also less visible processes going on. Inside aging brains there is another phenomenon at work, which may contribute to age-related brain defects. In a paper published online on April 7, 2013 in the journal Nature Neuroscience, Cold Spring Harbor Laboratory (CSHL) Associate Professor Joshua Dubnau and colleagues show that so-called "jumping genes," or transposons, increase in abundance and activity in the brains of fruit flies as they age. Originally discovered at CSHL by eventual Nobel Prize winner Professor Barbara McClintock (photo) while working on maize (corn) in the 1940s, transposons are typically repeat DNA sequences that insert themselves into the DNA of an animal or plant. The moniker "jumping genes" comes from the fact that, when activated, transposons can reinsert themselves, or transpose, into another part of the genome. In the course of doing so, they are thought to either provide variations in genetic function or, especially in the germline, induce potentially fatal disruptive defects. The lifespan of a fruit fly can be measured in days. The average fruit fly lives for somewhere between 40-50 days. But these flies provide a powerful model with which to get at the genetics of phenomena like aging and brain function, including memory. Dr. Dubnau's interest was piqued by an experiment in which his team showed that when the activity of a protein called Ago2 (Argonaute 2) was perturbed, so was long-term memory—which was tested using a trained Pavolvian response to smell. "This is a neurodegenerative defect that gets profoundly more apparent with age of the flies," notes Dr. Dubnau.

April 7th

Massive Study Reveals New Genes for Height and Obesity

An international research team has identified seven new gene loci linked to obesity. Researchers were also able to show that the genetic mechanisms that cause extreme obesity are similar to those that cause milder forms of overweight and obesity. The scientists were also able to identify four new gene loci for height. A total of more than 260,000 people were included in the study of the links between genes and obesity, which was published online on April 7, 2013 in Nature Genetics. The aim of the study was to identify new genes that increase the risk of obesity, but also to compare genetic factors that cause extreme obesity with those that are linked to rest of the body mass index (BMI) range. "We know from experience that genetic factors are important for the emergence of both milder and more extreme forms of obesity, but how much overlap there is between genes that are involved in extreme obesity and normal or slightly elevated BMI has not been examined systematically previously," says Dr. Erik Ingelsson, Professor at the Department of Medical Sciences and Science for Life Laboratory, Uppsala University, who coordinated the study. The researchers studied gene variants, or positions in the genetic code that differ between individuals. Many million such commonly occurring inherited differences are scattered throughout the genome. In the just published study, researchers identified loci (regions of the genome) that are linked to obesity through examining the relationship between different body measurements and 2.8 million gene variants in 168,267 participants. The scientists then carried out a targeted follow-up of the 273 gene variants with the strongest link to various body measurements in another 109,703 people.