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November 14th

Penguin Is Model for New Propulsion System

Back in 1991, Nature published a picture from the IMAX movie Antarctica, along with the caption: "Emperor penguins may be waddling jokes on land, but underwater they can turn into regular rockets…accelerating from 0 to 7 m/s in less than a second." That's all it took to inspire Flavio Noca, who at the time was a graduate student in Caltech's Aeronautics Department, and now teaches aerodynamics at the University of Applied Sciences Western Switzerland (hepia) and the Swiss Federal Institute of Technology (EPFL), to explore leveraging penguins' "rocket" properties to create new propulsion technologies with high maneuverability and improved hydrodynamic efficiency. At the American Physical Society's (APS) Division of Fluid Dynamics meeting, November 24 – 26, in Pittsburgh, Pennsylvania, Noca will present a penguin-inspired propulsion system that uses a novel spherical joint mechanism developed and manufactured by Bassem Sudki, a research assistant within Noca's aerodynamics group, under the supervision of Professor Michel Lauria who leads hepia's Robotics Laboratory. Based on a penguin's shoulder-and-wing system, the mechanism features a spherical joint that enables three degrees of freedom and a fixed center of rotation. "Unlike an animal shoulder joint, however, this spherical joint enables unlimited rotational range about the main shaft axis like a propeller," Noca said. To achieve this, they needed to overcome the technical challenges of spherical joints, such as the lack of rigidity and the inability to generate high torques. To understand the challenge involved, just try lifting a 10-pound weight on your hand with your arm extended. The researchers maneuvered around these challenges by choosing a parallel robotic architecture for this type of mechanism, because it enables rigidity as well as high actuation frequencies and amplitudes.

Annexin A5 Is Possible New Treatment for Sepsis

Sepsis is the leading cause of in-hospital death and there is no specific treatment for it. Now, research led by Dr. Qingping Feng of Western University (London, Canada) suggests a protein called recombinant human annexin A5 may have therapeutic potential for the treatment of this disease. The paper has been published in advance, online in Critical Care Medicine. Sepsis is caused by an overwhelming immune response to an existing infection. It's estimated there are 18 million cases annually worldwide. The mortality rate is 30 to 40 per cent for severe sepsis and 40 to 80 per cent for septic shock. Dr. Feng, a professor in the Departments of Physiology and Pharmacology, and Medicine at Western's Schulich School of Medicine & Dentistry and a scientist at Lawson Health Research Institute is particularly interested in how sepsis causes cardiac dysfunction. Annexin A5 is a lipid-binding protein produced by cells. Using mice with induced sepsis, Dr. Feng, Dr. Xiangru Lu, and Paul Arnold, M.Sc., studied the effects of annexin A5 on cardiac function and animal survival. "We treated the septic animals and to our surprise we found a dramatic, significant effect in improving cardiac function during sepsis and improved survival rates in the mice," says Dr. Feng. "We also found it helped even if administered hours after the septic infection. This is important because the delayed treatment simulates what usually happens in a clinical setting. The patient often has had sepsis for several hours, or a few days when they seek treatment." Annexin A5 is not currently used as a therapeutic agent, but its safety has been tested in humans. It's currently used in imaging studies to identify cells undergoing apoptosis (cell death). While this study looked at the heart, Dr.

Patients and Scientists Join Forces to Tackle Friedreich’s Ataxia with Gene Therapy Approach

In a November 14, 2013 press release, it was announced that The Spanish Federation of Ataxia (FEDAES)—in representation of the GENEFA Platform for a Friedreich's Ataxia cure—, the Babel Family association for biomedical research into Friedreich’s Ataxia, the “Centro de Biología Molecular Severo Ochoa” (CMBSO), and the Institute for Research in Biomedicine (IRB Barcelona) have signed an agreement through which these patients’ associations will fund, by means of donations, a three-year research project addressing Friedreich’s Ataxia. Friedreich’s Ataxia is a rare degenerative disease of the nervous system that affects coordination, balance, and movement. It is a monogenic disease, that is to say, it is caused by a defect in only one gene. Those affected by this disorder have inherited an altered frataxin gene from both parents. The project aims to develop molecular tools to transport a correct copy of the defective gene to all the cells of the body and particularly to a kind of neuron that undergoes degeneration and causes the disease. This approach seeks to restore the normal levels of frataxin and to stop the manifestation of the degenerative symptoms of the disease. The GENEFA Platform heads the money-raising campaign to collect the 300,000 euros required to develop this gene therapy project. Juan Carlos Baiges, in representation of FEDAES/GENEFA and the Babel Family for this project, expresses his enthusiasm, “it is the first step towards achieving an effective treatment based on solid basic research knowledge,” and adds, “we have a motivating project ahead that may lead us closer to a treatment.” Dr. Ernest Giralt, at IRB Barcelona, and Dr.

November 13th

Fungus Kills Ticks, May Benefit Sheep

Ticks may be facing a dangerous fate. In the TICLESS project, Bioforsk, the Norwegian Institute for Agricultural and Environmental Research, is hoping to determine whether fungus can kill ticks in sheep pastures, according to a November 12, 2013 press release. This would also benefit future hikers. Tick bites in sheep can lead to the disease tick-borne fever (TBF), which causes high fever and weakens the immune system. As a result of TBF, animals may become seriously ill from diseases they usually cope with. Bioforsk is therefore conducting field trials where the aim is to reduce tick populations in sheep grazing areas by using a tick pathogenic fungus called Metarhizium. Metarhizium occurs naturally in Norwegian soil and in the soils of many other countries worldwide where it has the potential to infect and kill ticks. When living organisms or "natural enemies" of a pest are utilized in order to reduce pest population levels, this is known as biological control. Dr. Ingeborg Klingen, Head of the Section of Invertebrate Pests at Bioforsk Plant Health and Plant Protection Division, and her group, are currently conducting field trials with BIPESCO 5 which is a formulation of an isolate of the tick pathogenic fungus, Metarhizium. “The fungus we are using in the trial is a natural enemy of insects and mites found in soil. What we do is to increase the natural fungal population by releasing it in large quantities. This type of biological control is known as augmentation biological control and is an alternative to chemical control”, says Dr. Klingen. “The death that awaits ticks exposed to this fungus, is inhumane; fungal spores land and germinate on the skin (cuticle) of the tick and then penetrate it before entering the tick body. The fungus then grows and proliferates inside the tick.

Engineered Fusion Protein Opens Door for Safer Gene Therapy‬

A protein engineered by researchers at KU Leuven that combines proteins active in HIV and Moloney murine leukemia virus (MLV) replication may lead to safer, more effective retroviral gene therapy. KU Leuven is located in Flanders, the Dutch-speaking region of Belgium. Gene therapy involves inserting healthy genetic material into a diseased cell. Using a carrier derived from a retrovirus, the genetic material is smuggled into a human cell where, once inside, it integrates itself into the cell’s DNA. But gene therapy is not without risks. If integrated too near a carcinogenic gene, the newly introduced genetic material can also induce disease-causing mutations. In gene therapy, the delivery vehicle is not the retrovirus itself, but a viral vector: a derivative form of the retrovirus that retains its proteins but not its nucleic acid. One of the most widely used viral vectors is derived from MLV. But this particular virus-borne carrier is both a weapon and a risk. It can cure disease but, if integrates in the wrong place in a cell’s DNA, it can also cause leukemia. A separate protein, which plays a role in HIV, does not have that problem. It only integrates itself in ‘safe’ places in the host cell’s DNA. The researchers put one and two together to create a safer viral vector: “We developed a fused protein with the head of the protein that HIV uses and the tail of the protein that MLV uses,” Dr. Rik Gijsbers explains. Their work was reported online on October 31, 2013 in Cell Reports, and the researchers say their engineered retroviral vector works: “Our experiments with cell cultures show that in the presence of this protein, the viral vector always inscribes itself in a safe place, just as it does in the HIV virus,” says Dr. Gijsbers.

Thin Invisibility Cloak Demonstrated for First Time

Invisibility cloaking is no longer the stuff of science fiction: two researchers in The Edward S. Rogers Sr. Department of Electrical & Computer Engineering have demonstrated an effective invisibility cloak that is thin, scalable and adaptive to different types and sizes of objects. Professor George Eleftheriades and Ph.D. student Michael Selvanayagam have designed and tested a new approach to cloaking—by surrounding an object with small antennas that collectively radiate an electromagnetic field. The radiated field cancels out any waves scattering off the cloaked object. Their paper was published online on November 12, 2013 in an open-access article in Physical Review X. “We’ve taken an electrical engineering approach, but that’s what we are excited about,” says Professor Eleftheriades. “It’s very practical.” Picture a mailbox sitting on the street. When light hits the mailbox and bounces back into your eyes, you see the mailbox. When radio waves hit the mailbox and bounce back to your radar detector, you detect the mailbox. Eleftheriades and Selvanyagam’s system wraps the mailbox in a layer of tiny antennas that radiate a field away from the box, cancelling out any waves that would bounce back. In this way, the mailbox becomes undetectable to radar. “We’ve demonstrated a different way of doing it,” says Professor Eleftheriades. “It’s very simple: instead of surrounding what you’re trying to cloak with a thick metamaterial shell, we surround it with one layer of tiny antennas, and this layer radiates back a field that cancels the reflections from the object.” Their experimental demonstration effectively cloaked a metal cylinder from radio waves using one layer of loop antennas.

Transcription Factor Study Yields Insight

In order to react effectively to changes in the surroundings, bacteria must be able to quickly turn specific genes on or off. Although the overall mechanisms behind gene regulation have long been known, the fine details have eluded scientists for decades. Researchers at Uppsala University in Sweden can now provide a picture of how proteins regulate genetic expression at the atomic level. Genes can be regarded as blueprints for all of the molecular machines—normally proteins—that perform the tasks an organism needs for survival. Under different living conditions, different types of proteins are needed to break down the available types of nutrients, for example. Because the surroundings can change rapidly, it is also important for bacteria and other organisms to be able to quickly reconfigure their biochemical operations in order to adapt to the new environment. This is done through regulation of the activity of proteins that already exist in the cell, but also by the binding of special proteins—transcription factors—to specific sites on the DNA, turning certain genes on or off, which in turn regulates the cell's production of various proteins. The latter might seem impossible, as an arbitrary transcription factor normally exists in just a handful of copies inside a bacterial cell, and one of them has to find a specific binding site on the DNA spiral, which contains some five million base pairs, in order to turn a gene on or off, says Dr. Erik Marklund, one of the lead authors of the new study. Roughly 40 years ago, it was observed that these transcription factors find their binding sites on DNA much more quickly than free diffusion in three dimensions would allow.

November 12th

Novel Therapies for Nicotine, Heroin, and Gambling Addiction Show Promise—Neuroscience 2013

Studies released today suggest promising new treatments for nicotine and heroin addiction, and further our understanding of pathological gambling and heroin abuse in those suffering chronic pain. This new knowledge, released at a Tuesday, November 12 press conference at Neuroscience 2013, the annual meeting of the Society for Neuroscience and the world’s largest source of emerging news about brain science and health, may one day lead to non-pharmaceutical interventions and therapies to treat addiction. 30,000 scientists are attending this meeting in San Diego. According to the World Health Organization, 15.3 million people worldwide suffer from drug use disorders. A variety of brain areas and processes play a role in addictive behaviors, complicating treatment and costing millions of dollars and lives each year. The studies described today contribute to an understanding of how compulsive disorders like addiction develop and provide new insight into methods to treat addictive behaviors . The new findings show that: magnetic stimulation of the brain helps some people decrease their smoking, and even quit altogether for up to six months after treatment (Abraham Zangen, abstract 635.03); stimulating an area of the brain associated with drug reward, the subthalamic nucleus, reduces rats’ motivation to take heroin (Carrie Wade, Ph.D., abstract 818.03); chronic pain leads rats already exposed to drugs to take more and higher doses of heroin, suggesting that people with addiction are more susceptible to overdose when in chronic pain (Lucia Hipolito, Ph.D., abstract 158.05).

Armadillos and Other Species Offer Clues to Human Brain Function and Vision Loss—Neuroscience 2013

Research released at a Monday, November 11 press conference reveals a new model for genetic eye disease and shows how animal models—from flies to armadillos and monkeys--can yield valuable information about the human brain. The findings were presented at Neuroscience 2013, the annual meeting of the Society for Neuroscience and the world’s largest source of emerging news about brain science and health. 30,000 scientists are attending this meeting. Animal models have long been central to how we understand the human brain, behavior, and nervous system due to similarities in many brain areas and functions across species. Almost every major medical advance in the last century was made possible by carefully regulated, humane animal research. Monday’s announced findings show that: the nine-banded armadillo may serve as a model for certain types of progressive blindness. The animal’s poor eyesight mimics many human disorders and may shed light on new treatment approaches for such diseases (Christopher Emerling, B.S., abstract 150.06); analysis of a baboon population reveals particular genes that may be involved in creating the “folds” in the structure of the brain. These findings provide information on how human genes may have evolved to create the brain’s shape and function (Elizabeth Atkinson, B.A., abstract 195.13); monkeys and humans use similar brain pathways while processing decisions. Detailed analyses of similarities and differences in brain wiring could provide new insights into decision-making in humans (Franz-Xaver Neubert, abstract 18.03). Other recent findings discussed show that: use of powerful genetic tools in fruit flies is helping to reveal the basic building blocks of brain circuitry and function.

Nicotinic Acetylcholine Receptors in Amygdala Could Be Anti-Depression Target—Neuroscience 2013

Decreasing a specific protein in the amygdala, an area of the brain involved in mood, creates antidepressant-like effects and reduces anxiety in mice. The findings, presented at a Monday, November 11Neuroscience 2013 press conference, the annual meeting of the Society for Neuroscience and the world’s largest source of emerging news about brain science and health, may help identify new molecular drug targets 30,000 scientists are attending this meeting. “Our data provide a new mechanism and location in the brain that can be used to study depression,” said lead author Yann Mineur, Ph.D., an Associate Research Scientist at Yale University School of Medicine. “These findings could lead to new tools to understand and diagnose depression, and might be the key to creating more effective antidepressants.” Previous studies show that drugs that block specific beta 2 nicotinic acetylcholine receptors (β2 nAChRs) can have antidepressant properties. To zero in on the role of this interaction, the researchers developed mice with localized reduction of β2 nAChRs expression and measured responses to social defeat stress tests. Dr. Mineur and his colleagues found that this change in the mouse amygdala appeared to protect against depression and anxiety in mice. The findings could guide researchers to a better understanding of the molecular mechanisms of depression and assist in the development of new drugs to treat mood disorders. When β2 nAChRs were knocked down in the hippocampus, there was no change in depression-like behavior or stress resilience in the social defeat test. These results suggest that decreasing nicotinic signaling through β2* nAChRs in the amygdala is antidepressant-like, likely due to the high level of tonic ACh input to this structure at baseline. The scientific presentation of Dr.