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Archive - 2013

March 28th

New Technologies Used to Combat Aquatic Invasive Species

A new research paper by a team of researchers from the University of Notre Dame's Environmental Change Initiative (ECI) and collaborators demonstrates how two cutting-edge technologies can provide a sensitive and real-time solution to screening real-world water samples for invasive species before they get into our country or before they cause significant damage. The paper was published online on March 22, 2013 in Conservation Letters. "Aquatic invasive species cause ecological and economic damage worldwide, including the loss of native biodiversity and damage to the world's great fisheries," Dr. Scott Egan, a research assistant professor with Notre Dame's Advanced Diagnostics and Therapeutics Initiative and a member of the research team, said. "This research combines two new, but proven technologies, environmental DNA (eDNA) and Light Transmission Spectroscopy (LTS), to address the growing problem of aquatic invasive species by increasing our ability to detect dangerous species in samples before they arrive or when they are still rare in their environment and have not yet caused significant damage." Egan points out that eDNA is a species surveillance tool that recognizes a unique advantage of aquatic sampling: water often contains microscopic bits of tissue in suspension, including the scales of fish, the exoskeletons of insects, and the sloughed cells of and tissues of aquatic species. These tissue fragments can be filtered from water samples and then a standard DNA extraction is performed on the filtered matter. The new sampling method for invasive species was pioneered by members of the Notre Dame Environmental Change Initiative, including Dr. David Lodge and Dr. Chris Jerde, Central Michigan University's Dr. Andrew Mahon, and The Nature Conservancy's Dr. Lindsay Chadderton. Dr.

Study Shows Brain Scans Might Predict Future Criminal Behavior

A new study conducted by The Mind Research Network (MRN) in Albuquerque, New Mexico, together with collaborators at Duke University, the University of New Mexico, the University of Massachusetts Medical School, and the University of California-Santa Barbara, shows that neuroimaging data can predict the likelihood of whether a criminal will reoffend following release from prison. The paper, which was published online on March 27, 2013 in PNAS, studied impulsive and antisocial behavior and centered on the anterior cingulate cortex (ACC), a portion of the brain that deals with regulating behavior and impulsivity. The study demonstrated that inmates with relatively low anterior cingulate activity were twice as likely to reoffend than inmates with high-brain activity in this region. "These findings have incredibly significant ramifications for the future of how our society deals with criminal justice and offenders," said Dr. Kent A. Kiehl, who was senior author on the study and is director of mobile imaging at MRN and an associate professor of psychology at the University of New Mexico. "Not only does this study give us a tool to predict which criminals may reoffend and which ones will not reoffend, it also provides a path forward for steering offenders into more effective targeted therapies to reduce the risk of future criminal activity." The study looked at 96 adult male criminal offenders aged 20-52 who volunteered to participate in research studies. This study population was followed over a period of up to four years after inmates were released from prison. "These results point the way toward a promising method of neuroprediction with great practical potential in the legal system," said Dr.

Common Gene Variants Explain 42 Percent of Individual Variation in Antidepressant Response

Antidepressants are commonly prescribed for the treatment of depression, but many individuals do not experience symptom relief from treatment. The National Institute of Mental Health's STAR*D study, the largest and longest study ever conducted to evaluate depression treatment, found that only approximately one-third of patients responded within their initial medication trial and approximately one-third of patients did not have an adequate clinical response after being treated with several different medications. Thus, identifying predictors of antidepressant response could help to guide the treatment of this disorder. A new study, published online on December 12, 2012 in Biological Psychiatry and printed in the April 1, 2013 issue of that journal, now shares progress in identifying genomic predictors of antidepressant response. Many previous studies have searched for genetic markers that may predict antidepressant response, but have done so despite not knowing the contribution of genetic factors. Dr. Katherine Tansey of the Institute of Psychiatry at King's College London and colleagues resolved to answer that question. "Our study quantified, for the first time, how much is response to antidepressant medication influenced by an individual's genetic make-up," said Dr. Tansey. To perform this work, the researchers estimated the magnitude of the influence of common genetic variants on antidepressant response using a sample of 2,799 antidepressant-treated subjects with major depressive disorder and genome-wide genotyping data. They found that genetic variants explain 42% of individual differences, and therefore, significantly influence antidepressant response. "While we know that there are no genetic markers with strong effect, this means that there are many genetic markers involved.

March 26th

Elsevier Launches Web-Based Data Mining/Visualization Software for Biologists

Elsevier, a world-leading provider of scientific, technical, and medical information products and services, announced on March 26, 2013 the launch of a web-based version of Pathway Studio (http://www.elsevier.com/pathway-studio), a research solution for biologists. Additionally, Pathway Studio now incorporates biological data from Elsevier’s biology journals in addition to journals obtained through collaboration with third-party publishers. The addition of this data to Pathway Studio results in a resource that is unparalleled in depth and coverage of molecular interactions with supporting evidence. The new web-based version broadly extends access to researchers to reveal new insights and to assist with critical decision making. “Currently, molecular facts are scattered in individual articles and researchers must gather and integrate these to advance new discovery,” said Jaqui Mason, Product Development Director for Biology Products at Elsevier. “Pathway Studio presents these facts in a graphical context to help researchers assemble biological models that can be applied to target discovery programs, identify potential diagnostics, and reposition drugs.

Researchers Re-Program Other Cells to Become Nerve Cells Directly in the Brain

The field of cell therapy, which aims to form new cells in the body in order to cure disease, has taken another important step in the development towards new treatments. A new report from researchers at Lund University in Sweden shows that it is possible to re-program other cells to become nerve cells, directly in the brain. Two years ago, researchers in Lund were the first in the world to re-program human skin cells, known as fibroblasts, to dopamine-producing nerve cells – without taking a detour via the stem cell stage. The research group has now gone a step further and shown that it is possible to re-programme both skin cells and support cells directly to nerve cells, in place in the brain. “The findings are the first important evidence that it is possible to re-program other cells to become nerve cells inside the brain,” said Dr. Malin Parmar, research group leader and Reader in Neurobiology. The researchers used genes designed to be activated or de-activated using a drug. The genes were inserted into two types of human cells: fibroblasts and glia cells – support cells that are naturally present in the brain. Once the researchers had transplanted the cells into the brains of rats, the genes were activated using a drug in the animals’ drinking water. The cells then began their transformation into nerve cells. In a separate experiment on mice, where similar genes were injected into the mice’s brains, the research group also succeeded in re-programming the mice’s own glia cells to become nerve cells. “The research findings have the potential to open the way for alternatives to cell transplants in the future, which would remove previous obstacles to research, such as the difficulty of getting the brain to accept foreign cells, and the risk of tumor development,” said Dr. Parmar.

Cal Tech Scientists Pinpoint Origin of Olfactory Neurons

When our noses pick up a scent, whether the aroma of a sweet rose or the sweat of a stranger at the gym, two types of sensory neurons are at work in sensing that odor or pheromone. These sensory neurons are particularly interesting because they are the only neurons in our bodies that regenerate throughout adult life—as some of our olfactory neurons die, they are soon replaced by newborns. Just where those neurons come from in the first place has long perplexed developmental biologists. Previous hypotheses about the origin of these olfactory nerve cells have given credit to embryonic cells that develop into skin or the central nervous system, where ear and eye sensory neurons, respectively, are thought to originate. But biologists at the California Institute of Technology (Caltech) have now found that neural-crest stem cells—multipotent, migratory cells unique to vertebrates that give rise to many structures in the body such as facial bones and smooth muscle—also play a key role in building olfactory sensory neurons in the nose. "Olfactory neurons have long been thought to be solely derived from a thickened portion of the ectoderm; our results directly refute that concept," says Dr. Marianne Bronner, the Albert Billings Ruddock Professor of Biology at Caltech and corresponding author of a paper published online in the open-access journal eLIFEon March 19, 2013 that outlines the findings. A related article (U. of Sheffield) was published online in eLIFE on March 26, 2013. eLIFE is backed by three of the most prestigious biomedical research funders in the world: the Howard Hughes Medical Institute, the Max Planck Society, and the Wellcome Trust.

March 25th

Akt Suppression May Prevent Herpes Virus Infections

Researchers at Albert Einstein College of Medicine of Yeshiva University in New York City have discovered a novel strategy for preventing infections due to the highly common herpes simplex viruses, the microbes responsible for causing genital herpes (herpes simplex virus 2) and cold sores (herpes simplex virus 1). The finding, published online on March 18, 2013 in The FASEB Journal, could lead to new drugs for treating or suppressing herpes virus infections. "We've essentially identified the molecular "key" that herpes viruses use to penetrate cell membranes and infect cells of the human body," said Betsy Herold, M.D., professor of pediatrics (infectious diseases), of microbiology & immunology and of obstetrics & gynecology and women's health at Einstein and attending physician of pediatrics, The Children's Hospital at Montefiore. Herpes viruses are known to infect skin cells as well as cells lining the cervix and the genital tract. A 2006 JAMA study estimated that nearly 60 percent of U.S. men and women between the ages of 14 and 49 carry the HSV-1 virus. The Centers for Disease Control (CDC) estimated that about 1 in 6 Americans (16.2 percent) between 14 and 49 are infected with herpes simplex virus type 2 (HSV-2), according to a 2010 national health survey. HSV-2 is a lifelong and incurable infection that can cause recurrent and painful genital sores and can make those infected with the virus two-to-three times more likely to acquire HIV, the virus that causes AIDS. Dr. Herold and her colleagues had previously shown that infection by the herpes viruses depends on calcium released within the cells. In this study, they found that calcium release occurs because the viruses activate a critical cell-signaling molecule called Akt at the cell membrane.

Possible Major Progress on Beta-Thalassemia, Hemochromatosis, and Polycythemia Vera

Two studies led by investigators at Weill Cornell Medical College in New York City shed light on the molecular biology of three blood disorders, leading to novel strategies to treat these diseases. The two new studies -- one published online on March 17, 2013 in Nature Medicine and the other published online on March 25, 2013 in an open-access article in the Journal of Clinical Investigation -- propose two new treatments for beta-thalassemia, a blood disorder which affects thousands of people globally every year. In addition, they suggest a new strategy to treat thousands of Caucasians of Northern European ancestry diagnosed with HFE-related hemochromatosis (i.e., hemochromatosis caused by a defect in the HFE gene) and a novel approach to the treatment of the rare blood disorder called polycythemia vera. These research insights were only possible because two teams that included 24 investigators at six American and European institutions decoded the body's exquisite regulation of iron, as well as its factory-like production of red blood cells. "When you tease apart the mechanisms leading to these serious disorders, you find elegant ways to manipulate the system," says Dr. Stefano Rivella, associate professor of genetic medicine in pediatrics at Weill Cornell Medical College. For example, Dr. Rivella says, two different gene mutations lead to different outcomes. In beta-thalassemia, patients suffer from anemia -- the lack of healthy red blood cells -- and, as a consequence, iron overload. In HFE-related hemochromatosis, patients suffer of iron overload. However, he adds, one treatment strategy that regulates the body's use of iron may work for both disorders.

T-Cell Therapy Eradicates an Aggressive Leukemia in Two Children

Two children with an aggressive form of childhood leukemia had a complete remission of their disease—showing no evidence of cancer cells in their bodies—after treatment with a novel cell therapy that reprogrammed their immune cells to rapidly multiply and destroy leukemia cells. A research team from The Children's Hospital of Philadelphia and the University of Pennsylvania published the case report of two pediatric patients online on March 25, 2013 in an open-access article in The New England Journal of Medicine. One of the patients, 7-year-old Emily Whitehead (photo), was featured in news stories in December 2012 after the experimental therapy led to her dramatic recovery after she relapsed following conventional treatment. Emily remains healthy and cancer-free, 11 months after receiving bioengineered T cells that zeroed in on a target found in this type of leukemia, called acute lymphoblastic leukemia (ALL). The other patient, a 10-year-old girl, who also had a complete response to the same treatment, suffered a relapse two months later when other leukemia cells appeared that did not harbor the specific cell receptor targeted by the therapy. "This study describes how these cells have a potent anticancer effect in children," said co-first author Stephan A. Grupp, M.D., Ph.D., of The Children's Hospital of Philadelphia, where both patients were treated in this clinical trial. "However, we also learned that in some patients with ALL, we will need to further modify the treatment to target other molecules on the surface of leukemia cells." Dr. Grupp is the director of Translational Research for the Center for Childhood Cancer Research at The Children's Hospital of Philadelphia, and a professor of Pediatrics at the Perelman School of Medicine at the University of Pennsylvania.

46-Gene Sequencing Test for Cancer Patients in UK’s National Health Service

The first multi-gene DNA sequencing test that can help predict cancer patients' responses to treatment has been launched in the National Health Service (NHS) in the UK, thanks to a partnership between scientists at the University of Oxford and the Oxford University Hospitals NHS Trust. The test uses the latest DNA sequencing techniques to detect mutations across 46 genes that may be driving cancer growth in patients with solid tumors. The presence of a mutation in a gene can potentially determine which treatment a patient should receive. The researchers say the number of genes tested marks a step change in introducing next-generation DNA sequencing technology into the NHS, and heralds the arrival of genomic medicine with whole genome sequencing of patients just around the corner. The many-gene sequencing test has been launched through the National Institute for Health Research (NIHR) Oxford Biomedical Research Centre (BRC), a collaboration between the Oxford University Hospitals NHS Trust and Oxford University to accelerate healthcare innovation, and which has partly funded this initiative. The BRC Molecular Diagnostics Centre carries out the test. The lab, based at Oxford University Hospitals, covers all cancer patients in the Thames Valley area. But the scientists are looking to scale this up into a truly national NHS service through the course of this year. The new £300 test could save significantly more in drug costs by getting patients on to the right treatments straightaway, reducing harm from side effects as well as the time lost before arriving at an effective treatment. “We are the first to introduce a multi-gene diagnostic test for tumor profiling on the NHS using the latest DNA sequencing technology,” says Dr.