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Archive - Nov 9, 2015

Starving Chicks Become Fat Birds! Disadvantaged Chicks Seem to Show “Memory of Early Hunger” and Tend to Overeat As Adults When Plentiful Food Available; Possible Human Analogy

A Newcastle University (UK) study has shown that baby starling birds that have a difficult start in life grow to be fatter and greedier than their more fortunate siblings. The researchers, led by Professor Melissa Bateson and Dr Clare Andrews, discovered that stress and other difficulties as a chick made a long-lasting impression on a starling's relationship with food. The new study, published in an open-access article in the November 2015 issue of Animal Behaviour and funded by the Biotechnology and Bilogical Sciences Research Council (BBSRC), showed that the smallest chicks in European starling families changed their adult feeding behavior, resulting in a fatter body composition in the fully developed birds. The article is titled “Early Life Adversity Increases Foraging and Information Gathering in European Starlings, Sturnus vulgaris.” Dr. Andrews, of the Newcastle University Centre for Behaviorr and Evolution said: "Building up body fat reserves as a safeguard against times of potential future famine is an evolved survival mechanism. What we have shown is that birds that had struggled against larger brothers or sisters for food early on were keener on finding food and tended to overeat when they became adults." "This study may also teach us something about ourselves as, surprisingly, there's evidence that obesity is common in people lacking a reliable supply of food. Perhaps people too have evolved to eat more and take more interest in food if worried where their next meal will come from." To ensure that some birds were disadvantaged by experiencing greater competition, smaller starling chicks were placed in a brood with significantly larger hatchlings.

Signaling Protein Tpl2 That Regulates Interferons Is Key to Immune Defense Against Influenza Infection; Tpl2 Knockout Mice Show 10-Fold Higher Influenza Virus Titers, Decreased Cytotoxic T-Cell Numbers, & Reduced Levels of Type III Interferons

Infectious disease researchers at the University of Georgia (UGA) have identified a signaling protein critical for host defense against influenza infection. The findings, published on xxxxxx in the open-access journal PLOS Pathogens, shed light on how a single component of the body's defense system promotes effective immunity against viral infections, particularly respiratory viruses that affect mucosal sites. The new article is titled “Tumor Progression Locus 2 Promotes Induction of IFNλ, Interferon-Stimulated Genes, and Antigen-Specific CD8+ T Cell Responses and Protects Against Influenza Virus.” The tumor progression locus 2 protein (Tpl2) is an important regulator of the immune response, controlling signaling downstream of cell-surface and intracellular receptors that recognize the presence of pathogens. Tpl2 regulates the production of a group of immune signaling proteins called interferons. Though interferon production is known to play a large role in host defense against viral infections, prior to this study little was known about how Tpl2 functions in that environment. The new study demonstrates a key role for Tpl2 in induction of anti-viral genes, including those for Type III interferons, a type of immune signaling protein, important in mediating antiviral responses. "Tpl2 regulates inflammation and inflammation is a necessary part of a host's defense against infection," said Wendy Watford (photo), Ph.D. (from Duke University), corresponding author on the study and an Associate Professor of Infectious Diseases in the UGA College of Veterinary Medicine. Ongoing projects in Dr. Watford's lab seek to understand how Tpl2 modulates the host immune response in different disease settings.

Extremely High Levels of Vitamin C (Equivalent to Levels in 300 Oranges) Impair Growth of Two Major Forms of Colorectal Cancer (KRAF-Mutant and BRAF-Mutant) in Cell Culture & Animal Model Tests

High levels of vitamin C kill certain kinds of colorectal cancers in cell cultures and mice, according to a new study from Weill Cornell Medicine investigators. The findings suggest that scientists might` one day harness vitamin C to develop targeted treatments. Colorectal cancer is the third most-common cancer diagnosed in the United States, with approximately 93,090 new cases each year. About half of those cases harbor mutations in the KRAS and BRAF genes; these forms of the disease are more aggressive and don't respond well to current therapies or chemotherapy. In a new study, published onlie on November 5, 2015 in an open-acces article in Science, a team of researchers from Weill Cornell Medicine, Cold Spring Harbor Laboratory, Tufts Medical Center, Harvard Medical School, and The Johns Hopkins Kimmel Cancer Center found that high doses of vitamin C (roughly equivalent to the levels found in 300 oranges) impaired the growth of KRAS-mutant and BRAF-mutant colorectal tumors in cultured cells and mice. The findings could lead to the development of new treatments and provide critical insights into who would most benefit from them. The Science article is titled “Vitamin C Selectively Kills KRAS and BRAF Mutant Colorectal Cancer Cells by Targeting GAPDH.” "Our findings provide a mechanistic rationale for exploring the therapeutic use of vitamin C to treat colorectal cancers that carry KRAS or BRAF mutations," said senior author Dr. Lewis Cantley, the Meyer Director of the Sandra and Edward Meyer Cancer Center and the Margaret and Herman Sokol Professor in Oncology Research at Weill Cornell Medicine. The conventional wisdom is that vitamin C improves health, in part because it can act as an antioxidant, preventing or delaying some types of cell damage. However, Dr.

Men with Thicker Cortex in Brain’s Fusiform Face Area (FFA) Are Better at Identifying Non-Living Objects; Those with Thinner Cortex in FFA Are Better at Identifying Faces and Living Objects

When you see a familiar face, when a bird-watcher catches a glimpse of a rare bird perched on a limb, or when a car-fancier spots a classic auto driving past, the same small region in the brain becomes engaged. For almost two decades, neuroscientists have known that this area, called the fusiform face area (FFA), plays a vital role in the brain's ability to recognize faces and objects that an individual has learned to identify. Now a new study, published online on October 6, 2015 in the Journal of Cognitive Neuroscience, has taken this one step farther by finding that the thickness of the cortex in the FFA (as measured using magnetic resonance imaging) can predict a person's ability to recognize faces and objects. The article is titled “Cortical Thickness in Fusiform Face Area Predicts Face and Object Recognition Performance.” "It is the first time we have found a direct relationship between brain structure and visual expertise," said Isabel Gauthier, Ph.D., David K. Wilson Professor of Psychology at Vanderbilt University, who directed the study. "It shows more clearly than ever that this part of the brain is relevant to both face and object recognition abilities." Relationships between cortical thickness and other types of processes, such as motor learning and acquisition of musical skills, have been observed before. The relationship seems relatively straightforward: the process of learning to type faster or play a violin causes the neurons in the relevant area of the cortex to make new connections, which causes the cortex to appear thicker. However, the link between cortical thickness and how well we recognize faces and objects turns out to have a surprising twist.

Helen Hobbs Awarded $3 Million 2016 Breakthrough Prize in Life Sciences for Transformative Genetics Research Techniques Developed and Used to ID Key Genes in Lipid Metabolism and Fatty Liver Disease; Mark Zuckerberg Helps Host Awards Ceremony

This year’s Breakthrough Prizes in Life Sciences of $3 million each have been awarded to five outstanding scientists, including Helen Hobbs, M.D., who is Director of the Eugene McDermott Center for Human Growth and Development at the University of Texas (UT) Southwestern, and also a Howard Hughes Medical Institute (HHMI) Investigator, in recognition of transformative genetics research techniques she developed and used to identify key genes involved in lipid metabolism and fatty liver disease. In addition to Dr. Hobbs, recipients of the 2016 Breakthrough PrizeS in Life sciences are Edward S. Boyden (MIT), Karl Deisseroth (Stanford, HHMI), John Hardy (University College London), and Svante Pääbo (Max Planck Institute for Evolutionary Anthropology). Please see the titles of the awards to the five recipients of the 2016 Breakthrough Prizes in Life Sciences at the end of this article. The Breakthrough Prize, an international award established in 2012 by Russian entrepreneur Yuri Milner, Google co-founder Sergey Brin, Facebook founder Mark Zuckerberg, and Alibaba founder Jack Ma, awards annual prizes of $3 million for ground-breaking discoveries in the fields of Mathematics, Physics, and Life Sciences. “Dr. Hobbs is an exceptional physician-scientist and a highly respected member of our faculty,” said Dr. Daniel K. Podolsky, President of UT Southwestern. “The Dallas Heart Study, which she pioneered and has led for the last 15 years, has proved to be a powerful resource for defining the genetic basis of human biology and disease, including mechanisms controlling cholesterol metabolism.” Dr. Podolsky holds the Philip O’Bryan Montgomery, Jr., M.D. Distinguished Presidential Chair in Academic Administration, and the Doris and Bryan Wildenthal Distinguished Chair in Medical Science.

Novel Fusion Protein Drug Targeted at Immune Checkpoint Inhibits Secretion of Disease-Related Inflammatory Cytokines in Co-Culture Cell Model for Rheumatoid Arthritis, Compugen Reports

Compugen Ltd. (NASDAQ: CGEN), a leading predictive drug discoverybeing held November 6-11 in San Francisco, California, the company has disclosed recent results from a translational company headquartered in Tel Aviv, Israel, announced, on November 9, 2015, that, in an oral presentation at the 2015 ACR/ARHP Annual Meeting study supporting the potential treatment of rheumatoid arthritis (RA) with Compugen’s RA candidate drug CGEN-15001. CGEN-15001 is an Fc fusion protein based on one of the multiple novel immune checkpoint candidates discovered by the Company. The translational study, conducted in collaboration with Professor Iain B. McInnes, M.D., Ph.D., from the University of Glasgow in Scotland, was designed to evaluate the potential to translate the efficacy of CGEN-15001, previously observed in animal models of RA disease, to human patients. Professor McInnes is a world-renowned clinician and scientist in the field of rheumatology and a member of Compugen’s scientific advisory board. He is Professor of Medicine, Muirhead Chair of Medicine, and Director of the Institute of Infection, Immunity, and Inflammation at the University of Glasgow. The study’s experimental design utilizes co-cultures of immune cells from individual RA patients that mimic the deleterious interaction of these cells within the joints of RA patients. This interaction drives secretion of pro-inflammatory proteins known as cytokines that have a major role in RA pathology, leading to chronic progressive joint inflammation and damage. Thus, these co-cultures provide a translational tool to evaluate the effect of potential drugs for treatment of RA.