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Archive - Jun 19, 2017

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Scientists Demonstrate Adaptation of Animal Vision in Extreme Cold Environments; Rhodopsin Evolves to Increase Reaction Rates

Cell biologists at the University of Toronto (U of T) have discovered animals can adapt their ability to see even with extreme changes in temperature. The researchers looked deeply into the eyes of catfish living in cold-water streams at altitudes of up to nearly three kilometers (1.6 miles) in the Andes Mountains to find out how. Their findings were published online on June 19, 2017 in PNAS. The article is titled “Evolution of Non-Spectral Rhodopsin Function at High Altitudes.” Vision is initiated when several chemical proteins in the retina are activated. It is a key sensory system that enables organisms to adapt to their environment, as how killer whales did to improve their ability to see underwater in predominantly blue-tinted light. Examining the impact of cold temperatures on the habitats of Andean catfishes, the team of researchers led by U of T evolutionary biologist Belinda Chang, PhD, studied the role of a protein known as rhodopsin that enables vision in dim light. The scientists found that rhodopsin serves another function as well: it accelerates the speed at which vision occurs among the fish living at the highest - and therefore coldest - elevations. "When we think about adaptations to the visual system, light and color are usually the first variables that come to mind," said Dr. Chang, Professor in the Departments of Ecology & Evolutionary Biology and Cell & Systems Biology at U of T. "These results add a new dimension to the question of how complex biological processes can adapt to extreme environments." Vision is critical for these nocturnal animals' survival. In the high-altitude fishes, the rates at which the chemical reactions involving the protein occurred, changed. The kinetic rates sped up in order to compensate for decreases in ambient temperature.

New Three-In-One Blood Test (Liquid Biopsy) Opens Door to Precision Medicine for Prostate Cancer; Test Picks Out Men for Treatment, Detects Early Signs of Resistance, and Monitors Cancer's Evolution Over Time

Scientists have developed a three-in-one blood test that could transform treatment of advanced prostate cancer through use of precision drugs designed to target mutations in the BRCA genes. By testing cancer DNA in the bloodstream, researchers found they could pick out which men with advanced prostate cancer were likely to benefit from treatment with exciting new drugs called PARP inhibitors. The scientists also used the test to analyze DNA in the blood after treatment had started, so people who were not responding could be identified and switched to alternative therapy in as little as four to eight weeks. And finally, they used the test to monitor a patient's blood throughout treatment, quickly picking up signs that the cancer was evolving genetically and might be becoming resistant to the drugs. The researchers, at The Institute of Cancer Research, London, and The Royal Marsden NHS Foundation Trust, say their test is the first developed for a precision prostate cancer therapy targeted at specific genetic faults within tumors. It could, in the future, allow the PARP inhibitor olaparib to become a standard treatment for advanced prostate cancer, by targeting the drug at the men most likely to benefit, picking up early signs that it might not be working, and monitoring for the later development of resistance. The study was published online on June 19, 2017 in Cancer Discovery.

Scientists Identify Single-Gene (CARD11) Mutations That Lead to Atopic Dermatitis; Mutations Lead to Defective T-Cell Signaling; Study Points to Possible Therapeutic Effect of Supplemental Glutamine

Researchers have identified mutations in a gene called CARD11 that lead to atopic dermatitis, or eczema, an allergic skin disease. Scientists from the National Institute of Allergy and Infectious Diseases (NIAID) and other institutions discovered the mutations in four unrelated families with severe atopic dermatitis and studied the resulting cell-signaling defects that contribute to allergic disease. Their findings, reported online on June 19, 2017 in Nature Genetics, also suggest that some of these defects potentially could be corrected by supplementation with the amino acid glutamine. The article is titled “Germline Hypomorphic CARD11 Mutations in Severe Atopic Disease.” The scientists analyzed the genetic sequences of patients with severe atopic dermatitis and identified eight individuals from four families with mutations in the CARD11 gene, which provides instructions for production of a cell-signaling protein of the same name. While some people with these mutations had other health issues, such as infections, others did not, implying that mutations in CARD11 could cause atopic dermatitis without leading to other medical issues often found in severe immune system syndromes. The scientists next set out to understand how the newly discovered CARD11 mutations contribute to atopic dermatitis. Each of the four families had a distinct mutation that affected a different region of the CARD11 protein, but all the mutations had similar effects on T-cell signaling. With cell culture and other laboratory experiments, the researchers determined that the mutations led to defective activation of two cell-signaling pathways, one of which typically is activated in part by glutamine.