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Archive - Aug 20, 2015

Profoundly Different Mechanism of Hummingbird Nectar Consumption Discovered; Tongue Acts As Pump, Not Capillary; 50 Years of Nectar-Hummingbird Co-Evolution Research Must Now Be Reconsidered

In a paper titled “Hummingbird Tongues Are Elastic Micropumps,” which is featured as the cover article of the August 22, 2015 print issue of Proceedings of the Royal Society B, Dr. Alejandro Rico Guevara and Dr. Margaret Rubega from the Department of Ecology and Evolutionary Biology and Dr, Tai-Hsi Fan from the School of Engineering, al at the University of Connecticut, say that fluid is actually drawn into the tongue by the elastic expansion of the tongues grooves after they are squeezed flat by the beak. The article was published online, ahead of print, on August 19, 2015. The new data shows that fifty years of research describing how hummingbirds and floral nectar have co-evolved will have to be reconsidered. What is actually taking place, the researcher report, is that during the off-loading of the nectar inside the bill, hummingbirds compress their tongues upon extrusion. The compressed tongue remains flattened until it contacts the nectar surface, after which the tongue reshapes, filling entirely with nectar. The expansive filling mechanism uses the elastic recovery properties of the groove walls to load nectar on the tongue in an order of magnitude that allows the hummingbirds to extract nectar at higher rates than are predicted by capillarity-based foraging models. Observations and measurements were taken from seven countries throughout the Americas where free-living, never handled hummingbirds were feeding at modified transparent feeders simulating nectar volumes and concentrations of hummingbird-pollenated flowers. The researchers measured 96 foraging bouts of 32 local birds belonging to 18 species from seven out the nine main hummingbird clads. In the hundreds of licks studied, the researchers observed capillarity only once, acting on a single tongue groove.

Sloan-Kettering Reports First “Basket” Study, Categorizing Specific Cancer Mutations and Responses to Targeted Drugs, Exclusive of Cancer Origin Site; Described As “First Deliverable of Precision Medicine”

Researchers from the Memorial Sloan Kettering Cancer Center (MSKCC) in New York City have announced results from the first published “basket” study, a new form of clinical trial design that explores responses to drugs based on the specific mutations in patients' tumors rather than the site where their cancer originated. Published in today’s (August 20, 2015 issue of the New England Journal of Medicine, the early phase II study, led by MSKCC Physician-in-Chief and Chief Medical Officer José Baselga, M.D., Ph.D., looked at the effect of vemurafenib (Zelboraf®) in multiple non-melanoma BRAFV600-mutated cancers in 122 patients from 23 centers around the world. The article is titled “Vemurafenib in Multiple Nonmelanoma Cancers with BRAFV600 Mutations.” “Vemurafenib previously has been proven to treat BRAFV600-mutated melanoma. People with lung, colorectal, and ovarian cancers were among those included in the study, as well as people with rare diseases, such as Erdheim-Chester disease. Until this point, the efficacy of vemurafenib in non-melanoma cancers has remained unexplored despite significant therapeutic potential. "This study is the first deliverable of precision medicine. We have proven that histology-independent, biomarker-selected basket studies are feasible and can serve as a tool for developing molecularly targeted cancer therapy," said Dr. Baselga, the study's senior author. "While we can -- and should -- be cautiously optimistic, this is what the future of precision medicine looks like." Basket studies permit the detection of early signals of activity across multiple tumor types simultaneously, while allowing for the possibility that tumor lineage might influence drug sensitivity.

Synthetic DNA Vaccine, for First Time, Induces Protective Immunity to MERS Coronavirus in Non-Human Primates

A novel synthetic DNA vaccine can, for the first time, induce protective immunity against the Middle East Respiratory Syndrome (MERS) coronavirus in animal species, reported researchers from the Perelman School of Medicine at the University of Pennsylvania. David B. Weiner, Ph.D., a Professor of Pathology and Laboratory Medicine, together with colleagues, published their work in the August 19, 2015 issue of Science Translational Medicine (STM). The article is titled “A Synthetic Consensus Anti–Spike Protein DNA Vaccine Induces Protective Immunity Against Middle East Respiratory Syndrome Coronavirus in Nonhuman Primates.” The experimental, preventive vaccine, given six weeks before exposure to the MERS virus, was found to fully protect rhesus macaques from disease. The vaccine also generated potentially protective antibodies in blood drawn from camels, the purported source of MERS transmission in the Middle East. MERS is caused by an emerging human coronavirus, which is distinct from the SARS coronavirus. Since its identification in 2012, MERS has been linked to over 1,300 infections and close to 400 deaths. It has occurred in the Arabian Peninsula, Europe, and in the U.S. The recent 2015 outbreak in South Korea was of great concern as the infection spread from a single patient to infect more than 181 people, resulting in hospital closings, severe economic impact, and more than 30 deaths. During this outbreak rapid human-to-human transmission was documented, with in-hospital transmission the most common route of infection. "The significant recent increase in MERS cases, coupled with the lack of effective antiviral therapies or vaccines to treat or prevent this infection, have raised significant concern," Dr. Weiner said.

Revolutionary Sepsis-Treatment Device Optimized by Wyss Institute/Harvard Scientists in Effort to Speed Clinical Adoption of Life-Saving Additional Approach to Curing Deadly Sepsis; Engineered FcMBL Protein Is Key

In 2014, a team of sciencitsts from the Wyss Institute for Biologically Inspired Engineering at Harvard University described the development of a new device to treat sepsis that works by mimicking our spleen. It cleanses pathogens and toxins from blood circulating through a dialysis-like circuit. Now, the Wyss Institute team has developed an improved device that synergizes with conventional antibiotic therapies and has been streamlined to better position it for near-term translation to the clinic. The improved design is described in the October 2015 issue (volume 67) of Biomaterials and is available online now. Sepsis is a common, and frequently fatal, medical complication that can occur when a person's body attempts to fight off serious infection. Resulting widespread inflammation can cause organs to shut down, blood pressure to drop, and the heart to weaken. This can lead to septic shock, and more than 30 percent of septic patients in the United States eventually die. In most cases, the pathogen responsible for triggering the septic condition is never pinpointed, so clinicians blindly prescribe an antibiotic course in a blanket attempt to stave off infectious bacteria and halt the body's dangerous inflammatory response. But sepsis can be caused by a wide-ranging variety of pathogens that are not susceptible to antibiotics, including viruses, fungi, and parasites. What's more, even when antibiotics are effective at killing invading bacteria, the dead pathogens fragment and release toxins into the patient's bloodstream.