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Archive - May 2018

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May 9th

Tick Exosomes May Aid Transmission of Viruses to Vertebrates

Scientists have shown for the first time that exosomes from tick cells can aid transmission of viral proteins and genetic material from arthropod to vertebrate host cells, according to research published on January 4, 2018 in PLOS Pathogens. The open-access article is titled “Exosomes Serve As Novel Modes of Tick-Borne Flavivirus Transmission from Arthropod to Human Cells and Facilitates Dissemination of Viral RNA and Proteins to the Vertebrate Neuronal Cells.” When ticks (Ixodes scapularis species; commonly known as deer ticks) bite humans or other vertebrates, they can transmit dangerous, brain-infecting viruses in the Flaviviridae viral family, such as tick-borne encephalitis virus (TBEV). However, the mechanisms underlying transmission of Flaviviridae from tick to vertebrate host are poorly understood. Previous studies have shown that some other pathogens use exosomes--tiny, membrane-bound spheres released from cells--to facilitate transmission and infection. Dr. Hameeda Sultana of Old Dominion University, Virginia, and colleagues hypothesized that tick-borne Flaviviridae viruses may use similar techniques. To investigate this hypothesis, the researchers infected cells from an Ixodes scapularis-derived cell line (ISE6) with tick-borne Langat virus (LGTV), which is closely related to TBEV but safer for laboratory work. Using cryo-electron microscopy, they showed that infected tick cells indeed produced exosomes, and further investigation showed that these contained LGTV RNA and proteins. Additional experiments using human and vertebrate cell lines revealed more about the role of exosomes in LGTV transmission. LGTV-carrying tick exosomes were able to infect keratinocytes, cells found at the outermost layer of human skin and human blood endothelial cells.

May 2nd

NIH Will Launch Hugely Ambitious “All of Us” Research Program on May 6; Program Seeks to Enroll One Million Volunteers from Diverse & Traditionally Under-Represented Backgrounds to Participate in Innovative Effort to Advance Precision Medicine

On Sunday, May 6, 2018, the National Institutes of Health (NIH) will open national enrollment for the All of Us Research Program (https://www.joinallofus.org/en) a momentous effort to advance individualized prevention, treatment, and care for people of all backgrounds. People ages 18 and older, regardless of health status, will be able to enroll. The official launch date will be marked by community events (https://launch.joinallofus.org/) in seven cities across the country, as well as an online event. Volunteers will join more than 25,000 participants already enrolled in All of Us as part of a year-long beta test to prepare for the program’s national launch. The overall aim is to enroll 1 million or more volunteers and over-sample communities that have been underrepresented in research to make the program the largest, most diverse resource of its kind. “All of Us is an ambitious project that has the potential to revolutionize how we study disease and medicine,” Health and Human Services Secretary Alex Azar said. “NIH’s unprecedented effort will lay the scientific foundation for a new era of personalized, highly effective health care. We look forward to working with people of all backgrounds to take this major step forward for our nation’s health.” Precision medicine is an emerging approach to disease treatment and prevention that considers differences in people’s lifestyles, environments, and biological makeup, including genes. With eyeglasses and hearing aids, we have long had customized solutions to individual needs. More recently, treating certain types of cancer is now possible with therapies targeted to patients’ DNA. Still, there are many unanswered questions leaving individuals, their families, their communities, and the health care community without good options.

May 2nd

Algorithms Applied to EEG Results for Infants Accurately Predict Risk of Autism Spectrum DIsorder; “Stunning” Results May Provide Basis for Early Intervention

Autism is challenging to diagnose, especially early in life. A new study published online on May 1, 2018 in Scientific Reports shows that inexpensive EEGs, which measure brain electrical activity, accurately predict or rule out autism spectrum disorder (ASD) in infants, even in some as young as 3 months. The open-access article is titled “EEG Analytics for Early Detection of Autism Spectrum Disorder: A Data-Driven Approach.” "EEGs are low-cost, non-invasive and relatively easy to incorporate into well-baby checkups," says Charles Nelson, PhD, Director of the Laboratories of Cognitive Neuroscience at Boston Children's Hospital and co-author of the study. "Their reliability in predicting whether a child will develop autism raises the possibility of intervening very early, well before clear behavioral symptoms emerge. This could lead to better outcomes and perhaps even prevent some of the behaviors associated with ASD." The study analyzed data from the Infant Sibling Project (now called the Infant Screening Project), a collaboration between Boston Children's Hospital and Boston University that seeks to map early development and identify infants at risk for developing ASD and/or language and communication difficulties. William Bosl, PhD, Associate Professor of Health Informatics and Clinical Psychology at the University of San Francisco, also affiliated with the Computational Health Informatics Program (CHIP) at Boston Children's Hospital, has been working for close to a decade on algorithms to interpret EEG signals, the familiar squiggly lines generated by electrical activity in the brain. Dr. Bosl's research suggests that even an EEG that appears normal contains "deep" data that reflect brain function, connectivity patterns, and structure that can be found only with computer algorithms. The Infant Screening Project provided Dr.

Low Levels of Vasopressin Hormone in Cerebrospinal Fluid Possible Biomarker for Low Sociability Seen in Autism Spectrum Disorder

One of the characteristics of children with autism spectrum disorder is reduced social ability. It's difficult to study the possible causes of social impairment in children, but a new study shows that rhesus macaques with low sociability also had low levels of the peptide vasopressin in cerebrospinal fluid, as did children with autism spectrum disorder. The study, by researchers at the California National Primate Research Center (CNPRC) at the University of California (UC), Davis and Stanford University, was published online on May 2, 2018 in the journal Science Translational Medicine. The article is titled “Arginine Vasopressin in Cerebrospinal Fluid Is a Marker of Sociality in Nonhuman Primates.” "At this point, we consider vasopressin concentrations to be a biomarker for low sociability," said John Capitanio, PhD, Professor of Psychology at UC Davis and a research scientist at the CNPRC. Dr. Capitanio studies the interplay between social behavior and health. Over several years, his team has assessed rhesus macaque monkeys born at the Center for sociability. The Center maintains large field corrals where the macaques live in extended large family groups with the same hierarchies and social behavior that they show in the wild.nAbout fifteen percent of the animals are classed as "low social": they spend less time interacting with others than most macaques. Dr. Capitanio has previously studied how this natural variation affects the course of infectious disease. Professor Karen Parker at the Stanford Department of Psychiatry and Behavioral Sciences, principal investigator on the project, is interested in why children with autism spectrum disorder have deficits in social ability.

April 30th

Designer Peptoids Mimic Surfactant Proteins & Reduce Surface Tension in the Lungs, Restoring Breathing Capacity in Injured Lungs in Rat Model—Results “Open Up New Frontiers”

A Stanford University researcher has bioengineered an effective protein mimic that restored breathing capacity to the injured lungs of rats, according to a new study. This synthetic product could lead to better, cheaper treatments for acute lung injury in humans. When used in the rats, it equaled or outperformed a costly animal-derived counterpart in several physiological measures, the study said. A paper describing the research was published online May 1 in Scientific Reports. The open-access article is titled “Effective in vivo treatment of acute lung injury with helical, amphipathic peptoid mimics of pulmonary surfactant proteins. Imagine the force you'd need to blow up a balloon whose surface area nearly matched that of a tennis court. Imagine further that the balloon has a pocked, moist inner surface and is made of exquisitely delicate material. That balloon is your lungs, and every breath you take is a miracle. What makes it possible is a thin coating of a soap-like film, or surfactant, that lowers the tension of the lung's inner surface, radically reducing the amount of force required to inhale. Without this surfactant, you couldn't breathe. "Lung surfactant is endowed with amazing biological properties," said Annelise Barron (photo), PhD, Associate Professor of Bioengineering at Stanford. "The key to this is the presence, in the surfactant, of two special proteins whose structures uniquely enable them to cut surface tension." But those same amazing structural properties, she said, also make these proteins difficult to synthesize and purify, and relatively unstable in solution, limiting shelf-life and increasing price. "One of them contains the most hydrophobic, or fat-resembling, stretch of chemical constituents of all known human proteins," Dr. Barron said.