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Archive - Jun 8, 2019

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Using MicroRNA from Exosomes to Detect Early Signs of Type 2 Diabetes in Teens-- Hyperglycemic Obese Teens Have Different Exosomes Than Normoglycemic Obese Teens, with MicroRNAs Targeting Carbohydrate Metabolism & Visceral Fat

Researchers know that exosomes, tiny subcellular membrane-bound nanoparticles released from fat cells (and all cells studied), travel through the bloodstream and body, regulating a variety of processes, from growth and development to metabolism. The exosomes are important in lean, healthy individuals in maintaining homeostasis, but when fat gets “sick,” the most common reason for this is too much weight gain—the exosomes from fat cells show an altered phenotype, becoming inflammatory, and they can disrupt how our organs function, from how our skeletal muscle and liver metabolize sugar to how our blood vessels process cholesterol. Robert J. Freishtat (photo), MD, MPH, the Chief of Emergency medicine at Children's National Health System and a Professor of Precision Medicine and Genomics at the George Washington University School of Medicine and Health Sciences, and Sheela N. Magge MD, MSCE, who is now the Director of Pediatric Endocrinology and an Associate Professor of Medicine at the Johns Hopkins School of Medicine, were curious about what this process looked like in teens who fell in the mid-range of obesity. Obesity is a major risk factor for insulin resistance and type 2 diabetes, but Dr. Freishtat and Dr. Magge wanted to know: Why do some teens with obesity develop type 2 diabetes over others? Why are some teens in this mid-range of obesity metabolically healthy while others have metabolic syndrome? Can fat in obese people become sick and drive disease? To test this, Dr. Freishtat and Dr. Magge worked with 55 obese adolescents, ages 12 to 17, as part of a study at Children's National Health System. The participants (32 obese normoglycemic youth and 23 obese hyperglycemic youth) were similar in age, sex, race, pubertal stage, body mass index, and overall fat mass.

Hepatitis C Virus (HCV) Inhibits Normal Immune Response by Triggering Suppressor of Cytokine Signaling (SOCS) Regulator Molecule

Scientists from Trinity College Dublin have discovered how the highly infectious and sometimes deadly hepatitis C virus (HCV) "ghosts" our immune system and remains undiagnosed in many people. The rsearchers reported their findings on June 5, 2019 in The FASEB Journal. The article is titled “The Hepatitis C Virus (HCV) Protein, P7, Suppresses Inflammatory Responses to Tumor Necrosis Factor (TNF)-α Via Signal Transducer and Activator of Transcription (STAT)3 and Extracellular Signal-Regulated Kinase (ERK)–Mediated Induction of Suppressor of Cytokine Signaling (SOCS)3.” HCV's main route of transmission is via infected blood, but over the past 40 years, the virus has accidentally been given to many patients across the world via infected blood products. The virus replicates particularly well in the liver, and the damage it causes makes it a leading cause of liver disease worldwide. Even though HCV can be deadly, initial infection is rarely accompanied by any obvious clinical symptoms for reasons that have, until now, remained unknown. As a result, it often goes undiagnosed for the first 6-12 months following infection. If left untreated, HCV spreads throughout the liver, stimulating a low-level inflammatory response. Over several months, these mild responses, accompanied by subsequent liver repair, result in fibrotic scarring of the liver. The liver's main job is to filter out toxins, but during HCV infection the build-up of fibrotic, non-functioning liver tissue, results in reduced liver function. Without a fully functioning liver, one major side-effect is the build-up of toxins, often manifest as "jaundice.” If patients do not realize they are infected with HCV, their first noticeable symptoms are the side-effects of liver fibrosis (such as jaundice).

Scientists Edge Closer to Root Causes of Multiple Sclerosis; Study of 32 Families Having Multiple Members with MS Demonstrates 12 Different Disease-Associated Candidate Genes; These Genes May Offer Guideposts to Development of Effective MS Treatment

An international team of researchers led by the University of British Columbia scientists has made a scientific advance they hope will lead to the development of preventative treatments for multiple sclerosis (MS). In a study published online on June 6, 2019 in PLOS Genetics, researchers found mutations in 12 genes believed to be largely responsible for the onset of MS in families with multiple members diagnosed with the disease. The open-access article is titled “Exome Sequencing in Multiple Sclerosis Families Identifies 12 Candidate Genes and Nominates Biological Pathways for the Genesis ff Disease.” "These genes are like a lighthouse illuminating where the root cause of MS is," said lead author Carles Vilariño-Güell, PhD, Assistant Professor in the UBC Faculty of Medicine's Department of Medical Genetics and a Michael Smith Scholar. MS is a disease that affects the central nervous system, in which cells from the immune system attack and damage the nerve cells' protective myelin sheath (see larger image at end). The disease often results in disability and can have a significant impact on quality of life. For this study, researchers sequenced all known genes in three or more MS patients from 34 families and examined the genetic variants in family members both affected by and unaffected by MS. By looking at the genes of 132 patients, they identified 12 genetic mutations that can lead to an overactive autoimmune system that attacks myelin, the insulating layer around nerves in the brain and spinal cord. Of people diagnosed with MS, only 13 per cent are believed to have a genetic form of the disease, but those presenting the mutations identified in this new study were estimated to have an up to 85 per cent chance of developing MS in their lifetime. Dr.