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Scorpion Venom Toxins Found to Have Components with Anti-Bacterial Activity; Stanford Scientists Synthesize These Components in the Lab; May Point Way to New Weapons Against Increasingly Drug-Resistant Bacteria

A scorpion native to Eastern Mexico may have more than just toxin in its sting. Researchers at Stanford University and in Mexico have found that the venom also contains two color-changing compounds that could help fight bacterial infections. The team not only isolated the compounds in the scorpion's venom, but also synthesized them in the lab and verified that the lab-made versions killed staphylococcus and drug-resistant tuberculosis bacteria in tissue samples and in mice. The findings, published online on June 10, 2019 in PNAS, highlight the potential pharmacological treasures awaiting discovery in the toxins of scorpions, snakes, snails, and other poisonous creatures. The PNAS article is titled “1,4-Benzoquinone Antimicrobial Agents Against Staphylococcus Aureus and Mycobacterium tuberculosis Derived from Scorpion Venom.” "By volume, scorpion venom is one of the most precious materials in the world. It would costs $39 million to produce a gallon of it," said study senior author Richard Zare (https://web.stanford.edu/group/Zarelab/about.html), PhD, who led the Stanford group. "If you depended only on scorpions to produce it, nobody could afford it, so it's important to identify what the critical ingredients are and be able to synthesize them." Dr. Zare worked with his colleagues in Mexico, including Lourival Possani, PhD, a Professor of Molecular Medicine at the National University of Mexico, whose students caught specimens of the scorpion Diplocentrus melici for study. "The collection of this species of scorpion is difficult because during the winter and dry seasons, the scorpion is buried," Dr. Possani said. "We can only find it in the rainy season." For the past 45 years, Dr. Possani has focused on identifying compounds with pharmacological potential in scorpion venom.

Rhes Protein Initiates Construction of Nanotubes That Enable Travel of Huntington’s Disease Protein from Cell to Cell

A toxic protein (huntingtin) linked to Huntington’s disease can move from neuron to neuron through a nanotube tunnel whose construction is initiated by a protein called Rhes, say scientists at Scripps Research-Florida. The finding, by Scripps Research neuroscientist Srinivasa Subramaniam, PhD, improves understanding of how and why this disease attacks and destroys certain brain cells. The research was published online on May 10, 2019 in Journal of Cell Biology. The article is titled “Rhes Travels from Cell to Cell and Transports Huntington Disease Protein Via TNT-Like Cellular Protrusions.” “We are excited about this result because it may explain why the patient gets the disease in this area of the brain called the striatum,” says Dr. Subramaniam, an Associate Professor in the Department of Neuroscience at Scripps Research-Florida. People with Huntington’s disease inherit a mutant gene that codes for an aberrant protein that is somehow complicit in destroying brain cells. Scientists discovered this protein in 1993, but are still piecing together its role in this degenerative disease. Scans show Huntington’s disease brains are shrunken and degraded. As the neurons deteriorate, people lose motor control, they can have emotional problems, and their thinking and memory suffer. Symptoms usually begin around age 30 to 40 and last 15 to 20 years until death. A rarer and more aggressive form of the disease affects children, cutting their childhood and their lives short. About 3 to 7 people out of 100,000 have the disease and it has mostly affected those with European ancestry. However, Dr. Subramaniam believes the disease is underreported in other areas, such as India. “There is a lot of stigma associated with the disease,” says Subramaniam.

Additional Findings Suggest Diet Changes Could Lead to Better Prevention and Management of Type 2 Diabetes

Could changing what we eat lower the chances of developing type 2 diabetes? Studies presented at Nutrition 2019 will examine how consuming certain foods, vitamins and even the order in which we eat can affect blood sugar levels and risk of developing 2 diabetes. Nutrition 2019 is being held June 8-11, 2019 at the Baltimore Convention Center. In a study of 2,717 young adults in the US with long-term follow-up, people who increased the amount of fruits, vegetables, whole grains, nuts and vegetable oils in their diet over 20 years had a 60 percent lower risk of type 2 diabetes compared to those with a small decrease in plant foods. The findings suggest that long-term shifts toward a more plant-centered diet could help prevent diabetes. Yuni Choi, PhD candidate, University of Minnesota-Twin Cities, will present this research on Tuesday, June 11, from 11 - 11:15 a.m. in the Baltimore Convention Center, Ballroom IV. The presentation is titled “Life Course Change Towards a Plant-Centered Diet and Incidence of Type 2 Diabetes: The Coronary Artery Risk Development in Young Adults (CARDIA) Study” (https://www.eventscribe.com/2019/ASN/fsPopup.asp?Mode=presInfo&Presentat...). Findings from a second study examining three large cohorts of US health professionals suggest that people with higher intakes of vitamins B2 and B6 from food or supplements have a lower risk for type 2 diabetes. The study, which included more than 200,000 people, also revealed that consuming higher levels of vitamin B12 from foods was associated with a higher type 2 diabetes risk, which may be due to consumption of animal products. Kim V. E. Braun, PhD, Erasmus University Medical Center, presented this research on Sunday, June 9, from 3:15 - 3:30 p.m. in the Baltimore Convention Center.

Large International Study Finds Diabetes Drug (Dulaglutide) Cuts Cardiovascular & Kidney Problems in Older Patients with Type 2 Diabetes; Dulaglutide Is Glucagon-Like Peptide-1 Receptor Agonist; Two Articles in The Lancet

A clinical trial that followed more than 9,900 people in 24 countries has found that the drug dulaglutide reduced cardiovascular events and kidney problems in middle-aged and older people with Type 2 diabetes. During more than five years of follow-up, cardiovascular events like heart attacks and strokes were reduced by 12% in people taking dulaglutide compared to people taking a placebo. This effect was seen in both men and women with or without previous cardiovascular disease. In addition, during the same period, the drug reduced the development of kidney disease by 15%. The trial was led by the Population Health Research Institute (PHRI) of McMaster University and Hamilton Health Sciences, both in Hamilton, Ontario, Canada. Two papers describing the cardiovascular and kidney results of the trial were published on June 9, 2019 in The Lancet from the study called the Researching Cardiovascular Events with a Weekly Incretin in Diabetes (REWIND) trial. The two articles are titled “Dulaglutide and Cardiovascular Outcomes in Type 2 Diabetes (REWIND): a Double-Blind, Randomised Placebo-Controlled Trial” and “Dulaglutide and Renal Outcomes in Type 2 Diabetes: an Exploratory Analysis of the REWIND Randomised, Placebo-Controlled Trial.” "Compared to others, people with diabetes have twice the rate of cardiovascular events like heart attacks and strokes, and up to 40% of people with diabetes develop kidney disease," said Hertzel C. Gerstein (photo), MD, principal investigator for the study, Professor of Medicine at McMaster and Deputy Director of the PHRI. "The REWIND trial shows that dulaglutide can safely reduce these events while improving diabetes control and modestly lowering weight and blood pressure in middle-aged people with Type 2 diabetes."

Experimental Drug Delays Type 1 Diabetes in People at High Risk; NIH-Funded Study Shows That Immunotherapy with Monoclonal Anti-CD3 Antibody (Teplizumab) Slows Progression to Clinical Disease by Two Years or More

A treatment affecting the immune system effectively slowed the progression to clinical type 1 diabetes in high-risk individuals, according to findings from National Institutes of Health-funded research. The study is the first to show that clinical type 1 diabetes can be delayed by two or more years among people who are at high risk. These results were published online on June 9, 2019 in The New England Journal of Medicine and presented at the American Diabetes Association Scientific Sessions (June 7-11) in San Francisco. The NEJM article is titled “An Anti-CD3 Antibody, Teplizumab, in Relatives at Risk for Type 1 Diabetes.” The study, involving treatment with an anti-CD3 monoclonal antibody (teplizumab), was conducted by Type 1 Diabetes TrialNet (https://www.trialnet.org/), an international collaboration aimed at discovering ways to delay or prevent type 1 diabetes. Researchers enrolled 76 participants ages 8-49 who were relatives of people with type 1 diabetes, had at least two types of diabetes-related autoantibodies (proteins made by the immune system), and abnormal glucose (sugar) tolerance. Participants were randomly assigned to either the treatment group, which received a 14-day course of teplizumab, or the control group, which received a placebo. All participants received glucose tolerance tests regularly until the study was completed, or until they developed clinical type 1 diabetes - whichever came first. During the trial, 72% of people in the control group developed clinical diabetes, compared to only 43% of the teplizumab group. The median time for people in the control group to develop clinical diabetes was just over 24 months, while those who developed clinical diabetes in the treatment group had a median time of 48 months before progressing to diagnosis.

Oral Administration of Antigen-Specific Exosomes Carrying MicroRNA-150 Suppresses Delayed-Type Hypersensitivity (DTH) Underlying Casein Allergy in Mouse Model; Results Suggest Possible Treatment Approach for Patients with Clinical Conditions Like Asthma

A publication in the April 23, 2019 issue of Nutrients presents new data, from the lab group of Philip Askenase (photo), MD, at the Yale University School of Medicine, describes the successful oral administration of suppressor T cell-derived exosomes strongly inhibiting immune inflammation in the skin. Exosomes are nano-sized, membrane-bounded vesicles secreted by cells, often to communicate between cells, mostly by exchange of RNAs. The article, which was included in Nutrients special issue "Cow's Milk and Allergy" is titled "Delayed-Type Hypersensitivity Underlying Casein Allergy Is Suppressed by Extracellular Vesicles Carrying miRNA-150." The results in this study were largely generated by visiting Professors Krzysztof Bryniarski and Katarzyna Nazimek from the Jagellonian College of Medicine in Krakow, Poland. The Askenase group studied allergic CD4pos T cell- and macrophage-orchestrated effector inflammation in the ear skin of mice that was strongly inhibited by oral administration of antigen-specific suppressor CD8pos T cell-derived exosomes delivering miRNA-150. Quantitated skin responses were measured kinetically over five days and the responses were to casein, a common protein of milk allergy. The antigen specificity was due to anti-casein antibody light chains coating the exosomes. This was demonstrated by flow cytometry, which also showed that the suppressive exosomes also expressed CD9, CD63, and CD81 (typical markers of classical exosomes) on their surfaces. The functioning exosomes were definitively identified by specific affinity column fractionation with beads linked to casein antigen and separately to anti-CD9. The exosomes were recovered and tested for function in vivo.

Millions of Cardiovascular Deaths Attributed to Not Eating Enough Fruits & Vegetables—New Study Tracks Toll of Suboptimal Fruit & Vegetable Intake By Region, Age, and Gender

Preliminary findings from a new study reveal that inadequate fruit and vegetable consumption may account for millions of deaths from heart disease and strokes each year. The study estimated that roughly 1 in 7 cardiovascular deaths could be attributed to not eating enough fruit and 1 in 12 cardiovascular deaths could be attributed to not eating enough vegetables. Low fruit intake resulted in nearly 1.8 million cardiovascular deaths in 2010, while low vegetable intake resulted in 1 million deaths, according to researchers. Overall, the toll of suboptimal fruit intake was almost double that of vegetables. The impacts were most acute in countries with the lowest average intakes of fruits and vegetables. "Fruits and vegetables are a modifiable component of diet that can impact preventable deaths globally," said lead study author Victoria Miller, PhD, a postdoctoral researcher at the Friedman School of Nutrition Science and Policy at Tufts University. "Our findings indicate the need for population-based efforts to increase fruit and vegetable consumption throughout the world." Dr. Miller presented the research findings at Nutrition 2019 (https://meeting.nutrition.org/), the American Society for Nutrition annual meeting, being held June 8-11, 2019 in Baltimore, Maryland. The title of her presentation (FS01-01-19)is “Estimated Global, Regional, and National Cardiovascular Disease Burdens Related to Fruit and Vegetable Consumption: An Analysis from the Global Dietary Database.”

Sun-Exposed Oyster Mushrooms Help Patients Fight Tuberculosis with Vitamin D

Tuberculosis (TB) remains one of the deadliest infectious diseases in low-income countries, with approximately 1.6 million people dying of the disease each year. In a new study, researchers show that sun-exposed oyster mushrooms offer a readily available source of vitamin D that can help TB patients respond better to anti-TB drugs by improving immune response. "TB is becoming more difficult to fight due to the emergence of drug-resistant strains, creating an urgent need for new treatments that can support first-line drugs," said TibebeSelassie Seyoum Keflie, a doctoral fellow at University of Hohenheim, in Stuttgart, Germany. "This source of vitamin D is ideal for low-income countries because mushrooms can easily be distributed and administered in a safe, low-cost, easy-to-replicate manner." Keflie, who performed the research with Hans Konrad Biesalski, PhD, at the University of Hohenheim, will present the research at Nutrition 2019 (https://meeting.nutrition.org/), the American Society for Nutrition annual meeting, held June 8-11, 2019 in Baltimore, Maryland. The title of the abstract (OR15-04-19) is “Vitamin D2 as Adjunctive Therapy of Tuberculosis” (https://www.eventscribe.com/2019/ASN/fsPopup.asp?Mode=presInfo&Presentat...). Studies have shown that vitamin D induces the body to form an antimicrobial compound that attacks the bacterial cause of TB. Although sun exposure can boost a person's vitamin D levels, it must be obtained through diet when sun exposure is scarce. The researchers used oyster mushrooms because they offer a cheap, safe, and readily available source of vitamin D that is easily absorbed by the body. Although fresh oyster mushrooms contain almost no vitamin D, the fungus produces it the after exposure to sunlight much like the human body.

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).

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