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Archive - Feb 28, 2018

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Single Non-Coding Nucleotide Difference Renders African Salmonella Variant Highly Lethal

Scientists at the University of Liverpool have identified a single genetic change in Salmonella that is playing a key role in the devastating epidemic of bloodstream infections currently killing approximately 400,000 people each year in sub-Saharan Africa. Invasive non-typhoidal Salmonellosis (iNTS) occurs when Salmonella bacteria, which normally cause gastrointestinal illness, enter the bloodstream and spread through the human body. The African iNTS epidemic is caused by a variant of Salmonella typhimurium (ST313) that is resistant to antibiotics and generally affects individuals with immune systems weakened by malaria or HIV. In a new study published online on February 27, 2018 in PNAS, a team of researchers led by Professor Jay Hinton at the University of Liverpool have identified a specific genetic change, a single-nucleotide polymorphism (SNP), that helps the African Salmonella to survive in the human bloodstream. The open-access article is titled “Role of a Single Noncoding Nucleotide in the Evolution of an Epidemic African Clade of Salmonella.” Professor Hinton explained: "Pinpointing this single letter of DNA is an exciting breakthrough in our understanding of why African Salmonella causes such a devastating disease, and helps to explain how this dangerous type of Salmonella evolved." SNPs represent a change of just one letter in the DNA sequence and there are thousands of SNP differences between different types of Salmonella. Until now, it has been hard to link an individual SNP to the ability of bacteria to cause disease. Using a type of RNA analysis called transcriptomics, the scientists identified SNPs that affected the level of expression of important Salmonella genes.

Study Suggests New Strategy Against Vascular Disease in Diabetes--Insulin-Mimicking Peptide Not Only Lowers Blood Sugars, But Also Slows Progression of Atherosclerosis In Mouse Model

Recent findings suggest a novel approach for protecting people with diabetes from their higher risk of advanced blood vessel disease, which sets the stage for early heart attacks and strokes. Cardiovascular problems from atherosclerosis - plaque-like lesions forming in artery walls - are the major cause of death in people with type 2 diabetes and metabolic syndrome. People with metabolic syndrome exceed the normal range for several clinical measurements: blood pressure, blood sugar levels, harmful lipids, body mass index, and belly fat. The researchers studied mice with metabolic syndrome. The mice were obese and had impaired glucose tolerance, a sign of pre-diabetes. In the study, an insulin-mimicking synthetic peptide called S597 was shown to both reduce blood sugar levels and slow the progression of atherosclerotic lesions. Insulin, even when it controls diabetes, does not prevent atherosclerosis. The findings were published in the February 26, 2018 issue of Diabetes. The article is titled “A Novel Strategy to Prevent Advanced Atherosclerosis and Lower Blood Glucose in a Mouse Model of Metabolic Syndrome.” The senior author is Karin E. Bornfeldt, University of Washington (UW) School of Medicine Professor of Medicine, Division of Metabolism, Endocrinology and Nutrition. Jenny Kanter, UW Research Assistant Professor of Medicine, was the lead author. They are scientists at the UW Medicine Diabetes Institute. The study was conducted as a research collaboration with Novo Nordisk A/S. Although S597 is composed of a single chain of amino acids and looks nothing like insulin, S597 can still activate insulin receptors. But, unlike insulin, it's more selective in what it turns on inside the cells.