You may have read about recent research, published in Science,Â describing a technique for revealingÂ which viruses have infected someone by scanning antiviral antibodies in the blood.
Emory immunologistsÂ have identified corresponding cells in which long-lived antibody production resides. A subset of plasma cells keep a catalog of how an adultâ€™s immune system responded to infections decades ago, in childhood encounters with measles or mumps viruses.
The results, published Tuesday, July 14 inÂ Immunity, could provide vaccine designers with a goalpost when aiming for long-lasting antibody production.
â€œIf youâ€™re developing a vaccine, you want to fill up this compartment with cells that respond to your target antigen,â€ says co-senior author F. Eun-Hyung Lee, MD, assistant professor of medicine at Emory University School of Medicine and director of Emory Healthcareâ€™s Asthma, Allergy and Immunology program.
The findings could advance investigation of autoimmune diseases such as lupus erythematosus or rheumatoid arthritis, by better defining the cells that produce auto-reactive antibodies.
Lee says that her team’s research on plasma cells in humansÂ provided insights unavailable from mice, since mice don’t live as long and their plasma cellsÂ also have a different patternÂ of protein markers.Â More here.
Non-alcoholic fatty liver disease (NAFLD) is one of the most common liver conditions in the United States, affecting 30 percent of the population, and increasing — and likely to catch up in prevalence with obesity and diabetes. In NAFLD, fat content of the liver is elevated to 6 percent or more in people who drink in moderation or not at all. Patients will first present with elevated liver enzyme values in blood tests, but then an imaging test or tissue biopsy may be ordered to evaluate the extent of the damage. NAFLD is mostly asymptomatic and is variable in severity; a majority of those afflicted do not need drug treatments. However, NAFLD is thought to be a preliminary condition that can eventually progress to severe manifestations, such as cirrhosis, hepatocellular carcinoma, and end stage liver failure.
Progression of liver disease, from NIDDK.
This is a guest post from Kristina Bargeron Clark, a MMG graduate student at Emory and communications chair for Women in Bio-Atlanta. Her website is www.inkcetera.org.
At Emory, Frank Anania, director of the Department of Medicineâ€™s Division of Digestive Diseases, and his colleagues are developing a tool to treat liver disease. A recent publication in the FASEB Journal describes their investigation into the potential for the hormone adiponectin to modulate liver fibrosis.
Adiponectin is produced by adipose tissue, but is known to decrease in overweight people with metabolic disease. Research by others indicates that it may prevent heart and kidney fibrosis. The Emory teamâ€™s studies were conducted to determine if adiponectin could also reduce liver fibrosis.
Neale Weitzmann and George Beck have been publishing a series of papers describingÂ how silica nanoparticles can increase bone mineral density in animals. Their findings could someday form the basis for a treatment for osteoporosis.
In 2012, we posted an article and video on this topic. We wanted to call attention to a few of theÂ team’sÂ recent papers, one of which probes the mechanism for aÂ remarkable phenomenon: how can very fine silica particles stimulate bone formation?
The particlesâ€™ properties seem to depend on their size: 50 nanometers wide â€“ smaller than a HIV or influenza vision.Â In a 2014 ACS Nano paper, Beck, Weitzmann and postdoc Shin-Woo Ha show that the particles interact with particular proteins involved in the process of autophagy, a process of â€œself digestionâ€ induced by stress.
â€œThese studies suggest that it is not the material per se that stimulates autophagy but rather size or shape,â€ they write. Read more
Severe sepsis, a consequence of the bodyâ€™s response to infection, is a major cause of death in hospitals. The earlier that doctors recognize that a patient has sepsis, the earlier the patient can be treated with antibiotics, fluids and other measures, and the better the chance of survival.
Thatâ€™s why critical care and emergency medicine researchers have been looking for ways to spotÂ whether someone coming to the hospitalÂ might haveÂ sepsis, even before arrival.
At Emory, Carmen Polito, Jonathan Sevransky and colleagues recently published a paper in the American Journal of Emergency Medicine on an emergency medical services screening tool for severe sepsis. Polito and Sevransky are in the division of pulmonary, allergy, critical care and sleep medicine in the Department of Medicine. The tool was evaluated based on Grady emergency medical services data from 2011 and 2012.
â€œSepsis is largely a face without a name in the EMS setting, â€œ Polito says. â€œThe goal of our study was to create a tool to assist EMS providers in naming this deadly condition at the point of first medical contact. Similar to other life-threatening, time-sensitive conditions like stroke and heart attack, naming sepsis is the first step in developing coordinated care pathways that focus on delivering rapid, life-saving treatment once the patient arrives at the hospital.â€
Cardiologist Bob Taylor and colleagues have a new paper in PLOS One this week, looking at the biomechanical forces behind plaque erosion.
Plaque erosion is a mechanism for blood clots formation in coronary arteries that is not as well-understood as its more explosive counterpart, plaque rupture. Plaque erosion disproportionally affects women more than men and is thought to account for most heart attacks in younger womenÂ (women younger than 50).
â€œWe believe that this work has implications for our better understanding of the underlying biology of coronary artery disease in women,â€ Taylor says. The first author of the paper isÂ biomedical engineering graduate student Ian Campbell, who now has his PhD. The team collaborated with cardiovascular pathologist Renu Virmani in Maryland.
Cardiologists have well-developedÂ ideas for how plaque rupture works*; see the concept of â€œvulnerable plaque.â€ Cholesterol and inflammatory cells build up in the coronary arteries over several years. At one point in a particular artery, the plaque has a core of dying inflammatory cells, covered by a fibrous cap. If the cap is thin (the patterns of blood flows near the cap influence this), there is a risk that the cap will break and the contents of the core will spill out, triggering a blood clot nearby.
Plaque erosion is more mysterious and can occur more gradually, the researchers have found. Read more