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Archive - Jul 31, 2014

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C. difficile Vaccine Proves Safe and 100 Percent Effective in Animal Models

An experimental vaccine protected 100 percent of animal models against the highly infectious and virulent bacterium, Clostridium difficile (image), which causes an intestinal disease that kills approximately 30,000 Americans annually. The research was published ahead of print on July 14, 2014 in Infection and Immunity. In the study, the vaccine protected the mice and non-human primates against the purified toxins produced by C. difficile, as well as from an orogastric spore infection, a laboratory model that mimics the human disease, after only two immunizations. "Animals that received two immunizations did not get sick or show signs of C. difficile-associated disease," says corresponding author Michele Kutzler, Ph.D., of Drexel University College of Medicine, Philadelphia. "While our research was conducted in animal models, the results are very translatable to the clinic," says Dr. Kutzler. "In some cases, patients who acquire C. difficile can develop serious complications including severe diarrhea, toxic megacolon, bowel perforation, multi-organ failure, and death. Once fully developed, our DNA vaccine could prevent the deadly effects of C. difficile infection when administered to hospital patients at risk of acquiring C. difficile." The protection following just two immunizations is especially important because the time window in humans between colonization with C. difficile and the onset of disease symptoms can be a mere 10-14 days, says Dr. Kutzler. The vaccine protects against the bacterial toxins by mustering anti-toxin neutralizing antibodies, says Dr. Kutzler. The cost of fighting the half million C. difficile infections that occur annually in the U.S. is estimated to be nearly $10 billion, most of which could be saved by a successful preventive vaccine, says Dr. Kutzler.

Researchers Uncover Cause of Gum Disease Related to Type 2 Diabetes

Going to the dentist isn't fun for anyone, but for those with periodontal disease related to type 2 diabetes, a new research discovery may have them smiling. In a report appearing in the August 2014 issue of the Journal of Leukocyte Biology, one of the most important blood cells involved in the human immune response, B cells (image), are shown to promote inflammation and bone loss in type 2 diabetes-associated periodontal disease. These findings support the idea that treatments that manipulate the responses of B cells may treat or prevent this complication. "Our study identified common inflammatory mechanisms shared by type 2 diabetes and periodontal disease. It paves the way for the development of novel therapeutics which aim to simultaneously treat both type 2 diabetes and its complications," said Min Zhu, Ph.D., a researcher involved in the work from the department of microbiology at Boston University School of Medicine in Boston, Massachusetts. To make this discovery, scientists used an experimental model (mouse model) of periodontal disease and applied it to two groups. The first group had a genetic alteration that knocked out all B cells. The second group had normal B cell levels. When fed a low-fat diet, without development of obesity and type 2 diabetes, both groups demonstrated a similar extent of oral bone loss and inflammation. However, when they were fed a high-fat diet, became obese, and developed type 2 diabetes, oral bone loss and inflammation occurred in the normal group with B cells, but did not develop in the group with the altered gene to knock out the B cells. This suggests that the B cell-response might be a viable target for pharmacological intervention in both type 2 diabetes and periodontal disease, as well as potentially in other type 2 diabetes complications.

Exploring 3-D Printing to Make Organs for Transplants

Printing whole new organs for transplants sounds like something out of a sci-fi movie, but the real-life budding technology could one day make actual kidneys, livers, hearts, and other organs for patients who desperately need them. In the American Chemical Society journal Langmuir, scientists reported online on July 8, 2014 new understanding about the dynamics of 3-D bioprinting that takes them a step closer to realizing their goal of making working tissues and organs on demand. Yong Huang and colleagues note that this idea of producing tissues and organs, or biofabricating, has the potential to address the shortage of organ donations. And biofabricated organs and tissues could even someday be made with a patient's own cells, lowering the risk of rejection. Today, more than 120,000 people are on waiting lists for donated organs, with most needing kidney transplants. But between January and April of this year, just short of 10,000 people received the transplant they needed. There are a few different biofabricating methods, but inkjet printing has emerged as a frontrunner. It's been used to print live cells, from hamster ovary cells to human fibroblasts, which are a common type of cell in the body. But no studies had been done to really understand how biological inks behave when they're dispensed through printer nozzles. Huang's team set out to fill that gap. They tested bioinks with different concentrations of mouse fibroblasts plus a hydrogel made out of sodium alginate. They discovered, among other findings, that adding more cells in the material reduces both the droplet size and the rate at which it gets dispensed. The new results will help scientists move forward with this promising technology.

Resistance to Key Malaria Drug Spreading at Alarming Rate in Southeast Asia

Resistance to artemisinin, the main drug to treat malaria, is now widespread throughout Southeast Asia, among the Plasmodium falciparum (P. falciparum) parasites (image) that cause the disease and is likely caused by a genetic mutation in the parasites. However, a six-day course of artemisinin-based combination therapy—as opposed to a standard three-day course—has proved highly effective in treating drug-resistant malaria cases, according to findings published today in the July 31, 2014 issue of the New England Journal of Medicine. The research was conducted by an international team of scientists including those from the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health. Previous clinical and laboratory studies suggest that P. falciparum parasites with a mutant version of a gene called K13-propeller are resistant to artemisinin. In the new study, researchers found that the geographic distribution of these mutant parasites in Western Cambodia corresponded with the recent spread of drug resistance among malaria patients in that region. Although artemisinin continued to effectively clear malaria infections among patients in this region, the parasites with the genetic mutation were eliminated more slowly, according to the authors. Slow-clearing infections strongly associated with this genetic mutation were found in additional areas, validating this marker of resistance outside of Cambodia. Artemisinin resistance is now firmly established in areas of Cambodia, Myanmar, Thailand, and Vietnam, according to the authors. As a potential treatment, the researchers tested a six-day course of artemisinin-based combination therapy in Western Cambodia and found the regimen to be effective in this region, where resistance has become the most problematic.

A New Way to Generate Insulin-Producing Cells in Type 1 Diabetes Using Peptide from Tree Frog

A new study by researchers at Sanford-Burnham Medical Research Institute (Sanford-Burnham) in La Jolla, California, has found that a peptide called caerulein can convert existing cells in the pancreas into those cells destroyed in type 1 diabetes-insulin-producing beta cells. The study, published online July 31, 2014 open-access article in Cell Death and Disease, suggests a new approach to treating the estimated 3 million people in the U.S., and over 300 million worldwide, living with type 1 diabetes. "We have found a promising technique for type 1 diabetics to restore the body's ability to produce insulin. By introducing caerulein to the pancreas, we were able to generate new beta cells—the cells that produce insulin—potentially freeing patients from daily doses of insulin to manage their blood-sugar levels." said Fred Levine, M.D., Ph.D., professor and director of the Sanford Children's Health Research Center at Sanford-Burnham. The study first examined how mice in which almost all beta cells were destroyed—similar to humans with type 1 diabetes—responded to injections of caerulein. In those mice, but not in normal mice, they found that caerulein caused existing alpha cells in the pancreas to differentiate into insulin-producing beta cells. Alpha cells and beta cells are both endocrine cells meaning they synthesize and secrete hormones—and they exist right next to one another in the pancreas in structures called islets. However, alpha cells do not normally become beta cells. The research team then examined human pancreatic tissue from type 1 diabetics, finding strong evidence that the same process induced by caerulein also occurred in the pancreases of those individuals.