Tumor cells have evolved a crafty scheme for protecting themselves from the killing power of the host immune system; in part, they disable the immune response. New studies implicate a receptor for prostaglandin E2 (PGE2) in this phenomenon of tumor-induced immune suppression. The findings, published in the March 1 Journal of Clinical Investigation, suggest that drugs that block the PGE2 receptor, called EP2, might restore the immune system’s tumor-killing capacity.
New research into the origin of kidney stone formation published in the March 1 issue of the Journal of Clinical Investigation may well change the direction of the most basic level of research in that area. The study will dispel the current beliefs of where stone formation begins, said the article’s lead author, adding that the research confirmed instead a hypothesis published in 1940 by Alexander Randall, M.D.
Eclampsia, the occurrence of often fatal seizures during pregnancy, is preceded by a condition called preeclampsia. Preeclampsia itself is a serious complication of pregnancy and affects up to 5% of pregnant women. Diagnosed in its early stages by elevated blood pressure and protein levels in the urine, it is the major cause of premature birth and perinatal child death and accounts for approximately 15% of all maternal deaths. Despite decades of intensive research, we still do not know what causes preeclampsia.
Genetic differences that prevent tiny blood vessels from relaxing may be one reason why some people have high blood pressure, or hypertension, according to research led by scientists at Washington University School of Medicine in St. Louis. The findings are published in the February issue of the Journal of Clinical Investigation. “These findings provide new insights into the cause of hypertension and how normal blood pressure is regulated,” says lead investigator Kendall J. Blumer, Ph.D., professor of cell biology and physiology. “This may lead to a way of determining the underlying cause of a person’s hypertension and the most effective treatment for that individual.”
Researchers have found that a recently discovered gene regulates HDL (high density lipoproteins) cholesterol, also known as “good” cholesterol. The study, published in the February issue of the Journal of Clinical Investigation, could lead to new therapies for heart disease, said lead author Thomas Quertermous, MD. “This is a significant and unexpected finding, and the gene is going to be a real target for the prevention and treatment of heart disease,” said Quertermous, the William G. Irwin Professor and chief of cardiovascular medicine at Stanford University School of Medicine. “This type of thing doesn’t happen every day.”
The hormone leptin, primarily produced in fat cells, helps regulate food intake, metabolism and reproduction. It has also been shown to promote and sustain the body’s immune response by binding to T lymphocytes – the frontline cells that protect against infection.
The disease experimental autoimmune encephalomyelitis (EAE) in mice is currently used by researchers as a model of human multiple sclerosis (MS). Italian researchers now reports that just prior to developing the clinical symptoms of EAE, mice experience a significant burst of leptin which correlates with a reduction in food intake and weight loss. Furthermore, subjecting mice to acute starvation, which prevents the production of leptin, was found to delay the onset and reduce the severity of disease.
A cousin to the anti-anxiety drug Valium has been shown in mice to reduce some of the symptoms associated with lupus. Lupus is an autoimmune condition in which the immune system attacks the body’s own tissues. “The best available therapies for lupus haven’t changed for many, many years,” says U-M’s Gary D. Glick, Ph.D., one of the lead authors on the study. “It’s a disease where the mechanisms that normally prevent the immune system from attacking components of one’s own body are defective. Because we do not yet understand what triggers lupus, it has been very difficult to develop lupus-specific therapies.”