apoptosis

Many medical conditions destroy nerve axons, the long wires that transmit signals to other parts of the body. Now, researchers have found a way the body can remove injured axons, identifying a potential target for new drugs that could prevent the inappropriate loss of axons and maintain nerve function.

A workhorse of modern biology is sick, and scientists couldn’t be happier. Researchers at Washington University School of Medicine in St. Louis and other institutions have found that the nematode C. elegans, a millimeter-long worm used extensively for decades to study many aspects of biology, gets naturally occurring viral infections.

This PET scan shows high levels of an anticancer agent in the tumor.Cancer cells keep growing because they don’t react to internal signals urging them to die. Now researchers at the School of Medicine have found an efficient way to get a messenger into cancer cells that forces them to respond to death signals. And they did it using one of the most sinister pathogens around — HIV.

Researchers linked anticancer agents to a PET tracer to deliver treatment directly to tumors in mice (red and yellow shows highest amounts of tracer).Cancer cells keep growing because they don’t react to internal signals urging them to die. Now researchers at Washington University School of Medicine in St. Louis have found an efficient way to get a messenger into cancer cells that forces them to respond to death signals. And they did it using one of the most sinister pathogens around — HIV.

Patients in intensive care units are kept alive with breathing machines, dialysis, tube feeding and other extraordinary measures until their bodies can begin to recover from critical illness or traumatic injury.Sepsis, sometimes called blood poisoning, is the leading cause of death among critically ill patients in the United States. For many years, scientists believed it was the result of an uncontrolled inflammatory response, but several studies that involved anti-inflammatory drugs were not successful at improving survival. Now, a research team led by Richard S. Hotchkiss, M.D., professor of anesthesiology and of medicine and associate professor of surgery and of molecular biology and pharmacology, and Irene E. Karl, Ph.D., research professor of medicine at Washington University School of Medicine in St. Louis have found that how immune cells die in sepsis might be a key to whether patients survive. When immune cells die through a process known as programmed cell death, or apoptosis, a patient’s chance of survival appears to be much lower than if cells die through a different mechanism called necrosis.