apoptosis
Researchers have found that blocking a kind of cell death called apoptosis in fibrotic diseases of the lung, also blocks the fibrosis, opening new ways of looking at treatment for lung diseases such as pulmonary fibrosis. The team examined how a molecule called TGF-beta causes apoptosis and abnormal scarring in the lungs. There are a variety of human diseases where normal tissue is replaced with scar tissue that doesn't function the same way as the original tissue. This results in dysfunction of the skin or other involved organ. People can develop fibrosis of the skin, which leads to conditions like sclerodoma, where the skin thickens. When this occurs in the lungs, it is called pulmonary fibrosis.
Researchers have successfully designed and improved a new type of cancer-killing compound by performing molecular surgery to stabilize the molecule so that it selectively triggers cell death. Using the biologically active portion of a protein that triggers apoptosis, the team successfully inserted non-natural amino acids into the peptide sequence and then performed a chemical reaction that created a ''staple'' within the molecule, resulting in its stabilization. The chemical approach they applied, called hydrocarbon stapling, permitted the researchers to overcome the tendency of short peptides to lose their critical three-dimensional structure -- and their ability to kill cells -- when removed from the context of the complete protein.
Treatment with a new dual cell cycle and angiogenesis pathway inhibitor blocks VEGF-induced vascular permeability, inhibits tumor growth and cell death, researchers said today. Runaway growth and tumor-induced angiogenesis (development of new blood vessels to supply the growing tumor with oxygen) are two major hallmarks of cancer.
An underlying principle of female reproductive biology appears to have been overturned by a new study. The investigators report that female mice retain the ability to make new egg cells well into adulthood. It has been believed that most female mammals are born with a finite supply of these cells, called oocytes, that are lost at a steady rate until the supply is exhausted, leading to menopause in women.
When recovering from a heart attack or stroke, the body must restore blood flow in order to resupply cells with oxygen. Ironically, the process of reoxygenation - so necessary for full recovery - also generates reactive oxygen species (ROS), molecules that induce apoptosis, or cellular death. Now, researchers have identified a biochemical strategy to block ROS - which effectively prevents cellular damage and death.
Researchers have for the first time described a method that Staphylococcus aureus (staph) infection uses to inactivate the body's immune system. A protein produced by the staph bacteria causes previously healthy B cells -- a specialized cell of the immune system -- to commit suicide, a process called apoptosis. "By the targeted elimination of disease-causing B cells, properly dosed injections of SpA may have the potential to control the over-activity of the immune system that causes damage in autoimmune diseases like lupus and in certain cancers," said Gregg Silverman, M.D., UCSD professor of medicine and senior author of the paper.
The method that Staphylococcus aureus (staph) infection uses to inactivate the body's immune response and cause previously healthy B cells to commit suicide, is described for the first time by researchers at the University of California, San Diego (UCSD) School of Medicine. Normally, B cells mount an early defense against invading bacteria. From this immunologic experience, memory B cells are developed with the ability to quickly recognize these antigens and destroy the bacteria if they return in the future. When staph infections occur, however, this important process for immune defense can be corrupted.
Scientists have discovered that the genetic mutation that causes the childhood cancer retinoblastoma routinely triggers fetal death and miscarriage in laboratory animals by disrupting the normal functions of the placenta, a finding that may force researchers to reevaluate the powerful Rb gene and the role it plays in causing cancer.
Researchers have found that a recently discovered gene plays an essential role in mediating apoptosis, or cell death, in colorectal cancer cells. The gene, PUMA, or p53 up-regulated modulator of apoptosis, is controlled by p53 ? a tumor-suppressing gene that prevents normal cells from turning into life-threatening tumor cells. Previous research has determined that damage to p53 is fundamental to the development of a vast majority of cancers, and inactivation of the growth-controlling function of p53 is critical to the growth and spread of most cancers.
A new study designed to find out why cells in the eye die when exposed to lead may provide novel therapies for retinal damage caused by injury or diseases such as diabetes and retinitis pigmentosa.
The study, published in the Feb. 4 issue of the Proceedings of the National Academy of Sciences, focused on identifying how low-level lead exposure during development in mice injures and eventually kills rod-shaped photoreceptor cells, or rods, in the eye. Rods are cells in the eye that help humans see in dim light. The other type of photoreceptors, or light-gathering cells, called cones are responsible for color and spatial vision. Cones are used primarily in daylight and for activities such as reading.
UCLA scientists report that 11 days of daily exercise and the Pritikin low-fat, high-fiber diet induce prostate cancer cells to die. The research, published in the new issue of the journal Cancer Causes and Control, is the first to show that diet and exercise can kill prostate cancer cells. "You can make changes in a short period of time that have a dramatic impact on your health ? in this case, on the growth and death of prostate tumor cells," said R. James Barnard, professor of physiological science at UCLA and lead investigator on the study.
Trimming the waistline may not be the only reason to cut calories after the New Year: Doing so also may protect the brain from aging. In the first study to look specifically at the effects of life-long calorie-restricted diets on brain cells, University of Florida researchers determined certain proteins linked to cell death that naturally increase with age were significantly reduced in the brains of rats whose calories were limited. More important, they found the levels of a beneficial protein known to provide potent protection against neuron death were twice as high in older rats whose calories were restricted by 40 percent.
The process that makes fireflies glow bright in the summer night can also shed light on how well new medicines work, showing immediately whether the drugs are effective at killing cells or causing other effects. That's the conclusion of a team of scientists who report that they have inserted the gene for a firefly's glow-producing molecule into mice with cancer, and kept it from producing its telltale beacon of light until the cells started to die in response to cancer treatment.
Researchers have discovered a cellular basis for what many have long suspected: Men, as well as women, have a reproductive clock that ticks down with age. A recent study revealed that sperm in men older than 35 showed more DNA damage than that of men in the younger age group. In addition, the older men's bodies appeared less efficient at eliminating the damaged cells, which could pass along problems to offspring
Fatty acids from fish oils and fatty fish can destroy the power station - the mitochondria- in certain types of cancer cells, making the cells commit suicide. These are the conclusions in a Norwegian researcher, who says polyunsaturated omega-3 fatty acid ingested by different leukemia/lymphoma cell lines can cause the cells to shut down.
