In the online May 2 issue of the journal Cell Metabolism, researchers at the University of California, San Diego School of Medicine publish three distinct articles exploring: the complex interactions of lipids and inflammation in insulin resistance the roles of omega 3 fatty acids and a particular gene in fighting inflammation how elevated levels of a particular protein might delay the muscle-destroying effects of amyotrophic lateral sclerosis. Type 2 diabetes has reached epidemic proportions around the world, fueled in large part by the equally alarming expansion of obesity as a global health problem. But while it's well-known that obesity is the most common cause of insulin resistance - the primary metabolic abnormality in type 2 diabetes - researchers have only recently begun to effectively parse the underlying, complicated relationships between lipids (fats and related molecules essential to cell structure and function) and chronic tissue inflammation (a key cause of obesity-induced insulin resistance).
One of the major routes of tumor cell dissemination to form metastasis at distant organs in the body is the lymphatic system. To study this process, still poorly understood, and to gain information on which tumors prefer this route for dissemination and how to block it, researchers of the Spanish National Cancer Research Center (CNIO), led by researcher Sagrario Ortega, have created transgenic mice in which, for the first time, the growth of the lymphatic vessels can be visualized in the whole animal, by a light-emitting reaction, as tumor progresses and forms metastasis. The technique is so sensitive that it allows monitoring those lymph nodes that are going to be invaded by tumor cells. The work is published in the journal PNAS (Proceedings of the National Academy of Sciences). The normal physiological function of the lymphatic vessels is to collect fluid, molecules and cells from tissues and transport them to the blood stream.
In children under the age of 2, respiratory syncytial virus (RSV) is a major cause of respiratory illness. However, Sylvia van den Hurk and her team at the University of Saskatchewan are closing in on a needle-free vaccine for the virus and clinical trials are expected to begin in about two years. Van den Hurk, explained: "It's one of the most important respiratory infections in young babies. And there's no vaccine." For the majority of children and adults, the virus may only produce symptoms of a common cold, such as runny nose, sore throat, mild headache, dry cough, and light fever. However, in young infants, RSV can cause pneumonia or bronchiolitis, with difficulty breathing, severe cough and high fever. The outlook is usually good when children have access to good care, including respirators to deliver supplementary oxygen, although when they don't have access to good care the outlook is a problem.
No Link Found Between Measles-Containing Vaccines And Increased Risk Of Febrile Seizures In Children 4-6
Vaccines for measles were not associated with an increased risk of febrile seizures* among 4-6 year olds during the six weeks after vaccination, according to a study by the Kaiser Permanente Vaccine Study Center that appears in the current issue of Pediatrics. Funded by the U.S. Centers for Disease Control, the study of 86, 750 children follows an earlier study published in Pediatrics that showed one particular combination of measles-containing vaccine - the measles, mumps, rubella and chickenpox containing vaccination (or MMRV) - was associated with an increased risk of febrile seizures in 1-to-2-year-old children, compared with same-day administration of the separate vaccine for MMR (measles, mumps, rubella) and the V (varicella) vaccine for chicken pox. This new study sought to evaluate, for the first time, the risk of febrile seizures following MMRV or separate MMR plus V vaccines among 4-6 year olds and found no increased risk of febrile seizures, said study lead author Nicola Klein, MD, PhD, co-director of the Kaiser Permanente Vaccine Study Center.
AUTOIMMUNITY Understanding bone loss in rheumatoid arthritis patients Rheumatoid arthritis causes joint stiffness and pain for over 2 million Americans. The disease is caused by an errant attack on healthy tissue by the body's immune system. Antibodies found in some patients target specific types of modified proteins, called citrullinated proteins, and are associated with an increased risk of bone destruction. Dr. Georg Schett and fellow researchers at University of Erlangen-Nuremberg in Germany suspected that these particular self-reactive antibodies directly influence bone loss that can sometimes occur in rheumatoid arthritis. They found that antibodies against citrullinated proteins bind to osteoclasts, specialized cells that break down bone tissue. In a mouse model system, they demonstrated that infusion of antibodies recognizing a cirtullinated protein activated osteoclasts and triggered bone resorption, resulting in the breakdown of bone and release of calcium.