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In Systemic Lupus Erythematosus Models, Novel DNA Vaccine Leads To Kidney Damage Prevention
DNA vaccination using lupus autoantigens and interleukin-10 (IL-10, a cytokine that plays an important role in regulating the immune system) has potential as a novel therapy to induce antigen specific tolerance and may help to prevent kidney damage in patients with systemic lupus erythematosus (SLE), according to a new study presented at EULAR 2009, the Annual Congress of the European League Against Rheumatism in Copenhagen, Denmark.

Instrumental Variable Analysis: Is The Cure Worse Than The Disease?
Causal inference is challenging in all non-experimental studies because of the possibility of hidden bias. Hidden bias may exist as a result of failure to control for unobservable factors, such as doctors" practice/prescription patterns.
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ENT And Allergy Initiates A 'First Of Its Kind' Self-Insured Medical Malpractice Program
ENT and Allergy Associates, LLP (ENTA), is pleased to announce the formation of OASIS (i.e., Otolaryngology, Allergy Specialty Insurance Services), a separate company that will be a vehicle to provide Otolaryngology and Allergy Specific medical malpractice coverage. OASIS, which will be domiciled in the State of Vermont, is the first RRG to provide medical malpractice coverage exclusively to ENT physicians and Allergists. ENTA decided to embark on this path as a means of stabilizing its malpractice premiums in the face of mounting deficits among the State"s largest carriers and the failure of the legislature to pass any meaningful tort reform. These factors will most likely result in substantial premium increases well into the future. In addition, ENTA, now a 96 physician practice, will be able to focus on controlling the risks unique to its specialty to ensure patient safety and physician compliance with its risk management policies.
Public Health

Role For Innate, Not Adaptive, Immunity Revealed By Autoinflammatory Disease Model

Researchers at the University of California, San Diego School of Medicine have developed the first mouse model for auto-inflammatory diseases, disorders that involve the over-activation of the body"s innate, primitive immune system. Their study, published early on-line in Cell Immunity on June 4, suggests that the innate - not adaptive - immune system drives auto-inflammatory diseases. The findings could open new therapeutic directions for research into disorders such as gout or inflammatory bowel disease. "Auto-inflammatory diseases are a relatively new classification of diseases that are different from autoimmune diseases or allergies," said Hal Hoffman, MD, associate professor of medicine at UC San Diego School of Medicine. Hoffman studies a group of rare, inherited auto-inflammatory conditions called Cryopyrin-Associated Periodic Syndromes (CAPS), which includes Familial Cold Auto-inflammatory Syndrome (FCAS) and Muckle-Wells Syndrome (MWS). Autoimmune diseases arise from an overactive response of the body"s adaptive, or acquired, immune system against substances and tissues normally present in the body. Allergies are also a product of the adaptive immune system, but in response to environmental substances. Both involve the action of lymphocytes such as B cells and T cells. The older innate immune system, on the other hand, recruits immune cells to sites of infection and inflammation, but doesn"t confer long-time protection. Pathogens evoke an inappropriate response that doesn"t involve antibodies or lymphocytes. With CAPS, Hoffman had earlier discovered that mutations of the NLRP3 gene caused the auto-inflammatory disease symptoms because the gene causes alterations in the protein called cryopyrin. Cryopyrin regulates the release of interleukin-1, an important mediator of fever and systemic inflammation during the body"s innate immune response, and alterations in cryopyrin lead to over-production of Il-1. Mutations in the NLRP3 gene are thought to result in inappropriate activation of a multi-protein complex called an inflammasome, leading to excessive Il-1í² release and manifestation of CAPS disease symptoms. Treatment with Il-1í² inhibitors reduces the inflammation and symptoms in auto-inflammatory diseases; however, NLRP3 may have other effects in addition to increased Il-1í². "Patients treated with the Il-1í² inhibitors got much better, but still exhibited some symptoms," said Hoffman. In order to examine the role of inflammatory mediators and adaptive immune responses in CAPS, the researchers developed two NLRP3 mutant knock-in mouse models. (In "knock-in" models, genetic information is inserted into a particular part of the genome; in contrast to "knock-out" mouse models, in which genetic information is removed.) These mice had systemic inflammation and poor growth, similar to some human patients. By mating these mice to mice with various gene mutant backgrounds, the scientists showed that CAPS requires an intact inflammasome, is only partially dependent on Il-1í² and is independent of T cells. Their findings may help lead to more effective treatments for CAPS syndromes. "The data shows that CAPS are true inflammasome-mediated diseases and that the adaptive immune system is not necessary for this disease," said Hoffman. "In the larger picture, our findings also suggest that innate and adaptive immune systems don"t necessarily always "cross talk" or communicate with one another." According to the researchers, given the importance of IL-- and the inflammasome to innate immunity, NLRP3 knock-in mice may be applied to the study of many diseases along the autoinflammatory-autoimmune spectrum. Notes: Additional contributors to the study include UCSD researchers Susannah D. Brydges, James L. Mueller, Matthew D. McGeough, Carla A. Pena, Amirhossein Misaghi, Chhavi Gandhi, Chris D. Putnam, David L. Boyle, Gary S. Firestein and Anthony A. Horner; Pejman Soroosh of the La Jolla Institute of Allergy and Immunology; and Wendy T. Watford, John J O"Shea and Daniel L. Kastner of the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS). Mueller and Putnam are also faculty members with the Ludwig Institute of Cancer Research. This work was funded by the National Institutes of Health and NIAMS. Dr. Hoffman has received consultant fees from Regeneron and Novartis Pharmaceuticals. Debra Kain University of California - San Diego


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