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Print ArticleResearchers at Cincinnati Children’s have issued the first study showing that a protein normally involved in blood clotting (fibrin), also plays an important role in the inflammatory response and development of rheumatoid arthritis. Inflammatory joint disease appears to be driven by the engagement of inflammatory cells with fibrin matrices through a specific integrin receptor, aMB2. Writing in the November issue of The Journal of Clinical Investigation, researchers suggest that therapies designed to interrupt the localized interaction of inflammatory cells and fibrin may help arthritis patients.
“Our study establishes that fibrin is a powerful, although context-dependent, determinant of inflammatory joint disease,” said Jay Degen, Ph.D., a researcher in Developmental Biology at Cincinnati Children’s and the study’s lead author. “These findings also suggest that pharmacologically interrupting the interaction of fibrin and aMB2 might be efficacious in the treatment of arthritic disease as well as many other inflammatory diseases, such as multiple sclerosis.”
Affecting 2.1 million people in the United States, rheumatoid arthritis is a painful and debilitating disease involving chronic inflammation, tissue degeneration, loss of cartilage and bone and ultimately loss of joint mobility and function, according to the National Institute of Arthritis and Musculoskeletal and Skin Diseases. Although the disease’s precise cause is not fully known, activation of specific components in the body’s immune system seem to play a major role in its onset and early progression, according to researchers. Fibrin deposits are a prominent feature of arthritic joints and the protein appears to be a link between systems that control inflammation and bleeding within joints. Dr. Degen and his colleagues explained that in arthritic joints, the mesh-like matrices formed by fibrin to create blood clots may control local activity of inflammatory cells as well as support inappropriate tissue reorganization.
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Arthritis is caused by noxious human pheromones, just like all the other autoimmune diseases. Soluble proteins, pheromone receptor proteins, attach transiently to much smaller pheromones, changing the protein's conformation. Pheromone receptor protein conformational change can desequester ions, altering potential difference across any nearby excitable membrane. The voltage change on a hyperpolarized membrane yields an epsp. Arthritis, like diabetes, atherosclerosis, multiple sclerosis, Alzheimer's disease, and many others, is an "intended" insult that degrades populations to better fit ecological circumstances. It's epigenetic. Pheromones can reach a cell and alter DNA function in the nucleus. Thus anti-epigenetic strategies, coupled with beneficial pheromone exposures (non-self human pheromonal skin surface lipids (700 + "butterfly pheromones") one, sebaleic acid is unique in all nature) should halt disease progression.
To prevent disease, we might try "shower caps" for "hot heads" who release noxious pheromone on angry emotion. We could attempt to prevent pheromone reception by warning people not to lacrimate emotional tears in proximity to "hot heads". The tears hold pheromone receptor proteins in them along with specialized mix of ionic species for sequestration/desequestration.
The upshot is that the "mistake" theory of arthritis and autoimmune disease is bankrupt. These autoimmune syndromes are purposeful devices that affect the human chemical ecology directly in feedback loops, just like hormones inside the body. We will go another hundred years of failure if the contemptible airheads at NIH aren't replaced with much smarter people.
I suggest lowering salaries across the board to discourage incompetent imbeciles seeking remuneration from filling most positions. Poverty is good for the soul. Abject poverty is good for creativity. Have lab-dwellers pay to heat their space in the building and let them buy podium time. Economics is a science, if you use it results will come. Use it not, and woe will persist and befall us all.
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