LYCOS RETRIEVER 
Inflammation: Swelling
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Acute inflammation normally resolves by mechanisms that have remained somewhat elusive. Emerging evidence now suggests that an active, coordinated program of resolution initiates in the first few hours after an inflammatory response begins. After entering tissues, granulocytes promote the switch of arachidonic acid–derived prostaglandins and leukotrienes to lipoxins, which initiate the termination sequence. Neutrophil recruitment ... ceases and programmed death by apoptosis is engaged. These events coincide with the biosynthesis, from omega-3 polyunsaturated fatty acids, of resolvins and protectins, which critically shorten the period of neutrophil infiltration by initiating apoptosis. Consequently, apoptotic neutrophils undergo phagocytosis by macrophages, leading to neutrophil clearance and release of anti-inflammatory and reparative cytokines such as transforming growth factor-Β1.
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Some studies show reducing inflammation may reduce the risk of Alzheimer's disease by as much as 33 percent. And after Alzheimer's sets in, causing plaque to form on the brain, inflammation can make the symptoms worse. The possible connection between inflammation and Alzheimer's is getting a lot of attention in research circles, so expect to hear more about it in the coming years.
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Acute inflammation is characterised by marked vascular changes, including vasodilation, increased permeability, and the slowing of blood flow, which are induced by the actions of various inflammatory mediators. Vasodilation occurs first at the arteriole level, progressing to the capillary level, and brings about a net increase in the amount of blood present, causing the redness and heat of inflammation. Increased permeability of the vessels results in the movement of plasma into the tissues, with resultant stasis due to the increase in the concentration of the cells within blood - a condition characterised by enlarged vessels packed with cells. Stasis allows leukocytes to marginate along the endothelium, a process critical to their recruitment into the tissues. Normal flowing blood prevents this, as the shearing force along the periphery of the vessels moves cells in the blood into the middle of the vessel.
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"Researchers are linking inflammation to an ever-wider array of chronic illnesses," reports Newsweek's Anne Underwood. "Suddenly medical puzzles seem to be fitting together, such as why hypertension puts patients at increased risk of Alzheimer's, or why rheumatoid-arthritis sufferers have higher rates of sudden cardiac death. They're all connected on some fundamental level."
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Gradually, researchers put together a new narrative for heart attacks and strokes: immune-system cells that cause inflammation burrow into the artery wall and begin gobbling up droplets of fat. These fat- filled cells form a plaque and inflammation thins its fibrous cap. Eventually, the cap ruptures, and the plaque's contents spill into the bloodstream - along with pro-inflammatory cytokines, which encourage clotting. Suddenly, the artery fills with a cloud of rapidly coagulating blood cells. If the cloud is large enough, it forms a clot that blocks the artery and causes a heart attack or stroke.
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Inflammation is perhaps best known for its destructive effects on bone and joint health and for the role it plays in arthritis. The cyclooxygenase-2 (COX-2) enzyme is known to produce pro-inflammatory prostaglandins, which ultimately result in the destruction of cartilage.7
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