Activation of the transcription factor NF-kappaB in the rat air pouch model of inflammation
Article Abstract:
A protein called nuclear factor kappa B (NF-kappaB) appears to be involved in inflammation, according to a study in rats. This protein activates specific genes, including the genes for interleukins 1 and 6, and tumor necrosis factor.
Publication Name: Annals of the Rheumatic Diseases
Subject: Health
ISSN: 0003-4967
Year: 2000
User Contributions:
Comment about this article or add new information about this topic:
Oxygen free radicals, inflammation, and synovitis: the current status
Article Abstract:
A free radical is a molecule with an unpaired electron that is very unstable and chemically reactive. Oxygen and hydrogen peroxide are sources of free radicals. Under normal conditions, polymorphonuclear leukocytes (a type of immune cell) produce oxygen free radicals that help kill microorganisms. However, free radicals can also cause damage to cell membranes, proteins, carbohydrates, and deoxyribonucleic acid (DNA), the genetic material of the cell. There is growing evidence that free radicals are involved in the inflammatory processes of joint diseases such as rheumatoid arthritis (RA). Several cells that accumulate in inflamed joints, such as polymorphonuclear leukocytes, are capable of producing free radicals; production appears to depend on the presence of iron. Free radicals have been shown to cause damage to cartilage tissue and structural proteins within the joint. Because oxygen levels tend to be low in inflamed joints, it is thought that joint damage may occur during the subsequent restoration of blood flow and oxygen supply. Exercise of an inflamed joint blocks off the blood supply and the restoration of circulation to the joint at the end of exercise results in the production of free radicals. Thus, bed rest has been shown to be effective in treating RA; overuse of a limb worsens the disease. Further investigation of the role of free radicals in human biology is required to develop better therapies for disease processes involving these highly reactive molecules. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: Annals of the Rheumatic Diseases
Subject: Health
ISSN: 0003-4967
Year: 1989
User Contributions:
Comment about this article or add new information about this topic:
Inactivation of antithrombin III in synovial fluid from patients with rheumatoid arthritis
Article Abstract:
The activity of antithrombin III (AT III) may be depressed in rheumatoid arthritic joints. AT III is a blood protein which inactivates thrombin, a key factor in blood coagulation. Researchers compared synovial fluid samples from rheumatoid, osteoarthritic, and normal joints. Although rheumatoid synovial fluid had more AT III, compared to fluid from joints with osteoarthritis, the AT III activity was decreased. Unopposed thrombin resulting from decreased AT III activity may increase inflammation, coagulation, and damage in rheumatoid joints.
Publication Name: Annals of the Rheumatic Diseases
Subject: Health
ISSN: 0003-4967
Year: 1998
User Contributions:
Comment about this article or add new information about this topic:
- Abstracts: Effect of the angiotensin-converting-enzyme inhibitor benazepril on the progression of chronic renal insufficiency
- Abstracts: Relation of race and sex to the use of reperfusion therapy in Medicare beneficiaries with acute myocardial infarction
- Abstracts: Treatment of acromegaly with the growth hormone-receptor antagonist pegvisomant. Growth hormone for the elderly?
- Abstracts: Lack of association of severe preeclampsia with maternal and fetal mutant alleles for tumor necrosis factor alpha and lymphotoxin alpha genes and plasma tumor necrosis factor alpha levels
- Abstracts: Hepatitis C virus infection in 'primary' Sjogren's syndrome: prevalence and clinical significance in a series of 90 patients