Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018099 (gout)
 5,192 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the past 20 years treatment appears to have had a major impact on all forms of cerebral vascular disease. Morbidity and mortality from strokes have declined nearly 50% in developed countries. Modern imaging techniques, methodology, and biostatistics have identified risk factors and refined clinical trials such that we question all previous studies of stroke management. Control of moderate and severe hypertension has significantly lowered stroke rates. In borderline and mild hypertension the decision to treat is influenced by other stroke risk factors including diabetes mellitus, cigarette smoking, ischaemic heart disease, plasma lipid levels, gout, haematocrit, and body weight. Current data indicate that anticoagulants are of no value, or hazardous, in atherothrombotic strokes; of unknown value in transient ischaemic attacks; of dubious value in evolving strokes; and beneficial in cardiac embolism. The cardiac causes, including mural thrombus, unstable arrhythmias, and mitral valve prolapse should be actively sought. Aspirin, as the prototype anti-platelet agent, holds promise in transient ischemic attacks and minor strokes at both small and moderate dosages. Ticlopine is now being critically evaluated in America. Use of cerebral vasodilators should be abandoned. Enthusiasm in the use of streptokinase and urokinase has been dampened by the conversion of ischemic infarcts into haemorrhagic infarcts. In subarachnoid haemorrhage epsilon-aminocaprioc acid is useful although hazardous, in preventing rebleeding. Certain calcium ion channel blockers are promising in the reduction of vasopasm. Since the November 1985 article in the new England Journal of Medicine on the failure of external-to-internal carotid arterial bypass to reduce the risk of ischemic stroke, the swing is back to conservative management.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Advances in the medical management of cerebral vascular disease. 331 47

During inflammatory processes, monocytes leave the blood stream at increased rates and enter inflammation tissue, where they undergo phenotypic transformation to mature macrophages with enhanced phagocytic activity. alpha-Actinin, a cytoskeletal protein, is present in focal adhesion complexes and left in the microenvironment as a result of cell movement. Mactinin, a 31 kDa amino-terminal fragment of alpha-actinin, is generated by the degradation of extracellular alpha-actinin by monocyte-secreted urokinase. We have previously demonstrated that mactinin promotes monocyte/macrophage maturation. We now report that 0.5-10 nM mactinin has significant chemotactic activity for monocytes. Mactinin seems to be present in inflammatory arthritis synovial fluid, because affinity-purified antisera reacted with a protein of the expected molecular mass in various types of arthritis fluids that were immunoaffinity-purified and subjected to Western analysis. Thus, six of seven samples from patients with psoriatic arthritis, reactive arthritis, gout, or ankylosing spondylitis contained mactinin at levels that are active in vitro. Initially, mactinin was not found in affinity-purified rheumatoid arthritis samples. However, it was detectable after the dissociation of immune complexes, suggesting that it was complexed to anti-microfilament auto-antibodies. In addition, mactinin was found in the lavage fluid from the arthritic knee joints of rabbits with antigen-induced arthritis and was absent from the contralateral control knee fluids. We conclude that mactinin is present in several types of inflammatory arthritis and might modulate mononuclear phagocyte response to inflammation.
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PMID:Mactinin: a modulator of the monocyte response to inflammation. 1293 95

Colchicine is an alkaloid widely used for the treatment of inflammatory diseases, such as gout. It suppresses cell division by inhibiting mitosis. We investigated the anticancer effects of colchicine on human hypopharyngeal cancer cells and the mechanisms underlying its anticancer effects. XTT cell proliferation assay showed that colchicine inhibited the growth and proliferation of human hypopharyngeal cancer cells (FaDu and SNU1041) in a dose- and time-dependent manner. Colchicine also inhibited the migration, invasion, and adhesion of hypopharyngeal cancer cells in a dose-dependent manner. The levels of mRNA expression and activity of matrix metalloproteinase-9 (MMP9) and urokinase-type plasminogen activator (uPA) decreased after treatment with colchicine. Further investigation revealed that colchicine inhibited the phosphorylation of the FAK/SRC complex and paxillin. Tumor volume ratios in colchicine-treated mice (0.1 mg/kg, every 2 days for 14 days) increased less than in control mice. To our knowledge, this is the first report showing that colchicine can suppress cell invasion, migration, and adhesion through reduced expression of MMP9, the uPA system, and the FAK/SRC complex. Colchicine has the potential to prevent disease progression in hypopharyngeal cancer and may have application as an adjunctive treatment.
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PMID:Anticancer Effects of Colchicine on Hypopharyngeal Cancer. 2906 10