Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0039483 (giant cell arteritis)
 3,204 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The mechanisms of formation, morphology and functions of macrophagal polykaryons are discussed. These giant multinuclear cells are formed by means of macrophagal cell fusion ("natural hybridization") and specialized on the extra- and intracellular processes of resorption of the foreign body and tissues of the proper organism. The formation of macrophagal polykaryons seems to be one of the possible manifestation of reactive histiocytosis in chronic inflammation and tumor growth. The role of macrophagal polykaryons in such disease as giant cell arteritis, giant cell granuloma and fibrohistiocytic tumors is considered in details. It is proposed that one and the same mechanism of regulations served as a basis of developing of both osteoclastic remodelling of the bone tissue (morphogenetic process) and resorption of the foreign body and tissues of the proper organism in inflammation in the process of evolution.
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PMID:[Macrophagal polykaryons]. 1082 32

Among matrix metalloproteinases (MMPs), the subfamily of gelatinases (MMP-2, MMP-9) is of particular interest due to their ability to degrade type IV collagen and other non-fibrillar collagen domains and proteins such as fibronectin and laminin. Whilst malignant cells often over-express various MMPs, the gelatinases have been most consistently detected in malignant tissues and associated with tumor growth, metastatic potential and angiogenesis. Radiosynthesis of carboxylic (1') and hydroxamic (2') MMPIs resulted in radiochemical yields of 70 +/- 5% (n = 6) and 60 +/- 5% (n = 4), respectively. Evaluation in A549-inoculated athymic mice showed a tumor uptake of 2. 0+/- 0.7%ID/g (3 h p.i.), a tumor/blood ratio of 0.5 and a tumor/muscle ratio of 4.6 at 48 h p.i. for 1'. For compound 2' a tumor uptake of 0.7 +/- 0.2%ID/g (3 h p.i.), a tumor/blood ratio of 1.2 and a tumor/muscle ratio of 1.8 at 24 h p.i. were observed. HPLC analysis of the blood (plasma) showed no dehalogenation or other metabolites of 1' 2 h p.i. For compound 2', 65.4% of intact compound was found in the blood (plasma) and one polar metabolite (31%) was detected whereas in the tumor 91.8% of the accumulated activity was caused by intact compound and only 8.1% by the metabolite. Planar imaging, using a Toshiba GCA-9300A/hg SPECT camera, showed that tumor tissue could be visualized and that image quality improved by decreasing specific activity resulting in lower liver uptake, indicating some degree of saturable binding in the liver. In vivo evaluation of these radioiodinated carboxylic and hydroxamic MMP inhibitor tracers revealed that MMP inhibitors could have potential as tumor imaging agents, but that further research is necessary.
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PMID:Valine-based biphenylsulphonamide matrix metalloproteinase inhibitors as tumor imaging agents. 1654 98

We observed that free bile acids (CA, DCA, and CDCA) inhibited the growth of cholangiocarcinoma cells by promoting cell apoptosis, while the conjugated bile acids (GCA, GDCA, and GCDCA) stimulated cell growth. Consistently, we found that GDCA stimulated tumor growth and CDCA decreased tumor growth in xenografted mice. Further, the phosphorylated IkB was downregulated by free bile acids, and was upregulated by the conjugated bile acids. IL-6 and COX-2 were decreased by the free bile acids and increased by the conjugated bile acids. Collectively, these results suggest that the bile acids regulate the growth of cholangiocarcinoma by modulating NF-kB pathway.
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PMID:Bile acids affect the growth of human cholangiocarcinoma via NF-kB pathway. 2336 50