Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023473 (chronic myeloid leukemia)
 18,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three patients who developed symptomatic, autoimmune-mediated thyroid dysfunction during treatment with interferon-alpha (IFN-alpha) for chronic active hepatitis C with liver cirrhosis, age-related macular degeneration with foveal involvement, and chronic myelogenous leukemia, respectively, are described. The first two patients developed autoimmune hypothyroidism that required thyroxine replacement, and the third developed autoimmune thyroiditis with transient thyrotoxicosis. The clinical manifestations were protean, and required a high index of suspicion for diagnosis, the failure of which led to significant morbidity. A literature review revealed that the mean incidence of IFN-alpha induced thyroid dysfunction was 6%. Spontaneous resolution occurred in more than half with discontinuation of IFN-alpha treatment. Hypothyroidism was induced more frequently than hyperthyroidism. At least one positive thyroid autoantibody titer was found in 17% of patients receiving IFN-alpha. Risk factors for developing thyroid dysfunction with IFN-alpha treatment were female sex, underlying malignancy or hepatitis C, higher doses of IFN-alpha for longer durations, combination immunotherapy (especially with interleukin-2), and the presence of thyroid autoantibodies prior to or during treatment.
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PMID:Interferon-alpha induced thyroid dysfunction: three clinical presentations and a review of the literature. 945 33

Action of N(epsilon)-(carboxymethyl)lysine-human serum albumin (CML-HSA) on neovascularization was investigated in cultured rat choroidal explant. Choroidal explants of normal male Wistar rats were cultured in fibrin gel with Dulbecco's modified Eagle medium containing fetal bovine serum in the presence or absence of CML-HSA. Migrated cells were budded from 2nd day in culture and developed from cultured choroidal explants in a time-dependent manner. Budded and developed cells from the choroidal explant had a feature of fibroblasts, which had attenuated long cytoplasmic processes, long ellipsoid nuclei and numerous membrane-bound polymorphic vesicles. Immunostaining of the attenuated cells in fibrin bed with CD34 (a marker protein of vascular endothelial cells and endothelial progenitor cells) failed to disclose positive result. However the cells which were isolated from fibrin bed by collagenase were specifically stained with anti-CD34 antibody. The isolated cells did not form tube-like structures on collagen gel by 3 weeks in culture. CML-HSA significantly increased the number of total isolated cells and CD34(+) cells as well as the number of vessel-like structures. These results indicate that CML-HSA overproduced immature blood vessels from cultured choroidal explants in fibrin gel, which consisted of CD34(+) cells. The CML-HSA-induced formation of immature blood vessel may be implicated in various choroidal diseases such as age-related macular degeneration.
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PMID:N(epsilon)-(carboxymethyl)lysine proliferated CD34(+) cells from rat choroidal explant in culture. 1534 Feb 23

N(epsilon)-(carboxymethyl)lysine (CML) adduct, a major structure of advanced glycation end product, facilitated production of immature microvessels from choroidal explant cultured in fibrin gel. The present study was investigated an action of endogenous CML adduct on neovascularization of cultured choroidal explants of aged Wistar rats with 9 months of age. The number of microvessels budded from explants was counted under optical microscope and used as an index of in vitro neovascularization. Aged choroidal explants increased the neovascularization in an age-dependent manner. Anti-CML antibody decreased age-facilitated neovascularization as well as CML-human serum albumin (HSA)-facilitated neovascularization. Both the aged explant and CML-HSA-treated explant significantly released vascular endothelial growth factor (VEGF), tumor necrosis factor (TNF) alpha and platelet-derived growth factor (PDGF)-B during the culture period. The release of TNF alpha and PDGF-B was earlier than that of VEGF from the aged explants. The antibodies against these factors decreased the CML-facilitated and age-facilitated neovascularization in the choroidal explants. The inhibitory capacity of anti-TNF alpha antibody was greater than those of anti-VEGF and anti-PDGF-B antibodies. In conclusion, endogenous CML adduct overproduced the neovascularization of the aged choroidal explant. The CML adduct releases TNF alpha which might induce the production and release of VEGF for the abnormal choroidal neovascularization in the patients of age-related macular degeneration.
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PMID:Overproduction of N(epsilon)-(carboxymethyl)lysine-induced neovascularization in cultured choroidal explant of aged rat. 1720 73