Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0019209 (hepatomegaly)
 5,798 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

NADPH-cytochrome P450 reductase (CPR) is an essential component for the function of many enzymes, including microsomal cytochrome P450 (P450) monooxygenases and heme oxygenases. In liver-Cpr-null (with liver-specific Cpr deletion) and Cpr-low (with reduced CPR expression in all organs examined) mouse models, a reduced serum cholesterol level and an induction of hepatic P450s were observed, whereas hepatomegaly and fatty liver were only observed in the liver-Cpr-null model. Our goal was to identify hepatic gene expression changes related to these phenotypes. Cpr-lox mice (with a floxed Cpr gene and normal CPR expression) were used as the control. Through microarray analysis, we identified many genes that were differentially expressed among the three groups of mice. We also recognized the 12 gene ontology terms that contained the most significantly changed gene expression in at least one of the two mouse models. We further uncovered potential mechanisms, such as an increased activation of constitutive androstane receptor and a decreased activation of peroxisomal proliferator-activated receptor-alpha by precursors of cholesterol biosynthesis, that underlie common changes (e.g. induction of multiple P450s and suppression of genes for fatty acid metabolism) in response to CPR loss in the two mouse models. Additionally, we observed model-specific gene expression changes, such as the induction of a fatty-acid translocase (Cd36 antigen) and the suppression of carnitine O-palmitoyltransferase 1 (Cpt1a) and acyl-CoA synthetase long chain family member 1 (Acsl1), that are potentially responsible for the severe hepatic lipidosis and an altered fatty acid profile observed in liver-Cpr-null mice.
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PMID:Hepatic gene expression changes in mouse models with liver-specific deletion or global suppression of the NADPH-cytochrome P450 reductase gene. Mechanistic implications for the regulation of microsomal cytochrome P450 and the fatty liver phenotype. 1600 52

In order to provide early intervention for coronary artery lesion (CAL) caused by Kawasaki Disease (KD), we analyzed clinical characteristics of typical and incomplete KD cases from 1998 to 2008 in Northwest and Central China. A total of 383 patients included 298 cases of typical KD and 85 cases of incomplete KD. The morbidity of incomplete KD was 28.5%, a percentage significantly lower than that of typical KD. The occurrence of bulbar conjunctiva congestion, erythra, crissum red, film-like decrustation, lip red, rhagades, raspberry tongue, bilateral toe-end decrustation, limb sclerosis, cervical lymph nodes enlargement, agitation and irritability in incomplete KD group was lower than that in the group of typical KD (p < 0.05); however, the occurrence of unilateral toe-end decrustation, scar reappearance erythema, malaise, fatigue, liver incidence was significant higher in incomplete KD group (p < 0.05). Based on lab assays and inspection index comparisons, the incomplete KD cases whose C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) were significantly increased, had significantly higher reduction in blood platelet (PLT). Interestingly, the KD patients with CPR higher than 30 mg/L, ESR higher than 40 mm/h, hepatomegaly and IVIG ineffectiveness, had higher incidence of CAL development. Altogether, our data have indicated differential clinical characteristics between incomplete KD and typical KD, and have identified several high risk factors of KD for CAL, such as hepatomegaly.
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PMID:Retrospective analysis of risk factors associated with Kawasaki disease in China. 2890 47