Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0008325 (cholecystitis)
 3,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

At an acute phlegmonous cholecystitis in the human being, certain changes in ultrastructure of organelles of hepatocytes and slight rearrangements in their surface are revealed. Destruction of microfilaments, hypertrophy and fragmentation are observed in Golgi complex (GC) and in the granular endoplasmic reticulum. The structure of the GC and of the endoplasmic reticulum demonstrates their active functional state, that is evidently manifested as a defensive reaction of the organism to the lesion.
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PMID:[Changes in the ultrastructure of human hepatocytes in acute phlegmonous cholecystitis]. 409 90

Destructive, inflammatory and sclerotic alterations of the hepatic tissue, increased content of lipid inclusions, lysosomes and microbodies in hepatocytes, vesiculation of the endoplasmic reticulum and depletion of ribosomal granules in it were revealed by morphological examinations of liver samples from the gall bladder bed from patients will rarely, frequently and continuously recurring chronic cholecystitis. A relationship between resorption of lipid structures, content of lysosomes and microbodies, and glycogen accumulation in hepatic cells was found. The destructive morphological changes correlated with reduced capacity of the liver to absorb radioactive label, an increase of alanine transaminase level in the blood, and decreased oxidative processes in the mitochondrial fraction of the liver. The results of the study attest to the involvement of the liver in the pathological process in accord with the rate of cholecystitis recurrency.
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PMID:[Structural and functional changes in the liver in chronic recurrent cholecystitis]. 722 81

The toxicity of atorvastatin (AT), an inhibitor of hydroxymethylglutaryl-coenzyme A reductase (HMG), was evaluated in beagle dogs. In 4 studies [2-wk rising dose (daily increasing doses for 1 wk; maintenance for 1 wk), 12-wk rising dose (daily dosing with weekly increases in dose), 2-wk toxicity (daily dosing for 2 wk; 3 dose levels), 13-wk toxicity (daily dosing for 13 wk; 3 dose levels)], dogs received up to 400 mg/kg orally. Doses of 180 mg/kg induced moribundity, necessitating euthanasia. Weight losses up to 26% were seen at doses > or = 150 mg/kg. Decreases in cholesterol levels were dose-related. Alanine and/or aspartate aminotransferase were increased at doses > or = 80 mg/kg; alkaline phosphatase was increased at doses > or = 150 mg/kg. Histopathologic findings were seen at > or = 150 mg/kg and included hepatocellular eosinophilia related to increased smooth endoplasmic reticulum and cholangiohepatitis and cholecystitis at 150 mg/kg in the 2-wk toxicity study; hepatocellular degeneration, centrilobular bridging, cholecystitis, hemorrhage in gallbladder and brain, demyelination of optic nerve, and skeletal muscle necrosis at > or = 280 mg/kg in the 12-wk rising dose study; and erosion and hemorrhage in large intestine, hepatocellular degeneration and necrosis, and inflammation and necrosis of gallbladder epithelium at 320 mg/kg in the 2-wk rising dose study. Doses up to 80 mg/kg for 13 wk did not induce histopathologic lesions in examined organs. AT effectively lowered serum cholesterol in normal lipidemic dogs. Toxicity at AT in dogs was similar to that with other inhibitors of HMG except that lenticular changes were not seen, significant hepatic, testicular, or neurological toxicity was associated only with high doses at AT, and skeletal muscle changes similar to those described in rats and rabbits were identified.
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PMID:Subchronic toxicity of atorvastatin, a hydroxymethylglutaryl-coenzyme A reductase inhibitor, in beagle dogs. 886 88