Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute pancreatitis was induced in mice by feeding with a choline-deficient ethionine-supplemented diet. All the mice developed acute pancreatitis, and approximately 80% of them died within 4 days. Stereomicroscopic and light microscopic examinations revealed that pancreatic necrosis and circulatory disturbance that were not apparent on day 1 were increased markedly on days 2 and 3. Serum levels of pancreatic enzymes were normal or reduced on day 1 but then increased to peak on day 3. Plasma 5-hydroxyindoleacetic acid levels, which may indicate serotonin release, were significantly increased on days 1 through 3. Pretreatment with D, L-p-chlorophenylalanine methylester hydrochloride (200-400 mg/kg) significantly attenuated the mortality of the mice with pancreatitis. Dose-dependent attenuation was also obtained with ketaserin (0. 01-10 mg/kg), cyproheptadine (0.01-10 mg/kg), pindolol (0.1-100 mg/kg) and NAN-190 (0.1-100 mg/kg), but not with 0.01 to 10 mg/kg of ICS205-930 or M-840, and the activities were significantly correlated with the binding affinities for serotonin2 receptor on the rat cerebral cortex. In addition, ketanserin or cyproheptadine attenuated the morphologic changes in the choline-deficient ethionine-supplemented diet mice at a dose (3.2 mg/kg) that hardly affected the serum enzyme levels. We propose that serotonin2 receptor activation plays an important role in the aggravation of diet-induced acute pancreatitis.
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PMID:Possible involvement of 5-HT2 receptor activation in aggravation of diet-induced acute pancreatitis in mice. 940 26

Most of proteins in human blood circulation are glycoproteins with one or more covalently linked N- or O-linked glycans. Sialic acid (SA) generally occurs as the terminal monosaccharide on the glycans. SA in glycoproteins modulates a wide range of physiological and pathological processes and has been routinely measured in hospital since 1950s. Increased serum SA levels have been associated with different types of cancers. However, a systematic comparison of the serum SA levels in different types of human diseases has not been reported. In current study, 160,537 clinical lab test results of serum SA levels from healthy individuals and patients with 64 different types of diseases during the past 5 years in our hospital were retrieved and analyzed. Based on the mean (SD), median, and p (-Log10p) values, we found that patients suffering 55 different types of cancer and noncancer diseases such as sepsis, pancreatitis, bone cancer, rheumatoid arthritis, pancreatic cancer, and encephalitis had significantly (p<0.05, -Log10p>1.30) increased median serum SA levels whereas patients suffering hepatic encephalopathy, cirrhosis, renal cyst, and hepatitis had significantly decreased median serum SA levels compared to that of healthy controls. Moreover, the greatest increase in the mean (SD) and -Log10p values was observed in sepsis and pancreatitis, respectively, but not in cancers. Thus, the regulations of serum SA levels were much more complicated than previously assumed. Understanding the molecular mechanisms behind these observations would make serum SA a useful biomarker to facilitate personalized diagnosis and treatment for patients with different diseases.
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PMID:The serum SA levels are significantly increased in sepsis but decreased in cirrhosis. 3090 61