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Biomedical subjects

T R Terry

Publications and source records attributed to T R Terry.

23 records · Page 2Linked to original sources
PubMed1986

Small bowel ulceration in patients receiving non-steroidal anti-inflammatory drugs for rheumatoid arthritis.

Evidence is presented for a non-specific ulcerative process in the small bowel of patients with rheumatoid arthritis. All three cases presented with lower gastrointestinal bleeding; on withdrawal of non-steroidal anti-inflammatory drugs no further bleeding occurred. Non-steroidal anti-inflammatory drugs may lead to small bowel ulceration in inhibiting mucosal glycoprotein synthesis and increasing intestinal permeability.

Aged↗
PubMed1985

The generation of lysolecithin by enterokinase in trypsinogen prophospholipase A2 lecithin mixtures, and its relevance to the pathogenesis of acute necrotising pancreatitis.

The cascade enterokinase-trypsinogen-prophospholipase A2 lecithin, generating trypsin, phospholipase A2 and lysolecithin, respectively, was studied in vitro using a novel phospholipase A2 assay. The rate of enterokinase catalysed activation of trypsinogen was maximal at 4 mmol/1 glycodeoxycholic acid; higher concentrations of bile salt progressively inhibited enterokinase activity. Net phospholipase A2 activity in reaction mixtures was critically dependent on the trypsin/prophospholipase A2 molar ratio. Lecithin hydrolysis by phospholipase A2 was dependent on the bile salt/lecithin molar ratio and was optimal at 1.25 to 1. The addition of enterokinase to lecithin and bile salt mixtures, containing trypsinogen and prophospholipase A2 at presumed pathophysiological concentrations, resulted in the generation of concentrations of lysolecithin lytic for pancreatic acinar cells within 5 min. These findings would support the concept that the entry of bile containing active enterokinase into the pancreatic duct system in vivo may in some cases be involved in the initiation of necrotising acute pancreatitis in man.

Acute Disease↗
PubMed1983

Biliary excretion of enterokinase in rats: studies in alcoholic rats with fatty liver.

Ethanol-associated fatty liver was induced in rats fed a nutritionally deficient liquid diet containing 36% of total calories as ethanol. Control rats received the same diet with sucrose substituted isocalorically for ethanol. After 40 days, hepatic lipid content of the ethanol-maintained animals was four-fold greater than controls and ultrastructural changes in hepatocytes were well established. Clearance of intravenously administered human enterokinase from the circulation as well as bile flow were, however, the same in both groups. The proportion of enterokinase appearing in catalytically active form in bile after intravenous injection was substantially greater in the ethanol-maintained animals than the isocaloric controls; the difference was highly significant (p less than 0.001) and reached two- to four-fold after 70 days on the diet. These findings would suggest that the ability of hepatocytes to degrade enterokinase cleared from the blood may be bypassed or impaired by prolonged ethanol consumption and a deficient diet. Catalytically active enterokinase in bile may participate in the development of some types of acute necrotising pancreatitis.

Animals↗