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)

Using a battery of 7 horseradish peroxidase marked lectins (WGA, RCA I, PHA, LCA, PNA, UEA I, LPA) or 2 unmarked lectins (Con A, VAA I) and HRP-marked antibodies, the binding to acinar cells with a postembedding technique on semithin sections of rat pancreatic tissue after olive-oil pancreatitis was studied light microscopically. The lectin binding of the normal healthy rat pancreatic tissue (Jonas et al. 1991) changed remarkably. Whereas the apical glycocalyx of acinar cells with the strong binding of WGA, RCA I, and PHA remained unchanged within the first 10 min of damage, the basolateral cell surface lost the typical specific binding of UEA I within the initial phase of pancreatitis just 2 min after injection of olive-oil. Con A and VAA I were found to be very reactive with the necrotic cells 60 min after administration of oil. The results were discussed in relation to the possible functions of the 2 main domains of the pancreatic acinar cell glycocalyx.
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PMID:Light and electron microscopic studies of lectin binding to the glycocalyx of rat pancreatic cells. II. Light microscopic changes after induction of an olive-oil pancreatitis. 128 45

The work was aimed at the elucidation of mechanisms of pathogenetic prevention of acute experimental pancreatitis induced according to the method of Arai. Pathological and biochemical examinations have shown that the application of PNA synthesis inhibitor 5-FU and cellular and intracellular membrane stabilizer-intralipid, infused at the beginning of the experiment, prevented the development of acute purulent pancreatitis.
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PMID:[Mechanisms of the pathogenetic prevention of acute pancreatitis in an experiment]. 362 Jun 45