Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017160 (gastroenteritis)
 11,398 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Norovirus (NV), a member of the family Caliciviridae, is one of the important causative agents of acute gastroenteritis. In the present study, we found that virus-like particles (VLPs) derived from genogroup II (GII) NV were bound to cell surface heparan sulfate proteoglycan. Interestingly, the VLPs derived from GII were more than ten times likelier to bind to cells than were those derived from genogroup I (GI). Heparin, a sulfated glycosaminoglycan, and suramin, a highly sulfated derivative of urea, efficiently blocked VLP binding to mammalian cell surfaces. The reagents known to bind to cell surface heparan sulfate, as well as the enzymes that specifically digest heparan sulfate, markedly reduced VLP binding to the cells. Treatment of the cells with chlorate revealed that sulfation of heparan sulfate plays an important role in the NV-heparan sulfate interaction. The binding efficiency of NV to undifferentiated Caco-2 (U-Caco-2) cells differed largely between GI NV and GII NV, whereas the efficiency of binding to differentiated Caco-2 (D-Caco-2) cells did not differ significantly between the two genogroups, although slight differences between strains were observed. Digestion with heparinase I resulted in a reduction of up to 90% in U-Caco-2 cells and a reduction of up to only 50% in D-Caco-2 cells, indicating that heparan sulfate is the major binding molecule for U-Caco-2 cells, while it contributed to only half of the binding in the case of D-Caco-2 cells. The other half of those VLPs was likely to be associated with H-type blood antigen, suggesting that GII NV has two separate binding sites. The present study is the first to address the possible role of cell surface glycosaminoglycans in the binding of recombinant VLPs of NV.
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PMID:Genogroup II noroviruses efficiently bind to heparan sulfate proteoglycan associated with the cellular membrane. 1504 97

A 86-year-old female with nonvalvular atrial fibrillation (NOVAF) who did not receive prophylactic anticoagulant treatment visited our hospital because of gastrointestinal symptoms. At first, acute gastroenteritis was suspected, but later she developed ileus and she was diagnosed with superior mesenteric artery occlusion (SMAO). We successfully performed the anesthetic management of this patient and subtotal resection of the small intestine was performed. Heparin was initiated after surgery, but she developed cerebral infarction later, and finally she died due to infection and anemia caused by melena. Although this patient was at high risk of thrombosis, she did not receive anticoagulant treatment. It might result in developing SMAO, and once SMAO occurred, thrombosis recurred even on anticoagulant treatment. This case suggested the importance of primary prevention of thrombosis in patients with NVAF.
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PMID:A Case of Superior Mesenteric Artery Occlusion Caused by Delayed Administration of Anticoagulants in a Patient with Nonvalvular Atrial Fibrillation. 2705 Aug 88