Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Distal splenorenal shunt (DSRS) is a once-only form of treatment. It is suitable for many black South Africans with non-cirrhotic variceal bleeding who cannot attend repeated follow-up sclerotherapy sessions. However, persistent hyperbilirubinaemia and encephalopathy may occur following DSRS in schistosomiasis. Forty-one consecutive patients with DSRS have been treated over a 7-year period. The causes of portal hypertension were schistosomiasis (32), portal vein thrombosis (8) and diffuse nodular hyperplasia (1). Operative mortality was 6%. Encephalopathy was observed in 1 patient. Galactose elimination capacity (GEC) and technetium-diethylenetriamine penta-acetic acid hepatic perfusion index (HPI) were used to assess liver function and hepatic perfusion pre- and postoperatively, respectively, in schistosomiasis. GEC was 348 +/- 37 (M +/- SD) before, compared with 343 +/- 67 postoperatively (P = 0.78). HPI showed long-term preservation of hepatopetal portal venous flow following DSRS. Morbidity and mortality were observed only in patients with schistosomiasis associated with hepatitis B chronic active hepatitis. DSRS is ideal treatment in selected patients with non-cirrhotic variceal bleeding.
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PMID:Distal splenorenal shunt for non-cirrhotic variceal bleeding in black South Africans. 759 1

Patients with an influenza virus infection can be complicated by acute encephalopathy and encephalitis. To investigate the immune reactions involved in the neurocomplication, mouse microglia and astrocytes were isolated, infected with human H1N1 and avian H5N1 influenza viruses, and examined for their immune responses. We observed homogeneously distributed viral receptors, sialic acid (SA)-alpha2,3-Galactose (Gal) and SA-alpha2,6-Gal, on microglia and astrocytes. Both viruses were replicative and productive in microglia and astrocytes. Virus-induced apoptosis and cytopathy in infected cells were observed at 24 h post-infection (p.i.). Expression of IL-1beta, IL-6 and TNF-alpha mRNA examined at 6 h and 24 h p.i. was up-regulated, and their expression levels were considerably higher in H5N1 infection. The amounts of secreted proinflammatory IL-1beta, IL-6 and TNF-alpha at 6 h and 24 h p.i. were also induced, with greater induction by H5N1 infection. This study is the first demonstration that both human H1N1 and avian H5N1 influenza viruses can infect mouse microglia and astrocytes and induce apoptosis, cytopathy, and proinflammatory cytokine production in them in vitro. Our results suggest that the direct cellular damage and the consequences of immunopathological injury in the CNS contribute to the influenza viral pathogenesis.
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PMID:Apoptosis and proinflammatory cytokine responses of primary mouse microglia and astrocytes induced by human H1N1 and avian H5N1 influenza viruses. 1844 41