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Intercellular adhesion molecule-1, strongly expressed on the interlobular and proliferating bile ducts in primary biliary cirrhosis, is important in the migration and adhesion of inflammatory cells from the circulation to these structures. A soluble form has been found to be elevated in serum in primary biliary cirrhosis. Our aim was to check on the role of soluble intercellular adhesion molecule-1 in primary biliary cirrhosis with particular reference to its specificity by comparison with other disease control groups and to assess its relationship with stage of disease activity, circulating lymphocyte activation and cholestasis. Soluble intercellular adhesion molecule-1 (enzyme-linked immunosorbent assay) and liver biochemistry were measured in 41 patients with primary biliary cirrhosis, 9 with primary sclerosing cholangitis, 12 with alcoholic liver disease and 17 healthy controls. In subgroups of patients with primary biliary cirrhosis, lymphocyte activation and hepatic bile acid uptake and excretory rates were determined. Soluble intercellular adhesion molecule-1 was significantly higher in all three disease groups. Levels in primary biliary cirrhosis and primary sclerosing cholangitis were similar and significantly higher than alcoholic liver disease. Soluble intercellular adhesion molecule-1 expression was greater in late primary biliary cirrhosis than early disease and correlated with histological progression. Correlations were also found with alkaline phosphatase, gamma-glutamyl transpeptidase and conjugated bilirubin. A trend toward an inverse correlation with hepatic excretory rate was found, but no correlation was detected with circulating lymphocyte interleukin-2 receptor expression.(ABSTRACT TRUNCATED AT 250 WORDS)

Increased serum gammaGT level in patients with chronic hepatitis C is associated with liver steatosis and fibrosis, and indicates more advanced liver disease rather than reflecting the cholestasis that often accompanies this condition.

The study will provide insights with regard to the design and use of online game-playing as a cost-effective approach to improve nutritional knowledge among university students.

Purpose Cancer cachexia (CC) is a syndrome characterised by an ongoing loss of skeletal muscle mass associated with reduced tolerance to treatment. This study explored the prevalence and severity of CC in advanced non-small cell lung cancer (NSCLC) patients and determined its relationship with chemotherapy outcomes. Methods CC was classified into a four-stage model: no cachexia, pre-cachexia (PC), cachexia and refractory cachexia (RC) with categorisation determined from biochemical and body composition and performance assessment. Associations between the stage of cachexia and chemotherapy outcomes including radiological response, the number of chemotherapy cycles completed and the number of cycles delayed or dose reduced were explored. Results Twenty-four patients were included with 4 (18%) classified as having no cachexia, 4 (18%) PC, 3 (14%) cachexia (13.6%), and 11 (50%) RC. No association was observed between the stage of cachexia and the radiological response to chemotherapy number of cycles delayed or the number of cycle's dose reduced; however, there was an association with the number of cycles completed (p = 0.030). An association between C-reactive protein (CRP) and the number of chemotherapy cycles completed (p = 0.044) and the number of dose reductions (p = 0.044) was also identified. Conclusions Limited conclusions can be drawn given the small sample size. However, the majority of patients presented with some degree of cachexia at diagnosis. A relationship was identified between the increasing severity of cachexia and a lower number of chemotherapy cycles completed, as well as between CRP and the number of chemotherapy cycles completed and the number of dose reductions required, and therefore warrants further exploration in larger studies.

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Previous studies have suggested that copper is incompletely incorporated into caeruloplasmin, the major plasma form of copper-transporting protein, in the genetic copper toxic condition, Wilson's disease. In this paper we have investigated the role of copper and caeruloplasmin in the abnormal biliary copper transport and characterizes Wilson's disease. Using SDS/PAGE and Western blotting, we have demonstrated the presence of holocaeruloplasmin in liver samples from patients with Wilson's disease (abnormal biliary copper excretion) and in control patients (normal biliary copper excretion). The presence of holocaeruloplasmin was also confirmed by measurement of caeruloplasmin oxidase activity using staining with o'Dianisidine. In contrast with the findings in liver tissue, holocaeruloplasmin was absent from bile from patients with Wilson's disease, but as expected it was present in the bile from control subjects. We have also identified and partially characterized a 189-200 kDa protein from purified human biliary canalicular membranes which binds copper and possesses caeruloplasmin-like activity when probed with a specific human anti-caeruloplasmin antibody. In conclusion, we have demonstrated that copper incorporation in caeruloplasmin is normal in patients with Wilson's disease contrary to previous reports. Secondly, we have shown that the defect in Wilson's disease appears to lie in the biliary canalicular excretion of holocaeruloplasmin resulting in its retention within the hepatocyte causing copper toxicosis. Finally we have identified and partially characterized a caeruloplasmin-binding protein from biliary canalicular membranes which may provide a link to the gene defect in Wilson's disease.