Polyadenylic-polyuridylic acid is a non-toxic double stranded complex of synthetic polyribonucleotides and a proved potent modulator of both humoral and cellular immune responses. The complex is also an inducer of interferon. Although results of direct determination of interferon in patients receiving the complex were negative,' in later studies we found an enhancement of interferon mediated protein kinase p67 K in mouse plasma and p72 K in human plasma in response to treatment with polyadenylic-polyuridylic acid.5 We have also reported that treatment of tumour bearing mice with the complex in association with cyclophosphamide results in a synergistic inhibition of tumour characterised by more retarded tumour growth, lower mortality, and a higher rate of tumour free survival than in mice treated with either agent alone. Furthermore, in these tumour bearing mice receiving such combined treatment there was a significant enhancement of natural killer (NK) cell activity.6 Recently we have studied in more detail the NK boosting effect of polyadenylic-polyuridylic acid in mice in parallel with an assay of an enzyme marker for the production and action of interferon-namely, 2-5 A synthetase. Enhanced NK cell activity accompanied increased activities of 2-5 A synthetase in mice treated with polyadenylic-polyuridylic acid.7 In patients an increase of NK cell activity as well as an increase of 2-5 A synthetase activity after one intravenous injection of 60 mg polyadenylic-polyuridylic acid was also observed (A G Hovanessian et al, paper in preparation). In view of these observations we hypothesise that interferon and NK cell activity probably play a part in the overall mechanism of action of polyadenylic-polyuridylic acid as an adjunct to surgery in breast cancer.Polyadenylic-polyuridylic acid appears to interact with many cell populations,8 so that its biological activity might therefore be exerted at different levels. Indeed, in patients 24 hours after a single intravenous injection of 30 mg of the complex we observed that the mean percentage of E rosette forming cells was significantly (p <0 001) higher than that found before the injection (60-8% v 51-0%), confirming our observation on T lymphocytes in mice.9The relevance of the biological effects to the therapeutic action so far observed remains to be determined. Reports suggest that the low incidence of ischaemic heart disease in Greenlandic Eskimos is related to the effect of a diet rich in eicosapentaenoic acid on platelet reactivity and plasma lipid concentrations. A double blind randomised investigation was therefore conducted of the effects on blood viscosity of dietary supplementation with an oil rich in this fatty acid (1-8 g/day, given as fish oil) and an eicosapentaenoic acid poor oil (as corn/olive oil)

C. difficile infections are associated with a significant increase in 30-day mortality, but not overall mortality. Risk factors of ICU admission and antibiotic exposure were associated with the diagnosis of CDI in cirrhosis patients. Hypoalbuminemia and ICU admission were found to be strong predictors of increased mortality in cirrhosis patients with CDI.

Historically, GAVE has been associated with connective tissue disease and liver disease. Based on these associations and its histologic appearance, GAVE has presumed to be caused by mechanical- and hormonally mediated injury. Recent findings have been notable for a clinical association with aspects of the metabolic syndrome. Therefore, the pathogenic etiology may be akin to aspects of the metabolic syndrome via microvascular injury and neoangiogenesis. The potential etiologies of GAVE include hypergastrinemia, mechanical injury, and microvascular injury with neovascular proliferation particularly in the metabolic syndrome. Further research is needed to evaluate these proposed mechanisms and potential targets for treatment.

These results confirm the association of gastric antral vascular ectasia with underlying cirrhosis and revealed a significant correlation of gastric antral vascular ectasia with features of metabolic syndrome such as diabetes, BMI, vascular disease, and nonalcoholic steatohepatitis cirrhosis. The pathophysiology of gastric antral vascular ectasia remains uncertain, but we speculate that it may be a manifestation of the metabolic syndrome.

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