Direct observation of many-electron magnetoconductivity in a nondegenerate 2D electron liquid.
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Biomedical subjects
Publications and source records attributed to A Blackburn.
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Studies show that the gastroduodenal mucosal barrier is damaged by pepsin under conditions in which it is resistant to acid alone. The continuous layer of adherent mucus gel provides a diffusion barrier to luminal pepsin, preventing its access to the underlying epithelium. Pepsin has mucolytic activity and will progressively digest the adherent mucus layer at its luminal surface, although normally this is balanced by secretion of new mucus to maintain a continuous barrier. In peptic ulcer disease the proportion of peptic activity in gastric juice attributable to pepsin type 1 is significantly raised (four to five-fold). Pepsin 1 has increased mucolytic activity compared with the major component, pepsin 3, both at the optimal pH of 2 (twofold increase in activity) and at higher pH values up to pH 5 (sixfold increase in activity at pH 4). Structural studies show that the gel forming polymeric mucin of the antral adherent mucus barrier is deficient in peptic ulcer disease. This breakdown of the mucus barrier in peptic ulcer patients can be attributed to the increased pepsin activity of gastric juice seen in this disease, although other explanations are also possible. The increased pepsin activity of gastric juice in peptic ulcer patients is compatible with the concept 'no acid, no pepsin, no ulcer'.
The clinical course of 29 liver graft recipients in the Cambridge/King's College Hospital series who have received cyclosporin A (CyA) for up to five years (median 40 months) was analysed with particular reference to the immunosuppressive effectiveness and adverse effects of the drug. Eight patients had been maintained on prednisolone and azathioprine for two to six years before treatment was changed to cyclosporin A and the remainder were started on cyclosporin A after operation. Results in both groups over a one to five year study period are similar, and showed that cyclosporin A was effective in maintaining adequate immunosuppression, allowing complete withdrawal of prednisolone in 16 patients. Episodes of rejection were observed in only three patients and in two of these it was of the chronic 'vanishing bile duct' variety. Some evidence of nephrotoxicity (serum creatinine greater than 150 mumol/l) occurred in 72 per cent (21 of 29 patients) but it was necessary to discontinue treatment in only two. Hypertension, occasionally of sudden onset, was found in nine patients and led to the withdrawal of the drug in two. Additional hypotensive drug treatment was required in five. In one other patient cyclosporin A was discontinued on account of severe headaches. Cyclosporin A was withdrawn in two further patients. Withdrawal led to considerable risk of acute rejection and increased doses of corticosteroids as well as substitution of azathioprine were required at that time.
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