Fractionation of the cell extract led to partial isolation of four protein fractions that are involved in the dissimilation of pyruvate into acetyl-CoA and formate: Enzyme I , molecular weight about 140000 ; enzyme 11, molecular weight about 30000, which requires an activation by ferrous ion and dithiols; enzyme 111, molecular weight 25000, which is a flavoprotein with flavin-mononucleotide as coenzyme ; and a hitherto less characterized fraction IV. The system in addition comprises the cofactors S-adenosylmethionine and thiamine diphosphate.Enzyme 111, fraction IV, and thiamine diphosphate could be replaced by the reagents cobaltous ion and thiols which form complexes of high reducing power. This part of the enzyme system obviously plays an auxiliary role, most likely by providing an appropriate redox potential via pyruvate as electron donor.The ability to dissimilate pyruvate was found to arise only and specifically from an interaction between enzyme I, ferrous ion-activated enzyme I1 and adenosylmethionine, in presence of either of t,he above auxiliary systems. Enzyme I is thereby converted into an active form, possibly by reduction, which alone is responsible for the catalysis of the pyruvate dissimilation reaction. The identification of this pyruvate formate-lyase was accomplished by sedimentation experiments in anaerobic sucrose gradients. As a substitute for the classical "clastic reaction", the semi-systematic term "pyruvate formate-lyase reaction", which will be used here, has recently been introduced to designate reaction (1) [5].I n sharp contrast to the well established mechanism and enzymology of pyruvate dehydrogenation in Escherichia coli [6], only a little information is available about the pyruvate dissimilation. The elucidation of its mechanism has been hampered mainly by the oxygen inhibition of the system [7,8] and the multiplicity of low and high molecular weight

In a multicentre single-blind study, ranitidine was compared to cimetidine as prophylactic treatment against stress-induced upper gastrointestinal bleeding in seriously ill patients in the intensive care unit (ICU). 380 patients entered the study. 192 patients were treated with ranitidine 50 mg q.i.d. as i.v. bolus followed by 150 mg orally twice daily. 188 patients received cimetidine 400 mg q.i.d. intravenously and 1,000 mg daily orally in divided doses. Five patients in the ranitidine group (2.6%) and 12 in the cimetidine group (6.4%) developed gastrointestinal bleeding definitely or possibly due to stress lesions. This difference was not significant. The incidence of stress erosions or ulcerations developing during the study was 11.8% for the ranitidine group and 18.3% for the cimetidine group (non-significant difference). Adverse events in the ranitidine group were nausea, tachycardia or vomiting in 4 patients. 5 cimetidine-treated patients developed cholestasis, and 5 additional central nervous system problems. The high degree of efficacy of both drugs compared very favourably with the high incidence of stress ulceration and hemorrhage in similar untreated populations.

No abstract

Between 1980 and 1987 a total of 17 patients were operated upon in curative intention of the Non-Hodgkin-Lymphoma of the stomach at our surgical department. Ten of these patients were within Ann-Arbor-Stage I, four within stage II/1 and the other three within stage II/2. In six cases we found low-malignant and in the other 11 cases high-malignant tumors. One patient died postoperatively after a myocardial infarction, one female died four months postoperatively in spite of chemotherapy of the disease. 15 patients (94%) are still alive today without any new symptoms of the disease, within a median average observation time of 40.6 months.

No abstract