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Biomedical subjects

G Brunner

Publications and source records attributed to G Brunner.

177 records · Page 10Linked to original sources

Omeprazole for peptic ulcer disease in pregnancy.

This report contains the observations of 9 women who received omeprazole for severe reflux disease during different stages of pregnancy. Four patients took omeprazole at the time of conception, and 3 of these patients continued omeprazole therapy without interruption until delivery. One patient discontinued therapy in the 8th week of pregnancy but had to take the drug again from the 28th week to delivery. The other 5 patients started therapy in weeks 24, 30, 33, 34 and 36 of pregnancy because of bleeding in 2 patients and unbearable H2 receptor refractory reflux symptoms in the other 3 patients. All patients were carefully monitored. In all cases omeprazole was well tolerated. No severe side effects were observed in any of the mothers or their newborns. No malfunctions or malformations were observed in the newborns. Follow-up of the children between 2 and 12 years showed normal development in all children. These data together with the data on 8 such pregnancies published by other authors suggest that omeprazole is safe when given during pregnancy at whatever phase.

Adult↗

Removal of excess inorganic phosphate by haemoperfusion with composite beads.

New composite beads, made by encapsulating hydrous zirconium oxide powder in agarose, are evaluated in vitro and in vivo for the removal of inorganic phosphate from the blood. Phosphate adsorption is rather good and calcium removal can be controlled. Thus, a 250 to 300 ml column is capable of reducing phosphate plasma level by some 5 mg per cent, thus making it attractive for the treatment of acute renal failure. Biocompatibility tests showed that supplementing the standard heparinization procedure by adding some citrate, as ACD, to the extracorporeal circuit greatly improves platelet and leucocyte count. No adverse haemodynamic effects were noted in repeated haemoperfusions of five dogs.

Acute Kidney Injury↗

Plasmin in pericellular proteolysis and cellular invasion.

Invasive tumor growth or severe inflammation is accompanied by the extravasation of fibrinogen from leaky or damaged blood vessels and the formation of a fibrin clot. The clot provides a matrix for the inward migration ('invasion,' 'infiltration') of tumor cells as well as inflammatory cells. The factors that govern the cell/fibrin interaction are not known. We have explored in vitro the possible role of the cell-surface-associated pathway of plasminogen activation in the adhesion of keratinocytes to fibrin and in the invasion of melanoma cells into fibrin gels. Our experiments provided evidence that generation of plasmin at the cell surface destabilizes the adhesive interaction between keratinocytes and fibrin, most likely by cleaving fibrin into fibrinopeptides and destroying its adhesive capacity. Moreover, we found that plasmin generated at the melanoma cell surface promotes the inward migration of these cells into three-dimensional fibrin matrices. In conclusion, the generation of plasmin at the cellular surface may be an important factor in pericellular proteolysis and the dynamic interaction between cells and fibrin-containing pericellular matrix under conditions of tumor invasion and inflammation.

Animals↗

Inhibition of glycosylphosphatidylinositol (GPI) phospholipase D by suramin-like compounds.

A number of proteins are found attached to the plasma membrane of mammalian cells by a glycosylphosphatidylinositol (GPI) anchor that can be cleaved by GPI specific phospholipase D (GPI-PLD). There are no known specific inhibitors of GPI-PLD. We examined some inhibitors of phosphatidylinositol specific phospholipase C (PI-PLC) for their ability to inhibit human serum and human bone marrow cell GPI-PLD. Azo analogues of suramin were found to be potent inhibitors of GPI-PLD. One compound had an IC50 of 3.7 microM that was 10-fold lower than the IC50 required to inhibit PI-PLC. The azo suramin analogues inhibited cancer cell growth at concentrations similar to those required to inhibit GPI-PLD, and below concentrations required to inhibit growth factor binding. It is possible that inhibition of cell growth might be related to the ability of the compounds to inhibit GPI-PLD.

Cell Division↗

Optimizing the intragastric pH as a supportive therapy in upper GI bleeding.

Acid inhibitory therapy has long been considered of no benefit for upper GI bleeding. The reason was that achlorhydria in the stomach could not be achieved with any single or combination of acid inhibitory drugs. The introduction of proton pump inhibitors has, for the first time, allowed the physician to temporarily achieve achlorhydria by large doses of intravenously applied proton pump inhibitors. The first placebo-controlled clinical trials have shown that, indeed, an intragastric pH of near 7 can significantly improve the clinical outcome of upper GI bleeding. Pharmacokinetic studies with proton pump inhibitors have shown that a bolus of 80 mg pantoprazole or omeprazole followed by immediate continuous infusion of eight mg per hour will result in an intragastric pH of 7 within 20 minutes. This intragastric pH optimizes the different steps of hemostasis in the stomach.

2-Pyridinylmethylsulfinylbenzimidazoles↗