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Biomedical subjects

J Keller

Publications and source records attributed to J Keller.

At least 271 records · Page 15Linked to original sources
PubMed1977

[Effect of drug therapy during pregnancy on the clotting potential of the newborn].

Drug therapy in mothers may lead to various disturbances of the hemostasis of the newborn. Some authors reported on severe hemorrhages in newborn after coumarin treatment of the mothers, others had not or only seldom observed such events. Our examination did not reveal any significant clotting disorders in 4 newborns whose mothers had received Athrombom. Perhaps the indandion derivative does not significantly penetrate the placental barrier. However, therapy with anticoagulants of the vitamin K antagonist type may be instituted during pregnancy only in cases where it is strictly indicated. Streptokinase and heparin will certainly not enter the fetal circulation, therefore they may be used without risk for the child. Furthermore the clinican must known severe bleeding conditions of the vitamin K deficiency type in newborns of mothers with anticonvulsive therapy. Preventive administration of vitamin K to pregnant women and newborns or, in the presence of bleedings, instantaneous and exact substitution may bring under control the critical situation. Acetylsalicylic acid given during the last weeks of pregnancy causes an inhibition of the aggregation of thrombocytes of the newborn. Bleedings occur only seldom. Other drugs administered during pregnancy may induce neonatal thrombocytopenia through immunological or toxic mechanisms, such for instance quinine, quinidine, tolbutamide and thiazides.

Aspirin↗
PubMed1976

D-Mannitol dehydrogenase from Absidia glauca. Purification, metabolic role, and subunit interactions.

When Absidia glauca was grown in minimal media with D-mannitol as the only source of carbon, an NAD+ specific D-mannitol dehydrogenase (EC 1.1.1.67) was induced. The crude extract also gave evidence of mannitol kinase, mannitol-1-phosphate dehydrogenase, phosphofructokinase, and L-iditol dehydrogenase activity. The heat labile purified preparation was judged enzymically homogeneous based on evidence derived from substrate specificity studies and activity staining, following disc gel electrophoresis. The enzymic monomer, with a weight of about 67000 daltons, slowly polymerizes when stored at -20 degrees C, giving a multiplicity of protein bands on electrophoresis distributed predominantly across a spectrum from dimer to pentamer, with enzymic activity resident predominantly in even multiples of the monomer. Depolymerization occurred rapidly (hours) when a frozen preparation was brought to and held between 4 and 20 degrees C. Aggregate fragmentation with sodium dodecyl sulfate showed a time-temperature dependence, terminating in a subunit component of 13000 daltons. pH optimum for polyol oxidation occurs at 9.6 (NaOH-glycine buffer) while ketose reduction proceeded most rapidly at pH 7.0-7.2 (phosphate buffer). A regulatory role is suggested for this enzyme based on dead-end inhibition by mannitol 1-phosphate, multiple enzyme forms, and its locus at the initiation site for mannitol utilization. The physiological relevance of low-temperature aggregation to regulatory control remains to be established.

Electrophoresis, Disc↗