The serini reaction

Zusammenfassung Der Mechanismus der Serini-Reaktion wird kurz erörtert und ein 17, 20-Oxyd als Zwischenprodukt vorgeschlagen. Das stereochemische Ergebnis der Reaktion soll von zwei Faktoren abhängig sein, und zwar: 1. von der Geometrie des « transition state » und 2. von der Konfiguration des Oxydrings. Ausgehend von diesen Überlegungen, kann vorausgesagt werden, daßReichsteins Substanz 0-Diacetat durch die Serini-Reaktion in ein 17-Iso-20-keton und nicht in ein 17-Normal-20-keton umgewandelt werden soll. Tatsächlich ist das 17-Isoallopregnanol-(3)-on-20 als einziges Produkt experimentell aufgefunden worden.     

Systematic pathway analysis using high-resolution fitness profiling of combinatorial gene deletions

Systematic genetic interaction studies have illuminated many cellular processes. Here we quantitatively examine genetic interactions among 26 Saccharomyces cerevisiae genes conferring resistance to the DNA-damaging agent methyl methanesulfonate (MMS), as determined by chemogenomic fitness profiling of pooled deletion strains. We constructed 650 double-deletion strains, corresponding to all pairings of these 26 deletions. The fitness of single- and double-deletion strains were measured in the presence and absence of MMS. Genetic interactions were defined by combining principles from both statistical and classical genetics. The resulting network predicts that the Mph1 helicase has a role in resolving homologous recombination-derived DNA intermediates that is similar to (but distinct from) that of the Sgs1 helicase. Our results emphasize the utility of small molecules and multifactorial deletion mutants in uncovering functional relationships and pathway order.     

Die Wirkung des Toluidinblaus und der Thrombokinase auf den Vorgang der Thrombininaktivierung

Summary The disappearance of thrombin—formed in the blood, or added to serum-follows a manomolecular reaction-type. Heparin increases the reaction-velocity of this thrombin-inactivating process.Our investigation established that toluidine blue or kinase, which, according to the literature, bind heparin, strongly reduce the speed of thrombin-inactivation too. Therefore the heparin-binding capacity of these substances is also manifested in the decrease of thrombin-inactivation.