Wiederherstellung des normalen Herzschlages nach elektrisch erzeugtem Kammerflimmern durch Adenosintriphosphorsäure

Summary (1) In the isolated mammalian heart (rabbit, cat, dog) electrically induced ventricular fibrillation is stopped in practically 100% of the cases by adenosin-triphosphoric acid (ATP) in doses of 0.25–20 mg, and the normal rhythm of the heart is permanently restored (as far as the experiment extends).(2) This effect of ATP follows from a primary blocking, which leads to a complete cessation of the activity of the ventricles with diastolic dilatation of the heart.(3) In as much as adenyl acid from yeast and adenosin (in large doses) also stop ventricular fibrillation, the energetic effect of ATP seems to be of no importance in stopping it; it is a specific effect of the adenyl compounds on the bundle ofHis.     

Genomic analysis of Bartonella identifies type IV secretion systems as host adaptability factors

The bacterial genus Bartonella comprises 21 pathogens causing characteristic intraerythrocytic infections. Bartonella bacilliformis is a severe pathogen representing an ancestral lineage, whereas the other species are benign pathogens that evolved by radial speciation. Here, we have used comparative and functional genomics to infer pathogenicity genes specific to the radiating lineage, and we suggest that these genes may have facilitated adaptation to the host environment. We determined the complete genome sequence of Bartonella tribocorum by shotgun sequencing and functionally identified 97 pathogenicity genes by signature-tagged mutagenesis. Eighty-one pathogenicity genes belong to the core genome (1,097 genes) of the radiating lineage inferred from genome comparison of B. tribocorum, Bartonella henselae and Bartonella quintana. Sixty-six pathogenicity genes are present in B. bacilliformis, and one has been lost by deletion. The 14 pathogenicity genes specific for the radiating lineage encode two laterally acquired type IV secretion systems, suggesting that these systems have a role in host adaptability.     

Inhibition of cytosolic rat hepatic glutathione S-transferase activities by bromosulfophthaleins

Summary The enzymatically catalyzed conjugation of glutathione with 1-chloro-2,4-dinitrobenzene and styrene-7,8-oxide is inhibited by tetrabromosulfophthalein in a non-competetive way, although tetrabromosulfophthalein itself is a substrate for glutathione S-transferases. Dibromosulfophthalein, which is not a substrate for glutathione S-transferases, inhibits the 1-chloro-2,4-dinitrobenzene conjugation competetively and the styrene-7,8-oxide conjugation non-competetively.