Inhibition of respiratory oxidation of reduced sulfur compounds by intact cells ofThiobacillus denitrificans (strain RT) grown on thiosulfate

Thiobacillus denitrificans strain RT, an obligate sulfur-oxidizing chemolithoautotroph, was grown under microaerophilic conditions with thiosulfate as the only energy source. The rates of tetrathionate, thiosulfate, elemental sulfur (S^o) and sulfite oxidation were measured respirometrically with an oxygen electrode, using actively growing cells. Cells oxidized thiosulfate, elemental sulfur (S^o) and sulfite, but not tetrathionate. The thiosulfateoxidizing activity and elemental sulfur-oxidizing activity (SOA) were almost totally inhibited by 50 M myxothiazol (>80%), an inhibitor of the quinone-cytochrome b region, and by 10 M of the uncoupler carbonyl cyanide m-chlorophenylhydrazone (CCCP) (>82%). Sulfite-oxidizing activity was also significantly inhibited (>60%) by 50 M myxothiazol and 10 M CCCP. 1 mM KCN totally inhibited (>90%) all respiratory activities. This study confirms that a sulfur-oxidizing activity appears during microaerophilic growth ofThiobacillus denitrificans strain RT on thiosulfate. The SOA is linked to the respiratory chain, probably releasing electrons in the quinone-cytochrome b region.To whom correspondence should be addressed. Submitted by R. Bachofen.     

The influence of GABA on discharges of cortical epileptogenic focus

Summary GABA, when applied locally, acted similarly on both primary and mirror cortical focus: the negative component of the spike discharge was suppressed or inverted in polarity, whereas the late slow negative wave was strongly potentiated. Recordings from deep cortical layers suggested a different origin of these 2 surface-negative components of focal discharges.     

Effects of angiotensin II and of an angiotensin II receptor antagonist on Simian virus 40-induced tumor growth in vivo

Summary The effects of angiotensin II and of the competitive angiotensin II receptor antagonist saralasin on in vivo tumor growth were investigated in hamsters. Angiotensin II strongly inhibited tumor growth while saralasin stimulated it, though the high dose used had partial agonistic angiotensin II-like actions. Lower doses of saralasin were without significant effect on tumor weights.Acknowledgments. These studies were supported by the Deutsche Forschungsgemeinschaft (DFG) within the SFB 90 Cardiovaskuläres System. Saralasin was a gift from Dr A.W. Castellion, Norwich Pharmacal Company, USA. We thank S. Thiele, P. Baumgärtl and D. Kurz for excellent technical assistance.     

Finding the mid-path

Computers have changed nearly every aspect of life in this world. Invented roughly fifty years ago, they now form the infrastructure on which government, business, and global communications rest. As our reliance on computers increases, so does the number and complexity of the applications and the number and quality of trained professionals that will be needed to support further progress. The United States already faces personnel shortages in some computer-related jobs, including university teaching. In the face of this evident and increasing need, we must think clearly about out expectations for computing professionals of all sorts and the way they are trained. In the forty years that I have been in the field, the focus in industry has changed from programming to software development. A gulf is growing between the skills that students build at a university and the needs of industry. This paper examines the nature and extent of the problem and suggests a variety of ways to address it.     

Stem cell division is regulated by the microRNA pathway

One of the key characteristics of stem cells is their capacity to divide for long periods of time in an environment where most of the cells are quiescent. Therefore, a critical question in stem cell biology is how stem cells escape cell division stop signals. Here, we report the necessity of the microRNA (miRNA) pathway for proper control of germline stem cell (GSC) division in Drosophila melanogaster. Analysis of GSCs mutant for dicer-1 (dcr-1), the double-stranded RNaseIII essential for miRNA biogenesis, revealed a marked reduction in the rate of germline cyst production. These dcr-1 mutant GSCs exhibit normal identity but are defective in cell cycle control. On the basis of cell cycle markers and genetic interactions, we conclude that dcr-1 mutant GSCs are delayed in the G1 to S transition, which is dependent on the cyclin-dependent kinase inhibitor Dacapo, suggesting that miRNAs are required for stem cells to bypass the normal G1/S checkpoint. Hence, the miRNA pathway might be part of a mechanism that makes stem cells insensitive to environmental signals that normally stop the cell cycle at the G1/S transition.