Effect of osmotic pressure, ionic strength and dibutyryl cyclic adenosine monophosphate on the adhesion of hen erythrocytes.

In the presence of lysolecithin at physiological pH it was found that the increase of ionic strength facilitates the adhesion of hen erythrocytes. In this medium, dibutyryl cyclic adenosine monophosphate (DBcAMP) increases the adhesion index of the cells. If the osmotic pressure is elevated without a proper increase of ionic strength, the lysolecithin induced hemolysis and adhesion are found to be lacking.     

Nitrogen economy of endolithic microbial communities in hot and cold deserts

The source of combined nitrogen in endolithic microbial communities was studied in samples from desert localities in North and South America, the Middle East, South Africa, and Antarctica. Nitrogen fixation (acetylene reduction) seems to occur only exceptionally. Evidence suggests that, in general, the nitrogen source for endolithic microorganisms in deserts is abiotically fixed nitrogen produced by atmospheric electric discharges (lightning or aurorae), conveyed to the rock by atmospheric precipitation. Nitrogen is apparently not a limiting factor in these low-productivity communities. An incomplete nitrogen cycle seems to be present which includes the following pathways: supply of nitrates and ammonia from the atmosphere; decomposition of organic matter to ammonia; reassimilation of ammonia; ammonia volatilization; loss of organic matter through weathering (only in certain Antarctic rocks); biological nitrogen fixation (exceptional).     

Endogenous bacteria-triggered inducible nitric oxide synthase activation protects the ovariectomized rat stomach

Under experimental circumstances, ovariectomy attenuates gastric mucosal injury where nitric oxide (NO)-mediated pathways are involved. In this study, we have examined the changes in constitutive (cNOS) and inducible NO synthase (iNOS) enzyme activities (assessed by the citrulline assay), and the role of endogenous bacteria in ovariectomy-provoked mucosal defence. Gastric lesions were induced by indomethacin (50 mg/kg, s.c.) over a 4 h period in sham-operated and ovariectomized female Wistar rats. Groups of animals received the wide-spectrum antibiotic ampicillin (800 mg/kg/day, p.o., for 3 days), and others were injected with bacterial endotoxin (E. coli, 3 mg/kg, i.v., 5 h before autopsy). We found that ovariectomy increased iNOS and decreased cNOS activity (resulting an elevated total gastric NOS level), and protected the stomach, effects reversed by ampicillin treatment. In ovary-intact rats, administration of bacterial endotoxin enhanced gastric iNOS activity and reduced lesion-formation. These results suggest that ovariectomy improves gastric mucosal defence perhaps by endogenous bacteria-triggered induction of iNOS.     

Pathological Phosphorylation Causes Neuronal Death: Effect of Okadaic Acid in Primary Culture of Cerebellar Granule Cells

We have investigated the role of protracted phosphatase inhibition and the consecutive protracted protein phosphorylation on neuronal viability. We found that in primary cultures of cerebellar granule neurons, the protracted (24-h) inhibition of the serine/threonine protein phosphatases 1 and 2A (EC 3.1.3.16) by treatment of the cultures with okadaic acid (OKA; 5-20 nM) caused neurotoxicity that could be inhibited by the protein kinase inhibitor 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H7) or by the previous down-regulation of the neuronal protein kinase C (PKC; ATP:protein phosphotransferase; EC 2.7.1.37). PKC was down-regulated by exposure of the cultures for 24 h to 100 nM phorbol 12-myristate 13-acetate (TPA). The effect of the drugs used in the viability studies on the pattern of protein phosphorylation was measured by quantitative autoradiography. In particular, the 50- and 80-kDa protein bands showed dramatic changes in the degree of phosphorylation: increase by OKA and brief TPA treatment; decrease by H7 or 24 h of TPA treatment; and inhibition of the OKA-induced increase by H7 or 24 h of TPA treatment. The results suggest that the protracted phosphorylation, in particular that mediated by PKC, may lead to neuronal death and are in line with our previous suggestion that prolonged PKC translocation is operative in glutamate neurotoxicity.