pneumoniae by serological analysis and polymerase chain reaction (PCR) to amplify a 277-base pair region of 16S rDNA gene of M. pneumoniae applied to throat swab specimens. Serological and/or PCR positive results diagnosed M. pneumoniae infection in 23 (30.7%) patients.”
“Two new diketopiperazine derivatives, bacillusamides A (1) and B (2), have been Isolated from the EtOAc extract of
the sea urchin-derived Bacillus sp along with the known cyclo(-L-pro-L-val-) (3), cyclo(-L-pro-L-tyr-) (4), cyclo(-L-pro-L-phe-) (5) These structures were elucidated by extensive spectroscopic methods click here Furthermore, the absolute configurations of the amino acid residues were determined using Marfey’s method Compound 1 displayed weak antifungal activity against Aspergillus niger”
“Actively respiring animal and plant tissues experience hypoxia because of mitochondrial O-2 consumption. Controlling oxygen balance is a critical issue that involves in mammals hypoxia-inducible factor (HIF) mediated transcriptional regulation, cytochrome oxidase (COX) subunit adjustment and nitric oxide (NO) as a mediator in vasodilatation and oxygen homeostasis. In plants,
NO, mainly derived from nitrite, is also an important signalling molecule. We describe here a mechanism by which mitochondrial respiration is adjusted to prevent a tissue to reach anoxia. During pea seed germination, the internal atmosphere was strongly hypoxic due to very active mitochondrial respiration. There was no sign of fermentation, suggesting selleck compound a down-regulation of O-2 consumption near anoxia. Mitochondria were found to finely regulate their surrounding O-2 level through selleck chemicals a nitrite-dependent NO production, which was ascertained using electron paramagnetic resonance (EPR) spin trapping of NO within membranes. At low O-2, nitrite is reduced into NO, likely at complex III, and in turn reversibly inhibits COX, provoking a rise to a higher steady state level
of oxygen. Since NO can be re-oxidized into nitrite chemically or by COX, a nitrite-NO pool is maintained, preventing mitochondrial anoxia. Such an evolutionarily conserved mechanism should have an important role for oxygen homeostasis in tissues undergoing hypoxia. (C) 2008 Elsevier B.V. All rights reserved.”
“HIF-1 alpha is a nuclear factor important in the transcription of genes controlling angiogenesis including vascular endothelial growth factor (VEGF). Both hypoxia and oxidative stress are known mechanisms for the induction of HIF-1 alpha. Oxidative stress and mitochondrial permeability transition (MPT) are mechanistically important in acetaminophen (APAP) toxicity in the mouse. MPT may occur as a result of oxidative stress and leads to a large increase in oxidative stress. We previously reported the induction of HIF-1 alpha in mice with APAP toxicity and have shown that VEGF is important in hepatocyte regeneration following APAP toxicity.