ABSTRACT
Three novel bacterial strains, PVAS-1(T), B3W22(T) and B8W22(T), were isolated from cryotubes used to collect air samples at altitudes of between 27 and 41 km. Based on phenotypic characteristics, chemotaxonomic features, DNA-DNA hybridization with the nearest phylogenetic neighbours and phylogenetic analysis based on partial 16S rRNA gene sequences (PVAS-1(T), 1196 nt; B3W22(T), 1541 nt; B8W22(T), 1533 nt), the three strains were identified as representing novel species, and the names proposed are Janibacter hoylei sp. nov. (type strain PVAS-1(T) =MTCC 8307(T) =DSM 21601(T) =CCUG 56714(T)), Bacillus isronensis sp. nov. (type strain B3W22(T) =MTCC 7902(T) =JCM 13838(T)) and Bacillus aryabhattai sp. nov. (type strain B8W22(T) =MTCC 7755(T) =JCM 13839(T)).
Subject(s)
Actinomycetales/classification , Actinomycetales/isolation & purification , Air Microbiology , Air/analysis , Bacillus/isolation & purification , Equipment and Supplies/microbiology , Actinomycetales/genetics , Bacillus/classification , Bacillus/genetics , DNA, Bacterial/genetics , DNA, Ribosomal/genetics , Molecular Sequence Data , Phylogeny , RNA, Ribosomal, 16S/geneticsABSTRACT
Monoclonal antibodies were raised to the idiotype of a gonadotropin releasing hormone (GnRH) specific antibody, one of which was found to bind specifically to GnRH receptors present on pituitary gonadotrophs, placental syncytiotrophoblasts and testicular Leydig cells. These observations were confirmed by Western and ligand blotting as well as by the ability of the antibody to induce an increase in intracellular Ca++ in a mouse gonadotroph cell-line viz., alpha T3-1.
Subject(s)
Antibodies, Anti-Idiotypic , Antibodies, Monoclonal , Gonadotropin-Releasing Hormone/immunology , Pituitary Gland/chemistry , Receptors, LHRH/analysis , Aged , Animals , Antibodies, Anti-Idiotypic/metabolism , Antibodies, Anti-Idiotypic/pharmacology , Antibodies, Monoclonal/metabolism , Antibodies, Monoclonal/pharmacology , Antibody Specificity , Blotting, Western , Calcium/metabolism , Cell Line , Enzyme-Linked Immunosorbent Assay , Female , Gonadotropin-Releasing Hormone/antagonists & inhibitors , Gonadotropin-Releasing Hormone/pharmacology , Humans , Leydig Cells/chemistry , Male , Mice , Mice, Inbred BALB C , Rats , Receptors, LHRH/metabolism , Sheep , Trophoblasts/chemistryABSTRACT
BACKGROUND: Previous studies have demonstrated that ischemic preconditioning prevents lethal cell injury and, as a consequence, limits infarct size in rat heart. Although both apoptosis and necrosis have been shown to contribute to myocardial cell death after myocardial ischemia and reperfusion, the ability of ischemic preconditioning to prevent programmed cell death remains unknown. METHODS AND RESULTS: To test the hypothesis that ischemic preconditioning reduces irreversible ischemic injury in part by decreasing apoptosis, rats that underwent ischemic preconditioning and controls were subjected to 30 minutes of left coronary artery occlusion followed by 180 minutes of reperfusion. Ischemic preconditioning was achieved by five 5-minute cycles of ischemia, each followed by 5 minutes of reperfusion. Infarct size, determined by dual staining with triphenyltetrazolium chloride and phthalocyanine blue dye, was significantly reduced in preconditioned compared with nonpreconditioned rats (11.4+/-1.4% versus 58.7+/-1.4%; n=20 in each group; P<.001; infarct size/risk area). Genomic DNA from preconditioned hearts showed little or no oligonucleosome-sized fragments (200-bp multiples), whereas genomic DNA from nonpreconditioned hearts showed a typical nucleosome fragmentation. The TUNEL assay localized fewer and sparsely stained nuclei within the infarct zone of ischemic preconditioned hearts compared with nonpreconditioned hearts. Consistent with these findings, the number of cytosolic histone-associated low-molecular-weight DNA fragments was significantly decreased in preconditioned hearts compared with controls (0.17+/-0.02 versus 1.07+/-0.09 U; n=10 in each group; P<.001; absorbance 405 nm/490 nm). CONCLUSIONS: This study suggests that ischemic preconditioning reduces irreversible ischemic injury in part by decreasing apoptosis after prolonged ischemia and reperfusion.
