Finally, a refined pharmacophore model was generated using the most active compounds 2, 12c and 22c via application of HipHop program. (C) 2013 find more Elsevier Masson SAS. All rights reserved.”
“Introduction: Microsporidia constitute the most common black fly pathogens, although the species’ diversity, seasonal occurrence and transmission mechanisms remain poorly understood. Infections by this agent

are often chronic and non-lethal, but they can cause reduced fecundity and decreased longevity. The objective of this study was to identify microsporidia infecting Simulium (Chirostilbia) pertinax (Kollar, 1832) larvae from Caraguatatuba, State of Sao Paulo, Brazil, by molecular and morphological characterization. Methods: Larvae were collected at a single point in a stream in a rural area of the city and were kept under artificial aeration until analysis. Polydispyrenia spp. infection was characterized by the presence of Tipifarnib at least 32 mononuclear spores measuring 6.9 +/- 1.0 x 5.0 +/- 0.7 mu m in persistent sporophorous vesicles. Similarly, Amblyospora spp. were characterized

by the presence of eight uninucleate spores measuring 4.5 x 3.5 mu m in sporophorous vesicles. Results: The molecular analysis confirmed the presence of microsporidian DNA in the 8 samples (prevalence of 0.51%). Six samples (Brazilian larvae) were related to Polydispyrenia simulii and Caudospora palustris reference sequences but in separate clusters. One sample was clustered with Amblyospora spp. Edhazardia aedis was the positive control taxon. Selleckchem Epigenetic inhibitor Conclusions: Samples identified as Polydispyrenia spp. and Amblyospora spp. were grouped with P. simulii and Amblyospora spp.,

respectively, corroborating previous results. However, the 16S gene tree showed a considerable distance between the black fly-infecting Amblyospora spp. and the mosquito-infecting spp. This distance suggests that these two groups are not congeneric. Additional genomic region evaluation is necessary to obtain a coherent phylogeny for this group.”
“Many cancer drugs are toxic to cells by activating apoptotic pathways. Previous studies have shown that mitochondria have key roles in apoptosis in mammalian cells, but the role of mitochondrial DNA (mtDNA) copy number variation in the pathogenesis of tumor cell apoptosis remains largely unknown. We used the HEp-2, HNE2, and A549 tumor cell lines to explore the relationship between mtDNA copy number variation and cell apoptosis. We first induced apoptosis in three tumor cell lines and one normal adult human skin fibroblast cell line (HSF) with cisplatin (DDP) or doxorubicin (DOX) treatment and found that the mtDNA copy number significantly increased in apoptotic tumor cells, but not in HSF cells. We then downregulated the mtDNA copy number by transfection with shRNA-TFAM plasmids or treatment with ethidium bromide and found that the sensitivity of tumor cells to DDP or DOX was significantly increased.