Measuring impact of New Mexico prekindergarten on standardized test scores and high school graduation using propensity score matching.

The long-term impact of prekindergarten programs is an important consideration given the trend of dedicating more resources to these programs. However, long-term impact of prekindergarten programs is not well-understood and recent studies have shown preschool effectiveness can vary across states and programs. A state run prekindergarten program in New Mexico was examined using propensity score matching to minimize selection bias. The research revealed a number of long-term impacts corresponding with prekindergarten participation for the cohort including a 9.7 percentage point increase in high school graduation rates and improved reading and math proficiency at third, sixth, and eighth grades. Considerations for future research and challenges in implementing prekindergarten programs are discussed.

Salmonella enterica prevalence in leatherback sea turtles (Dermochelys coriacea) in St. Kitts, West Indies.

Salmonella spp. are gram-negative bacteria capable of causing diseases in a wide range of aquatic and terrestrial animals, including humans. Sea and terrestrial turtles have been recognized as carriers of this zoonotic pathogen. In this project, conventional and molecular diagnostic methods were combined to investigate the prevalence of Salmonella enterica in leatherback sea turtles (Dermochelys coriacea) that used the island of St. Kitts, West Indies as a nesting ground during 2011 (n = 21). Isolates obtained from selective media were screened and colonies suspected of being Salmonella spp. were confirmed by fluorescence resonance energy transfer polymerase chain reaction. The prevalence of S. enterica within this sample population during this period was found to be 14.2%. Moreover, due to the increasing risk of antibiotic resistance in enteric bacteria, antimicrobial susceptibility was investigated in all recovered Salmonella spp. isolates utilizing the broth microdilution method. All isolates were susceptible to the lowest concentration of kanamycin, gentamicin, ciprofloxacin, enrofloxacin, nalidixic acid, and trimethoprim/sulfamethoxazole tested. Further research should be pursued to understand the interaction of this bacterial pathogen with the environment, host, and other microbial communities, and to further develop faster, more sensitive, and more specific diagnostic methods.

4-hydroxy nimesulide effects on mitochondria and HepG2 cells. A comparison with nimesulide.

We previously reported that the nonsteroidal anti-inflammatory drug, nimesulide (N-[4-nitro-2-phenoxyphenyl]-methanesulfonamide), is an uncoupler and oxidizes NAD(P)H in isolated rat liver mitochondria, triggering mitochondrial Ca2+ efflux or, if this effect is inhibited, eliciting mitochondrial permeability transition (Mingatto et al., Br. J. Pharmacol. 131:1154-1160, 2000). We presently demonstrated that nimesulide's hydroxylated metabolite (4-hydroxy nimesulide) lacks the uncoupling property of the parent drug, while keeping its ability to oxidize mitochondrial NADPH. In the presence of 10 microM Ca2+, low (5-50 microM) concentrations of 4-hydroxy nimesulide elicited mitochondrial permeability transition, as assessed by cyclosporin A-sensitive mitochondrial swelling, associated with mitochondrial Ca2+ efflux/membrane potential dissipation (Deltapsi), apparently occurring on account of the oxidation of mitochondrial protein thiols; no involvement of reactive oxygen species was observed. While nimesulide (0.5 or 1 mM, 30 h incubation) did not lead to significant HepG2 cell death, 4-hydroxy nimesulide caused a low extent (approximately 15%) of cell necrosis, partly prevented by cyclosporine A, suggesting the involvement of mitochondrial permeability transition. Both nimesulide and 4-hydroxy nimesulide caused NADPH oxidation and Deltapsi dissipation in HepG2 cells. Because such Deltapsi dissipation induced by the metabolite was almost completely inhibited by cyclosporine A, it probably results from the mitochondrial permeability transition. Therefore, mitochondrial permeability transition, in apparent association with NADPH oxidation, constitutes the most probable cause of HepG2 cell death elicited by 4-hydroxy nimesulide.

Apoptotic effect of ethanol is potentiated by caffeine-induced calcium release in rat astrocytes.

In this study, we investigated agents that increased intracellular calcium levels and their correlation with apoptotic cell death induction. We used rat astrocytes to investigate the increase in cytosolic Ca2+ (Ca(c)2+) and apoptosis induction by drugs that mobilize Ca2+ from different sources. We observed that thapsigargin (Thap), caffeine (Caff) and FCCP which caused similar increases in Ca(c)2+ levels (30-40%), also induced similar apoptotic rates (30-35%). On the other hand, antimycin (Anti), staurosporine (STS) and ethanol (Eth) promoted higher increases in Ca(c)2+ (55-65 %) and higher apoptotic rates (55-85%). Eth induced cell death in a concentration- and time-dependent manner. After treatment with Eth plus Caff for 6, 12 and 24 h, these effects were strongly potentiated. Results suggest that there might be a correlation between Ca(c)2+ increase and the rate of apoptosis. It is possible that Eth induces cell death by activation of more than one pathway and Ca2+ might be one of the elements involved. The present work indicates that Ca2+ can potentiate death by ethanol in rat astrocytes.