Perinatal and Socioeconomic Risk Factors for Variable and Persistent Cognitive Delay at 24 and 48 Months of Age in a National Sample

The objective of this paper is to examine patterns of cognitive delay at 24 and 48 months and quantify the effects of perinatal and sociodemographic risk factors on persistent and variable cognitive delay. Using data from 7,200 children in the Early Childhood Longitudinal Study, Birth Cohort (ECLS-B), multiple logistic regression models identified significant predictors of low cognitive functioning at 24 and 48 months. Additional multiple logistic models predicting cognitive delay at 48 months were estimated separately for children with and without delay at 24 months. Of the nearly 1,000 children delayed at 24 months, 24.2% remained delayed by 48 months; 7.9% of the children not delayed at 24 months exhibited delay at 48 months. Low and very low birthweight increased cognitive delay risk at 24, but not 48 months. Low maternal education had a strongly increasing effect (OR = 2.3 at 24 months, OR = 13.7 at 48 months), as did low family income (OR = 1.4 at 24 months, OR = 7.0 at 48 months). Among children delayed at 24 months, low maternal education predicted delay even more strongly at 48 months (OR = 30.5). Low cognitive functioning is highly dynamic from 24 to 48 months. Although gestational factors including low birthweight increase children’s risk of cognitive delay at 24 months, low maternal education and family income are more prevalent in the pediatric population and are much stronger predictors of both persistent and emerging delay between ages 24 and 48 months

Role of the H-2s haplotype in survival of mice after infection with Trypanosoma cruzi.

In studies of the resistance of inbred mice to infection with Trypanosoma cruzi Peru, mouse strain B10.S was the only strain which survived the infection resulting from the inoculation of 10(3) trypomastigotes. This is the only inbred mouse strain studied to survive infection. To investigate the effect of the H-2 haplotype on survival, C57BL/10 congenic mouse strains bearing H-2S recombinant haplotypes and mouse strains A.SWSn/J and SJL/J were tested for their ability to overcome the T. cruzi infection. None of the recombinant strains tested, including B10.S(7R), B10.S(8R), B10.S(9R), and B10.HTT, survived the infection, indicating that at least two or more regions of the H-2 locus must be H-2S to ensure survival. Strains A.SWSn/J and SJL/J with the H-2S haplotype did not survive, indicating that the genetic background outside the H-2 complex also influences survival. The congenic F1 hybrid (C57BL/10 X B10.S) F1 exhibited intermediate survival levels when compared with the parental strains, indicating that H-2S survival is affected by gene dosage. The F1 hybrid strain [B10.S(7R) X B10.S(8R)]F1, which possesses the complete H-2S haplotype in the trans configuration, did not survive T. cruzi infection, suggesting that H-2S-mediated survival does not operate by trans complementation

East–west, collectivist-individualist: A cross-cultural examination of temperament in toddlers from Chile, Poland, South Korea, and the U.S.

The present study examined toddler temperament across Chilean, South Korean, Polish, and U.S. samples, providing an opportunity to examine both collectivist-individualist and East-West contrasts. The effect of culture on the three factor and 18 dimension scores provided by the Early Childhood Behavior Questionnaire were investigated. Results provide evidence of cross-cultural differences between the four samples. Chilean toddlers scored significantly higher than U.S., Polish, and South Korean children on the overall factor of Negative Affectivity, as well as higher than the Polish and South Korean samples on the Surgency factor. South Korean toddlers scored significantly higher on the factor of Effortful Control, and two related dimensions, than U.S., Polish, or Chilean samples. Results are discussed in terms of the apparent roles of individualism/collectivism and East-West distinctions in shaping temperament development

Physical conditions in star-forming regions around S235

Gas density and temperature in star forming regions around Sh2-235 are derived from ammonia line observations. This information is used to evaluate formation scenarios and to determine evolutionary stages of the young embedded clusters S235 East1, S235 East2, and S235 Central. We also estimate the gas mass in the embedded clusters and its ratio to the stellar mass. S235 East1 appears to be less evolved than S235 East2 and S235 Central. In S235 East1 the molecular gas mass exceeds that in the other clusters. Also, this cluster is more embedded in the parent gas cloud than the other two. Comparison with a theoretical model shows that the formation of these three clusters could have been stimulated by the expansion of the Sh2-235 HII region (hereafter S235) via a collect-and-collapse process, provided the density in the surrounding gas exceeds $3\cdot10^3$ cm$^{-3}$, or via collapse of pre-existing clumps. The expansion of S235 cannot be responsible for star formation in the southern S235 A-B region. However, formation of the massive stars in this region might have been triggered by a large-scale supernova shock. Thus, triggered star formation in the studied region may come in three varieties, namely collect-and-collapse and collapse of pre-existing clumps, both initiated by expansion of the local HII regions, and triggering by an external large-scale shock. We argue that the C235 A HII region expands into a highly non-uniform medium with increasing density. It is too young to trigger star formation in its vicinity by a collect-and-collapse process. There is an age spread inside the S235 A-B region. Massive stars in the S235 A-B region are considerably younger than lower mass stars in the same area. This follows from the estimates of their ages and the ages of associated HII regions.Comment: 17 pages, 9 figures, accepted to MNRA

Genetic characterization of glucose transporter function in Leishmania mexicana

Both insect and mammalian life cycle stages of Leishmania mexicana take up glucose and express all three isoforms encoded by the LmGT glucose transporter gene family. To evaluate glucose transporter function in intact parasites, a null mutant line has been created by targeted disruption of the LmGT locus that encompasses the LmGT1, LmGT2, and LmGT3 genes. This Δlmgt null mutant exhibited no detectable glucose transport activity. The growth rate of the Δlmgt knockout in the promastigote stage was reduced to a rate comparable with that of WT cells grown in the absence of glucose. Δlmgt cells also exhibited dramatically reduced infectivity to macrophages, demonstrating that expression of LmGT isoforms is essential for viability of amastigotes. Furthermore, WT L. mexicana were not able to grow as axenic culture form amastigotes if glucose was withdrawn from the medium, implying that glucose is an essential nutrient in this life cycle stage. Expression of either LmGT2 or LmGT3, but not of LmGT1, in Δlmgt null mutants significantly restored growth as promastigotes, but only LmGT3 expression substantially rescued amastigote growth in macrophages. Subcellular localization of the three isoforms was investigated in Δlmgt cells expressing individual LmGT isoforms. Using anti-LmGT antiserum and GFP-tagged LmGT fusion proteins, LmGT2 and LmGT3 were localized to the cell body, whereas LmGT1 was localized specifically to the flagellum. These results establish that each glucose transporter isoform has distinct biological functions in the parasite