39 research outputs found

    Maternal smoking during pregnancy and scholastic achievement in childhood: evidence from the LIFECOURSE cohort study.

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    To access publisher's full text version of this article, please click on the hyperlink in Additional Links field or click on the hyperlink at the top of the page marked FilesResearch on the impact of maternal smoking during pregnancy (MSDP) on scholastic achievement in the offspring has shown conflicting findings. The objective of this study was to assess the impact of MSDP on scholastic achievement in a birth cohort of children in 4th, 7th and 10th grades.We analysed data from the LIFECOURSE study, a cohort study of risk and protective factors in all children born in Reykjavik, Iceland, in the year 2000 (N = 1151, girls = 49.3%). Retrospective registry data for 2014-2015 were merged with prospective survey data that were collected in April 2016. Data on MSDP were assessed during regular antenatal visits at the end of the first trimester. Standardized academic achievement scores were obtained from official school transcripts. Data were analysed using OLS regressions that were entered in three hierarchical blocks.Children of mothers who smoked tobacco during the first trimester consistently revealed between 5% and 7% lower scores on standardized academic achievement in 4th, 7th and 10th grade (∼6-8 points on a normally distributed 120 point scale) than those of mothers who had not smoked tobacco during this period (P < 0.05). These findings held after controlling for several factors associated with the time of birth (e.g. birth weight, maternal age at birth, birth order, parental cohabitation and household income), as well as the year of scholastic assessment (parental cohabitation, household income and parental education).Maternal smoking during pregnancy was negatively related to scholastic achievement in the offspring during 4th, 7th and 10th grade.European Research Counci

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

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    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

    Brain Research to Ameliorate Impaired Neurodevelopment - Home-based Intervention Trial (BRAIN-HIT)

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    <p>Abstract</p> <p>Background</p> <p>This randomized controlled trial aims to evaluate the effects of an early developmental intervention program on the development of young children in low- and low-middle-income countries who are at risk for neurodevelopmental disability because of birth asphyxia. A group of children without perinatal complications are evaluated in the same protocol to compare the effects of early developmental intervention in healthy infants in the same communities. Birth asphyxia is the leading specific cause of neonatal mortality in low- and low-middle-income countries and is also the main cause of neonatal and long-term morbidity including mental retardation, cerebral palsy, and other neurodevelopmental disorders. Mortality and morbidity from birth asphyxia disproportionately affect more infants in low- and low-middle-income countries, particularly those from the lowest socioeconomic groups. There is evidence that relatively inexpensive programs of early developmental intervention, delivered during home visit by parent trainers, are capable of improving neurodevelopment in infants following brain insult due to birth asphyxia.</p> <p>Methods/Design</p> <p>This trial is a block-randomized controlled trial that has enrolled 174 children with birth asphyxia and 257 without perinatal complications, comparing early developmental intervention plus health and safety counseling to the control intervention receiving health and safety counseling only, in sites in India, Pakistan, and Zambia. The interventions are delivered in home visits every two weeks by parent trainers from 2 weeks after birth until age 36 months. The primary outcome of the trial is cognitive development, and secondary outcomes include social-emotional and motor development. Child, parent, and family characteristics and number of home visits completed are evaluated as moderating factors.</p> <p>Discussion</p> <p>The trial is supervised by a trial steering committee, and an independent data monitoring committee monitors the trial. Findings from this trial have the potential to inform about strategies for reducing neurodevelopmental disabilities in at-risk young children in low and middle income countries.</p> <p>Trial Registration</p> <p>Clinicaltrials.gov NCT00639184</p

    Saccharomyces cerevisiae Tti2 Regulates PIKK Proteins and Stress Response

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    The TTT complex is composed of the three essential proteins Tel2, Tti1, and Tti2. The complex is required to maintain steady state levels of phosphatidylinositol 3-kinase-related kinase (PIKK) proteins, including mTOR, ATM/Tel1, ATR/Mec1, and TRRAP/Tra1, all of which serve as regulators of critical cell signaling pathways. Due to their association with heat shock proteins, and with newly synthesized PIKK peptides, components of the TTT complex may act as cochaperones. Here, we analyze the consequences of depleting the cellular level of Tti2 in Saccharomyces cerevisiae. We show that yeast expressing low levels of Tti2 are viable under optimal growth conditions, but the cells are sensitive to a number of stress conditions that involve PIKK pathways. In agreement with this, depleting Tti2 levels decreased expression of Tra1, Mec1, and Tor1, affected their localization and inhibited the stress responses in which these molecules are involved. Tti2 expression was not increased during heat shock, implying that it does not play a general role in the heat shock response. However, steady state levels of Hsp42 increase when Tti2 is depleted, and tti2L187P has a synthetic interaction with exon 1 of the human Huntingtin gene containing a 103 residue polyQ sequence, suggesting a general role in protein quality control. We also find that overexpressing Hsp90 or its cochaperones is synthetic lethal when Tti2 is depleted, an effect possibly due to imbalanced stoichiometry of a complex required for PIKK assembly. These results indicate that Tti2 does not act as a general chaperone, but may have a specialized function in PIKK folding and/or complex assembly
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