Effects of a summer school-readiness programme on measures of literacy and behaviour growth: a pilot study

Young children enter kindergarten with varying levels of readiness and abilities to learn. One factor that contributes to lower levels of school readiness is poverty. One timely, cost-effective, and feasible strategy to boost school readiness, regardless of exposure to high-quality preschool is to leverage the summer months prior to kindergarten entry and provide comprehensive, evidence-based programming immediately before the school year begins. The current study implemented a community-based summer programme targeted at improving school readiness for 25 four- and five-year-old children in a low-income community. Across the 9-week study, children participated in two types of early literacy activities and the Incredible Years social/emotional learning curriculum. Results indicate that participants demonstrated significant growth across three early literacy skills and were rated as overall stable regarding their behaviour across the summer. These results are discussed along with implications and future directions in this line of research.     

Changes in iodine status among US adults, 2001–2012

Urinary iodine concentrations (UICs) in the US have been reported to be stable since 1988–1994, although those in selected subgroups remained low. We aimed to investigate iodine status among adults (≥20 years) by two different criteria of assessing iodine deficiency in population. Utilizing National Health and Nutrition Examination Surveys 2001–2012, we conducted linear logistic regressions adjusting for covariates. The prevalence of <50?μg/L UIC was higher in women than in men; increased from 11.6% (2001–2004) to 13.2% (2009–2012) at the national level and in young adults, non-Hispanic blacks (NHBs) and non-users of iodine-containing supplements (all, p?<0.05); the adjusted odds ratios (95%CI) in young adults (1.54 [1.11–2.15], p =?0.0007) and NHBs (1.70 [1.15–2.52], p =?0.0078). Median UICs confirm women and NHBs being in borderline iodine status. Recognizing the critical consequence of iodine deficiency particularly in women and NHBs, regular monitoring of iodine status is important for public health in the US.     

Protein kinase Cδ mediates trimethyltin-induced neurotoxicity in mice in vivo via inhibition of glutathione defense mechanism

We investigated whether protein kinase C (PKC) is involved in trimethyltin (TMT)-induced neurotoxicity. TMT treatment (2.8 mg/kg, i.p.) significantly increased PKCδ expression out of PKC isozymes (i.e., α, βI, βII, δ, and ?) in the hippocampus of wild-type (WT) mice. Consistently, treatment with TMT resulted in significant increases in cleaved PKCδ expression. Genetic or pharmacological inhibition (PKCδ knockout or rottlerin) was less susceptible to TMT-induced seizures than WT mice. TMT treatment increased glutathione oxidation, lipid peroxidation, protein oxidation, and levels of reactive oxygen species. These effects were more pronounced in the WT mice than in PKCδ knockout mice. In addition, the ability of TMT to induce nuclear translocation of Nrf2, Nrf2 DNA-binding activity, and upregulation of γ-glutamylcysteine ligase was significantly increased in the PKCδ knockout mice and rottlerin (10 or 20 mg/kg, p.o. × 6)-treated WT mice. Furthermore, neuronal degeneration (as shown by nuclear chromatin clumping and TUNEL staining) in WT mice was most pronounced 2 days after TMT. At the same time, TMT-induced inhibition of phosphoinositol 3-kinase (PI3K)/Akt signaling was evident, thereby decreasing phospho-Bad, expression of Bcl-xL and Bcl-2, and the interaction between phospho-Bad and 14-3-3 protein, and increasing Bax expression and caspase-3 cleavage were observed. Rottlerin or PKCδ knockout significantly protected these changes in anti- and pro-apoptotic factors. Importantly, treatment of the PI3K inhibitor LY294002 (0.8 or 1.6 µg, i.c.v.) 4 h before TMT counteracted protective effects (i.e., Nrf-2-dependent glutathione induction and pro-survival phenomenon) of rottlerin. Therefore, our results suggest that down-regulation of PKCδ and up-regulations of Nrf2-dependent glutathione defense mechanism and PI3K/Akt signaling are critical for attenuating TMT neurotoxicity.