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Objective To assess the relationship between cerebral oxygenation in the first 72 h of life and neurodevelopmental impairment (NDI) at 2 years corrected age in former premature infants. Study design Prospective observational cohort study of 127 infants

Objective we sought to determine the degree to which cognitive reserve, as assessed by the Test of Premorbid Functioning in combination with demographic variables, could act as a buffer against the effect of traumatic brain injury (TBI) on cognitive test performance. Method retrospective analysis of a cohort of 121 persons with TBI who completed the Wechsler Adult Intelligence Scale-Fourth Edition (WAIS-IV) within 1-12 months after injury. Results regression analyses indicated that cognitive reserve was a statistically significant predictor of all postinjury WAIS-IV factor index scores, after controlling for various premorbid and comorbid confounding variables. Only for Processing Speed did injury severity make an additional statistically significant contribution to the prediction model. Conclusions cognitive reserve has a protective effect with regard to the impact of TBI on cognitive test performance but this effect is imperfect and does not completely negate the effect of injury severity.

Successful implementation of chlorination for disinfecting community water systems in developing countries faces obstacles, with rejection of chlorinous flavor as a significant factor. Determining consumers' abilities to accurately detect chlorine in treated water is important to identifying acceptable chlorination levels that are also effective for water disinfection. Chlorine detection sensitivity was tested in untrained Ecuadorian consumers with limited prior experience with chlorinated water and US consumers with extensive prior experience with chlorinated water. Water samples with free chlorine concentrations up to 3.0 mg/L were presented for flavor testing. Ecuadorian consumers showed higher sensitivity, being able to detect chlorination at 2.0 and 3.0 mg/L, while US consumers did not reliably detect chlorine presence for any concentration levels. Additionally, Ecuadorian consumers' rejection of water samples depended on chlorination, showing a statistically significant increase in rejections of samples with chlorine concentrations above 1.0 mg/L. On the other hand, although US consumers rejected more samples overall, their tendency to reject did not vary as a function of chlorination levels. This study demonstrated that limited experience with chlorination is a critical factor for accurate chlorine flavor detection in drinking water. This article has been made Open Access thanks to the generous support of a global network of libraries as part of the Knowledge Unlatched Select initiative.

Induction of heme oxygenase-1 (HO-1) has been demonstrated to result in chronic weight loss in several rodent models of obesity. However, the specific contribution of the HO metabolite, carbon monoxide (CO) to this response remains unknown. In this study, we determined the effect of chronic low level administration of a specific CO donor on the progression of obesity and its effects on metabolism and adipocyte biology in mice fed a high-fat diet. Experiments were performed on C57BL/6J mice fed a high-fat diet (60%) from 4 weeks until 30 weeks of age. Mice were administered either the CO donor, carbon monoxide releasing molecules (CORM)-A1 (5 mg kg−1, intraperitoneally every other day) or the inactive form of the drug (iCORM-A1). Body weights were measured weekly and fasted blood glucose, insulin as well as body composition were measured every 6 weeks. Food intake, O2 consumption, CO2 production, activity and body heat production were measured at 28 weeks after start of the experimental protocol. Chronic CORM-A1 attenuated the development of high fat induced obesity from 18 weeks until the end of the study. Chronic CORM-A1 treatment in mice fed a high-fat diet resulted in significant decreases in fasted blood glucose, insulin and body fat and increased O2 consumption and heat production as compared with mice treated with iCORM-A1. Chronic CORM-A1 treatment also resulted in a significant decrease in adipocyte size and an increase in adipocyte number and in NRF-1, PGC-1α and UCP1 protein levels in epidydmal fat. Our results demonstrate that chronic CO treatment prevents the development of high-fat diet induced obesity via stimulation of metabolism and remodeling of adipocytes.