Background Short sleep is associated with obesity and may alter the endocrine regulation of hunger and appetite. Objective To test the hypothesis that the curtailment of human sleep could promote excessive energy intake. Design Eleven healthy volunteers (5F/6M; mean ± SD age 39 ± 5y; BMI 26.5 ± 1.5 kg/m2) completed in random order two 14-day stays in the sleep laboratory with ad lib access to palatable food and 5.5- or 8.5-hour bedtimes. The primary endpoints were the calories from meals and snacks consumed during each bedtime condition. Additional measures included total energy expenditure and 24-hour profiles of serum leptin and ghrelin. Results Sleep was reduced by 122 ± 25 min/night during the 5.5-hour bedtime condition. While meal intake remained similar (P=0.51), sleep restriction was accompanied by increased consumption of calories from snacks (1087 ± 541 vs. 866 ± 365 kcal/day; P=0.026) with higher carbohydrate content (65 vs. 61%; P=0.04), particularly during the period from 19:00 to 7:00. These changes were not associated with a significant increase in energy expenditure during the 5.5-h (2526 ± 537 kcal/d) vs. 8.5-h bedtime period (2390 ± 369 kcal/d, P=0.58) and there were no significant differences in serum leptin and ghrelin between the two sleep conditions. Conclusions The results indicate that recurrent bedtime restriction can modify the amount, composition, and distribution of human food intake, and support the notion that sleeping short hours in an obesity-promoting environment may facilitate the excessive consumption of energy from snacks, but not meals.

The metabolic syndrome and its individual components are common in PCOS, particularly among women with the highest insulin levels and BMI. Hyperinsulinemia is a likely common pathogenetic factor for both PCOS and the metabolic syndrome.

There is a need to develop early biomarkers of acute kidney injury following cardiac surgery, where morbidity and mortality are increased by its presence. Plasma cystatin C (CyC) and plasma and urine Neutrophil Gelatinase Associated Lipocalin (NGAL) have been shown to detect kidney injury earlier than changes in plasma creatinine in critically ill patients. In order to determine the utility of urinary CyC levels as a measure of kidney injury, we prospectively collected plasma and urine from 72 adults undergoing elective cardiac surgery for analysis. Acute kidney injury was defined as a 25% or greater increase in plasma creatinine or renal replacement therapy within the first 72 hours following surgery. Plasma CyC and NGAL were not useful predictors of acute kidney injury within the first 6 hours following surgery. In contrast, both urinary CyC and NGAL were elevated in the 34 patients who later developed acute kidney injury, compared to those with no injury. The urinary NGAL at the time of ICU arrival and the urinary CyC level 6 hours after ICU admission were most useful for predicting acute kidney injury. A composite time point consisting of the maximum urinary CyC achieved in the first 6 hours following surgery outperformed all individual time points. Our study suggests that urinary CyC and NGAL are superior to conventional and novel plasma markers in the early diagnosis of acute kidney injury following adult cardiac surgery.

Although the reciprocal effects of parenting and child behavior have long been recognized, the emphasis of empirical study in the field of developmental psychopathology has been on parenting effects on children. For girls in particular, little is known about unique parenting effects on conduct problems in comparison to depression, or vice versa. In the current study, data from the large-scale (n = 2,451) Pittsburgh Girls Study were used to examine the reciprocal relations between parenting and child behavior over a six year period (child ages 7-12 years). Girls and their caregivers (85% of whom were biological mothers) were interviewed annually in their homes. Girls reported on symptoms of conduct disorder and depression, and caregivers reported on level of parent-child warmth and use of harsh punishment. The results of generalized estimating equation regression models demonstrated that both parenting behaviors were uniquely predictive of changes in girls' conduct problems and depressed mood. When the effects of race and poverty on these associations were controlled for, both parenting effects on girls' conduct problems remained significant, but only low parental warmth remained as a significant predictor of depressed mood. Girls' conduct problems, but not depressed mood, predicted changes in harsh punishment over time. The small effect of girls' depressed mood, on changes in parental warmth, was further weakened when socio-demographic factors were also included in the model.

BackgroundWorldwide, approximately two billion people are chronically infected with Toxoplasma gondii with largely unknown consequences.MethodsTo better understand long-term effects and pathogenesis of this common, persistent brain infection, mice were infected at a time in human years equivalent to early to mid adulthood and studied 5–12 months later. Appearance, behavior, neurologic function and brain MRIs were studied. Additional analyses of pathogenesis included: correlation of brain weight and neurologic findings; histopathology focusing on brain regions; full genome microarrays; immunohistochemistry characterizing inflammatory cells; determination of presence of tachyzoites and bradyzoites; electron microscopy; and study of markers of inflammation in serum. Histopathology in genetically resistant mice and cytokine and NRAMP knockout mice, effects of inoculation of isolated parasites, and treatment with sulfadiazine or αPD1 ligand were studied.ResultsTwelve months after infection, a time equivalent to middle to early elderly ages, mice had behavioral and neurological deficits, and brain MRIs showed mild to moderate ventricular dilatation. Lower brain weight correlated with greater magnitude of neurologic abnormalities and inflammation. Full genome microarrays of brains reflected inflammation causing neuronal damage (Gfap), effects on host cell protein processing (ubiquitin ligase), synapse remodeling (Complement 1q), and also increased expression of PD-1L (a ligand that allows persistent LCMV brain infection) and CD 36 (a fatty acid translocase and oxidized LDL receptor that mediates innate immune response to beta amyloid which is associated with pro-inflammation in Alzheimer's disease). Immunostaining detected no inflammation around intra-neuronal cysts, practically no free tachyzoites, and only rare bradyzoites. Nonetheless, there were perivascular, leptomeningeal inflammatory cells, particularly contiguous to the aqueduct of Sylvius and hippocampus, CD4+ and CD8+ T cells, and activated microglia in perivascular areas and brain parenchyma. Genetically resistant, chronically infected mice had substantially less inflammation.ConclusionIn outbred mice, chronic, adult acquired T. gondii infection causes neurologic and behavioral abnormalities secondary to inflammation and loss of brain parenchyma. Perivascular inflammation is prominent particularly contiguous to the aqueduct of Sylvius and hippocampus. Even resistant mice have perivascular inflammation. This mouse model of chronic T. gondii infection raises questions of whether persistence of this parasite in brain can cause inflammation or neurodegeneration in genetically susceptible hosts.