Neurodevelopmental outcomes in CDH survivors: A single institution's experience.

PURPOSE: Survivors of congenital diaphragmatic hernia (CDH) face high morbidity. We studied the neurodevelopmental outcomes of CDH survivors at a single institution. METHODS: CDH survivors born July 2006-March 2016 at a free-standing children's hospital were reviewed. Neurodevelopment was assessed using the Peabody Developmental Motor Scales (PDMS-2) broken into gross, fine, and total motor quotients. Data collected included prenatal variables (liver herniation, defect laterality, observed:expected total fetal lung volume (o:eTFLV) on MRI), birth demographics (sex, race, estimated gestational age (EGA), birth weight (BtWt), 5 min APGAR, associated anomalies), and therapies/hospital course (HFOV/HFJV, ECMO, timing of repair, pulmonary hypertension (PHTN) severity, length of stay, ventilator days). Variables were analyzed using mixed linear modeling. RESULTS: Sixty-eight children were included. Most patients had left-sided CDH (55/68, 81%) without liver herniation (42/68, 62%). ECMO utilization was 25/68 (37%). The mean [95% confidence interval] gross motor quotient for the entire cohort was 87 [84-91], fine motor quotient was 92 [88-96], and total motor quotient was 88 [84-93], representing below average, average, and below average functioning, respectively. o:eTFLV predicted fine motor quotient among prenatal variables. Associated anomalies and ECMO use predicted all quotients in the final model. CONCLUSIONS: Associated anomalies and ECMO use predict neurodevelopmental delay in CDH survivors. TYPE OF STUDY: Retrospective observational study; Prognostic. LEVEL OF EVIDENCE: II.

Application of the Environmental Assessment Tool (EAT) as a process measure for a worksite weight management intervention.

OBJECTIVE: To assess the ability of the Environmental Assessment Tool (EAT) to detect changes over time in workplace physical and social environmental supports for physical activity and nutrition; and predict employee engagement, behavior changes, and biometrics. METHODS: Analyses utilized site-level (n = 12) EAT scores. Differences-in-difference regressions tested changes in EAT scores over time across treatment sites. Generalized linear mixed models examined the ability of site-level EAT scores to predict individual-level outcomes. RESULTS: Overall, the EAT captured changes in the workplace environmental supports for health promotion over time. However, the ability of EAT scores to predict intervention outcomes was weak. CONCLUSIONS: The EAT is a useful tool for monitoring changes in workplace environments over time. Further research is needed regarding the dose or intensity of environmental intervention needed to affect changes in employee behaviors and biometrics.

Development of the Environmental Assessment Tool (EAT) to measure organizational physical and social support for worksite obesity prevention programs.

OBJECTIVE: To describe the development, reliability, and validity of the Environmental Assessment Tool (EAT) for assessing worksite physical and social environmental support for obesity prevention. METHODS: The EAT was developed using a multistep process. Inter-rater reliability was estimated via Kappa and other measures. Concurrent and predictive validity were estimated using site-level correlations and person-level multiple regression analyses comparing EAT scores and employee absenteeism and health care expenditures. RESULTS: Results show high inter-rater reliability and concurrent validity for many measures and predictive validity for absenteeism expenditures. CONCLUSIONS: The primary use of the EAT is as a physical and social environment assessment tool for worksite obesity prevention efforts. It can be used as a reliable and valid means to estimate relationships between environmental interventions and absenteeism and medical expenditures, provided those expenditures are for the same year that the EAT is administered.

Leptin resistance in mice is determined by gender and duration of exposure to high-fat diet.

Mice fed a high-fat diet are reported to be resistant to peripheral injections of leptin. We previously failed to induce leptin resistance in female mice fed a high-fat diet for 15 weeks. Therefore, we measured the responsiveness to peripheral infusions (10 microg/day) of leptin, and the responsiveness to third ventricle injections of leptin (1 microg) in male and female NIH Swiss mice fed low-fat (10% kcal) or high-fat (45% kcal) diets. Male and female 15-week-old mice that had been fed low- or high-fat diet from 10 days of age lost fat during a 13-day intraperitoneal infusion of leptin and lost weight in response to a single central injection of leptin. Fifteen-week-old male mice fed a high-fat diet for 5 weeks did not lose body fat during a peripheral infusion of leptin and did not lose weight in response to a central injection of leptin. Female mice fed high-fat diet for 5 weeks remained leptin-responsive. Weight loss was achieved without a significant voluntary decrease in food intake, suggesting that both peripherally and centrally administered leptin increases energy expenditure. These results demonstrate that the development of leptin resistance in NIH Swiss mice fed a high-fat diet is dependent upon the gender of the mice and either the duration of exposure to high-fat diet or the age at which the mice are first exposed to the diet.

Method of leptin dosing, strain, and group housing influence leptin sensitivity in high-fat-fed weanling mice.

High-fat diets are reported to induce resistance to peripherally administered leptin. In an attempt to develop a model of juvenile diet-induced obesity, mice were weaned onto high-fat diet. Male and female, 35-day-old, C57BL/6J high-fat (45% kcal fat) diet-fed mice housed individually on grid floors did not decrease food intake or body weight in response to intraperitoneal (30 microg), lateral ventricle (5 microg), or third ventricle (0.5 microg) injections of leptin. Body weight and fat were significantly reduced by 13-day intraperitoneal infusions of 10 microg leptin/day, which doubled circulating leptin. Leptin infusion also reduced body fat in weanling, high-fat diet-fed NIH Swiss mice. Group housing mice on bedding prevented loss of fat in high-fat diet-fed male and female NIH Swiss and female C57BL/6J mice. These results indicate that peripherally infused leptin reduces fat in part by increasing thermogenesis and that inhibition of food intake in high-fat diet-fed mice requires either chronic activation of central leptin receptors or is independent of receptors that inhibit feeding in response to an acute central injection of leptin.