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Structural analyses were performed using immunofluorescent staining against Ki67 and CD31 to investigate phenotypic outcomes at both timepoints. RESULTS RNA-seq and IPA analyses revealed differential expression of transcripts and pathway interactions related to placental vascular development and tissue morphology in obese placentae at term, including downregulation of Muc15, Cnn1, and Acta2. Pdgfb, which is implicated in labyrinthine layer development, was downregulated in obese placentae at E13. This was consistent with the morphological evidence of reduced labyrinth zone (LZ) size, as well as lower fetal weight at both timepoints irrespective of offspring sex. CONCLUSIONS Maternal obesity results in abnormal placental LZ development and impaired vascularization, which may mediate the observed FGR through reduced transfer of nutrients across the placenta.BACKGROUND/OBJECTIVES The winter holiday season in the United States, which spans mid-November to mid-January, contributes to over half of annual body weight gain. Selleck Pexidartinib Although self-reported data have linked this weight change to both increased energy intake and reduced physical activity, objective techniques have never been used; and thus, the actual cause of holiday weight gain is controversial. Here, we aimed to determine changes in components of energy balance leading to the holiday weight gain. METHODS Body weight change was compared between the pre-holiday (mid-September to mid-November) and the holiday period (mid-November to early January). Total energy expenditure (TEE) was measured using doubly labeled water during holiday time (early to mid-December). Subjective (ratings) and physiological (appetite-regulating hormones) measures of appetite, eating-away-from-home frequency, and incentive salience of food pictures were also evaluated. RESULTS In 23 obese adults (87% female), body weight change during the holidays (0.41 ± 0.42 kg) was significantly higher (P = 0.02) than the body weight change during the pre-holiday period (-0.86 ± 0.42 kg). TEE was unchanged during the two periods, suggesting no role of energy expenditure on weight gain. However, participants reported lower satisfaction after a meal pre-load which was significantly correlated with increased body weight during the holiday period. An increase in number of episodes of eating at sit-down restaurants was also reported during that period. Overall, these changing behaviors were supported by a non-significant increase in energy intake (+80 kcal/day, P = 0.07) observed during the study holiday period. CONCLUSION We conclude that a decrease in energy expenditure does not result in the weight increase, but that increase in food intake is the more likely cause. Our data imply that compromised internal satiety mechanisms in presence of external food cues and diet-related behavioral variables during the holidays may influence weight gain.BACKGROUND/OBJECTIVES Physical activity is beneficial to lipid profiles; however, the association between sedentary behavior and sleep and pediatric dyslipidemia remains unclear. We aimed to investigate whether sedentary behavior or sleep predicted lipid profiles in children over a 2-year period. SUBJECTS/METHODS Six hundered and thirty children from the QUALITY cohort, with at least one obese parent, were assessed prospectively at ages 8-10 and 10-12 years. Measures of sedentary behavior included self-reported TV viewing and computer/video game use. Seven-day accelerometry was used to derive sedentary behavior and sleep duration. Adiposity was assessed using DEXA scans. Twenty-four-hour dietary recalls yielded estimates of carbohydrate and fat intake. Outcomes included fasting total cholesterol, triglycerides, HDL and LDL-cholesterol. Multivariable models were adjusted for adiposity and diet. RESULTS At both Visit 1 (median age 9.6 year) and Visit 2 (median age 11.6 year), children were of normal weight (55%), overweight (22%), or obese (22%). Every additional hour of TV viewing at Visit 1 was associated with a 7.0% triglyceride increase (95% CI 3.5, 10.6; P  less then  0.01) and 2.6% HDL decrease (95% CI -4.2, -0.9; P  less then  0.01) at Visit 2; findings remained significant after adjusting for adiposity and diet. Every additional hour of sleep at Visit 1 predicted a 4.8% LDL decrease (95% CI -9.0, -0.5; P = 0.03) at Visit 2, after adjusting for fat intake; this association became nonsignificant once controlling for adiposity. CONCLUSIONS Longer screen time during childhood appears to deteriorate lipid profiles in early adolescence, even after accounting for other major lifestyle habits. There is preliminary evidence of a deleterious effect of shorter sleep duration, which should be considered in further studies.Limited therapeutic options are available for advanced-stage hepatocellular carcinoma owing to its poor diagnosis. Drug resistance to sorafenib, the only available targeted agent, is commonly reported. The comprehensive elucidation of the mechanisms underlying sorafenib resistance may thus aid in the development of more efficacious therapeutic agents. To clarify the signaling changes contributing to resistance, we applied quantitative phosphoproteomics to analyze the differential phosphorylation changes between parental and sorafenib-resistant HuH-7 cells. Consequently, an average of ~1500 differential phosphoproteins were identified and quantified, among which 533 were significantly upregulated in resistant cells. Further bioinformatic integration via functional categorization annotation, pathway enrichment and interaction linkage analysis led to the discovery of alterations in pathways associated with cell adhesion and motility, cell survival and cell growth and the identification of a novel target, EphA2, in resistant HuH-7R cells. In vitro functional analysis indicated that the suppression of EphA2 function impairs cell proliferation and motility and, most importantly, overcomes sorafenib resistance. The attenuation of sorafenib resistance may be achieved prior to its development through the modulation of EphA2 and the subsequent inhibition of Akt activity. Binding analyses and in silico modeling revealed a ligand mimic lead compound, prazosin, that could abate the ligand-independent oncogenic activity of EphA2. Finally, data obtained from in vivo animal models verified that the simultaneous inhibition of EphA2 with sorafenib treatment can effectively overcome sorafenib resistance and extend the projected survival of resistant tumor-bearing mice. Thus our findings regarding the targeting of EphA2 may provide an effective approach for overcoming sorafenib resistance and may contribute to the management of advanced hepatocellular carcinoma.Selleck Pexidartinib