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An effective behavior change program is the first line of prevention for youth obesity. However, effectiveness in prevention of adolescent obesity requires several approaches, with special attention paid to disordered eating behaviors and psychological support, among other environmental factors. The aim of this systematic review is to compare the impact of two types of obesity prevention programs, inclusive of behavior change components, on weight outcomes. “Energy-balance” studies are aimed at reducing calories from high-energy sources and increasing physical activity (PA) levels, while “shared risk factors for obesity and eating disorders” focus on reducing disordered eating behaviors to promote a positive food and eating relationship. A systematic search of ProQuest, PubMed, PsycInfo, SciELO, and Web of Science identified 8825 articles. Thirty-five studies were included in the review, of which 20 regarded “energy-balance” and 15 “shared risk factors for obesity and eating disorders”. “Energy-balance” studies were unable to support maintenance weight status, diet, and PA. check details “Shared risk factors for obesity and eating disorders” programs also did not result in significant differences in weight status over time. However, the majority of “shared risk factors for obesity and eating disorders” studies demonstrated reduced body dissatisfaction, dieting, and weight-control behaviors. Research is needed to examine how a shared risk factor approach can address both obesity and eating disorders.The size (grain size and specimen size) effect makes traditional macroscopic forming technology unsuitable for a microscopic forming process. In order to investigate the size effect on mechanical properties and deformation behavior, pure copper wires (diameters range from 50 μm to 500 μm) were annealed at different temperatures to obtain different grain sizes. The results show that a decrease in wire diameter leads to a reduction in tensile strength, and this change is pronounced for large grains. The elongation of the material is in linear correlation to size factor D/d (diameter/grain size), i.e., at the same wire diameter, more grains in the section bring better plasticity. This phenomenon is in relationship with the ratio of free surface grains. A surface model combined with the theory of single crystal and polycrystal is established, based on the relationship between specimen/grain size and tensile property. The simulated results show that the flow stress in micro-scale is in the middle of the single crystal model (lower critical value) and the polycrystalline model (upper critical value). Moreover, the simulation results of the hybrid model calculations presented in this paper are in good agreement with the experimental results.When considering connexin expression and regulation, the epidermis of the skin is one of the most complex tissues found in mammals even though it largely contains a single cell type, the keratinocyte. In the rodent epidermis, up to 9 connexin family members have been detected at the mRNA level. Many of these connexins are temporally and spatially regulated in coordination with keratinocyte progenitor cell differentiation and migration from the stratum basale to form the stratum spinosum and stratum granulosum layers before finally forming the stratum corneum. Cx43 is the principal connexin found in basal keratinocytes and to a lesser degree found in keratinocytes that have begun to differentiate where Cx26, Cx30 and Cx31 become prevalent. Here we show that the CRISPR-Cas9 ablation of Cx43 reduces overall gap junction coupling in monolayer cultures of rat epidermal keratinocytes (REKs) and dysregulates the differentiation of REKs when grown in organotypic cultures. Natively found in differentiated keratinocytes, Cx31 readily assembles into gap junctions when expressed in REKs where it can extensively co-assemble into the same gap junctions with co-expressed Cx30. Time-lapse imaging indicated that many Cx31 gap junctions are mobile within the plasma membrane undergoing both fusion and fission events. Finally, the persistence of pre-existing Cx31 gap junctions in the presence of the protein trafficking blocker, brefeldin A, is longer than that found for Cx43 gap junctions indicating that it has a distinctly different life expectancy in REKs. Collectively, this study highlights the importance of Cx43 in rodent keratinocyte differentiation and suggests that Cx31 acquires life-cycle properties that are distinct from Cx43.Knowledge regarding the involvement of sweetness perception on energy intake is scarce. Here, the impact of glucose and sucrose sweetness, beyond their caloric load, on subsequent food intake and biomarkers of satiation was evaluated by co-administration of the sweet taste receptor inhibitor lactisole. A total of 27 healthy, male subjects received solutions of either 10% glucose w/o 60 ppm lactisole or 10% sucrose w/o 60 ppm lactisole. Subsequent food intake from a standardized breakfast was evaluated 2 h after receiving the respective test solution. Changes in postprandial plasma concentrations of cholecystokinin, ghrelin, and serotonin were determined over a period of 120 min, as was the body temperature. Administration of lactisole to the sucrose solution increased the energy intake from the subsequent standardized breakfast by 12.9 ± 5.8% (p = 0.04), led to a decreased Δ AUC of the body core temperature by 46 ± 20% (p = 0.01), and time-dependently reduced Δ serotonin plasma concentrations (-16.9 ± 6.06 ng/mL vs. -0.56 ± 3.7 ng/mL after sucrose administration, p = 0.03). The present study shows that lactisole increases energy intake and decreases plasma serotonin concentrations as well as body core temperature induced by sucrose, but not glucose. This finding may be associated with the different binding affinities of sucrose and glucose to the sweet taste receptor.miR-22 is one of the most abundant miRNAs in the liver and alterations of its hepatic expression have been associated with the development of hepatic steatosis and insulin resistance, as well as cancer. However, the pathophysiological roles of miR-22-3p in the deregulated hepatic metabolism with obesity and cancer remains poorly characterized. Herein, we observed that alterations of hepatic miR-22-3p expression with non-alcoholic fatty liver disease (NAFLD) in the context of obesity are not consistent in various human cohorts and animal models in contrast to the well-characterized miR-22-3p downregulation observed in hepatic cancers. To unravel the role of miR-22 in obesity-associated NAFLD, we generated constitutive Mir22 knockout (miR-22KO) mice, which were subsequently rendered obese by feeding with fat-enriched diet. Functional NAFLD- and obesity-associated metabolic parameters were then analyzed. Insights about the role of miR-22 in NAFLD associated with obesity were further obtained through an unbiased proteomic analysis of miR-22KO livers from obese mice.