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Traditional bullying and cyberbullying are common problems faced by today's youth. Research seeking to explain bullying perpetration has often invoked Agnew's general strain theory (GST). However, research to date has often explored within a given study only a single emotion at a time that can result from strain. Further, prior research has tended to take the causal ordering arguments of GST at face value. The current study seeks to focus on the correlation of strains related to socioeconomics with traditional and cyberbullying perpetration and negative emotions. Utilizing the Add Health data and path modeling in Mplus, results suggest that socioeconomic strain positively correlates with bullying perpetration and recent negative emotions. However, results suggest a potential causal chain that is the opposite of an expectation of GST, with bullying perpetration potentially affecting negative emotions, and not the other way around. Implications of the results for theory and policy are discussed. [ABSTRACT FROM AUTHOR]

[This corrects the article DOI: 10.1016/j.molmet.2013.10.005.].

Circadian rhythms control metabolism and energy homeostasis, but the role of the skeletal muscle clock has never been explored. We generated conditional and inducible mouse lines with muscle-specific ablation of the core clock gene Bmal1. Skeletal muscles from these mice showed impaired insulin-stimulated glucose uptake with reduced protein levels of GLUT4, the insulin-dependent glucose transporter, and TBC1D1, a Rab-GTPase involved in GLUT4 translocation. Pyruvate dehydrogenase (PDH) activity was also reduced due to altered expression of circadian genes Pdk4 and Pdp1, coding for PDH kinase and phosphatase, respectively. PDH inhibition leads to reduced glucose oxidation and diversion of glycolytic intermediates to alternative metabolic pathways, as revealed by metabolome analysis. The impaired glucose metabolism induced by muscle-specific Bmal1 knockout suggests that a major physiological role of the muscle clock is to prepare for the transition from the rest/fasting phase to the active/feeding phase, when glucose becomes the predominant fuel for skeletal muscle.

Bullying victimization can have serious consequences for adolescents. This article examines the association between traditional and cyberbullying victimization, depressive symptoms, and suicidality in a national school-based sample, utilizing general strain theory (GST) as a guide to how these variables might relate to each other. We additionally examine whether the associations between these variables differ by gender. Results suggest that traditional and cyberbullying victimization have significant, positive associations with both depressive symptoms and suicidality. Results are partly supportive of the full model suggested by GST, with the associations between bullying and suicidality being weakened in some models when accounting for depressive symptoms. Gender differences also emerge. These findings are discussed in relation to their relevance for policy and theory. [ABSTRACT FROM AUTHOR]

Research has shown that military combat experience can shape later mental health in a negative fashion and increase subsequent antisocial behaviors. Limited research to date has attempted to explore if military combat experience is related to antisocial behaviors because it increases the likelihood of negative mental health states. Using general strain theory (GST) as a guide, the current study offers a preliminary test of how military combat experience, negative mental health, with a focus on depressive symptoms and posttraumatic stress disorder (PTSD), and antisocial behavior, with a focus on criminal behavior, might relate together in a single theoretically informed model. Results from the Add Health sample suggest that military combat experience correlates with depressive symptoms, PTSD, and crime. Further, results suggest that PTSD, but not depressive symptoms, could potentially act as a mediator between military combat experience and subsequent criminal behavior. Implications for theory and policy are discussed. [ABSTRACT FROM AUTHOR]

Intracellular calcium influences an array of pathways and affects cellular processes. With the rapidly progressing research investigating the molecular identity and the physiological roles of the mitochondrial calcium uniporter (MCU) complex, we now have the tools to understand the functions of mitochondrial Ca 2+ in the regulation of pathophysiological processes. Herein, we describe the role of key MCU complex components in insulin resistance in mouse and human adipose tissue. Adipose tissue gene expression was analyzed from several models of obese and diabetic rodents and in 72 patients with obesity as well as in vitro insulin-resistant adipocytes. Genetic manipulation of MCU activity in 3T3-L1 adipocytes allowed the investigation of the role of mitochondrial calcium uptake. In insulin-resistant adipocytes, mitochondrial calcium uptake increased and several MCU components were upregulated. Similar results were observed in mouse and human visceral adipose tissue (VAT) during the progression of obesity and diabetes. Intriguingly, subcutaneous adipose tissue (SAT) was spared from overt MCU fluctuations. Furthermore, MCU expression returned to physiological levels in VAT of patients after weight loss by bariatric surgery. Genetic manipulation of mitochondrial calcium uptake in 3T3-L1 adipocytes demonstrated that changes in mitochondrial calcium concentration ([Ca 2+ ] mt ) can affect mitochondrial metabolism, including oxidative enzyme activity, mitochondrial respiration, membrane potential, and reactive oxygen species formation. Finally, our data suggest a strong relationship between [Ca 2+ ] mt and the release of IL-6 and TNFα in adipocytes. Altered mitochondrial calcium flux in fat cells may play a role in obesity and diabetes and may be associated with the differential metabolic profiles of VAT and SAT., (Copyright © 2017 the American Physiological Society.)

Circadian rhythms control metabolism and energy homeostasis, but the role of the skeletal muscle clock has never been explored. We generated conditional and inducible mouse lines with muscle-specific ablation of the core clock gene Bmal1. Skeletal muscles from these mice showed impaired insulin-stimulated glucose uptake with reduced protein levels of GLUT4, the insulin-dependent glucose transporter, and TBC1D1, a Rab-GTPase involved in GLUT4 translocation. Pyruvate dehydrogenase (PDH) activity was also reduced due to altered expression of circadian genes Pdk4 and Pdp1, coding for PDH kinase and phosphatase, respectively. PDH inhibition leads to reduced glucose oxidation and diversion of glycolytic intermediates to alternative metabolic pathways, as revealed by metabolome analysis. The impaired glucose metabolism induced by muscle-specific Bmal1 knockout suggests that a major physiological role of the muscle clock is to prepare for the transition from the rest/fasting phase to the active/feeding phase, when glucose becomes the predominant fuel for skeletal muscle.