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In this article we examine whether different agents of socialization--family, school, and peers--are differentially associated with offending among different immigrant groups. Our expectation is to find that the association between delinquent friends and offending is stronger for first- and second-generation immigrants than for youths of native Swedish background. We use data from four nationally representative self-report studies of 21,504 adolescents with an average age of 15 years in Sweden. The results show that both first- and second-generation immigrants report committing more offenses than natives. The association is rather weak and the two predictors account for only a marginal amount of the variance in total offending. The results also show that the association between delinquent friends and offending is stronger for both first- and second-generation immigrants than for natives.

This study examines the association between number of siblings and delinquency, adjusting for family relations and demographic variables. Data is based on a nationally representative school survey in Sweden consisting of approximately 25,000 youths. The results show a positive association for those having five or more siblings (IRR = 1.533, p = <.001), whereas one or two siblings is negatively associated with delinquency compared to those having no siblings. These results remain stable after adjusting for family relations. This study underscores the importance of further exploring the variation and direction of the association between the number of siblings and delinquency, as well as deepening our understanding of the various theoretical mechanisms through which the number of siblings is associated with delinquent behaviour. [ABSTRACT FROM AUTHOR]

The Liver Kinase B1 (LKB1) tumor suppressor acts as a metabolic energy sensor to regulate AMP-activated protein kinase (AMPK) signaling and is commonly mutated in various cancers, including non-small cell lung cancer (NSCLC). Tumor cells deficient in LKB1 may be uniquely sensitized to metabolic stresses, which may offer a therapeutic window in oncology. To address this question we have explored how functional LKB1 impacts the metabolism of NSCLC cells using 13C metabolic flux analysis. Isogenic NSCLC cells expressing functional LKB1 exhibited higher flux through oxidative mitochondrial pathways compared to those deficient in LKB1. Re-expression of LKB1 also increased the capacity of cells to oxidize major mitochondrial substrates, including pyruvate, fatty acids, and glutamine. Furthermore, LKB1 expression promoted an adaptive response to energy stress induced by anchorage-independent growth. Finally, this diminished adaptability sensitized LKB1-deficient cells to combinatorial inhibition of mitochondrial complex I and glutaminase. Together, our data implicate LKB1 as a major regulator of adaptive metabolic reprogramming and suggest synergistic pharmacological strategies for mitigating LKB1-deficient NSCLC tumor growth.

Continuous de novo fatty acid synthesis is a common feature of cancer that is required to meet the biosynthetic demands of a growing tumor. This process is controlled by the rate-limiting enzyme acetyl-CoA carboxylase (ACC), an attractive but traditionally intractable drug target. Here we provide genetic and pharmacological evidence that in preclinical models ACC is required to maintain the de novo fatty acid synthesis needed for growth and viability of non-small-cell lung cancer (NSCLC) cells. We describe the ability of ND-646-an allosteric inhibitor of the ACC enzymes ACC1 and ACC2 that prevents ACC subunit dimerization-to suppress fatty acid synthesis in vitro and in vivo. Chronic ND-646 treatment of xenograft and genetically engineered mouse models of NSCLC inhibited tumor growth. When administered as a single agent or in combination with the standard-of-care drug carboplatin, ND-646 markedly suppressed lung tumor growth in the Kras;Trp53-/- (also known as KRAS p53) and Kras;Stk11-/- (also known as KRAS Lkb1) mouse models of NSCLC. These findings demonstrate that ACC mediates a metabolic liability of NSCLC and that ACC inhibition by ND-646 is detrimental to NSCLC growth, supporting further examination of the use of ACC inhibitors in oncology.

Contextual research on delinquency is primarily based on the idea that residential areas provide a major ecological setting that (indirectly) shapes observed differences in delinquency. Just like neighborhoods, schools differ in terms of their level of structural characteristics such as the concentration of immigrant children and children from disrupted families. Such characteristics may also shape delinquency. The present study aims to test the relationship between structural characteristics of schools and child antisocial behavior, using a sample of elementary school children (N = 779, aged 10-12 years in the urban context of Ghent, Belgium). This study found that the concentration of children from disrupted families has an independent effect on child delinquency, independent of social bonds, moral cognitions, and moral emotions. The contextual effect is fully mediated by exposure to peer delinquency.

This study examines the effects on adolescent offending of lifestyle risk and the individual propensity to offend. It is assumed that lifestyle risk will have a more important effect on offending for those individuals with high levels of individual propensity, whereas for individuals with low levels of individual propensity it is assumed that a risky lifestyle will not, or will only marginally, influence their involvement in offending. The data are drawn from two different samples of young adolescents in Antwerp, Belgium (N = 2,486), and Halmstad, Sweden (N = 1,003). The data provide strong support for the hypothesis that the effect of lifestyle risk is dependent on the strength or weakness of individual propensity, indicating that lifestyle risk has a stronger effect on delinquency for individuals with a high propensity to offend. The similarity of the results across two independent samples suggests the findings are stable. (Contains 5 notes, 2 tables, and 1 figure.)

Investigated gender differences in adolescent drug use in terms of parental monitoring and peer deviance. Surveys of Swedish adolescents indicated that girls were more highly monitored than boys, and boys were more exposed to deviant peers than girls. There was a significant interaction for parental monitoring and peer deviance for the sample as a whole. The effect of this interaction was greater among females. (Contains references.) (SM)