Temple University

About: Temple University is a education organization based out in Philadelphia, Pennsylvania, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 32154 authors who have published 64375 publications receiving 2219828 citations.

Affiliation With Antisocial Peers, Susceptibility to Peer Influence, and Antisocial Behavior During the Transition to Adulthood

Abstract: Developmental theories suggest that affiliation with deviant peers and susceptibility to peer influence are important contributors to adolescent delinquency, but it is unclear how these variables impact antisocial behavior during the transition to adulthood, a period when most delinquent individuals decline in antisocial behavior. Using data from a longitudinal study of 1,354 antisocial youth, the present study examined how individual variation in exposure to deviant peers and resistance to peer influence affect antisocial behavior from middle adolescence into young adulthood (ages 14 to 22 years). Whereas we find evidence that antisocial individuals choose to affiliate with deviant peers, and that affiliating with deviant peers is associated with an individual's own delinquency, these complementary processes of selection and socialization operate in different developmental periods. In middle adolescence, both selection and socialization serve to make peers similar in antisocial behavior, but from ages 16 to 20 years, only socialization appears to be important. After age 20, the impact of peers on antisocial behavior disappears as individuals become increasingly resistant to peer influence, suggesting that the process of desistance from antisocial behavior may be tied to normative changes in peer relations that occur as individuals mature socially and emotionally.

Crisis in the IS field? A critical reflection on the state of the discipline

Abstract: This paper explores the issue of whether the field of IS is in crisis. To do so, the paper first starts by looking back on where the field has come from. Next, it assesses the status of the IS field by exploring where the field is now. That our current status remains a ‘fragmented adhocracy’ suggests the field may indeed be in crisis or headed for a crisis. This is compounded by the fact that there are two different views on the state of the IS field, each posing its own set of threats. One is the external view of the community (the view of IS from outside the academic field); the other is the internal view (the view from inside the IS community). By analyzing these two views, a better understanding of the problems the field faces emerges. In the next part of the paper, some thoughts are presented on where might the field go from here for overcoming its internal communication deficit. The paper proposes four different types of knowledge for structuring an IS Body of Knowledge (BoK) and following on from that, the value of creating a common BoK for the field. Lastly, the implications arising from the paper’s analysis are explored. More specifically, the paper considers various options that are available for overcoming the internal communications deficit the IS field faces. These include changing the way the field thinks about generalizations, changing the institutional publication practices, focusing more on understanding the field’s organizational stakeholders, and developing new knowledge creation and transformation networks. If IS as a field can overcome its internal communications deficits, it might ultimately contribute to the societal challenge of developing a deliberative cyber democracy and thereby help to address the social communication deficit which is a feature of modern mass societies.

Ca2+- and mitochondrial-dependent cardiomyocyte necrosis as a primary mediator of heart failure

Abstract: Loss of cardiac myocytes in heart failure is thought to occur largely through an apoptotic process. Here we show that heart failure can also be precipitated through myocyte necrosis associated with Ca2+ overload. Inducible transgenic mice with enhanced sarcolemmal L-type Ca2+ channel (LTCC) activity showed progressive myocyte necrosis that led to pump dysfunction and premature death, effects that were dramatically enhanced by acute stimulation of β-adrenergic receptors. Enhanced Ca2+ influx–induced cellular necrosis and cardiomyopathy was prevented with either LTCC blockers or β-adrenergic receptor antagonists, demonstrating a proximal relationship among β-adrenergic receptor function, Ca2+ handling, and heart failure progression through necrotic cell loss. Mechanistically, loss of cyclophilin D, a regulator of the mitochondrial permeability transition pore that underpins necrosis, blocked Ca2+ influx–induced necrosis of myocytes, heart failure, and isoproterenol-induced premature death. In contrast, overexpression of the antiapoptotic factor Bcl-2 was ineffective in mitigating heart failure and death associated with excess Ca2+ influx and acute β-adrenergic receptor stimulation. This paradigm of mitochondrial- and necrosis-dependent heart failure was also observed in other mouse models of disease, which supports the concept that heart failure is a pleiotropic disorder that involves not only apoptosis, but also necrotic loss of myocytes in association with dysregulated Ca2+ handling and β-adrenergic receptor signaling.