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.

Rumination as a common mechanism relating depressive risk factors to depression.

Abstract: Rumination was examined as a potential common mechanism linking risk factors with depression. Initially nondepressed individuals (N = 137) were assessed for presence of a ruminative response style and 4 other hypothesized risk factors for depression. They were followed for 2.5 years. Negative cognitive styles, self-criticism, dependency, neediness, and history of past depression were all significantly associated with rumination. Rumination mediated the predictive relationships of all risk factors except dependency with the number of prospective Diagnostic and Statistical Manual of Mental Disorders (3rd ed., rev.; American Psychiatric Association, 1987) major depressive episodes (MDEs; definite and subthreshold) during the follow-up period. In contrast, private self-consciousness did not mediate any relationships between risk factors and subsequent MDEs. Thus, rumination, as a special kind of self-focus, may act as a general proximal mechanism through which other vulnerability factors affect depression.

FEAR OF CRIME IN URBAN RESIDENTIAL NEIGHBORHOODS: Implications of Between‐ and Within‐Neighborhood Sources for Current Models

Abstract: Current work on fear of crime centers largely around three dominant theoretical models: indirect victimization, community concern, and incivilities. Previous work (Taylor and Hale 1986) confirms th...

Dimensions of information systems success

Abstract: The value added by an organization’s IT assets is a critical concern to both research and practice. Not surprisingly, a large number of IS effectiveness measures can be found in the IS literature. What is not clear in the literature is what measures are appropriate in a particular context. In this paper we propose a two-dimensional matrix for classifying IS Effectiveness measures. The first dimension is the type of system studied. The second dimension is the stakeholder in whose interests the system is being evaluated. The matrix was tested by using it to classify IS effectiveness measures from 186 empirical papers in three major IS journals for the last nine years. The results indicate that the classifications are meaningful. Hence, the IS Effectiveness Matrix provides a useful guide for conceptualizing effectiveness measurement in IS research, and for choosing appropriate measures, both for research and practice.

The role of experience in spatial test performance: A meta-analysis

Abstract: The hypothesis that spatial ability is, in part, experientially determined, and that sex differences in spatial ability can be explained by sex differences in spatial experience, can be studied in a correlational manner by examining the relationship between spatial activity participation and spatial ability test performance for males and females. Alternatively, an experimental training situation, comparing male and female susceptibility to training, has been proposed to test the hypothesis that environment has an impact on spatial skills and sex differences in ability. Both lines of research are reviewed here, through the use of meta-analytic techniques. The first meta-analysis reveals a weak but reliable relationship between spatial activity participation and spatial ability. This relationship appears similar for males and females. The second meta-analysis reveals that spatial ability test performance can be improved by training for both sexes. This improvement does not appear different for males and females, however, contrary to a predominant hypothesis in the literature. Training to asymptote may be a better test of the relevance of differential experience to sex differences. Content and duration of training are also discussed as important factors in the effectiveness of training.

Central role of the P2Y12 receptor in platelet activation

Abstract: The vessel wall contains a continuous lining of endothelium that serves as a barrier between the circulating platelets and the prothrombotic subendothelial matrix (1). Upon vessel injury, the endothelial layer is disrupted and the circulating platelets are exposed to subendothelial proteins such as vWF, collagen, and vitronectin, among others (1). The platelets initially interact with the subendothelium through adhesive receptors, such as GPIb-IX-V receptors, that mediate rolling and tethering of the platelets to vWF at the site of vascular injury. Next, the platelet collagen receptors α2β1 and GPVI mediate a more firm adhesion and cause further platelet activation. These initial interactions with the subendothelium cause the release of contents from the platelet dense granules, which contain platelet agonists such as ADP, and the α-granules, which contain fibrinogen, factor V, and P-selectin (1). The release of the granule contents causes further platelet activation, but it also fuels the coagulation response as a result of the release of factor V and fuels the inflammatory response through the exposure of P-selectin on the platelet surface. The platelet also generates lipid mediators such as thromboxane A2. ADP elicits its effects on the platelet through the P2Y1 and P2Y12 receptors (2), whereas thromboxane A2 activates the thromboxane-prostanoid (TP) receptor on the platelet surface (1). The released dense granule contents cause further platelet activation and recruitment of circulating platelets to the site of injury. Platelets interacting with these mediators also undergo platelet shape change, a process of actin cytoskeletal reorganization that changes the platelets from a disc shape to a round shape with long, filopodial extensions that form a meshwork of platelets in the platelet plug (3). Also, tissue factor is exposed, which initiates the coagulation response that results in formation of thrombin. Thrombin activates platelets via interactions with the proteinase-activated receptor-1 (PAR1) and PAR4 receptors (4) and also cleaves fibrinogen to form fibrin. Fibrin further stabilizes the accumulating platelet plug at the site of injury, resulting in a stable hemostatic plug. Interactions of the platelets with collagen, vWF, ADP, thromboxane A2, and thrombin cause intracellular platelet signaling that leads to the activation of the heterodimeric integrin αIIbβ3, also known as the fibrinogen receptor (5). The intracellular platelet signaling from these agonists causes the fibrinogen receptor to change from a low-affinity state to a high-affinity state that binds fibrinogen (6). Fibrinogen binds to the platelets via the activated fibrinogen receptor, and this cross-linking of platelets to fibrinogen results in platelet aggregates that accumulate and arrest bleeding at the site of injury (Figure ​(Figure1).1). Thus, platelet activation is the product of many signals originating from many receptors, which each contribute to the formation of a platelet plug. Figure 1 The hemostatic process. Upon vessel injury, platelets roll and become tethered to the vessel wall by interactions with vWF and collagen (noted as black strands). These interactions cause platelet shape change, and release of ADP from dense granules. The ... Pathophysiologic conditions, such as atherosclerotic plaque rupture, can lead to aberrant platelet activation resulting in arterial thrombosis, which can cause myocardial infarction and ischemic stroke (6). The importance of ADP in this process has been demonstrated both by antiplatelet drugs that target the P2Y12 receptor (2) and by patients with dysfunctional P2Y12 receptors (7). Antagonism of the P2Y12 receptor with either ticlopidine or clopidogrel is clinically effective in the prevention of myocardial infarction, ischemic stroke, and vascular death (8). Despite the established role of the P2Y12 receptor in the hemostatic response, the full implications of P2Y12 receptor antagonism in the prevention of thrombosis remain incompletely understood. It is hoped that more clinically effective P2Y12 antagonists will prevent the incidence of ischemic events that stem from aberrant platelet activation and therefore will be used as improved and suitable treatments for thrombosis.