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.

Making Space: The Development of Spatial Representation and Reasoning

Abstract: Spatial competence is a central aspect of human adaptation. To understand human cognitive functioning, we must understand how people code the locations of things, how they navigate in the world, and how they represent and mentally manipulate spatial information. Until recently three approaches have dominated thinking about spatial development. Followers of Piaget claim that infants are born without knowledge of space or a conception of permanent objects that occupy space. They develop such knowledge through experience and manipulation of their environment. Nativists suggest that the essential aspects of spatial understanding are innate and that biological maturation of specific brain areas can account for whatever aspects of spatial development are not accounted for at birth. The Vygotskan approach emphasizes the cultural transmission of spatial skills. Nora Newcombe and Janellen Huttenlocher argue for an interactionist approach to spatial development that incorporates and integrates essential insights of the classic three approaches. They show how biological preparedness interacts with the spatial environment that infants encounter after birth to create spatial development and mature spatial competence. Topics covered include spatial coding during infancy and childhood; the early origins of coding distance in continuous space, of coding location with respect to distal external landmarks, and of hierarchical combination of information; the mental processes that operate on stored spatial information; spatial information as encoded in models and maps; and spatial information as encoded in language. In conclusion, the authors discuss their account of spatial development in relation to various approaches to cognitive development in other domains, including quantitative development, theory of mind, and language acquisition.

Negative Cognitive Styles and Stress-Reactive Rumination Interact to Predict Depression: A Prospective Study

Abstract: Research on cognitive theories of depression has identified negative cognitive styles and rumination in response to depressed mood as risk factors for depressive episodes. In addition, a general self-focusing style has been suggested to increase vulnerability to depression. The present study used a behavioral high-risk paradigm to test whether the interaction of negative cognitive styles and rumination predicted the prospective onset, number, and duration of depressive episodes in a sample of 148 initially nondepressed undergraduates over a 2.5-year follow-up. In addition, rumination was assessed specifically as the tendency to focus on maladaptive self-referential thoughts following stressful events (stress-reactive rumination; SRR). The principal hypotheses tested were (1) the interaction of negative cognitive styles and SRR increases risk for developing depressive episodes as well as longer duration depressive episodes; and (2) this interaction would not be obtained when a trait measure of general self-focus or a measure of rumination in response to depressed mood is used instead of the measure of SRR. After controlling for subsyndromal depressive symptoms and the main effects of negative cognitive styles and SRR, the interaction of negative cognitive styles and SRR was found to predict the prospective onset, number, and duration of major depressive and hopelessness depressive episodes. These interactions were not obtained when other measures of trait self-focus and depressive rumination were used instead of SRR.

Alternative splicing in concert with protein intrinsic disorder enables increased functional diversity in multicellular organisms

Abstract: Alternative splicing of pre-mRNA generates two or more protein isoforms from a single gene, thereby contributing to protein diversity. Despite intensive efforts, an understanding of the protein structure–function implications of alternative splicing is still lacking. Intrinsic disorder, which is a lack of equilibrium 3D structure under physiological conditions, may provide this understanding. Intrinsic disorder is a common phenomenon, particularly in multicellular eukaryotes, and is responsible for important protein functions including regulation and signaling. We hypothesize that polypeptide segments affected by alternative splicing are most often intrinsically disordered such that alternative splicing enables functional and regulatory diversity while avoiding structural complications. We analyzed a set of 46 differentially spliced genes encoding experimentally characterized human proteins containing both structured and intrinsically disordered amino acid segments. We show that 81% of 75 alternatively spliced fragments in these proteins were associated with fully (57%) or partially (24%) disordered protein regions. Regions affected by alternative splicing were significantly biased toward encoding disordered residues, with a vanishingly small P value. A larger data set composed of 558 SwissProt proteins with known isoforms produced by 1,266 alternatively spliced fragments was characterized by applying the pondr vsl1 disorder predictor. Results from prediction data are consistent with those obtained from experimental data, further supporting the proposed hypothesis. Associating alternative splicing with protein disorder enables the time- and tissue-specific modulation of protein function needed for cell differentiation and the evolution of multicellular organisms.

Apoptotic signaling by c-MYC

Abstract: c-MYC has a pivotal function in growth control, differentiation and apoptosis, and its abnormal expression is associated with many tumors. Overexpression of c-MYC sensitizes cells to apoptosis by a variety of stimuli. The decision of a cell to undergo apoptosis and how this apoptotic response is regulated by c-MYC depends on the specific cell type and the physiological status of the cell. Multiple cooperating molecular pathways of cell survival and apoptosis determine whether a cell lives or dies, and understanding how c-MYC interfaces with these pathways to influence the survival of cells is important to understand normal and abnormal development, tumor initiation and progression, and response of tumors to different treatment regimens. This article will provide an overview of the function of the tumor suppressor gene product p53 in the c-MYC-mediated apoptotic response and how c-MYC amplifies the intrinsic mitochondrial pathway and triggers and/or amplifies the death receptor pathways. Finally, a model for how deregulated c-MYC prematurely triggers the normal apoptotic response associated with terminal myeloid differentiation while also blocking the differentiation program is presented.