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Institution

Temple University

EducationPhiladelphia, Pennsylvania, United States
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.


Papers
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Journal ArticleDOI
TL;DR: Patients’ perceptions about their involvement in care appeared to be related to their attitudes about their illnesses as well as to recovery and further research is needed to determine the factors that influence these role perceptions.
Abstract: Objective:The purpose of this study was to explore the relationships among patients’ perceptions about the roles they played during medical visits, their subsequent attitudes about their illnesses and treatments, and their self-rated improvement.

354 citations

Journal ArticleDOI
TL;DR: It is demonstrated that ligation of macrophage Fcγ receptors (FcγR) can lead to a reversal ofmacrophage proinflammatory responses by inducing an upregulation of interleukin (IL)-10, with a reciprocal inhibition of IL-12 production.
Abstract: Macrophages can respond to a variety of infectious and/or inflammatory stimuli by secreting an array of proinflammatory cytokines, the overproduction of which can result in shock or even death. In this report, we demonstrate that ligation of macrophage Fcγ receptors (FcγR) can lead to a reversal of macrophage proinflammatory responses by inducing an upregulation of interleukin (IL)-10, with a reciprocal inhibition of IL-12 production. IL-10 upregulation was specific to FcγR ligation, since the ligation of the Mac-1 receptor did not alter IL-10 production. The identification of the specific FcγR subtype responsible for IL-10 upregulation was determined in gene knockout mice. Macrophages from mice lacking the FcR γ chain, which is required for assembly and signaling by FcγRI and FcγRIII, failed to upregulate IL-10 in response to immune complexes. However, mice lacking either the FcγRII or the FcγRIII were fully capable of upregulating IL-10 production, implicating FcγRI in this process. The biological consequences of FcγRI ligation were determined in both in vitro and in vivo models of inflammation and sepsis. In all of the models tested, the ligation of FcγR promoted the production of IL-10 and inhibited the secretion of IL-12. This reciprocal alteration in the pattern of macrophage cytokine production illustrates a potentially important role for FcγR-mediated clearance in suppressing macrophage proinflammatory responses.

353 citations

Journal ArticleDOI
TL;DR: It is concluded that physiologically elevated levels of FFa could potentially be responsible for a large part of the peripheral insulin resistance in patients with non-insulin-dependent diabetes mellitus.
Abstract: It was the aim of this study to determine whether FFA inhibit insulin-stimulated whole body glucose uptake and utilization in patients with non-insulin-dependent diabetes. We performed five types of isoglycemic (approximately 11mM) clamps: (a) with insulin; (b) with insulin plus fat/heparin; (c) with insulin plus glycerol; (d) with saline; (e) with saline plus fat/heparin and two types of euglycemic (approximately 5mM) clamps: (a) with insulin; (b) with insulin plus fat/heparin. During these studies, we determined rates of glucose uptake, glycolysis (both with 3[3H] glucose), glycogen synthesis (determined as glucose uptake minus glycolysis), carbohydrate oxidation (by indirect calorimetry) and nonoxidative glycolysis (determined as glycolysis minus carbohydrate oxidation). Fat/heparin infusion did not affect basal glucose uptake, but inhibited total stimulated (insulin stimulated plus basal) glucose uptake by 40-50% in isoglycemic and in euglycemic patients at plasma FFA concentration of approximately 950 and approximately 550 microM, respectively. In isoglycemic patients, the 40-50% inhibition of total stimulated glucose uptake was due to near complete inhibition of the insulin-stimulated part of glucose uptake. Proportional inhibition of glucose uptake, glycogen synthesis, and glycolysis suggested a major FFA-mediated defect involving glucose transport and/or phosphorylation. In summary, fat produced proportional inhibitions of insulin-stimulated glucose uptake and of intracellular glucose utilization. We conclude, that physiologically elevated levels of FFa could potentially be responsible for a large part of the peripheral insulin resistance in patients with non-insulin-dependent diabetes mellitus.

353 citations

Journal ArticleDOI
TL;DR: It is conclusively demonstrated that metabolic efficiency is not necessarily or exclusively related to obesity.

353 citations

Journal ArticleDOI
TL;DR: This study highlights the importance of social contingency in interactions for language learning and informs the literature on learning through screen media as the first study to examine word learning through video chat technology.
Abstract: Language learning takes place in the context of social interactions, yet the mechanisms that render social interactions useful for learning language remain unclear. This study focuses on whether social contingency might support word learning. Toddlers aged 24–30 months (N = 36) were exposed to novel verbs in one of three conditions: live interaction training, socially contingent video training over video chat, and noncontingent video training (yoked video). Results suggest that children only learned novel verbs in socially contingent interactions (live interactions and video chat). This study highlights the importance of social contingency in interactions for language learning and informs the literature on learning through screen media as the first study to examine word learning through video chat technology.

353 citations


Authors

Showing all 32360 results

NameH-indexPapersCitations
Robert J. Lefkowitz214860147995
Rakesh K. Jain2001467177727
Virginia M.-Y. Lee194993148820
Yury Gogotsi171956144520
Timothy A. Springer167669122421
Ralph A. DeFronzo160759132993
James J. Collins15166989476
Robert J. Glynn14674888387
Edward G. Lakatta14685888637
Steven Williams144137586712
Peter Buchholz143118192101
David Goldstein1411301101955
Scott D. Solomon1371145103041
Donald B. Rubin132515262632
Jeffery D. Molkentin13148261594
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202366
2022335
20213,475
20203,281
20193,166
20183,019