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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.


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Journal ArticleDOI
TL;DR: Using samples of undergraduates and a sample of clients with social anxiety disorder, it is found that the reverse-scored items show a strong relationship with the normal personality characteristic of extraversion, suggesting that the reversed items of the SIAS may primarily assess extraversion.

305 citations

Journal ArticleDOI
TL;DR: In this article, the authors investigated the effects of repeated testing and training on mental rotation skills in both men and women with higher or lower spatial experience, and found that videogame training has effects on performance and leads to transfer.
Abstract: This study addressed questions about improvement in mental rotation skills: (1) whether growth trajectories differ for men and women with higher or lower spatial experience, (2) whether videogame training has effects on performance and leads to transfer, (3) whether effects of repeated testing or training effects are durable and (4) whether transfer is durable Undergraduates participated in repeated testing on the MRT or played the videogame Tetris Analyses showed large improvements in mental rotation with both repeated testing and training; these gains were maintained several months later MRT scores of men and women did not converge, but men showed faster initial growth and women showed more improvement later Videogame training showed greater initial growth than repeated testing alone, but final performance did not differ Effects of videogame training transferred to other spatial tasks exceeding the effects of repeated testing, and this transfer advantage was still evident after several months Copyright © 2007 John Wiley & Sons, Ltd

305 citations

Journal ArticleDOI
TL;DR: The objective is to evaluate the efficacy of acid‐suppressive therapy with the proton pump inhibitor esomeprazole on the signs and symptoms of chronic posterior laryngitis (CPL) in patients with suspected reflux lARYngitis.
Abstract: Objective: To evaluate the efficacy of acid-suppressive therapy with the proton pump inhibitor esomeprazole on the signs and symptoms of chronic posterior laryngitis (CPL) in patients with suspected reflux laryngitis. Study Design: Prospective, multicenter, randomized, parallel-group trial that compared twice-daily esomeprazole 40 mg with placebo for 16 weeks. Methods: Eligible patients had a history of one or more CPL symptoms (throat clearing, cough, globus, sore throat, or hoarseness) and laryngoscopic signs indicating reflux laryngitis based on CPL index (CPLI) scores measured during a screening laryngoscopy. Patients were randomized to treatment if their 7-day screening diary-card recordings showed a cumulative primary symptom score of 9 or higher and they had 3 or more days with moderately severe symptoms based on a 7-point scale. Efficacy was assessed by changes in symptoms as recorded by patients and investigators and by changes in CPLI scores based on laryngoscopic examinations. Results: The patients' primary CPL symptom at final visit (primary efficacy end point) was resolved in 14.7% (14/95) and 16.0% (8/50) of patients in the esomeprazole and placebo groups, respectively (P = .799). Esomeprazole and placebo were not significantly different for change from baseline to the final visit in mean total CPLI (–1.66 ± 2.13 vs. –2.0 ± 2.55, respectively; P = .446) or any other secondary efficacy end points based on patient diary card or investigator assessments. Conclusion: This study provides no evidence of a therapeutic benefit of treatment with esomeprazole 40 mg twice daily for 16 weeks compared with placebo for signs and symptoms associated with CPL.

305 citations

Journal ArticleDOI
TL;DR: An unexpected functional link between IL-6, a major stem cell signaling pathway, and the TGF-β signaling pathway is revealed in the modulation of mammalian HCC, a lethal cancer of the foregut.
Abstract: Cancer stem cells (CSCs) are critical for the initiation, propagation, and treatment resistance of multiple cancers. Yet functional interactions between specific signaling pathways in solid organ “cancer stem cells,” such as those of the liver, remain elusive. We report that in regenerating human liver, two to four cells per 30,000–50,000 cells express stem cell proteins Stat3, Oct4, and Nanog, along with the prodifferentiation proteins TGF-β-receptor type II (TBRII) and embryonic liver fodrin (ELF). Examination of human hepatocellular cancer (HCC) reveals cells that label with stem cell markers that have unexpectedly lost TBRII and ELF. elf+/− mice spontaneously develop HCC; expression analysis of these tumors highlighted the marked activation of the genes involved in the IL-6 signaling pathway, including IL-6 and Stat3, suggesting that HCC could arise from an IL-6-driven transformed stem cell with inactivated TGF-β signaling. Similarly, suppression of IL-6 signaling, through the generation of mouse knockouts involving a positive regulator of IL-6, Inter-alpha-trypsin inhibitor-heavy chain-4 (ITIH4), resulted in reduction in HCC in elf+/− mice. This study reveals an unexpected functional link between IL-6, a major stem cell signaling pathway, and the TGF-β signaling pathway in the modulation of mammalian HCC, a lethal cancer of the foregut. These experiments suggest an important therapeutic role for targeting IL-6 in HCCs lacking a functional TGF-β pathway.

305 citations

Journal ArticleDOI
TL;DR: These studies indicate that the nuclear protein encoded by the c-myb protooncogene is required for maintenance of proliferation in certain leukemia cell lines, and support the hypothesis that development and maintenance of a malignant phenotype requires a multiplicity of interrelated genetic events.
Abstract: To study the role of the protooncogene c-myb in regulating myeloid leukemia cell proliferation and differentiation, we exposed cells of the human leukemia lines HL-60, ML-3, KG-1, and KG-1a to an oligodeoxynucleotide complementary to an 18-base-pair (bp) sequence of c-myb-encoded mRNA This treatment resulted in a significant decrease in cell proliferation in all of the lines, which was most marked in HL-60 cells After 5 days in culture, in several separate experiments with different oligomer preparations, 75% growth inhibition was observed in c-myb antisense treated cells in comparison to untreated HL-60 cells Two c-myb antisense oligomers of identical length with either 2- or 4-bp mismatches had no effect on cell growth nor did an 18-bp c-myb sense or myeloperoxidase antisense oligomer The effect of a c-myc antisense oligomer (18 bp) on the growth of HL-60, KG-1, and KG-1a cells was also studied This oligomer had much less inhibitory effect on cell proliferation than did the c-myb antisense sequence Interestingly, although c-myc antisense treatment induced maturation of HL-60 cells while it inhibited cell proliferation, such an effect was not noted in c-myb antisense treated cells These studies indicate that the nuclear protein encoded by the c-myb protooncogene is required for maintenance of proliferation in certain leukemia cell lines In compared to c-myc protein suggest that, at least in HL-60 cells, c-myc amplification or N-ras activation may not be sufficient to maintain the leukemic growth in the absence of c-myb protein These findings support the hypothesis that development and maintenance of a malignant phenotype requires a multiplicity of interrelated genetic events

305 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