Institution
Temple University
Education•Philadelphia, 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.
Topics: Population, Poison control, Anxiety, Health care, Receptor
Papers published on a yearly basis
Papers
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TL;DR: The research thus far appears most consistent in supporting the role of depression in predicting generated stress, although more research is still required.
522 citations
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TL;DR: The p53-mediated up-regulation of Bax may provide at least a partial explanation for the more rapid rate of apoptosis induced by p53 compared to by TGF beta 1, as well as for the ineffectiveness of ectopoic Bcl-2 to abrogate p53 -mediated apoptosis.
Abstract: Recently, both Bcl-2, which promotes cell survival, and Bax, which promotes cell death, have been implicated as major players in the control of apoptotic pathways, and it has been suggested that the ratio of Bcl-2 and Bax protein controls the relative susceptibility of cells to death stimuli. We have used M1 myeloid leukemia cells and genetically engineered M1 variants as a model system to study apoptosis induced by two distinct apoptotic stimuli. This includes apoptosis induced by activation of wild type p53 function of a temperature sensitive p53 transgene expressed in M1 cells, which do not express endogenous p53, and apoptosis induced by TGF beta 1. It is shown that the kinetics of apoptosis induced by p53 is more rapid than apoptosis induced by TGF beta 1. It is also shown that ectopic expression of Bcl-2, at levels which blocked TGF beta 1-induced apoptosis of M1 cells, delayed, but did not block, p53-induced apoptosis. Both p53 and TGF beta 1 down-regulated endogenous Bcl-2 expression, but only p53 up-regulated Bax expression, where bax has been identified as a p53 immediate early response gene. Thus, the p53-mediated up-regulation of Bax may provide at least a partial explanation for the more rapid rate of apoptosis induced by p53 compared to by TGF beta 1, as well as for the ineffectiveness of ectopoic Bcl-2 to abrogate p53-mediated apoptosis. These findings provide first insights to the molecular mechanisms which mediate p53-induced apoptosis, identifying bax and bcl-2 as p53 regulated genes, and serve as a paradigm of how the intracellular balance of Bcl-2 to Bax is differentially altered by distinct death stimuli.
520 citations
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TL;DR: The neglect syndrome per se, rather than overall stroke severity, predicts poor outcome in right hemisphere stroke.
Abstract: Objective: To assess the relative frequency of occurrence of motor, perceptual, peripersonal, and personal neglect subtypes, the association of neglect and other related deficits (e.g., deficient nonlateralized attention, anosognosia), and the neuroanatomic substrates of neglect in patients with right hemisphere stroke in rehabilitation settings. Methods: The authors assessed 166 rehabilitation inpatients and outpatients with right hemisphere stroke with measures of neglect and neglect subtypes, attention, motor and sensory function, functional disability, and family burden. Detailed lesion analyses were also performed. Results: Neglect was present in 48% of right hemisphere stroke patients. Patients with neglect had more motor impairment, sensory dysfunction, visual extinction, basic (nonlateralized) attention deficit, and anosognosia than did patients without neglect. Personal neglect occurred in 1% and peripersonal neglect in 27%, motor neglect in 17%, and perceptual neglect in 21%. Neglect severity predicted scores on the Functional Independence Measure and Family Burden Questionnaire more accurately than did number of lesioned regions. Conclusions: The neglect syndrome per se, rather than overall stroke severity, predicts poor outcome in right hemisphere stroke. Dissociations between tasks assessing neglect subtypes support the existence of these subtypes. Finally, neglect results from lesions at various loci within a distributed system mediating several aspects of attention and spatiomotor performance.
520 citations
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TL;DR: While the agrammatics were distinguishable from the nonagrammatic patients on most measures, both nonfluent groups showed comparable reductions in the structural complexity of their propositional utterances.
519 citations
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TL;DR: A two‐level model called VSL1, which consists of two specialized predictors, one of which was optimized for long disordered regions (>30 residues) and the other for short dis ordered regions (≤30 residues), and has achieved the highest accuracy yet and significantly improved performance on shortdisordered regions.
Abstract: During the past few years we have investigated methods to improve predictors of intrinsically disordered regions longer than 30 consecutive residues. Experimental evidence, however, showed that these predictors were less successful on short disordered regions, as observed two years ago during the fifth Critical Assessment of Techniques for Protein Structure Prediction (CASP5). To address this shortcoming, we developed a two-level model called VSL1 (CASP6 id: 193-1). At the first level, VSL1 consists of two specialized predictors, one of which was optimized for long disordered regions (>30 residues) and the other for short disordered regions (< or =30 residues). At the second level, a meta-predictor was built to assign weights for combining the two first-level predictors. As the results of the CASP6 experiment showed, this new predictor has achieved the highest accuracy yet and significantly improved performance on short disordered regions, while maintaining high performance on long disordered regions.
519 citations
Authors
Showing all 32360 results
Name | H-index | Papers | Citations |
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Robert J. Lefkowitz | 214 | 860 | 147995 |
Rakesh K. Jain | 200 | 1467 | 177727 |
Virginia M.-Y. Lee | 194 | 993 | 148820 |
Yury Gogotsi | 171 | 956 | 144520 |
Timothy A. Springer | 167 | 669 | 122421 |
Ralph A. DeFronzo | 160 | 759 | 132993 |
James J. Collins | 151 | 669 | 89476 |
Robert J. Glynn | 146 | 748 | 88387 |
Edward G. Lakatta | 146 | 858 | 88637 |
Steven Williams | 144 | 1375 | 86712 |
Peter Buchholz | 143 | 1181 | 92101 |
David Goldstein | 141 | 1301 | 101955 |
Scott D. Solomon | 137 | 1145 | 103041 |
Donald B. Rubin | 132 | 515 | 262632 |
Jeffery D. Molkentin | 131 | 482 | 61594 |