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, Context (language use), Medicine
Papers published on a yearly basis
Papers
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TL;DR: A review of the cell signaling pathways involved in cancer development and proliferation, and which are targeted by curcumin, suggests this polyphenol compound, alone or combined with other agents, could represent an effective drug for cancer therapy.
Abstract: Curcumin, a polyphenol extracted from Curcuma longa in 1815, has gained attention from scientists worldwide for its biological activities (e.g., antioxidant, anti-inflammatory, antimicrobial, antiviral), among which its anticancer potential has been the most described and still remains under investigation. The present review focuses on the cell signaling pathways involved in cancer development and proliferation, and which are targeted by curcumin. Curcumin has been reported to modulate growth factors, enzymes, transcription factors, kinase, inflammatory cytokines, and proapoptotic (by upregulation) and antiapoptotic (by downregulation) proteins. This polyphenol compound, alone or combined with other agents, could represent an effective drug for cancer therapy.
442 citations
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TL;DR: This work focuses on improving sequence-based predictions of long (>30 amino acid residues) regions lacking specific 3-D structure by means of four new neural-network-based Predictors Of Natural Disordered Regions (PONDRs): VL3, VL 3H, V l3P, and Vl3E.
Abstract: Protein existing as an ensemble of structures, called intrinsically disordered, has been shown to be responsible for a wide variety of biological functions and to be common in nature. Here we focus on improving sequence-based predictions of long (>30 amino acid residues) regions lacking specific 3-D structure by means of four new neural-network-based Predictors Of Natural Disordered Regions (PONDRs): VL3, VL3H, VL3P, and VL3E. PONDR VL3 used several features from a previously introduced PONDR VL2, but benefitted from optimized predictor models and a slightly larger (152 vs. 145) set of disordered proteins that were cleaned of mislabeling errors found in the smaller set. PONDR VL3H utilized homologues of the disordered proteins in the training stage, while PONDR VL3P used attributes derived from sequence profiles obtained by PSI-BLAST searches. The measure of accuracy was the average between accuracies on disordered and ordered protein regions. By this measure, the 30-fold cross-validation accuracies of VL3, VL3H, and VL3P were, respectively, 83.6 +/- 1.4%, 85.3 +/- 1.4%, and 85.2 +/- 1.5%. By combining VL3H and VL3P, the resulting PONDR VL3E achieved an accuracy of 86.7 +/- 1.4%. This is a significant improvement over our previous PONDRs VLXT (71.6 +/- 1.3%) and VL2 (80.9 +/- 1.4%). The new disorder predictors with the corresponding datasets are freely accessible through the web server at http://www.ist.temple.edu/disprot.
441 citations
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TL;DR: The studies imply that histone release contributes to death in inflammatory injury and in chemical-induced cellular injury, both of which are mediated in part through the TLRs.
Abstract: We previously reported that extracellular histones are major mediators of death in sepsis. Infusion of extracellular histones leads to increased cytokine levels. Histones activate TLR2 and TLR4 in a process that is enhanced by binding to DNA. Activation of TLR4 is responsible for the histone-dependent increase in cytokine levels. To study the impact of histone release on pathology we used two models: a Con A-triggered activation of T cells to mimic sterile inflammation, and acetaminophen to model drug-induced tissue toxicity. Histones were released in both models and anti-histone Abs were protective. TLR2- or TLR4-null mice were also protected. These studies imply that histone release contributes to death in inflammatory injury and in chemical-induced cellular injury, both of which are mediated in part through the TLRs.
440 citations
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TL;DR: The results of the study strongly support the idea that circulatory support with an LVAD improves myocyte contractile properties and increases beta-adrenergic responsiveness.
Abstract: Background—The failing myocardium is characterized by decreased force production, slowed relaxation, and depressed responses to β-adrenergic stimulation. In some heart failure patients, heart function is so poor that a left ventricular assist device (LVAD) is inserted as a bridge to transplantation. In the present research, we investigated whether circulatory support with an LVAD influenced the functional properties of myocytes from the failing heart. Methods and Results—Myocytes were isolated from human explanted failing hearts (HF-myocytes) and failing hearts with antecedent LVAD support (HF-LVAD-myocytes). Studies of myocyte function indicated that the magnitude of contraction was greater (9.6±0.7% versus 6.9±0.5% shortening), the time to peak contraction was significantly abbreviated (0.37±0.01 versus 0.75±0.04 seconds), and the time to 50% relaxation was reduced (0.55±0.02 versus 1.45±0.11 seconds) in the HF-LVAD-myocytes compared with the HF-myocytes (P<0.05). The HF-LVAD-myocytes had larger contrac...
439 citations
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TL;DR: Attention to the psychological aspects of breast cancer risk will be critical in the development of risk-counseling programs that incorporate testing for the recently cloned breast cancer susceptibility gene, BRCA1 (and BRCa2 when that gene has also been cloned).
Abstract: Background Studies have shown that a majority of women with a family history of breast cancer have exaggerated perceptions of their own risk of this disease and experience excessive anxiety. In response to the need to communicate more accurate risk information to these women, specialized programs for breast cancer risk counseling have been initiated in medical centers across the United States. Purpose Our purpose was 1) to evaluate the impact of a standardized protocol for individualized breast cancer risk counseling on comprehension of personal risk among first-degree relatives of index breast cancer patients and 2) to identify women most and least likely to benefit from such counseling. Methods This study is a prospective randomized trial comparing individualized breast cancer risk counseling to general health counseling (control). We studied 200 women aged 35 years and older who had a family history of breast cancer in a first-degree relative. Women with a personal history of cancer were excluded. Risk comprehension was assessed as the concordance between perceived "subjective" lifetime breast cancer risk and estimated "objective" lifetime risk. Results The results of logistic regression analysis showed that women who received risk counseling were significantly more likely to improve their risk comprehension, compared with women in the control condition (odds ratio [OR] = 3.5; 95% confidence interval [CI] = 1.3-9.5; P = .01). However, in both groups, about two thirds of women continued to overestimate their lifetime risks substantially following counseling. Examination of subjects by treatment interaction effects indicated that risk counseling did not produce improved comprehension among the large proportion of women who had high levels of anxious preoccupation with breast cancer at base line (P = .02). In addition, white women were less likely to benefit than African-American women (OR = 0.34; 95% CI = 0.11-0.99; P = .05). Conclusion Efforts to counsel women about their breast cancer risks are not likely to be effective unless their breast cancer anxieties are also addressed. Implications Attention to the psychological aspects of breast cancer risk will be critical in the development of risk-counseling programs that incorporate testing for the recently cloned breast cancer susceptibility gene, BRCA1 (and BRCA2 when that gene has also been cloned).
438 citations
Authors
Showing all 32360 results
Name | H-index | Papers | Citations |
---|---|---|---|
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 |