Institution
University of Alabama at Birmingham
Education•Birmingham, Alabama, United States•
About: University of Alabama at Birmingham is a education organization based out in Birmingham, Alabama, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 38523 authors who have published 86775 publications receiving 3930642 citations. The organization is also known as: UAB & The University of Alabama at Birmingham.
Topics: Population, Poison control, Transplantation, Health care, Immune system
Papers published on a yearly basis
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Northwestern University1, Seattle Cancer Care Alliance2, Case Western Reserve University3, Washington University in St. Louis4, Ohio State University5, Stanford University6, University of California, San Diego7, Brigham and Women's Hospital8, Memorial Sloan Kettering Cancer Center9, University of Colorado Boulder10, University of Texas MD Anderson Cancer Center11, Mayo Clinic12, Fox Chase Cancer Center13, Harvard University14, Duke University15, University of Pennsylvania16, Vanderbilt University17, Yale University18, City of Hope National Medical Center19, University of Wisconsin-Madison20, University of Michigan21, University of California, San Francisco22, Johns Hopkins University23, University of South Florida24, University of Alabama at Birmingham25, University of Utah26, Roswell Park Cancer Institute27, National Comprehensive Cancer Network28
TL;DR: The NCCN Guidelines specific to the workup and treatment of patients with recurrent/stage IV breast cancer are discussed in this article.
Abstract: This selection from the NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines) for Bladder Cancer focuses on the clinical presentation and workup of suspected bladder cancer, treatment of non-muscle-invasive urothelial bladder cancer, and treatment of metastatic urothelial bladder cancer because important updates have recently been made to these sections. Some important updates include recommendations for optimal treatment of non-muscle-invasive bladder cancer in the event of a bacillus Calmette-Guerin (BCG) shortage and details about biomarker testing for advanced or metastatic disease. The systemic therapy recommendations for second-line or subsequent therapies have also been revised. Treatment and management of muscle-invasive, nonmetastatic disease is covered in the complete version of the NCCN Guidelines for Bladder Cancer available at NCCN.org. Additional topics covered in the complete version include treatment of nonurothelial histologies and recommendations for nonbladder urinary tract cancers such as upper tract urothelial carcinoma, urothelial carcinoma of the prostate, and primary carcinoma of the urethra.
1,018 citations
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TL;DR: It is reported that glycogen synthase kinase 3 differentially regulates TLR-mediated production of pro- and anti-inflammatory cytokines in mice receiving lipopolysaccharide and mediated protection from endotoxin shock.
Abstract: The cellular mechanisms that directly regulate the inflammatory response after Toll-like receptor (TLR) stimulation are unresolved at present. Here we report that glycogen synthase kinase 3 (GSK3) differentially regulates TLR-mediated production of pro- and anti-inflammatory cytokines. Stimulation of monocytes or peripheral blood mononuclear cells with TLR2, TLR4, TLR5 or TLR9 agonists induced substantial increases in interleukin 10 production while suppressing the release of proinflammatory cytokines after GSK3 inhibition. GSK3 regulated the inflammatory response by differentially affecting the nuclear amounts of transcription factors NF-κB subunit p65 and CREB interacting with the coactivator CBP. Administration of a GSK3 inhibitor potently suppressed the proinflammatory response in mice receiving lipopolysaccharide and mediated protection from endotoxin shock. These findings demonstrate a regulatory function for GSK3 in modulating the inflammatory response.
1,016 citations
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Denver Health Medical Center1, University of Colorado Denver2, University of Minnesota3, University of Alabama at Birmingham4, University of California, Los Angeles5, Veterans Health Administration6, Temple University7, University of Michigan8, University of California, San Francisco9, Regions Hospital10, Mayo Clinic11, University of Pittsburgh12, University of Maryland, Baltimore13, University of Manitoba14
TL;DR: Among selected subjects with COPD, azithromycin taken daily for 1 year, when added to usual treatment, decreased the frequency of exacerbations and improved quality of life but caused hearing decrements in a small percentage of subjects.
Abstract: A total of 1577 subjects were screened; 1142 (72%) were randomly assigned to receive azithromycin, at a dose of 250 mg daily (570 participants), or placebo (572 participants) for 1 year in addition to their usual care. The rate of 1-year follow-up was 89% in the azithromycin group and 90% in the placebo group. The median time to the first exac erbation was 266 days (95% confidence interval [CI], 227 to 313) among participants receiving azithromycin, as compared with 174 days (95% CI, 143 to 215) among par ticipants receiving placebo (P<0.001). The frequency of exacerbations was 1.48 exacerba tions per patient-year in the azithromycin group, as compared with 1.83 per patient-year in the placebo group (P = 0.01), and the hazard ratio for having an acute exacerbation of COPD per patient-year in the azithromycin group was 0.73 (95% CI, 0.63 to 0.84; P<0.001). The scores on the St. George’s Respiratory Questionnaire (on a scale of 0 to 100, with lower scores indicating better functioning) improved more in the azithro mycin group than in the placebo group (a mean [±SD] decrease of 2.8±12.8 vs. 0.6±11.4, P = 0.004); the percentage of participants with more than the minimal clinically important difference of −4 units was 43% in the azithromycin group, as compared with 36% in the placebo group (P = 0.03). Hearing decrements were more common in the azithromycin group than in the placebo group (25% vs. 20%, P = 0.04). Conclusions Among selected subjects with COPD, azithromycin taken daily for 1 year, when added to usual treatment, decreased the frequency of exacerbations and improved quality of life but caused hearing decrements in a small percentage of subjects. Although this intervention could change microbial resistance patterns, the effect of this change is not known. (Funded by the National Institutes of Health; ClinicalTrials.gov number, NCT00325897.)
1,013 citations
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TL;DR: It is demonstrated that the delivery of H2S at the time of reperfusion limits infarct size and preserves left ventricular (LV) function in an in vivo model of myocardial ischemia-reperfusion (MI-R) and that either administration of H 2S or the modulation of endogenous production may be of clinical benefit in ischemic disorders.
Abstract: The recent discovery that hydrogen sulfide (H2S) is an endogenously produced gaseous second messenger capable of modulating many physiological processes, much like nitric oxide, prompted us to investigate the potential of H2S as a cardioprotective agent. In the current study, we demonstrate that the delivery of H2S at the time of reperfusion limits infarct size and preserves left ventricular (LV) function in an in vivo model of myocardial ischemia-reperfusion (MI-R). This observed cytoprotection is associated with an inhibition of myocardial inflammation and a preservation of both mitochondrial structure and function after I-R injury. Additionally, we show that modulation of endogenously produced H2S by cardiac-specific overexpression of cystathionine γ-lyase (α-MHC-CGL-Tg mouse) significantly limits the extent of injury. These findings demonstrate that H2S may be of value in cytoprotection during the evolution of myocardial infarction and that either administration of H2S or the modulation of endogenous production may be of clinical benefit in ischemic disorders.
1,012 citations
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TL;DR: Five resistant variants isolated from patients undergoing therapy with the protease inhibitor MK-639 exhibited cross-resistance to all members of a panel of six structurally diverse protease inhibitors, suggesting that com-bination therapy with multiple protease inhibition may not prevent loss of antiviral activity resulting from resistance selection.
Abstract: INHIBITORS of the human immunodeficiency virus type 1 (HIV-1) protease have entered clinical study as potential therapeutic agents for HIV-1 infection. The clinical efficacy of HIV-1 reverse transcriptase inhibitors has been limited by the emergence of resistant viral variants. Similarly, variants expressing resistance to protease inhibitors have been derived in cell culture1-10. We now report the characterization of resistant variants isolated from patients undergoing therapy with the protease inhibitor MK-639 (formerly designated L-735,524). Five of these variants, isolated from four patients, exhibited cross-resistance to all members of a panel of six structurally diverse protease inhibitors. This suggests that com-bination therapy with multiple protease inhibitors may not prevent loss of antiviral activity resulting from resistance selection. In addition, previous therapy with one compound may abrogate the benefit of subsequent treatment with a second inhibitor.
1,006 citations
Authors
Showing all 38940 results
Name | H-index | Papers | Citations |
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Rudolf Jaenisch | 206 | 606 | 178436 |
Joel Schwartz | 183 | 1149 | 109985 |
Tadamitsu Kishimoto | 181 | 1067 | 130860 |
Jasvinder A. Singh | 176 | 2382 | 223370 |
Gregg L. Semenza | 168 | 502 | 130316 |
David R. Jacobs | 165 | 1262 | 113892 |
Hua Zhang | 163 | 1503 | 116769 |
David R. Holmes | 161 | 1624 | 114187 |
David Cella | 156 | 1258 | 106402 |
Elaine S. Jaffe | 156 | 828 | 112412 |
Michael A. Matthay | 151 | 998 | 98687 |
Lawrence Corey | 146 | 773 | 78105 |
Barton F. Haynes | 144 | 911 | 79014 |
Douglas D. Richman | 142 | 633 | 82806 |
Kjell Fuxe | 142 | 1479 | 89846 |