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 & Medicine. 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, Medicine, Cancer, Poison control, Health care
Papers published on a yearly basis
Papers
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Johns Hopkins University1, University of Utah2, University of South Florida3, Fox Chase Cancer Center4, Roswell Park Cancer Institute5, Brigham and Women's Hospital6, Duke University7, City of Hope National Medical Center8, University of California, San Francisco9, University Of Tennessee System10, University of Michigan11, Memorial Sloan Kettering Cancer Center12, Stanford University13, Harvard University14, University of Alabama at Birmingham15, Ohio State University16, Houston Methodist Hospital17, Seattle Cancer Care Alliance18
TL;DR: The NCCN Clinical Practice Guidelines in Oncology for Small Cell Lung Cancer (SCLC) focus on extensive-stage SCLC because it occurs more frequently than limited-stage disease as discussed by the authors.
Abstract: Neuroendocrine tumors account for approximately 20% of lung cancers; most (≈15%) are small cell lung cancer (SCLC). These NCCN Clinical Practice Guidelines in Oncology for SCLC focus on extensive-stage SCLC because it occurs more frequently than limited-stage disease. SCLC is highly sensitive to initial therapy; however, most patients eventually die of recurrent disease. In patients with extensive-stage disease, chemotherapy alone can palliate symptoms and prolong survival in most patients; however, long-term survival is rare. Most cases of SCLC are attributable to cigarette smoking; therefore, smoking cessation should be strongly promoted.
514 citations
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University of Alabama at Birmingham1, Ohio State University2, St Thomas' Hospital3, University of Florida4, Medical University of South Carolina5, Emory University Hospital6, Memorial Hospital of South Bend7, Hospital of the University of Pennsylvania8, Medtronic plc9, Brigham and Women's Hospital10
TL;DR: The implantable continuous hemodynamic monitor-guided care did not significantly reduce total HF-related events compared with optimal medical management, and additional trials will be necessary to establish the clinical benefit of implantable Continuous Hemodynamic Monitor-guided Care in patients with advanced HF.
513 citations
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Columbia University1, Yale University2, Peking University3, Shanghai Jiao Tong University4, University of Alabama at Birmingham5, University of Tennessee6, Icahn School of Medicine at Mount Sinai7, Istituto Giannina Gaslini8, University of Calgary9, University of Parma10, University of Brescia11, University of Foggia12, University of Turin13
TL;DR: Three independent loci in the major histocompatibility complex, as well as a common deletion of CFHR1 and CFHR3 at chromosome 1q32 and a locus at chromosome 22q12 that each surpassed genome-wide significance, explain 4–7% of the disease variance and up to a tenfold variation in interindividual risk.
Abstract: We carried out a genome-wide association study of IgA nephropathy, a major cause of kidney failure worldwide. We studied 1,194 cases and 902 controls of Chinese Han ancestry, with targeted follow up in Chinese and European cohorts comprising 1,950 cases and 1,920 controls. We identified three independent loci in the major histocompatibility complex, as well as a common deletion of CFHR1 and CFHR3 at chromosome 1q32 and a locus at chromosome 22q12 that each surpassed genome-wide significance (P values for association between 1.59 × 10⁻²⁶ and 4.84 × 10⁻⁹ and minor allele odds ratios of 0.63-0.80). These five loci explain 4-7% of the disease variance and up to a tenfold variation in interindividual risk. Many of the alleles that protect against IgA nephropathy impart increased risk for other autoimmune or infectious diseases, and IgA nephropathy risk allele frequencies closely parallel the variation in disease prevalence among Asian, European and African populations, suggesting complex selective pressures.
513 citations
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University of California, San Francisco1, Stanford University2, George Washington University3, Memorial Hospital of South Bend4, Duke University5, University of Alabama at Birmingham6, Johns Hopkins University7, Hartford Hospital8, Université de Montréal9, University of Ottawa10, University of Minnesota11, National Institutes of Health12
TL;DR: In postmenopausal women with coronary disease, neither HRT nor antioxidant vitamin supplements provide cardiovascular benefit and a potential for harm was suggested with each treatment.
Abstract: ContextHormone replacement therapy (HRT) and antioxidant vitamins are widely
used for secondary prevention in postmenopausal women with coronary disease,
but no clinical trials have demonstrated benefit to support their use.ObjectiveTo determine whether HRT or antioxidant vitamin supplements, alone or
in combination, influence the progression of coronary artery disease in postmenopausal
women, as measured by serial quantitative coronary angiography.Design, Setting, and PatientsThe Women's Angiographic Vitamin and Estrogen (WAVE) Trial, a randomized,
double-blind trial of 423 postmenopausal women with at least one 15% to 75%
coronary stenosis at baseline coronary angiography. The trial was conducted
from July 1997 to January 2002 in 7 clinical centers in the United States
and Canada.InterventionsPatients were randomly assigned in a 2 × 2 factorial design to
receive either 0.625 mg/d of conjugated equine estrogen (plus 2.5 mg/d of
medroxyprogesterone acetate for women who had not had a hysterectomy), or
matching placebo, and 400 IU of vitamin E twice daily plus 500 mg of vitamin
C twice daily, or placebo.Main Outcome MeasureAnnualized mean (SD) change in minimum lumen diameter (MLD) from baseline
to concluding angiogram of all qualifying coronary lesions averaged for each
patient. Patients with intercurrent death or myocardial infarction (MI) were
imputed the worst rank of angiographic outcome.ResultsThe mean (SD) interval between angiograms was 2.8 (0.9) years. Coronary
progression, measured in mean (SD) change, worsened with HRT by 0.047 (0.15)
mm/y and by 0.024 (0.15) mm/y with HRT placebo (P =
.17); and for antioxidant vitamins by 0.044 (0.15) mm/y and with vitamin placebo
by 0.028 (0.15) mm/y (P = .32). When patients with
intercurrent death or MI were included, the primary outcome showed an increased
risk for women in the active HRT group (P = .045),
and suggested an increased risk in the active vitamin group (P = .09). Fourteen patients died in the HRT group and 8 in the HRT
placebo group (hazard ratio [HR], 1.8; 95% confidence interval [CI], 0.75-4.3),
and 16 in the vitamin group and 6 in the vitamin placebo group (HR, 2.8; 95%
CI, 1.1-7.2). Death, nonfatal MI, or stroke occurred in 26 HRT patients vs
15 HRT controls (HR, 1.9; 95% CI, 0.97-3.6) and in 26 vitamin patients and
18 vitamin controls (HR, 1.5; 95% CI, 0.80-2.9). There was no interaction
between the 2 treatment interventions.ConclusionIn postmenopausal women with coronary disease, neither HRT nor antioxidant
vitamin supplements provide cardiovascular benefit. Instead, a potential for
harm was suggested with each treatment.
513 citations
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University of Genoa1, Istituto Giannina Gaslini2, Karolinska Institutet3, University of Ljubljana4, University of Pennsylvania5, Cincinnati Children's Hospital Medical Center6, Albert Einstein College of Medicine7, Jaslok Hospital8, Aichi Medical University9, University of Calgary10, Hacettepe University11, University of Zurich12, Bristol Royal Hospital for Children13, University of Toronto14, Mount Sinai Hospital15, University of Washington16, Katholieke Universiteit Leuven17, Utrecht University18, University of Alabama at Birmingham19
TL;DR: Criteria for the classification of macrophage activation syndrome (MAS) in patients with systemic juvenile idiopathic arthritis (JIA) is developed.
Abstract: To develop criteria for the classification of macrophage activation syndrome (MAS) in patients with systemic juvenile idiopathic arthritis (JIA). A multistep process, based on a combination of expert consensus and analysis of real patient data, was conducted. A panel of 28 experts was first asked to classify 428 patient profiles as having or not having MAS, based on clinical and laboratory features at the time of disease onset. The 428 profiles comprised 161 patients with systemic JIA-associated MAS and 267 patients with a condition that could potentially be confused with MAS (active systemic JIA without evidence of MAS, or systemic infection). Next, the ability of candidate criteria to classify individual patients as having MAS or not having MAS was assessed by evaluating the agreement between the classification yielded using the criteria and the consensus classification of the experts. The final criteria were selected in a consensus conference. Experts achieved consensus on the classification of 391 of the 428 patient profiles (91.4%). A total of 982 candidate criteria were tested statistically. The 37 best-performing criteria and 8 criteria obtained from the literature were evaluated at the consensus conference. During the conference, 82% consensus among experts was reached on the final MAS classification criteria. In validation analyses, these criteria had a sensitivity of 0.73 and a specificity of 0.99. Agreement between the classification (MAS or not MAS) obtained using the criteria and the original diagnosis made by the treating physician was high (κ=0.76). We have developed a set of classification criteria for MAS complicating systemic JIA and provided preliminary evidence of its validity. Use of these criteria will potentially improve understanding of MAS in systemic JIA and enhance efforts to discover effective therapies, by ensuring appropriate patient enrollment in studies.
512 citations
Authors
Showing all 38940 results
Name | H-index | Papers | Citations |
---|---|---|---|
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 |