Institution
Georgetown University
Education•Washington D.C., District of Columbia, United States•
About: Georgetown University is a education organization based out in Washington D.C., District of Columbia, United States. It is known for research contribution in the topics: Population & Cancer. The organization has 23377 authors who have published 43718 publications receiving 1748598 citations. The organization is also known as: GU & Georgetown.
Topics: Population, Cancer, Breast cancer, Health care, Politics
Papers published on a yearly basis
Papers
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19 Nov 2003TL;DR: Results suggest that the ensemble method learns drifting concepts almost as well as the base algorithms learn each concept individually, which is the best overall results for these problems to date.
Abstract: Algorithms for tracking concept drift are important for many applications. We present a general method based on the weighted majority algorithm for using any online learner for concept drift. Dynamic weighted majority (DWM) maintains an ensemble of base learners, predicts using a weighted-majority vote of these "experts", and dynamically creates and deletes experts in response to changes in performance. We empirically evaluated two experimental systems based on the method using incremental naive Bayes and incremental tree inducer [ITI] as experts. For the sake of comparison, we also included Blum's implementation of weighted majority. On the STAGGER concepts and on the SEA concepts, results suggest that the ensemble method learns drifting concepts almost as well as the base algorithms learn each concept individually. Indeed, we report the best overall results for these problems to date.
435 citations
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TL;DR: It is concluded that different subtypes of excitatory amino acid recognition sites are associated with inositol phospholipid metabolism in primary cultures of cerebellar granule cells.
Abstract: L-Glutamic, L-aspartic acids and a number of their structural analogs, including quisqualic, kainic, ibotenic, quinolinic, and N-methyl-D- aspartic (NMDA) acids, increase inositol phospholipid hydrolysis when added to primary cultures of cerebellar granule cells, as is reflected by an enhanced formation of 3H-inositolmonophosphate (3H-IP1) in the presence of Li+ L-Glutamic acid also enhances the formation of the initial products of inositol phospholipid hydrolysis, 3H-inositol di- (3H-IP2) and triphosphate (3H-IP3) In the absence of extracellular Ca2+, L-glutamic acid fails to enhance 3H-IP1 formation, but still increases 3H-IP2 and 3H-IP3 formation The stimulation of 3H-IP1 formation elicited by L-glutamic acid is reduced by DL-2-amino-5- phosphonovaleric acid (APV) and gamma-glutamylglycine and, to a lesser extent, by 2,3-cis-piperidindicarboxylic acid (PDA) The stimulation of 3H-IP1 formation by kainic acid is antagonized by PDA and gamma- glutamylglycine, but it is almost unaffected by APV The increase in 3H- IP1 formation elicited by quisqualic acid is not reduced by any of the dicarboxylic amino acid receptor antagonists that we have tested We conclude that different subtypes of excitatory amino acid recognition sites are associated with inositol phospholipid metabolism in primary cultures of cerebellar granule cells
434 citations
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University of Bonn1, Cardiff University2, Harvard University3, Eli Lilly and Company4, State University of New York Upstate Medical University5, NorthShore University HealthSystem6, University of California, San Diego7, National Institutes of Health8, Stanford University9, University of North Carolina at Chapel Hill10, Trinity College, Dublin11, Radboud University Nijmegen12, University of Pennsylvania13, University of St Andrews14, University of Western Australia15, University of California, Los Angeles16, Washington University in St. Louis17, University of Pittsburgh18, Johns Hopkins University19, Icahn School of Medicine at Mount Sinai20, University of Illinois at Urbana–Champaign21, University of Helsinki22, Université de Montréal23, University of Washington24, University of Toronto25, Vanderbilt University26, McMaster University27, University of Oslo28, University of Edinburgh29, University of Michigan30, University College London31, GlaxoSmithKline32, Indiana University33, Virginia Commonwealth University34, VU University Amsterdam35, University of Iowa36, University of California, San Francisco37, Howard University38, Institute of Physics39, QIMR Berghofer Medical Research Institute40, Columbia University41, Pfizer42, Rush University Medical Center43, Mayo Clinic44, Georgetown University45, Karolinska Institutet46, National Institute for Health and Welfare47, University of Queensland48, University of Aberdeen49, North Carolina State University50
TL;DR: GWAS methods have detected a remarkable number of robust genetic associations for dozens of common diseases and traits, leading to new pathophysiological hypotheses, although only small proportions of genetic variance have been explained thus far and therapeutic applications will require substantial further effort.
Abstract: Objective: The authors conducted a review of the history and empirical basis of genomewide association studies (GWAS), the rationale for GWAS of psychiatric disorders, results to date, limitations, and plans for GWAS meta-analyses. Method: A literature review was carried out, power and other issues discussed, and planned studies assessed. Results: Most of the genomic DNA sequence differences between any two people are common (frequency >5%) single nucleotide polymorphisms (SNPs). Because of localized patterns of correlation (linkage disequilibrium), 500,000 to 1,000,000 of these SNPs can test the hypothesis that one or more common variants explain part of the genetic risk for a disease. GWAS technologies can also detect some of the copy number variants (deletions and duplications) in the genome. Systematic study of rare variants will require large-scale resequencing analyses. GWAS methods have detected a remarkable number of robust genetic associations for dozens of common diseases and traits, leading to new pathophysiological hypotheses, although only small proportions of genetic variance have been explained thus far and therapeutic applications will require substantial further effort. Study design issues, power, and limitations are discussed. For psychiatric disorders, there are initial significant findings for common SNPs and for rare copy number variants, and many other studies are in progress. Conclusions: GWAS of large samples have detected associations of common SNPs and of rare copy number variants with psychiatric disorders. More findings are likely, since larger GWAS samples detect larger numbers of common susceptibility variants, with smaller effects. The Psychiatric GWAS Consortium is conducting GWAS meta-analyses for schizophrenia, bipolar disorder, major depressive disorder, autism, and attention deficit hyperactivity disorder. Based on results for other diseases, larger samples will be required. The contribution of GWAS will depend on the true genetic architecture of each disorder.
434 citations
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University of North Carolina at Chapel Hill1, University of California, San Francisco2, Duke University3, Harvard University4, University of Texas MD Anderson Cancer Center5, Washington University in St. Louis6, Georgetown University7, Indiana University – Purdue University Indianapolis8, Baylor College of Medicine9, University of Alabama at Birmingham10, Johns Hopkins University11, Mayo Clinic12, University of Utah13
TL;DR: Despite strong preclinical data, combination cetuximab plus carboplatin in metastatic TNBC produced responses in fewer than 20% of patients.
Abstract: Purpose Epidermal growth factor receptor (EGFR) is a targetable receptor frequently overexpressed in basal-like breast cancer, which comprises most triple-negative breast cancers (TNBCs), the only subtype without established targeted therapy. Patients and Methods In this randomized phase II trial, patients with metastatic TNBC received anti-EGFR antibody cetuximab (400 mg/m2 load then 250 mg/m2 per week intravenously [IV]) alone, with carboplatin (area under the curve of 2, once per week IV) added after progression or as concomitant therapy from the beginning. Response rate (RR) was the primary end point; others included time to progression (TTP), overall survival (OS), and toxicity. Embedded correlative studies included molecular subtyping on archival tissue. Fresh tumor tissue before and after 7 to 14 days of therapy was used for microarray analyses exploring EGFR pathway activity and inhibition. Results In 102 patients with TNBC, RRs were 6% (two of 31) to cetuximab and 16% (four of 25) to cetuximab pl...
433 citations
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Henry Ford Health System1, University of Utah2, Johns Hopkins University3, Virginia Mason Medical Center4, University of Chicago5, Veterans Health Administration6, Saint Louis University7, Pomona College8, Eastern Virginia Medical School9, Cincinnati Children's Hospital Medical Center10, Wayne State University11, Georgetown University12, Wake Forest Baptist Medical Center13, Morehouse School of Medicine14, Florida Atlantic University15, Louisiana State University16
TL;DR: This clinical practice guideline was undertaken to optimize the care of patients with AR by addressing quality improvement opportunities through an evaluation of the available evidence and an assessment of the harm-benefit balance of various diagnostic and management options.
Abstract: Objective. Allergic rhinitis (AR) is one of the most common diseases affecting adults. It is the most common chronic disease in children in the United States today and the fifth most common chronic disease in the United States overall. AR is estimated to affect nearly 1 in every 6 Americans and generates $2 to $5 billion in direct health expenditures annually. It can impair quality of life and, through loss of work and school attendance, is responsible for as much as $2 to $4 billion in lost productivity annually. Not surprisingly, myriad diagnostic tests and treatments are used in managing this disorder, yet there is considerable variation in their use. This clinical practice guideline was undertaken to optimize the care of patients with AR by addressing quality improvement opportunities through an evaluation of the available evidence and an assessment of the harm-benefit balance of various diagnostic and management options. Purpose. The primary purpose of this guideline is to address quality improvement opportunities for all clinicians, in any setting, who are likely to manage patients with AR as well as to optimize patient care, promote effective diagnosis and therapy, and reduce harmful or unnecessary variations in care. The guideline is intended to be applicable for both pediatric and adult patients with AR. Children under the age of 2 years were excluded from the clinical practice guideline because rhinitis in this population may be different than in older patients and is not informed by the same evidence base. The guideline is intended to focus on a limited number of quality improvement opportunities deemed most important by the working group and is not intended to be a comprehensive reference for diagnosing and managing AR. The recommendations outlined in the guideline are not intended to represent the standard of care for patient management, nor are the recommendations intended to limit treatment or care provided to individual patients. Action Statements. The development group made a strong recommendation that clinicians recommend intranasal steroids for patients with a clinical diagnosis of AR whose symptoms affect their quality of life. The development group also made a strong recommendation that clinicians recommend oral second-generation/less sedating antihistamines for patients with AR and primary complaints of sneezing and itching. The panel made the following recommendations: (1) Clinicians should make the clinical diagnosis of AR when patients present with a history and physical examination consistent with an allergic cause and 1 or more of the following symptoms: nasal congestion, runny nose, itchy nose, or sneezing. Findings of AR consistent with an allergic cause include, but are not limited to, clear rhinorrhea, nasal congestion, pale discoloration of the nasal mucosa, and red and watery eyes. (2) Clinicians should perform and interpret, or refer to a clinician who can perform and interpret, specific IgE (skin or blood) allergy testing for patients with a clinical diagnosis of AR who do not respond to empiric treatment, or when the diagnosis is uncertain, or when knowledge of the specific causative allergen is needed to target therapy. (3) Clinicians should assess patients with a clinical diagnosis of AR for, and document in the medical record, the presence of associated conditions such as asthma, atopic dermatitis, sleep-disordered breathing, conjunctivitis, rhinosinusitis, and otitis media. (4) Clinicians should offer, or refer to a clinician who can offer, immunotherapy (sublingual or subcutaneous) for patients with AR who have inadequate response to symptoms with pharmacologic therapy with or without environmental controls.
433 citations
Authors
Showing all 23641 results
Name | H-index | Papers | Citations |
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Cyrus Cooper | 204 | 1869 | 206782 |
David Cella | 156 | 1258 | 106402 |
Carl H. June | 156 | 835 | 98904 |
Ichiro Kawachi | 149 | 1216 | 90282 |
Judy Garber | 147 | 756 | 79157 |
Bernard J. Gersh | 146 | 973 | 95875 |
Edward G. Lakatta | 146 | 858 | 88637 |
Eugene C. Butcher | 146 | 446 | 72849 |
Mark A. Rubin | 145 | 699 | 95640 |
Richard B. Devereux | 144 | 962 | 116403 |
Robert H. Purcell | 139 | 666 | 70366 |
Eric P. Winer | 139 | 751 | 71587 |
Richard L. Huganir | 137 | 425 | 61023 |
Rasmus Nielsen | 135 | 556 | 84898 |
Henry T. Lynch | 133 | 925 | 86270 |