Institution
National Jewish Health
Healthcare•Denver, Colorado, United States•
About: National Jewish Health is a healthcare organization based out in Denver, Colorado, United States. It is known for research contribution in the topics: T cell & Asthma. The organization has 883 authors who have published 833 publications receiving 79201 citations. The organization is also known as: National Jewish Medical and Research Center.
Topics: T cell, Asthma, Population, Lung, Antigen
Papers published on a yearly basis
Papers
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TL;DR: Initiating HAART atCD4 cell counts ≥200 cells/mm3 reduced the incidence and risk of the 3 comorbid conditions and for anemia and peripheral neuropathy as well by starting at CD4 counts ≥350 cells/MM3.
Abstract: Background: US guidelines recommend deferring initiation of highly active antiretroviral therapy (HAART) for most patients with CD4 counts >350 cells/mm 3 in part because of concerns about antiretroviral toxicity. Methods: Incidence rates of peripheral neuropathy, anemia, and renal insufficiency in a cohort of 2165 patients followed more than 3 years (mean) were analyzed in multivariate Cox proportional hazards models by CD4 cell counts at initiation of HAART. A nested cohort of 895 patients restricted to study participants who did or did not start HAART within a CD4 cell count stratum were also compared. Results: Incidence and risks of all 3 comorbidities decreased with initiation of HAART at CD4 counts >200 cells/mm 3 versus <200 cells/mm 3 . Incidence and risks of renal insufficiency were similar with HAART initiation at CD4 counts ≥ 350 cells/mm 3 versus 200 to 349 cells/mm 3 , but risk of peripheral neuropathy and anemia were further decreased in persons starting HAART at a CD4 count ≥350 cells/mm 3 . The incidence of these conditions was highest during the first 6 months of treatment at any CD4 cell count and declined up to 19-fold with further therapy. Discussion: Initiating HAART at CD4 cell counts ≥200 cells/mm 3 reduced the incidence and risk of the 3 comorbid conditions and for anemia and peripheral neuropathy as well by starting at CD4 counts ≥350 cells/mm 3 . The incidence of each condition decreased rapidly and remained low with increasing time on HAART.
83 citations
TL;DR: In summary, acute exposure to O(3) induces AHR, neutrophilic inflammation, epithelial damage, and IL-1, and anIL-1Ra effectively prevents the development of altered airway function, inflammation, and structural damage.
Abstract: The role of an interleukin (IL)-1 receptor antagonist (IL-1Ra) on the development of airway hyperresponsiveness (AHR) and airway inflammation following acute O(3) exposure in mice was investigated. Exposure of C57/BL6 mice to O(3) at a concentration of 2.0 ppm or filtered air for 3 h resulted in increases in airway responsiveness to inhaled methacholine (MCh) 8 and 16 h after the exposure, and an increase in neutrophils in the bronchoalveolar lavage (BAL) fluid. IL-1beta expression, assessed by gene microarray, was increased 2-fold 4 h after O(3) exposure, and returned to baseline levels by 24 h. Levels of IL-1beta in lung homogenates were also increased 8 h after O(3) exposure. Administration of (human) IL-1Ra before and after O(3) exposure prevented development of AHR and decreased BAL fluid neutrophilia. Increases in chemokine levels in lung homogenates, tumor necrosis factor-alpha, MIP-2, and keratinocyte chemoattractant following O(3) exposure were prevented by IL-1Ra. Inhalation of dexamethasone, an inhibitor of IL-1 production, blocked the development of AHR, BAL fluid neutrophilia, and decreased levels of IL-1 following O(3) exposure. In summary, acute exposure to O(3) induces AHR, neutrophilic inflammation, epithelial damage, and IL-1. An IL-1Ra effectively prevents the development of altered airway function, inflammation, and structural damage.
83 citations
Vanderbilt University1, University of Colorado Denver2, National Jewish Health3, Brigham and Women's Hospital4, Oklahoma Medical Research Foundation5, University of Ulsan6, University of Edinburgh7, University of Nottingham8, Imperial College London9, University of Pittsburgh10, University of California, San Francisco11, University of Chicago12, University of Virginia13, University of Pennsylvania14, Ege University15, Royal Prince Alfred Hospital16, Monash University17, Paris Diderot University18, Cambridge University Hospitals NHS Foundation Trust19, University of Barcelona20, University of Iceland21, Columbia University22, Harvard University23, Aarhus University Hospital24, National Autonomous University of Mexico25, Cork University Hospital26, University College Dublin27, First Faculty of Medicine, Charles University in Prague28, University of British Columbia29, Tokyo Medical and Dental University30, University of Western Australia31, Brown University32, Inova Fairfax Hospital33, Gazi University34, University of Alabama at Birmingham35, University of Duisburg-Essen36, Trinity College, Dublin37, University of Genoa38, University of Minnesota39, University of Washington40
TL;DR: A limited number of common and rare variants contribute to the risk of idiopathic pulmonary fibrosis in each of the resequencing regions; these genetic variants focus on biological mechanisms of host defense and cell senescence.
Abstract: Rationale: Several common and rare genetic variants have been associated with idiopathic pulmonary fibrosis, a progressive fibrotic condition that is localized to the lung.Objectives: To develop an...
81 citations
Journal Article•
Georgetown University Medical Center1, University of Pennsylvania2, University of Cincinnati3, Icahn School of Medicine at Mount Sinai4, Medical University of South Carolina5, Georgetown University6, Case Western Reserve University7, National Jewish Health8, University of Iowa9, Johns Hopkins University10, Harvard University11
TL;DR: A "global" approach to the sarcoidosis patient, including careful assessment of dyspnea and health related quality of life, as well as of lung function and radiographic changes, and any extrathoracic involvement is important, not only in management of the individual patient, but should also prove beneficial in assessing outcomes in clinical trials in the future.
Abstract: Aim To assess lung involvement and the association of demographic and psychosocial factors with respiratory health in 736 persons with sarcoidosis at enrollment in A Case Control Etiologic Study of Sarcoidosis (ACCESS). Methods 736 patients with biopsy diagnosis of sarcoidosis within 6 months of enrollment were studied at 10 US centers. Lung involvement was evaluated by chest radiography, spirometry and dyspnea questionnaire. Demographics, number of involved extrathoracic organ systems, comorbidities, and health-related quality of life (HRQL) were assessed. Results 95% of patients had lung involvement. 8% were Scadding Stage 0, 40% I, 37% II, 10% III, and 5% IV 51% reported dyspnea. Increasing radiographic lung stage was associated with decreasing Forced Vital Capacity (FVC) (p or = 40, African-American race, body mass index > or = 30kg/m2, and CES-D scores > 9 were associated with decreased FVC and greater dyspnea. Impaired spirometry and greater dyspnea were associated with poorer quality of life. Conclusion A "global" approach to the sarcoidosis patient, including careful assessment of dyspnea and health related quality of life, as well as of lung function and radiographic changes, and any extrathoracic involvement, is important, not only in management of the individual patient, but should also prove beneficial in assessing outcomes in clinical trials in the future.
81 citations
TL;DR: The mechanisms of S. aureus colonization and infection are examined, of which the most important are defective skin barrier function, increased S.aureus adherence, and the decreased innate immune responses found in AD skin.
Abstract: The role of staphylococcal superantigens in the pathophysiology of atopic dermatitis (AD) has been the focus of intense interest during the past decade Although the increased prevalence of Staphylococcus aureus and its bacterial toxins in AD skin is well established, exploitation of the known mechanisms of superantigens in this disease for the development of novel therapies remains an active area of research With the emergence of multi-drug resistant S aureus, the need for a better understanding of the pathophysiology of bacterial superantigens in AD has become increasingly important This review examines the mechanisms of S aureus colonization and infection, of which the most important are defective skin barrier function, increased S aureus adherence, and the decreased innate immune responses found in AD skin The contribution of superantigens to the pathophysiology of AD is then discussed Important immunologic mechanisms in this context include the role of superantigens in promoting T helper-2 skin inflammation, IgE production, T-regulatory cell subversion, expansion and migration of skin-homing T cells, and IgE anti-superantigen production Lastly, these findings are discussed with reference to current therapeutic approaches, of which the most important include anti-inflammatory and antimicrobial medications, and future strategies, which are expected to consist of immune-modulators and synthetic antibacterials
80 citations
Authors
Showing all 901 results
| Name | H-index | Papers | Citations |
|---|---|---|---|
| Thomas V. Colby | 126 | 501 | 60130 |
| John W. Kappler | 122 | 464 | 57541 |
| Donald Y.M. Leung | 121 | 614 | 50873 |
| Philippa Marrack | 120 | 416 | 54345 |
| Jeffrey M. Drazen | 117 | 693 | 52493 |
| Peter M. Henson | 112 | 369 | 54246 |
| David A. Schwartz | 110 | 958 | 53533 |
| David A. Lynch | 108 | 714 | 59678 |
| Norman R. Pace | 101 | 297 | 50252 |
| Kevin K. Brown | 100 | 387 | 47219 |
| Stanley J. Szefler | 99 | 554 | 37481 |
| Erwin W. Gelfand | 99 | 675 | 36059 |
| James D. Crapo | 98 | 473 | 37510 |
| Yang Xin Fu | 97 | 390 | 33526 |
| Stephen D. Miller | 94 | 433 | 30499 |