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: Asthma & T cell. 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: Asthma, T cell, Population, Antigen, Lung
Papers published on a yearly basis
Papers
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TL;DR: The CT features presented in this article represent the typical features associated with each entity and can help to narrow the differential diagnosis of bronchiolitis.
Abstract: OBJECTIVE. The purpose of this article is to describe and illustrate the clinical, pathologic, and imaging features of the inflammatory and fibrotic forms of bronchiolitis. The CT features presented in this article represent the typical features associated with each entity.CONCLUSION. Direct signs of bronchiolitis include centrilobular nodules and tree-in-bud pattern. Indirect signs include mosaic attenuation and air trapping. Although classic examples of each entity exist, there can be substantial overlap in the appearances, and distinguishing among these entities is not always possible. When high-resolution CT features overlap, clinical details will usually help to narrow the differential diagnosis.
107 citations
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TL;DR: It is suggested that Ag-primed CD8+ T cells are required for the full development of AHR and airway inflammation, which appears to be associated with IL-13 production from these primed T cells.
Abstract: The role of Th2/CD4 T cells, which secrete IL-4, IL-5, and IL-13, in allergic disease is well established; however, the role of CD8+ T cells (allergen-induced airway hyperresponsiveness (AHR) and inflammation) is less clear. This study was conducted to define the role of Ag-primed CD8+ T cells in the development of these allergen-induced responses. CD8-deficient (CD8−/−) mice and wild-type mice were sensitized to OVA by i.p. injection and then challenged with OVA via the airways. Compared with wild-type mice, CD8−/− mice developed significantly lower airway responsiveness to inhaled methacholine and lung eosinophilia, and exhibited decreased IL-13 production both in vivo, in the bronchoalveolar lavage (BAL) fluid, and in vitro, following Ag stimulation of peribronchial lymph node (PBLN) cells in culture. Reconstitution of sensitized and challenged CD8−/− mice with allergen-sensitized CD8+ T cells fully restored the development of AHR, BAL eosinophilia, and IL-13 levels in BAL and in culture supernatants from PBLN cells. In contrast, transfer of naive CD8+ T cells or allergen-sensitized CD8+ T cells from IL-13-deficient donor mice failed to do so. Intracellular cytokine staining of lung as well as PBLN T cells revealed that CD8+ T cells were a source of IL-13. These data suggest that Ag-primed CD8+ T cells are required for the full development of AHR and airway inflammation, which appears to be associated with IL-13 production from these primed T cells.
107 citations
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Harvard University1, National Jewish Health2, Oregon Health & Science University3, University of Florida4, Mount Sinai St. Luke's and Mount Sinai Roosevelt5, Beaumont Hospital6, University of Nebraska Omaha7, University of California, San Francisco8, University of Texas at Tyler9, Cleveland Clinic10, Medical University of South Carolina11, University of Utah12
TL;DR: In subjects severely deficient in AAT, men, individuals with symptoms of chronic bronchitis and/or a past diagnosis of asthma or pneumonia may benefit from closer monitoring and potentially earlier treatment.
Abstract: Rationale: Severe alpha 1-antitrypsin deficiency
is an autosomal recessive genetic condition associated
with an increased, but variable, risk for chronic
obstructive pulmonary disease (COPD).
Objective: To assess the impact of chronic
bronchitis, pneumonia, asthma, and sex on the
development of COPD in individuals with severe alpha 1-
antitrypsin deficiency.
Methods: The Alpha 1-Antitrypsin Genetic Modifier Study
is a multi-center family-based cohort study designed to
study the genetic and epidemiological determinants of
COPD in alpha 1-antitrypsin deficiency. 378
individuals (age range: 33-80), confirmed to be
homozygous for the SERPINA1 Z mutation, were included in
the analyses.
Measurements and Main Results: The primary
outcomes of interest were a quantitative outcome, forced
expiratory volume in one second (FEV1) as a percent of
predicted, and a qualitative outcome, severe airflow
obstruction (FEV1 < 50% predicted). In multivariate
analysis of the overall cohort, cigarette smoking, sex,
asthma, chronic bronchitis and pneumonia were risk
factors for reduced FEV1 percent predicted and severe
airflow obstruction (p<0.01). Index cases had lower FEV1
values, higher smoking histories, and more reports of
asthma, pneumonia, and asthma before age 16 compared to
non-index cases (p<0.01). Men had lower pre and post-
bronchodilator FEV1 percent predicted measures than
women (p<0.0001); the lowest FEV1 values were observed
in men reporting a history of childhood asthma (26.9%
+9.1). This trend for more severe obstruction in men
remained when index and non-index groups were examined
separately, with males representing the majority of non-
index individuals with airflow obstruction (71%).
Chronic bronchitis (OR 3.8, CI: 1.8-12.0) and a
physician9s report of asthma (OR 4.2, CI: 1.4-13.1) were
predictors of severe airflow obstruction in multivariate
analysis of non-index men not women.
Conclusion: In individuals with severe alpha 1-
antitrypsin deficiency, sex, asthma, chronic bronchitis
and pneumonia are risk factors for severe COPD, in
addition to cigarette smoking. These results suggest
that amongst severely AAT deficient subjects, men,
individuals with symptoms of asthma or chronic
bronchitis, and/or a past diagnosis of pneumonia may
benefit from closer monitoring and potentially earlier
treatment.
107 citations
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TL;DR: Airway disease and emphysema detected by CT scanning are inversely related in patients with severe COPD and airway wall phenotypes were influenced by gender and associated with lung function in subjects with severe emphySEma.
107 citations
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TL;DR: Polymorphisms of the β2-AR may influence airway responses to regular inhaled β-agonist treatment as well as as-needed albuterol use.
Abstract: Background: Regular use of inhaled β-adrenergic agonists may have adverse effects in some asthma patients. Polymorphisms of the β2-adrenergic receptor (β2-AR)
107 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 |