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: Serum Gal-3 levels are associated with multiple indices of RV function and morphology, and may represent a novel biomarker for RV remodeling and associated ECM turnover in PAH.
Abstract: The response of the right ventricle (RV) to pulmonary arterial hypertension (PAH) involves changes in contractile function, chamber size, hypertrophy, and extracellular matrix (ECM). Galectin-3 (Gal-3) is a mediator of myocardial ECM metabolism and biomarker for left heart remodeling, yet its ability to reflect RV remodeling is unknown. We hypothesized that serum Gal-3 levels correlate with RV morphology and function in PAH, and that Gal-3 is associated with circulating markers of ECM. Fifteen subjects with PAH and 10 age-matched controls underwent same-day echocardiography, cardiac magnetic resonance (CMR) imaging, and phlebotomy for Gal-3 and ECM biomarkers including N-terminal propeptide of type III collagen type (PIIINP), tissue inhibitor of metalloproteinase-1 (TIMP-1), and hyaluronic acid (HA). RV ejection fraction, end diastolic volume index, end systolic volume index, and mass index were calculated using CMR. Echocardiography was used to estimate RV systolic pressure and measure RV strain. Serum Gal-3, TIMP-1, and HA levels were all significantly increased in PAH subjects when compared to controls. Gal-3 correlated with RV ejection fraction (ρ -0.44, p 0.03), end diastolic volume index (ρ 0.42, p 0.03), end systolic volume index (ρ 0.44, p 0.027), mass index (ρ 0.47, p 0.016), systolic pressure (ρ 0.55, p < 0.001), and strain (ρ 0.43, p 0.03). Gal-3 levels positively correlated with the ECM markers TIMP-1 and HA but not with PIIINP. In conclusion, Gal-3 levels are associated with multiple indices of RV function and morphology. Gal-3 may represent a novel biomarker for RV remodeling and associated ECM turnover in PAH.
53 citations
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10 Feb 2005TL;DR: In this article, novel inhibitors of the alternative complement pathway and particularly, novel anti-factor B antibodies are proposed to reduce or prevent airway hyperresponsiveness and/or airway inflammation by selectively inhibiting the Alternative complement pathway, thereby treating diseases in which such conditions play a role.
Abstract: Disclosed are novel inhibitors of the alternative complement pathway and particularly, novel anti-factor B antibodies. Also disclosed is the use of such inhibitors to reduce or prevent airway hyperresponsiveness and/or airway inflammation by selectively inhibiting the alternative complement pathway, thereby treating diseases in which such conditions play a role. Also disclosed is the use of such inhibitors to reduce or prevent other diseases and conditions, including ischemia-reperfusion injury, by inhibition of the alternative complement pathway.
53 citations
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TL;DR: In this article, a bradykinin antagonist dimer, CU201, inhibited the growth of SCLC and NSCLC cell lines with or without multidrug-resistant proteins and was 10-fold more potent with a longer plasma half-life than SPDs.
Abstract: All small cell (SCLCs) and many non-small cell lung cancers (NSCLCs) have neuroendocrine features including production of neuropeptides and cell surface receptors creating autocrine and paracrine growth loops. Neuropeptides bind to a family of 7-transmembrane receptors and activate heterotrimeric G proteins consisting of Gαq and Gα12,13. Substance P derivatives (SPDs) induced apoptosis and inhibited growth of lung cancer cells by discoordinately inhibiting Gαq and stimulating Gα12,13. However, these SPDs had low potency and short half-lives. In this report we show that a bradykinin antagonist dimer, CU201, inhibited the growth of SCLC and NSCLC cell lines with or without multidrug-resistant proteins and was 10-fold more potent with a longer plasma half-life than SPDs. Bradykinin agonists in either monomeric or dimeric form and monomeric bradykinin antagonist have no effect on lung cancer cell growth. The dimeric linking moiety of the two molecules was created, requiring a sufficient number of carbon chains to provide critical spacing between the two antagonists. CU201 inhibited intracellular Ca2+ release in response to bradykinin, indicating blockage of the Gαq signal, and stimulated c-Jun kinases, indicating stimulation of the Gα12,13 pathway. CU201-induced apoptosis was preceded by unique changes in apparent nuclear DNA binding and by c-Jun kinase and caspase-3 activation. At the concentration at which CU201 inhibited the growth of the cancer cells, it had no effect on the growth of normal lung cells in vitro. CU201 and similar compounds offer hope of becoming a new form of targeted therapy for tumors with neuroendocrine properties.
53 citations
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TL;DR: RSV-induced airway dysfunction is, at least in part, due to an imbalance in sensory neuropeptide expression in the airways, and Restoration of this balance may be beneficial for the treatment of RSV-mediatedAirway dysfunction.
Abstract: The mechanisms by which respiratory syncytial virus (RSV) infection causes airway hyperresponsiveness (AHR) are not fully established. We hypothesized that RSV infection may alter the expression of...
53 citations
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TL;DR: AATD remains a devastating illness for many of those affected as reflected in a high incidence of transplantation for liver and lung disease, and the clinical characteristics of diseased individuals in North America are reviewed.
Abstract: Background: α1-Antitrypsin deficiency (AATD) is an uncommon genetic disease which occurs in 1–2.5% of Americans with chronic obstructive pulmonary disease (COPD). Little
52 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 |