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Results: 21 to 30 of 122

Publication Record


Bone morphogenetic protein type I receptor antagonists decrease growth and induce cell death of lung cancer cell lines.
Langenfeld E, Hong CC, Lanke G, Langenfeld J
(2013) PLoS One 8: e61256
MeSH Terms: Bone Morphogenetic Protein 2, Bone Morphogenetic Protein Receptors, Type I, Bronchi, Cell Death, Cell Line, Tumor, Cell Proliferation, Cell Survival, Clone Cells, Endothelial Cells, Epithelial Cells, Gene Knockdown Techniques, Humans, Inhibitor of Differentiation Proteins, Lung Neoplasms, Pyrazoles, Pyrimidines, Signal Transduction, Smad Proteins
Show Abstract · Added September 20, 2013
Bone morphogenetic proteins (BMPs) are highly conserved morphogens that are essential for normal development. BMP-2 is highly expressed in the majority of non-small cell lung carcinomas (NSCLC) but not in normal lung tissue or benign lung tumors. The effects of the BMP signaling cascade on the growth and survival of cancer cells is poorly understood. We show that BMP signaling is basally active in lung cancer cell lines, which can be effectively inhibited with selective antagonists of the BMP type I receptors. Lung cancer cell lines express alk2, alk3, and alk6 and inhibition of a single BMP receptor was not sufficient to decrease signaling. Inhibition of more than one type I receptor was required to decrease BMP signaling in lung cancer cell lines. BMP receptor antagonists and silencing of BMP type I receptors with siRNA induced cell death, inhibited cell growth, and caused a significant decrease in the expression of inhibitor of differentiation (Id1, Id2, and Id3) family members, which are known to regulate cell growth and survival in many types of cancers. BMP receptor antagonists also decreased clonogenic cell growth. Knockdown of Id3 significantly decreased cell growth and induced cell death of lung cancer cells. H1299 cells stably overexpressing Id3 were resistant to growth suppression and induction of cell death induced by the BMP antagonist DMH2. These studies suggest that BMP signaling promotes cell growth and survival of lung cancer cells, which is mediated through its regulation of Id family members. Selective antagonists of the BMP type I receptors represents a potential means to pharmacologically treat NSCLC and other carcinomas with an activated BMP signaling cascade.
1 Communities
1 Members
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18 MeSH Terms
Risk of childhood asthma following infant bronchiolitis during the respiratory syncytial virus season.
James KM, Gebretsadik T, Escobar GJ, Wu P, Carroll KN, Li SX, Walsh EM, Mitchel EF, Sloan C, Hartert TV
(2013) J Allergy Clin Immunol 132: 227-9
MeSH Terms: Adult, Asthma, Bronchiolitis, Child, Child, Preschool, Cohort Studies, Female, Humans, Male, Respiratory Syncytial Virus Infections, Risk
Added May 27, 2014
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1 Members
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11 MeSH Terms
A 75-year-old man with progressive bronchioalveolar carcinoma.
Baikadi M, Lovly C, Horn L, Reckamp KL, Noonan K, Laskin J, Morris GJ
(2013) Semin Oncol 40: e1-8
MeSH Terms: Adenocarcinoma, Bronchiolo-Alveolar, Disease Progression, Humans, Lung Neoplasms, Male, Mutation, Proto-Oncogene Proteins, Proto-Oncogene Proteins p21(ras), ras Proteins
Added March 5, 2014
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2 Members
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9 MeSH Terms
Time to explore preventive and novel therapies for bronchiolitis obliterans syndrome after allogeneic hematopoietic stem cell transplantation.
Sengsayadeth SM, Srivastava S, Jagasia M, Savani BN
(2012) Biol Blood Marrow Transplant 18: 1479-87
MeSH Terms: Adrenal Cortex Hormones, Antineoplastic Agents, Bronchiolitis Obliterans, Chronic Disease, Combined Modality Therapy, Graft vs Host Disease, Hematopoietic Stem Cell Transplantation, Humans, Immunosuppressive Agents, Leukotriene Antagonists, Lung, Lung Transplantation, Photopheresis, Practice Guidelines as Topic, Transplantation, Homologous
Show Abstract · Added March 5, 2014
Although allogeneic hematopoietic stem cell transplant (allo-HSCT) is performed to treat otherwise incurable and fatal diseases, transplantation itself can lead to life-threatening complications due to organ damage. Pulmonary complications remain a significant barrier to the success of allo-HSCT. Lung injury, a frequent complication after allo-HSCT, and noninfectious pulmonary deaths account for a significant proportion of non-relapse mortality. Bronchiolitis obliterans syndrome (BOS) is a common and potentially devastating complication. BOS is now considered a diagnostic criterion of chronic graft-versus-host-disease (cGVHD), and National Institutes of Health (NIH) consensus has been published to establish guidelines for diagnosis and monitoring of BOS. It usually occurs within the first 2 years but may develop as late as 5 years after transplantation. Recent prevalence estimates suggest that BOS is likely underdiagnosed, and when severe BOS does occur, current treatments have been largely ineffective. Prevention and effective novel approaches remain the primary tools in the clinician's arsenal in managing BOS. This article provides an overview of the currently available and novel strategies for BOS, and we also discuss specific preventive interventions to reduce severe BOS after allo-HSCT. Therapeutic trials continue to be needed for this orphan disease.
Published by Elsevier Inc.
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1 Members
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15 MeSH Terms
Natural-source d-α-tocopheryl acetate inhibits oxidant stress and modulates atopic asthma in humans in vivo.
Hoskins A, Roberts JL, Milne G, Choi L, Dworski R
(2012) Allergy 67: 676-82
MeSH Terms: Adult, Antioxidants, Asthma, Bronchial Provocation Tests, Bronchoalveolar Lavage Fluid, Cytokines, Female, Humans, Immunoglobulin E, Male, Oxidative Stress, Tocopherols, Treatment Outcome, Young Adult
Show Abstract · Added March 26, 2014
BACKGROUND - Asthma is associated with oxidant stress and diminished antioxidant defenses. Yet, the mechanistic role of oxidant stress and antioxidant supplementation in human asthmatics remains uncertain. We determined the effect of high doses of the antioxidant natural-source d-α-tocopheryl acetate for 16 weeks on allergen-induced airway oxidant stress, inflammation, and bronchial responsiveness to methacholine and allergen in atopic asthmatics in vivo.
METHODS - Thirty-three mild atopic asthmatics underwent bronchoscopy with baseline bronchoalveolar lavage and segmental allergen challenge. The allergen-challenged airway was lavaged 24 h later. At least 3 weeks later, patients underwent inhaled challenges with methacholine and specific allergen. Volunteers took 1500 IU of natural-source d-α-tocopheryl acetate daily for at least 16 weeks. At the end of the treatment, the two bronchoscopies and inhaled methacholine and allergen challenges were repeated. F(2)-isoprostanes, specific markers of oxidant stress, and selected Th1 and Th2 cytokines were analyzed in the lavage fluid.
RESULTS - Following supplementation of natural-source d-α-tocopheryl acetate, plasma concentrations of α-tocopherol increased and γ-tocopherol decreased. Both baseline and allergen-induced F(2)-isoprostanes significantly decreased, providing biochemical evidence for an antioxidant effect. Natural-source d-α-tocopheryl acetate reduced allergen-provoked concentrations of interleukin 3 and interleukin 4 and augmented levels of interleukin 12 in bronchoalveolar lavage fluid. Natural-source d-α-tocopheryl acetate improved airway responsiveness to methacholine but did not alter airway reactivity to specific allergen.
CONCLUSIONS - Inhibition of oxidant stress by natural-source d-α-tocopheryl acetate modulates allergic inflammation and airway hyperresponsiveness in human atopic asthmatics in vivo. These results need to be confirmed by a randomized placebo-controlled trial.
© 2012 John Wiley & Sons A/S.
1 Communities
1 Members
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14 MeSH Terms
Smoking attenuates transforming growth factor-β-mediated tumor suppression function through downregulation of Smad3 in lung cancer.
Samanta D, Gonzalez AL, Nagathihalli N, Ye F, Carbone DP, Datta PK
(2012) Cancer Prev Res (Phila) 5: 453-63
MeSH Terms: Acetylation, Adenocarcinoma, Animals, Apoptosis, Blotting, Western, Bronchi, Carcinoma, Squamous Cell, Cell Proliferation, Cells, Cultured, Down-Regulation, Enzyme-Linked Immunosorbent Assay, Epithelial Cells, Histones, Humans, Immunoenzyme Techniques, Immunoprecipitation, Lung Neoplasms, Mice, Mice, Nude, Phosphorylation, Protein Binding, RNA, Messenger, Real-Time Polymerase Chain Reaction, Signal Transduction, Smad3 Protein, Small Cell Lung Carcinoma, Smoking, Survival Rate, Tissue Array Analysis, Transcription, Genetic, Transforming Growth Factor beta
Show Abstract · Added June 14, 2013
Epidemiologic studies have shown that most cases of lung cancers (85%-90%) are directly attributable to cigarette smoking. Although much information has been gained about the effects of cigarette smoking on various signaling pathways causing lung cancer, nothing is known about the effect of cigarette smoking on the TGF-β-induced tumor suppressor function in lung cancer. To address this issue, lung adenocarcinoma A549 and immortalized bronchial epithelial HPL1A cells were chronically treated with cigarette smoke condensate (CSC) and dimethyl sulfoxide (as a control) to mimic the conditions of long-term cigarette smoking. Prolonged exposure of these cells to CSC resulted in a decrease in Smad3 and Smad4 complex formation and TGF-β-mediated transcription due to reduced expression of Smad3. Long-term CSC treatment reduced apoptosis, increased cell viability, decreased TGF-β-mediated growth inhibition, and enhanced tumorigenicity. The decrease in apoptosis is due to the upregulation of Bcl-2, which is a downstream target of Smad3. Re-expression of Smad3 in the CSC-treated cells restored TGF-β signaling, increased apoptosis, and decreased cell viability and tumorigenicity. Withdrawal of CSC treatment resulted in the restoration of Smad3 expression, reduction in cell viability, and increased TGF-β-mediated growth inhibition. Expression of Smad3 is lower in lung tumors of current smokers than that observed in never-smokers. Collectively, these data provide evidence that cigarette smoking promotes tumorigenicity partly by abrogating TGF-β-mediated growth inhibition and apoptosis by reducing expression of Smad3.
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31 MeSH Terms
Noninvasive testing of lung function and inflammation in pediatric patients with acute asthma exacerbations.
Arnold DH, Gebretsadik T, Abramo TJ, Hartert TV
(2012) J Asthma 49: 29-35
MeSH Terms: Academic Medical Centers, Adolescent, Age Factors, Airway Resistance, Asthma, Breath Tests, Bronchitis, Child, Child, Preschool, Cohort Studies, Disease Progression, Emergency Service, Hospital, Female, Follow-Up Studies, Forced Expiratory Volume, Humans, Male, Nitric Oxide, Predictive Value of Tests, Prospective Studies, Respiratory Function Tests, Risk Assessment, Severity of Illness Index, Sex Factors, Spirometry, Urban Population
Show Abstract · Added May 27, 2014
OBJECTIVE - There is limited information on performance rates for tests of lung function and inflammation in pediatric patients with acute asthma exacerbations. We sought to examine how frequently pediatric patients with acute asthma exacerbations could perform noninvasive lung function and exhaled nitric oxide (FE(NO)) testing and participant characteristics associated with successful performance.
METHODS - We studied a prospective convenience sample aged 5-17 years with acute asthma exacerbations in a pediatric emergency department. Participants attempted spirometry for percent predicted forced expiratory volume in 1 second (%FEV(1)), airway resistance (Rint), and FE(NO) testing before treatment. We examined overall performance rates and the associations of age, gender, race, and baseline acute asthma severity score with successful test performance.
RESULTS - Among 573 participants, age was (median [interquartile range]) 8.8 [6.8, 11.5] years, 60% were male, 57% were African-American, and 58% had Medicaid insurance. Tests were performed successfully by the following [n (%)]: full American Thoracic Society-European Respiratory Society criteria spirometry, 331 (58%); Rint, 561 (98%); and FE(NO), 354 (70% of 505 attempted test). Sixty percent with mild-moderate exacerbations performed spirometry compared to 17% with severe exacerbations (p = .0001). Participants aged 8-12 years (67%) were more likely to perform spirometry than those aged 5-7 years (48%) (OR = 2.23, 95% CI: 1.45-3.11) or 13-17 years (58%) (OR = 1.61, 95% CI: 1.00-2.59).
CONCLUSIONS - There is clinically important variability in performance of these tests during acute asthma exacerbations. The proportion of patients with severe exacerbations able to perform spirometry (17%) limits its utility. Almost all children with acute asthma can perform Rint testing, and further development and validation of this technology is warranted.
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26 MeSH Terms
Effects of experimental asthma on inflammation and lung mechanics in sickle cell mice.
Pritchard KA, Feroah TR, Nandedkar SD, Holzhauer SL, Hutchins W, Schulte ML, Strunk RC, Debaun MR, Hillery CA
(2012) Am J Respir Cell Mol Biol 46: 389-96
MeSH Terms: Airway Resistance, Anemia, Sickle Cell, Animals, Asthma, Bronchial Hyperreactivity, Bronchial Provocation Tests, Bronchoalveolar Lavage Fluid, Bronchoconstrictor Agents, Colorimetry, Cytokines, Disease Models, Animal, Enzyme-Linked Immunosorbent Assay, Eosinophils, Hemoglobin A, Hemoglobin, Sickle, Humans, Immunoglobulin E, Inflammation Mediators, L-Lactate Dehydrogenase, Lung, Methacholine Chloride, Mice, Mice, Inbred C57BL, Mice, Transgenic, Ovalbumin, Pneumonia, Positive-Pressure Respiration, Vascular Endothelial Growth Factor A
Show Abstract · Added November 27, 2013
Experimental asthma increases eosinophil and collagen deposition in the lungs of sickle cell disease (SCD) mice to a greater extent than in control mice. However, the effects of asthma on inflammation and airway physiology remain unclear. To determine effects of asthma on pulmonary inflammation and airway mechanics in SCD mice, hematopoietic stem cell transplantation was used to generate chimeric SCD and hemoglobin A mice. Experimental asthma was induced by sensitizing mice with ovalbumin (OVA). Airway mechanics were assessed using forced oscillation techniques. Mouse lungs were examined histologically and physiologically. Cytokine, chemokine, and growth factors in bronchoalveolar lavage fluid were determined by multiplex. IgE was quantified by ELISA. LDH was quantified using a colorimetric enzymatic assay. At baseline (nonsensitized), chimeric SCD mice developed hemolytic anemia with sickled red blood cells, mild leukocytosis, and increased vascular endothelial growth factor and IL-13 compared with chimeric hemoglobin A mice. Experimental asthma increased perialveolar eosinophils, plasma IgE, and bronchoalveolar lavage fluid IL-1β, IL-4, IL-6, and monocyte chemotactic protein 1 in chimeric hemoglobin A and SCD mice. IFN-γ levels were reduced in both groups. IL-5 was preferentially increased in chimeric SCD mice but not in hemoglobin A mice. Positive end-expiratory pressures and methacholine studies revealed that chimeric SCD mice had greater resistance in large and small airways compared with hemoglobin A mice at baseline and after OVA sensitization. SCD alone induces a baseline lung pathology that increases large and small airway resistance and primes the lungs to increased inflammation and airway hyperresponsiveness after OVA sensitization.
1 Communities
1 Members
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28 MeSH Terms
Constrictive bronchiolitis in soldiers returning from Iraq and Afghanistan.
King MS, Eisenberg R, Newman JH, Tolle JJ, Harrell FE, Nian H, Ninan M, Lambright ES, Sheller JR, Johnson JE, Miller RF
(2011) N Engl J Med 365: 222-30
MeSH Terms: Adult, Afghan Campaign 2001-, Bronchioles, Bronchiolitis Obliterans, Exercise Test, Exercise Tolerance, Follow-Up Studies, Humans, Iraq War, 2003-2011, Lung, Military Personnel, Prevalence, Respiratory Function Tests, Tomography, X-Ray Computed, United States
Show Abstract · Added March 2, 2014
BACKGROUND - In this descriptive case series, 80 soldiers from Fort Campbell, Kentucky, with inhalational exposures during service in Iraq and Afghanistan were evaluated for dyspnea on exertion that prevented them from meeting the U.S. Army's standards for physical fitness.
METHODS - The soldiers underwent extensive evaluation of their medical and exposure history, physical examination, pulmonary-function testing, and high-resolution computed tomography (CT). A total of 49 soldiers underwent thoracoscopic lung biopsy after noninvasive evaluation did not provide an explanation for their symptoms. Data on cardiopulmonary-exercise and pulmonary-function testing were compared with data obtained from historical military control subjects.
RESULTS - Among the soldiers who were referred for evaluation, a history of inhalational exposure to a 2003 sulfur-mine fire in Iraq was common but not universal. Of the 49 soldiers who underwent lung biopsy, all biopsy samples were abnormal, with 38 soldiers having changes that were diagnostic of constrictive bronchiolitis. In the remaining 11 soldiers, diagnoses other than constrictive bronchiolitis that could explain the presenting dyspnea were established. All soldiers with constrictive bronchiolitis had normal results on chest radiography, but about one quarter were found to have mosaic air trapping or centrilobular nodules on chest CT. The results of pulmonary-function and cardiopulmonary-exercise testing were generally within normal population limits but were inferior to those of the military control subjects.
CONCLUSIONS - In 49 previously healthy soldiers with unexplained exertional dyspnea and diminished exercise tolerance after deployment, an analysis of biopsy samples showed diffuse constrictive bronchiolitis, which was possibly associated with inhalational exposure, in 38 soldiers.
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15 MeSH Terms
Relationship of maternal vitamin D level with maternal and infant respiratory disease.
Carroll KN, Gebretsadik T, Larkin EK, Dupont WD, Liu Z, Van Driest S, Hartert TV
(2011) Am J Obstet Gynecol 205: 215.e1-7
MeSH Terms: Adult, African Americans, Asthma, Bronchiolitis, European Continental Ancestry Group, Female, Humans, Infant, Male, Risk Factors, Vitamin D
Show Abstract · Added March 21, 2014
OBJECTIVE - The objective of the study was to investigate the association of maternal vitamin D and maternal asthma and infant respiratory infection severity.
STUDY DESIGN - The study included cross-sectional analyses of 340 mother-infant dyads enrolled from September to May 2004-2008 during an infant viral respiratory infection. Maternal vitamin D levels were determined from enrollment blood specimens. At enrollment, we determined self-reported maternal asthma and infant respiratory infection severity using a bronchiolitis score. We assessed the association of maternal vitamin D levels and maternal asthma and infant bronchiolitis score in race-stratified multivariable regression models.
RESULTS - The cohort was 70% white, 19% African American, and 21% had asthma. Overall, the median maternal vitamin D level was 20 ng/mL (interquartile range, 14-28). Among white women, a 14 ng/mL increase in vitamin D was associated with a decreased odds of asthma (adjusted odds ratio, 0.54; 95% confidence interval, 0.33-0.86). Maternal vitamin D was not associated with infant bronchiolitis score.
CONCLUSION - Higher maternal vitamin D levels were associated with decreased odds of asthma.
Copyright © 2011 Mosby, Inc. All rights reserved.
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11 MeSH Terms