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[PMID]:29208260
[Au] Autor:Fu T; Wang L; Zeng Q; Zhang Y; Sheng B; Han L
[Ad] Endereço:Department of Respiration, the 1st People's Hospital of Jining, Jining, China.
[Ti] Título:Ghrelin Ameliorates Asthma by Inhibiting Endoplasmic Reticulum Stress.
[So] Source:Am J Med Sci;354(6):617-625, 2017 12.
[Is] ISSN:1538-2990
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: This study aimed to confirm the ameliorative effect of ghrelin on asthma and investigate its mechanism. MATERIALS AND METHODS: The murine model of asthma was induced by ovalbumin (OVA) treatment and assessed by histological pathology and airway responsiveness to methacholine. The total and differential leukocytes were counted. Tumor necrosis factor α, interferon γ, interleukin-5 and interleukin-13 levels in bronchoalveolar lavage fluid were quantified by commercial kits. The protein levels in pulmonary tissues were measured by Western blot analysis. RESULTS: Ghrelin ameliorated the histological pathology and airway hyperresponsiveness in the OVA-induced asthmatic mouse model. Consistently, OVA-increased total and differential leukocytes and levels of tumor necrosis factor α, interferon γ, interleukin-5 and interleukin-13 in bronchoalveolar lavage fluid were significantly attenuated by ghrelin. Ghrelin prevented the increased protein levels of the endoplasmic reticulum stress markers glucose regulated protein 78 and CCAAT/enhancer binding protein homologous protein and reversed the reduced levels of p-Akt in asthmatic mice. CONCLUSIONS: Ghrelin might prevent endoplasmic reticulum stress activation by stimulating the Akt signaling pathway, which attenuated inflammation and ameliorated asthma in mice. Ghrelin might be a new target for asthma therapy.
[Mh] Termos MeSH primário: Antiasmáticos/uso terapêutico
Asma/tratamento farmacológico
Retículo Endoplasmático/efeitos dos fármacos
Grelina/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Antiasmáticos/farmacologia
Asma/patologia
Asma/fisiopatologia
Western Blotting
Líquido da Lavagem Broncoalveolar/química
Líquido da Lavagem Broncoalveolar/citologia
Modelos Animais de Doenças
Grelina/farmacologia
Queratinas/análise
Pulmão/efeitos dos fármacos
Pulmão/patologia
Masculino
Cloreto de Metacolina/farmacologia
Camundongos
Camundongos Endogâmicos C57BL
Estresse Fisiológico/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-Asthmatic Agents); 0 (Ghrelin); 0W5ETF9M2K (Methacholine Chloride); 68238-35-7 (Keratins)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171207
[St] Status:MEDLINE


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[PMID]:29211208
[Au] Autor:Meneghini AC; Paulino ACB; Pereira LP; Vianna EO
[Ad] Endereço:MSc. Doctoral Student, Department of Social Medicine, Faculdade de Medicina de Ribeirão Preto (FMRP), Universidade de São Paulo (USP), Ribeirão Preto (SP), Brazil.
[Ti] Título:Accuracy of spirometry for detection of asthma: a cross-sectional study.
[So] Source:Sao Paulo Med J;135(5):428-433, 2017 Sep-Oct.
[Is] ISSN:1806-9460
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Asthma is a chronic inflammatory disease with airway hyperresponsiveness. Spirometry is the most commonly used test among asthmatic patients. Another functional test used for diagnosing asthma is the bronchial challenge test. The aim of this study was to analyze the accuracy of spirometry for detecting asthma in the general population. DESIGN AND SETTING: Cross-sectional study with data analysis to evaluate the accuracy of spirometry through calculating sensitivity, specificity and predictive values and through the kappa agreement test. METHODS: Subjects who constituted a birth cohort were enrolled at the age of 23 to 25 years. Spirometric abnormality was defined as reduced forced expiratory volume in one second, i.e. lower than 80% of the predicted value. Measurement of bronchial responsiveness was performed by means of the bronchial challenge test with methacholine. The gold-standard diagnosis of asthma was defined as the presence of bronchial hyperresponsiveness in association with respiratory symptoms. RESULTS: Asthma was detected in 200 subjects (10.4%) out of the sample of 1922 individuals. Spirometric abnormality was detected in 208 subjects (10.9%) of the sample. The specificity of spirometric abnormality for detecting asthma was 90%, sensitivity was 23%, positive predictive value was 22%, and negative predictive value was 91%. The kappa test revealed weak agreement of 0.13 (95% confidence interval, CI: 0.07-0.19) between spirometry and the diagnosis of asthma. CONCLUSION: Spirometry, as a single test, has limitations for detecting asthma in the general population.
[Mh] Termos MeSH primário: Asma/diagnóstico
Espirometria
[Mh] Termos MeSH secundário: Adolescente
Asma/epidemiologia
Brasil/epidemiologia
Testes de Provocação Brônquica
Broncoconstritores
Criança
Pré-Escolar
Estudos Transversais
Feminino
Seres Humanos
Lactente
Masculino
Cloreto de Metacolina
Valor Preditivo dos Testes
Sensibilidade e Especificidade
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bronchoconstrictor Agents); 0W5ETF9M2K (Methacholine Chloride)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180123
[Lr] Data última revisão:
180123
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171207
[St] Status:MEDLINE


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[PMID]:28068846
[Au] Autor:Haddad L; Corriveau S; Rousseau E; Blouin S; Pasquier JC; Ponsot Y; Roy-Lacroix MÈ
[Ad] Endereço:a Department of Obstetrics and Gynecology , Urology Division, Centre Hospitalier Universitaire de Sherbrooke , Sherbrooke , Québec , Canada.
[Ti] Título:Impact of tamsulosin and nifedipine on contractility of pregnant rat ureters in vitro .
[So] Source:J Matern Fetal Neonatal Med;31(2):191-196, 2018 Jan.
[Is] ISSN:1476-4954
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: To evaluate the in vitro effect of tamsulosin and nifedipine on the contractility of pregnant rat ureters and to perform quantitative analysis of the pharmacological effects. Medical expulsive therapy (MET) is commonly used to treat urolithiasis. However, this treatment is seldom used in pregnant women since no studies support this practice. METHODS: This was an in vitro study on animal tissue derived from pregnant Sprague-Dawley rats. A total of 124 ureteral segments were mounted in an organ bath system and contractile response to methacholine (MCh) was assessed. Tamsulosin or nifedipine were added at cumulative concentrations (0.001-1 µM). The area under the curve (AUC) from isometric tension measurements was calculated. The effect of pharmacological agents and the respective controls were assessed by calculating the AUC for each 5-min interval. Statistical analyses were performed using the Mann-Whitney-Wilcoxon nonparametric test. RESULTS: Both drugs displayed statistically significant inhibitory activity at concentrations of 0.1 and 1 µM for tamsulosin and 1 µM for nifedipine when calculated as the AUC as compared to DMSO controls. CONCLUSION: Tamsulosin and nifedipine directly inhibit MCh-induced contractility of pregnant rat ureters. Further work is needed to determine the clinical efficacy of these medications for MET in pregnancy.
[Mh] Termos MeSH primário: Nifedipino/farmacologia
Sulfonamidas/farmacologia
Ureter/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Feminino
Cálculos Renais
Cloreto de Metacolina/farmacologia
Gravidez
Ratos
Ratos Sprague-Dawley
Ureter/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Sulfonamides); 0W5ETF9M2K (Methacholine Chloride); G3P28OML5I (tamsulosin); I9ZF7L6G2L (Nifedipine)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170111
[St] Status:MEDLINE
[do] DOI:10.1080/14767058.2017.1280017


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[PMID]:28749975
[Au] Autor:Davis JS; Sun M; Kho AT; Moore KG; Sylvia JM; Weiss ST; Lu Q; Tantisira KG
[Ad] Endereço:Channing Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, United States of America.
[Ti] Título:Circulating microRNAs and association with methacholine PC20 in the Childhood Asthma Management Program (CAMP) cohort.
[So] Source:PLoS One;12(7):e0180329, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Circulating microRNAs (miRNA) are promising biomarkers for human diseases. Our study hypothesizes that circulating miRNA would reveal candidate biomarkers related to airway hyperresponsiveness (AHR) and provide biologic insights into asthma epigenetic influences. METHODS: Serum samples obtained at randomization for 160 children in the Childhood Asthma Management Program were profiled using a TaqMan miRNA array set. The association of the isolated miRNA with methacholine PC20 was assessed. Network and pathway analyses were performed. Functional validation of two significant miRNAs was performed in human airway smooth muscle cells (HASMs). RESULTS: Of 155 well-detected circulating miRNAs, eight were significantly associated with PC20 with the strongest association with miR-296-5p. Pathway analysis revealed miR-16-5p as a network hub, and involvement of multiple miRNAs interacting with genes in the FoxO and Hippo signaling pathways by KEGG analysis. Functional validation of two miRNA in HASM showed effects on cell growth and diameter. CONCLUSION: Reduced circulatory miRNA expression at baseline is associated with an increase in PC20. These miRNA provide biologic insights into, and may serve as biomarkers of, asthma severity. miR-16-5p and -30d-5p regulate airway smooth muscle phenotypes critically involved in asthma pathogenesis, supporting a mechanistic link to these findings. Functional ASM phenotypes may be directly relevant to AHR.
[Mh] Termos MeSH primário: Asma/sangue
Asma/genética
Cloreto de Metacolina/farmacologia
MicroRNAs/sangue
[Mh] Termos MeSH secundário: Proliferação Celular
Tamanho Celular
Criança
Estudos de Coortes
Intervalos de Confiança
Feminino
Seres Humanos
Análise dos Mínimos Quadrados
Modelos Lineares
Pulmão/patologia
Masculino
Miócitos de Músculo Liso/metabolismo
Miócitos de Músculo Liso/patologia
Reprodutibilidade dos Testes
Software
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (MicroRNAs); 0W5ETF9M2K (Methacholine Chloride)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171009
[Lr] Data última revisão:
171009
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0180329


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[PMID]:28596292
[Au] Autor:Kistemaker LEM; Oenema TA; Baarsma HA; Bos IST; Schmidt M; Facchinetti F; Civelli M; Villetti G; Gosens R
[Ad] Endereço:Department of Molecular Pharmacology, University of Groningen, The Netherlands; l.e.m.kistemaker@rug.nl.
[Ti] Título:The PDE4 inhibitor CHF-6001 and LAMAs inhibit bronchoconstriction-induced remodeling in lung slices.
[So] Source:Am J Physiol Lung Cell Mol Physiol;313(3):L507-L515, 2017 Sep 01.
[Is] ISSN:1522-1504
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Combination therapy of PDE4 inhibitors and anticholinergics induces bronchoprotection in COPD. Mechanical forces that arise during bronchoconstriction may contribute to airway remodeling. Therefore, we investigated the impact of PDE4 inhibitors and anticholinergics on bronchoconstriction-induced remodeling. Because of the different mechanism of action of PDE4 inhibitors and anticholinergics, we hypothesized functional interactions of these two drug classes. Guinea pig precision-cut lung slices were preincubated with the PDE4 inhibitors CHF-6001 or roflumilast and/or the anticholinergics tiotropium or glycopyorrolate, followed by stimulation with methacholine (10 µM) or TGF-ß (2 ng/ml) for 48 h. The inhibitory effects on airway smooth muscle remodeling, airway contraction, and TGF-ß release were investigated. Methacholine-induced protein expression of smooth muscle-myosin was fully inhibited by CHF-6001 (0.3-100 nM), whereas roflumilast (1 µM) had smaller effects. Tiotropium and glycopyrrolate fully inhibited methacholine-induced airway remodeling (0.1-30 nM). The combination of CHF-6001 and tiotropium or glycopyrrolate, in concentrations partially effective by themselves, fully inhibited methacholine-induced remodeling in combination. CHF-6001 did not affect airway closure and had limited effects on TGF-ß -induced remodeling, but rather, it inhibited methacholine-induced TGF-ß release. The PDE4 inhibitor CHF-6001, and to a lesser extent roflumilast, and the LAMAs tiotropium and glycopyrrolate inhibit bronchoconstriction-induced remodeling. The combination of CHF-6001 and anticholinergics was more effective than the individual compounds. This cooperativity might be explained by the distinct mechanisms of action inhibiting TGF-ß release and bronchoconstriction.
[Mh] Termos MeSH primário: Remodelação das Vias Aéreas/efeitos dos fármacos
Broncoconstrição/efeitos dos fármacos
Antagonistas Colinérgicos/farmacologia
Nucleotídeo Cíclico Fosfodiesterase do Tipo 4/metabolismo
Pulmão/efeitos dos fármacos
Pulmão/fisiopatologia
Inibidores da Fosfodiesterase 4/farmacologia
Sulfonamidas/farmacologia
para-Aminobenzoatos/farmacologia
[Mh] Termos MeSH secundário: Aminopiridinas
Animais
Benzamidas
Ciclopropanos
Interações Medicamentosas
Glicopirrolato/farmacologia
Cobaias
Masculino
Cloreto de Metacolina/farmacologia
Brometo de Tiotrópio/farmacologia
Fator de Crescimento Transformador beta/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3,5-dichloro-4-(2-(3-(cyclopropylmethoxy)-4-(difluoromethoxy)phenyl)-2-(3-(cyclopropylmethoxy)-4-(methylsulfonamido)benzoyloxy)ethyl)pyridine 1-oxide); 0 (Aminopyridines); 0 (Benzamides); 0 (Cholinergic Antagonists); 0 (Cyclopropanes); 0 (Phosphodiesterase 4 Inhibitors); 0 (Sulfonamides); 0 (Transforming Growth Factor beta); 0 (para-Aminobenzoates); 0P6C6ZOP5U (Roflumilast); 0W5ETF9M2K (Methacholine Chloride); EC 3.1.4.17 (Cyclic Nucleotide Phosphodiesterases, Type 4); V92SO9WP2I (Glycopyrrolate); XX112XZP0J (Tiotropium Bromide)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170918
[Lr] Data última revisão:
170918
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170610
[St] Status:MEDLINE
[do] DOI:10.1152/ajplung.00069.2017


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[PMID]:28546155
[Au] Autor:Xu Y; Cardell LO
[Ad] Endereço:Division of Ear, Nose, and Throat Diseases, Department of Clinical Sciences, Intervention and Technology, Karolinska Institutet, Stockholm, Sweden; and yuan.xu@ki.se.
[Ti] Título:Long-term nicotine exposure dampens LPS-induced nerve-mediated airway hyperreactivity in murine airways.
[So] Source:Am J Physiol Lung Cell Mol Physiol;313(3):L516-L523, 2017 Sep 01.
[Is] ISSN:1522-1504
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Nicotine is a major component of cigarette smoke. It causes addiction and is used clinically to aid smoke cessation. The aim of the present study is to investigate the effect of nicotine on lipopolysaccharide (LPS)-induced airway hyperreactivity (AHR) and to explore the potential involvement of neuronal mechanisms behind nicotine's effects in murine models in vivo and in vitro. BALB/c mice were exposed to nicotine in vivo via subcutaneous Alzet osmotic minipumps containing nicotine tartate salt solution (24 mg·kg ·day ) for 28 days. LPS (0.1 mg/ml, 20 µl) was administered intranasally for 3 consecutive days during the end of this period. Lung functions were measured with flexiVent. For the in vitro experiments, mice tracheae were organcultured with either nicotine (10 µM) or vehicle (DMSO, 0.1%) for 4 days. Contractile responses of the tracheal segments were measured in myographs following electric field stimulation (EFS; increasing frequencies of 0.2 to 12.8 Hz) before and after incubation with 10 µg/ml LPS for 1 h. Results showed that LPS induced AHR to methacholine in vivo and increased contractile responses to EFS in vitro. Interestingly, long-term nicotine exposure markedly dampened this LPS-induced AHR both in vitro and in vivo. Tetrodotoxin (TTX) inhibited LPS-induced AHR but did not further inhibit nicotine-suppressed AHR in vivo. In conclusion, long-term nicotine exposure dampened LPS-induced AHR. The effect of nicotine was mimicked by TTX, suggesting the involvement of neuronal mechanisms. This information might be used for evaluating the long-term effects of nicotine and further exploring of how tobacco products interact with bacterial airway infections.
[Mh] Termos MeSH primário: Hiper-Reatividade Brônquica/patologia
Pulmão/patologia
Tecido Nervoso/efeitos dos fármacos
Nicotina/farmacologia
[Mh] Termos MeSH secundário: Animais
Líquido da Lavagem Broncoalveolar
Colágeno/metabolismo
Estimulação Elétrica
Feminino
Inflamação/patologia
Lipopolissacarídeos
Pulmão/efeitos dos fármacos
Cloreto de Metacolina/farmacologia
Camundongos
Camundongos Endogâmicos BALB C
Técnicas de Cultura de Órgãos
Mecânica Respiratória/efeitos dos fármacos
Tetrodotoxina/toxicidade
Fatores de Tempo
Receptor 4 Toll-Like/metabolismo
Traqueia/efeitos dos fármacos
Traqueia/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Lipopolysaccharides); 0 (Toll-Like Receptor 4); 0W5ETF9M2K (Methacholine Chloride); 4368-28-9 (Tetrodotoxin); 6M3C89ZY6R (Nicotine); 9007-34-5 (Collagen)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170918
[Lr] Data última revisão:
170918
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170527
[St] Status:MEDLINE
[do] DOI:10.1152/ajplung.00222.2016


  7 / 5002 MEDLINE  
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[PMID]:28514613
[Au] Autor:Cahill KN; Katz HR; Cui J; Lai J; Kazani S; Crosby-Thompson A; Garofalo D; Castro M; Jarjour N; DiMango E; Erzurum S; Trevor JL; Shenoy K; Chinchilli VM; Wechsler ME; Laidlaw TM; Boyce JA; Israel E
[Ad] Endereço:From Brigham and Women's Hospital, Harvard Medical School, Boston (K.N.C., H.R.K., J.C., J.L., A.C.-T., D.G., T.M.L., J.A.B., E.I.), and Novartis Institutes for BioMedical Research, Cambridge (S.K.) - both in Massachusetts; Washington University, St. Louis (M.C.); University of Wisconsin, Madison (N
[Ti] Título:KIT Inhibition by Imatinib in Patients with Severe Refractory Asthma.
[So] Source:N Engl J Med;376(20):1911-1920, 2017 05 18.
[Is] ISSN:1533-4406
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Mast cells are present in the airways of patients who have severe asthma despite glucocorticoid treatment; these cells are associated with disease characteristics including poor quality of life and inadequate asthma control. Stem cell factor and its receptor, KIT, are central to mast-cell homeostasis. We conducted a proof-of-principle trial to evaluate the effect of imatinib, a KIT inhibitor, on airway hyperresponsiveness, a physiological marker of severe asthma, as well as on airway mast-cell numbers and activation in patients with severe asthma. METHODS: We conducted a randomized, double-blind, placebo-controlled, 24-week trial of imatinib in patients with poorly controlled severe asthma who had airway hyperresponsiveness despite receiving maximal medical therapy. The primary end point was the change in airway hyperresponsiveness, measured as the concentration of methacholine required to decrease the forced expiratory volume in 1 second by 20% (PC ). Patients also underwent bronchoscopy. RESULTS: Among the 62 patients who underwent randomization, imatinib treatment reduced airway hyperresponsiveness to a greater extent than did placebo. At 6 months, the methacholine PC increased by a mean (±SD) of 1.73±0.60 doubling doses in the imatinib group, as compared with 1.07±0.60 doubling doses in the placebo group (P=0.048). Imatinib also reduced levels of serum tryptase, a marker of mast-cell activation, to a greater extent than did placebo (decrease of 2.02±2.32 vs. 0.56±1.39 ng per milliliter, P=0.02). Airway mast-cell counts declined in both groups. Muscle cramps and hypophosphatemia were more common in the imatinib group than in the placebo group. CONCLUSIONS: In patients with severe asthma, imatinib decreased airway hyperresponsiveness, mast-cell counts, and tryptase release. These results suggest that KIT-dependent processes and mast cells contribute to the pathobiologic basis of severe asthma. (Funded by the National Institutes of Health and others; ClinicalTrials.gov number, NCT01097694 .).
[Mh] Termos MeSH primário: Asma/tratamento farmacológico
Mesilato de Imatinib/uso terapêutico
Mastócitos/metabolismo
Inibidores de Proteínas Quinases/uso terapêutico
[Mh] Termos MeSH secundário: Adulto
Asma/imunologia
Asma/fisiopatologia
Hiper-Reatividade Brônquica/tratamento farmacológico
Testes de Provocação Brônquica
Contagem de Células
Método Duplo-Cego
Feminino
Volume Expiratório Forçado/efeitos dos fármacos
Seres Humanos
Mesilato de Imatinib/efeitos adversos
Masculino
Cloreto de Metacolina
Meia-Idade
Inibidores de Proteínas Quinases/efeitos adversos
Qualidade de Vida
Triptases/sangue
Triptases/secreção
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Protein Kinase Inhibitors); 0W5ETF9M2K (Methacholine Chloride); 8A1O1M485B (Imatinib Mesylate); EC 3.4.21.59 (Tryptases)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171118
[Lr] Data última revisão:
171118
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170518
[Cl] Clinical Trial:ClinicalTrial
[St] Status:MEDLINE
[do] DOI:10.1056/NEJMoa1613125


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[PMID]:28419121
[Au] Autor:Char JE; Dunn C; Davies Z; Milla C; Moss RB; Wine JJ
[Ad] Endereço:Cystic Fibrosis Research Laboratory, Stanford University, Stanford, California, United States of America.
[Ti] Título:The magnitude of ivacaftor effects on fluid secretion via R117H-CFTR channels: Human in vivo measurements.
[So] Source:PLoS One;12(4):e0175486, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We optically measured effects of orally available ivacaftor (Kalydeco®) on sweat rates of identified glands in 3 R117H subjects, each having a unique set of additional mutations, and compared them with 5 healthy control subjects tested contemporaneously. We injected ß-adrenergic agonists intradermally to stimulate CFTR-dependent 'C-sweat' and methacholine to stimulate 'M-sweat', which persists in CF subjects. We focused on an R117H-7T/F508del subject who produced quantifiable C-sweat off ivacaftor and was available for 1 blinded, 3 off ivacaftor, and 3 on ivacaftor tests, allowing us to estimate in vivo fold-increase in sweat rates produced by ivacaftor's effect on the open probability (PO) of R117H-CFTR. Measured sweat rates must be corrected for sweat losses. With estimated sweat losses of 0.023 to 0.08 nl·gland-1·min-1, ivacaftor increased the average C-sweat rates 3-7 fold, and estimated function as % of WT were 4.1-12% off ivacaftor and 21.9-32% on ivacaftor (larger values reflect increased loss estimates). Based on single tests, an R117H-7T/ R117H-7T subject showed 6-9% WT function off ivacaftor and 28-43% on ivacaftor. Repeat testing of an R117H-5T/F508del subject detected only trace responding to ivacaftor. We conclude that in vivo, R117H PO is strongly increased by ivacaftor, but channel number, mainly determined by variable deletion of exon 10, has a marked influence on outcomes.
[Mh] Termos MeSH primário: Aminofenóis/farmacologia
Regulador de Condutância Transmembrana em Fibrose Cística/metabolismo
Mutação
Quinolonas/farmacologia
Suor/secreção
Sudorese/efeitos dos fármacos
[Mh] Termos MeSH secundário: Administração Oral
Agonistas Adrenérgicos beta/administração & dosagem
Agonistas Adrenérgicos beta/farmacologia
Adulto
Aminofenóis/administração & dosagem
Análise de Variância
Agonistas dos Canais de Cloreto/administração & dosagem
Agonistas dos Canais de Cloreto/farmacologia
Regulador de Condutância Transmembrana em Fibrose Cística/genética
Éxons/genética
Feminino
Deleção de Genes
Seres Humanos
Injeções Intradérmicas
Ativação do Canal Iônico/efeitos dos fármacos
Ativação do Canal Iônico/genética
Masculino
Cloreto de Metacolina/administração & dosagem
Cloreto de Metacolina/farmacologia
Agonistas Muscarínicos/administração & dosagem
Agonistas Muscarínicos/farmacologia
Quinolonas/administração & dosagem
Sudorese/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic beta-Agonists); 0 (Aminophenols); 0 (Chloride Channel Agonists); 0 (Muscarinic Agonists); 0 (Quinolones); 0W5ETF9M2K (Methacholine Chloride); 126880-72-6 (Cystic Fibrosis Transmembrane Conductance Regulator); 1Y740ILL1Z (ivacaftor)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170522
[Lr] Data última revisão:
170522
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170419
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0175486


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[PMID]:28408655
[Au] Autor:Borander AK; Voie ØA; Longva K; Danielsen TE; Grahnstedt S; Sandvik L; Kongerud J; Sikkeland LIB
[Ad] Endereço:Department of Environmental and Occupational Medicine, Oslo University Hospital, Ullevål, Oslo, Norway.
[Ti] Título:Military small arms fire in association with acute decrements in lung function.
[So] Source:Occup Environ Med;74(9):639-644, 2017 Sep.
[Is] ISSN:1470-7926
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: After introduction of unleaded ammunition, Norwegian Armed Forces received reports of acute respiratory symptoms in soldiers after exposure to fumes from firing the standard weapon, HK416. The aim of the present study was to examine lung function before and after exposure to fumes from HK416 in a double-blinded standardised study design using three different types of ammunition. METHODS: Fifty-four healthy, non-smoking male volunteers (19-62 years) fired the weapons for 60 min with either leaded, unleaded or 'modified' unleaded ammunition. Gaseous and particulate emissions were monitored. Spirometry and exhaled nitric oxide (eNO) were performed within 14 days before (T0), shortly after (T1) and 24 hours after (T2) shooting. Methacholine provocation and diffusing capacity of carbon monoxide (DLCO) were carried out at T0 and T2. RESULTS: The mean forced expiratory volume in 1 s on a group level was significantly reduced both at T1 and T2 compared with T0, with means and 95% CI of 226 mL (158 to 294 mL) and 285 mL (218 to 351 mL), respectively. The same significant pattern was seen for DLCO, forced vital capacity and eNO. The methacholine test indicated a slight increase in bronchial hyper-reactivity. However, there were no significant differences between types of ammunition used. CONCLUSION: Exposure to fumes from military weapons might be a respiratory hazard for soldiers who do live-fire training regularly or are in a closed combat environment.
[Mh] Termos MeSH primário: Poluentes Atmosféricos/efeitos adversos
Armas de Fogo
Chumbo/efeitos adversos
Pulmão/efeitos dos fármacos
Militares
Exposição Ocupacional/efeitos adversos
[Mh] Termos MeSH secundário: Adulto
Brônquios/efeitos dos fármacos
Brônquios/fisiopatologia
Monóxido de Carbono/metabolismo
Método Duplo-Cego
Expiração
Volume Expiratório Forçado
Gases/efeitos adversos
Seres Humanos
Pulmão/fisiopatologia
Masculino
Cloreto de Metacolina/farmacologia
Meia-Idade
Óxido Nítrico/metabolismo
Noruega
Material Particulado/efeitos adversos
Espirometria
Capacidade Vital
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Air Pollutants); 0 (Gases); 0 (Particulate Matter); 0W5ETF9M2K (Methacholine Chloride); 2P299V784P (Lead); 31C4KY9ESH (Nitric Oxide); 7U1EE4V452 (Carbon Monoxide)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170901
[Lr] Data última revisão:
170901
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170415
[St] Status:MEDLINE
[do] DOI:10.1136/oemed-2016-104207


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[PMID]:28360111
[Au] Autor:Larcombe AN; Janka MA; Mullins BJ; Berry LJ; Bredin A; Franklin PJ
[Ad] Endereço:Telethon Kids Institute, University of Western Australia, Subiaco, Western Australia, Australia; alexander.larcombe@telethonkids.org.au.
[Ti] Título:The effects of electronic cigarette aerosol exposure on inflammation and lung function in mice.
[So] Source:Am J Physiol Lung Cell Mol Physiol;313(1):L67-L79, 2017 Jul 01.
[Is] ISSN:1522-1504
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Electronic cigarette usage is increasing worldwide, yet there is a paucity of information on the respiratory health effects of electronic cigarette aerosol exposure. This study aimed to assess whether exposure to electronic cigarette (e-cigarette) aerosol would alter lung function and pulmonary inflammation in mice and to compare the severity of any alterations with mice exposed to mainstream tobacco smoke. Female BALB/c mice were exposed for 8 wk to tobacco smoke, medical air (control), or one of four different types of e-cigarette aerosol. E-cigarette aerosols varied depending on nicotine content (0 or 12 mg/ml) and the main excipient (propylene glycol or glycerin). Twenty-four hours after the final exposure, we measured pulmonary inflammation, lung volume, lung mechanics, and responsiveness to methacholine. Mice exposed to tobacco cigarette smoke had increased pulmonary inflammation and responsiveness to methacholine compared with air controls. Mice exposed to e-cigarette aerosol did not have increased inflammation but did display decrements in parenchymal lung function at both functional residual capacity and high transrespiratory pressures. Mice exposed to glycerin-based e-cigarette aerosols were also hyperresponsive to methacholine regardless of the presence or absence of nicotine. This study shows, for the first time, that exposure to e-cigarette aerosol during adolescence and early adulthood is not harmless to the lungs and can result in significant impairments in lung function.
[Mh] Termos MeSH primário: Aerossóis/efeitos adversos
Sistemas Eletrônicos de Liberação de Nicotina/efeitos adversos
Inflamação/patologia
Inflamação/fisiopatologia
Pulmão/patologia
Pulmão/fisiopatologia
[Mh] Termos MeSH secundário: Resistência das Vias Respiratórias/efeitos dos fármacos
Animais
Peso Corporal/efeitos dos fármacos
Elasticidade
Feminino
Capacidade Residual Funcional/efeitos dos fármacos
Cromatografia Gasosa-Espectrometria de Massas
Mediadores da Inflamação/metabolismo
Cloreto de Metacolina/farmacologia
Camundongos Endogâmicos BALB C
Tamanho do Órgão
Pletismografia
Hipersensibilidade Respiratória/complicações
Hipersensibilidade Respiratória/patologia
Hipersensibilidade Respiratória/fisiopatologia
Fumar/efeitos adversos
Tórax/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aerosols); 0 (Inflammation Mediators); 0W5ETF9M2K (Methacholine Chloride)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170401
[St] Status:MEDLINE
[do] DOI:10.1152/ajplung.00203.2016



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