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[PMID]:27775689
[Au] Autor:Yang J; Wang T; Li Y; Yao W; Ji X; Wu Q; Han L; Han R; Yan W; Yuan J; Ni C
[Ad] Endereço:Department of Occupational Medicine and Environmental Health and Key Laboratory of Modern Toxicology of Ministry of Education, School of Public Health, Nanjing Medical University, Nanjing, China.
[Ti] Título:Earthworm extract attenuates silica-induced pulmonary fibrosis through Nrf2-dependent mechanisms.
[So] Source:Lab Invest;96(12):1279-1300, 2016 12.
[Is] ISSN:1530-0307
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Silicosis is an occupational pulmonary fibrosis caused by inhalation of silica (SiO ) and there are no ideal drugs to treat this disease. Earthworm extract (EE), a natural nutrient, has been reported to have anti-inflammatory, antioxidant, and anti-apoptosis effects. The purpose of the current study was to test the protective effects of EE against SiO -induced pulmonary fibrosis and to explore the underlying mechanisms using both in vivo and in vitro models. We found that treatment with EE significantly reduced lung inflammation and fibrosis and improved lung structure and function in SiO -instilled mice. Further mechanistic investigations revealed that EE administration markedly inhibited SiO -induced oxidative stress, mitochondrial apoptotic pathway, and epithelial-mesenchymal transition in HBE and A549 cells. Furthermore, we demonstrate that Nrf2 activation partly mediates the interventional effects of EE against SiO -induced pulmonary fibrosis. Our study has identified EE to be a potential anti-oxidative, anti-inflammatory, and anti-fibrotic drug for silicosis.
[Mh] Termos MeSH primário: Antioxidantes/uso terapêutico
Modelos Animais de Doenças
Pulmão/efeitos dos fármacos
Materia Medica/uso terapêutico
Oligoquetos/química
Fibrose Pulmonar/prevenção & controle
Silicose/tratamento farmacológico
Extratos de Tecidos/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Anti-Inflamatórios não Esteroides/administração & dosagem
Anti-Inflamatórios não Esteroides/farmacologia
Anti-Inflamatórios não Esteroides/uso terapêutico
Antioxidantes/administração & dosagem
Antioxidantes/farmacologia
Apoptose/efeitos dos fármacos
Linhagem Celular
Células Cultivadas
Transição Epitelial-Mesenquimal/efeitos dos fármacos
Injeções Intraperitoneais
Pulmão/metabolismo
Pulmão/patologia
Pulmão/fisiopatologia
Masculino
Materia Medica/administração & dosagem
Materia Medica/farmacologia
Camundongos Endogâmicos C57BL
Fator 2 Relacionado a NF-E2/agonistas
Fator 2 Relacionado a NF-E2/antagonistas & inibidores
Fator 2 Relacionado a NF-E2/genética
Fator 2 Relacionado a NF-E2/metabolismo
Estresse Oxidativo/efeitos dos fármacos
Fibrose Pulmonar/etiologia
Fibrose Pulmonar/imunologia
Interferência de RNA
Distribuição Aleatória
Mucosa Respiratória/citologia
Mucosa Respiratória/efeitos dos fármacos
Mucosa Respiratória/metabolismo
Mucosa Respiratória/patologia
Silicose/metabolismo
Silicose/patologia
Silicose/fisiopatologia
Organismos Livres de Patógenos Específicos
Extratos de Tecidos/administração & dosagem
Extratos de Tecidos/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Antioxidants); 0 (Materia Medica); 0 (NF-E2-Related Factor 2); 0 (Tissue Extracts)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE
[do] DOI:10.1038/labinvest.2016.101


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[PMID]:27773453
[Au] Autor:Liu Y; Vela M; Rudakevych T; Wigfield C; Garrity E; Saunders MR
[Ad] Endereço:Pritzker School of Medicine, University of Chicago, Chicago, Illinois, USA.
[Ti] Título:Patient factors associated with lung transplant referral and waitlist for patients with cystic fibrosis and pulmonary fibrosis.
[So] Source:J Heart Lung Transplant;36(3):264-271, 2017 Mar.
[Is] ISSN:1557-3117
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Since 2005, the Lung Allocation Score (LAS) has prioritized patient benefit and post-transplant survival, reducing waitlist to transplant time to <200 days and decreasing mortality on the waitlist. A current challenge is the wait for the waitlist-the time between the patient's transplant-eligible diagnosis and waitlist registration. METHODS: We investigated whether sociodemographic (age, sex, race, insurance, marital status, median household income) and clinical (forced expiratory volume in 1 second [FEV ] percent of predicted, body mass index, depression/anxiety, alcohol/substance misuse, absolute/relative contraindications) factors influenced referral and waitlist registration. We conducted a retrospective cohort study through chart review of hospitalized patients on the University of Chicago general medicine service from 2006 to 2014 who met transplant-eligible criteria and ICD-9 billing codes for cystic fibrosis (CF) and pulmonary fibrosis (PF). We analyzed the times from transplant eligibility to referral, work-up and waitlisting using Kaplan-Meier curves and log-rank tests. RESULTS: Overall, the referral rate for transplant-eligible patients was 64%. Of those referred, approximately 36% reach the lung transplant waitlist. Referred CF patients were significantly more likely to reach the transplant waitlist than PF patients (CF 60% vs PF 22%, p < 0.05). In addition, CF patients had a shorter wait from transplant eligibility to waitlist than PF patients (329 vs 2,369 days, respectively [25th percentile], p < 0.05). Patients with PF and CF both faced delays from eligibility to referral and waitlist. CONCLUSIONS: Quality improvement efforts are needed to better identify and refer appropriate patients for lung transplant evaluation. Targeted interventions may facilitate more efficient evaluation completion and waitlist appearance.
[Mh] Termos MeSH primário: Fibrose Cística/cirurgia
Transplante de Pulmão/métodos
Fibrose Pulmonar/cirurgia
Encaminhamento e Consulta/estatística & dados numéricos
Listas de Espera
[Mh] Termos MeSH secundário: Centros Médicos Acadêmicos
Adulto
Estudos de Coortes
Comorbidade
Fibrose Cística/diagnóstico
Fibrose Cística/mortalidade
Feminino
Rejeição de Enxerto
Sobrevivência de Enxerto
Seres Humanos
Cobertura do Seguro
Estimativa de Kaplan-Meier
Transplante de Pulmão/mortalidade
Masculino
Meia-Idade
Seleção de Pacientes
Fibrose Pulmonar/diagnóstico
Fibrose Pulmonar/mortalidade
Testes de Função Respiratória
Estudos Retrospectivos
Medição de Risco
Índice de Gravidade de Doença
Estatísticas não Paramétricas
Análise de Sobrevida
Estados Unidos
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


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[PMID]:29364918
[Au] Autor:Chamorro V; Morales-Cano D; Milara J; Barreira B; Moreno L; Callejo M; Mondejar-Parreño G; Esquivel-Ruiz S; Cortijo J; Cogolludo Á; Barberá JA; Perez-Vizcaino F
[Ad] Endereço:Departamento de Farmacología. Facultad de Medicina, Universidad Complutense de Madrid, Madrid, Spain.
[Ti] Título:Riociguat versus sildenafil on hypoxic pulmonary vasoconstriction and ventilation/perfusion matching.
[So] Source:PLoS One;13(1):e0191239, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Current treatment with vasodilators for pulmonary hypertension associated with respiratory diseases is limited by their inhibitory effect on hypoxic pulmonary vasoconstriction (HPV) and uncoupling effects on ventilation-perfusion (V'/Q'). Hypoxia is also a well-known modulator of the nitric oxide (NO) pathway, and may therefore differentially affect the responses to phosphodiesterase 5 (PDE5) inhibitors and soluble guanylyl cyclase (sGC) stimulators. So far, the effects of the sGC stimulator riociguat on HPV have been poorly characterized. MATERIALS AND METHODS: Contraction was recorded in pulmonary arteries (PA) in a wire myograph. Anesthetized rats were catheterized to record PA pressure. Ventilation and perfusion were analyzed by micro-CT-SPECT images in rats with pulmonary fibrosis induced by bleomycin. RESULTS: The PDE5 inhibitor sildenafil and the sGC stimulator riociguat similarly inhibited HPV in vitro and in vivo. Riociguat was more effective as vasodilator in isolated rat and human PA than sildenafil. Riociguat was ≈3-fold more potent under hypoxic conditions and it markedly inhibited HPV in vivo at a dose that barely affected the thromboxane A2 (TXA2) mimetic U46619-induced pressor responses. Pulmonary fibrosis was associated with V'/Q' uncoupling and riociguat did not affect the V'/Q' ratio. CONCLUSION: PDE5 inhibitors and sGC stimulators show a different vasodilator profile. Riociguat was highly effective and potentiated by hypoxia in rat and human PA. In vivo, riociguat preferentially inhibited hypoxic than non-hypoxic vasoconstriction. However, it did not worsen V'/Q' coupling in a rat model of pulmonary fibrosis.
[Mh] Termos MeSH primário: Hipóxia/tratamento farmacológico
Hipóxia/fisiopatologia
Artéria Pulmonar/efeitos dos fármacos
Artéria Pulmonar/fisiopatologia
Pirazóis/farmacologia
Pirimidinas/farmacologia
Citrato de Sildenafila/farmacologia
Vasodilatadores/farmacologia
Relação Ventilação-Perfusão/efeitos dos fármacos
[Mh] Termos MeSH secundário: Idoso
Animais
Modelos Animais de Doenças
Ativadores de Enzimas/farmacologia
Feminino
Seres Humanos
Hipertensão Pulmonar/tratamento farmacológico
Hipertensão Pulmonar/fisiopatologia
Técnicas In Vitro
Masculino
Meia-Idade
Inibidores da Fosfodiesterase 5/farmacologia
Fibrose Pulmonar/tratamento farmacológico
Fibrose Pulmonar/fisiopatologia
Ratos
Ratos Wistar
Guanilil Ciclase Solúvel/metabolismo
Vasoconstrição/efeitos dos fármacos
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Enzyme Activators); 0 (Phosphodiesterase 5 Inhibitors); 0 (Pyrazoles); 0 (Pyrimidines); 0 (Vasodilator Agents); BW9B0ZE037 (Sildenafil Citrate); EC 4.6.1.2 (Soluble Guanylyl Cyclase); RU3FE2Y4XI (riociguat)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180125
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191239


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[PMID]:28468623
[Au] Autor:Murray LA; Dunmore R; Camelo A; Da Silva CA; Gustavsson MJ; Habiel DM; Hackett TL; Hogaboam CM; Sleeman MA; Knight DA
[Ad] Endereço:Respiratory, Inflammation and Autoimmunity, MedImmune Ltd, Granta Park, Cambridge, CB21 6GH, United Kingdom. murrayl@medimmune.com.
[Ti] Título:Acute cigarette smoke exposure activates apoptotic and inflammatory programs but a second stimulus is required to induce epithelial to mesenchymal transition in COPD epithelium.
[So] Source:Respir Res;18(1):82, 2017 May 03.
[Is] ISSN:1465-993X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Smoking and aberrant epithelial responses are risk factors for lung cancer as well as chronic obstructive pulmonary disease and idiopathic pulmonary fibrosis. In these conditions, disease progression is associated with epithelial damage and fragility, airway remodelling and sub-epithelial fibrosis. The aim of this study was to assess the acute effects of cigarette smoke on epithelial cell phenotype and pro-fibrotic responses in vitro and in vivo. RESULTS: Apoptosis was significantly greater in unstimulated cells from COPD patients compared to control, but proliferation and CXCL8 release were not different. Cigarette smoke dose-dependently induced apoptosis, proliferation and CXCL8 release with normal epithelial cells being more responsive than COPD patient derived cells. Cigarette smoke did not induce epithelial-mesenchymal transition. In vivo, cigarette smoke exposure promoted epithelial apoptosis and proliferation. Moreover, mimicking a virus-induced exacerbation by exposing to mice to poly I:C, exaggerated the inflammatory responses, whereas expression of remodelling genes was similar in both. CONCLUSIONS: Collectively, these data indicate that cigarette smoke promotes epithelial cell activation and hyperplasia, but a secondary stimulus is required for the remodelling phenotype associated with COPD.
[Mh] Termos MeSH primário: Transição Epitelial-Mesenquimal/efeitos dos fármacos
Doença Pulmonar Obstrutiva Crônica/fisiopatologia
Fibrose Pulmonar/induzido quimicamente
Mucosa Respiratória/efeitos dos fármacos
Mucosa Respiratória/fisiopatologia
Fumaça/efeitos adversos
Produtos do Tabaco/envenenamento
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Seres Humanos
Camundongos
Camundongos Endogâmicos C57BL
Doença Pulmonar Obstrutiva Crônica/induzido quimicamente
Doença Pulmonar Obstrutiva Crônica/patologia
Fibrose Pulmonar/patologia
Fibrose Pulmonar/fisiopatologia
Mucosa Respiratória/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Smoke)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1186/s12931-017-0565-2


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[PMID]:28463231
[Au] Autor:Gaskill CF; Carrier EJ; Kropski JA; Bloodworth NC; Menon S; Foronjy RF; Taketo MM; Hong CC; Austin ED; West JD; Means AL; Loyd JE; Merryman WD; Hemnes AR; De Langhe S; Blackwell TS; Klemm DJ; Majka SM
[Ad] Endereço:Department of Medicine, Division of Allergy, Pulmonary and Critical Care Medicine or Division of Cardiovascular Medicine, Vanderbilt University Medical Center, Nashville, Tennessee USA.
[Ti] Título:Disruption of lineage specification in adult pulmonary mesenchymal progenitor cells promotes microvascular dysfunction.
[So] Source:J Clin Invest;127(6):2262-2276, 2017 Jun 01.
[Is] ISSN:1558-8238
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Pulmonary vascular disease is characterized by remodeling and loss of microvessels and is typically attributed to pathological responses in vascular endothelium or abnormal smooth muscle cell phenotypes. We have challenged this understanding by defining an adult pulmonary mesenchymal progenitor cell (MPC) that regulates both microvascular function and angiogenesis. The current understanding of adult MPCs and their roles in homeostasis versus disease has been limited by a lack of genetic markers with which to lineage label multipotent mesenchyme and trace the differentiation of these MPCs into vascular lineages. Here, we have shown that lineage-labeled lung MPCs expressing the ATP-binding cassette protein ABCG2 (ABCG2+) are pericyte progenitors that participate in microvascular homeostasis as well as adaptive angiogenesis. Activation of Wnt/ß-catenin signaling, either autonomously or downstream of decreased BMP receptor signaling, enhanced ABCG2+ MPC proliferation but suppressed MPC differentiation into a functional pericyte lineage. Thus, enhanced Wnt/ß-catenin signaling in ABCG2+ MPCs drives a phenotype of persistent microvascular dysfunction, abnormal angiogenesis, and subsequent exacerbation of bleomycin-induced fibrosis. ABCG2+ MPCs may, therefore, account in part for the aberrant microvessel function and remodeling that are associated with chronic lung diseases.
[Mh] Termos MeSH primário: Células Mesenquimais Estromais/fisiologia
Microvasos/fisiopatologia
[Mh] Termos MeSH secundário: Membro 2 da Subfamília G de Transportadores de Cassetes de Ligação de ATP/metabolismo
Animais
Receptores de Proteínas Morfogenéticas Ósseas Tipo II/metabolismo
Diferenciação Celular
Linhagem da Célula
Células Cultivadas
Seres Humanos
Pulmão/irrigação sanguínea
Camundongos Transgênicos
Microvasos/patologia
Neovascularização Patológica/metabolismo
Pericitos/fisiologia
Estabilidade Proteica
Fibrose Pulmonar/metabolismo
Fibrose Pulmonar/patologia
Vasoconstrição
Via de Sinalização Wnt
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ATP Binding Cassette Transporter, Sub-Family G, Member 2); 0 (Abcg2 protein, mouse); EC 2.7.11.30 (Bmpr2 protein, mouse); EC 2.7.11.30 (Bone Morphogenetic Protein Receptors, Type II)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE


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[PMID]:29278701
[Au] Autor:Chen C; Wang YY; Wang YX; Cheng MQ; Yin JB; Zhang X; Hong ZP
[Ad] Endereço:School of Pharmaceutical Sciences & Yunnan Key Laboratory of Pharmacology for Natural Products, Kunming Medical University, Kunming, Yunnan, China; Department of Urological Surgery, The 1st Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China.
[Ti] Título:Gentiopicroside ameliorates bleomycin-induced pulmonary fibrosis in mice via inhibiting inflammatory and fibrotic process.
[So] Source:Biochem Biophys Res Commun;495(4):2396-2403, 2018 01 22.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Pulmonary fibrosis (PF) is a chronic and ultimately fatal interstitial lung disease of various causes. The advent of nintedanib and pirfenidone provides treatment options for PF patients for the first time. However, the adverse effects of the two drugs such as gastrointestinal disorders and hepatic dysfunction often lead to treatment discontinuation. Gentiopicroside (GPS) is a natural secoiridoid glycoside from gentian species of medicinal plants, and has a variety of pharmacological activities, including hepatoprotective and cholagogic, anti-inflammatory, antinociceptive, and smooth muscle relaxing activities. The present study aimed to investigate the therapeutical effects of GPS on bleomycin (BLM)-induced PF in mice. Severe lung inflammation and fibrosis were observed in BLM-treated mice. GPS significantly ameliorated inflammatory and fibrotic responses in lungs of PF mice which were confirmed by histopathological examinations including light microscopy and transmission electron microscopy. Additionally, GPS significantly decreased the levels of inflammatory cytokines including TNF-α and IL-1ß in bronchoalveolar lavage fluid and reduced the content of hydroxyproline in lungs of PF mice. Furthermore, GPS significantly downregulated the expression of TGF-ß1 and CTGF in lungs of PF mice. In vitro, GPS inhibited epithelial-mesenchymal transition of A549 cells stimulated by TGF-ß1, in a dose-dependent manner. Our findings suggest that GPS has the potential as an ideal drug candidate for PF, as it has both anti-inflammatory and anti-fibrotic effects. Alveolar epithelial cells and TGF-ß1 may be the main target cells and molecule of GPS on BLM-induced PF, respectively.
[Mh] Termos MeSH primário: Glucosídeos Iridoides/administração & dosagem
Pulmão/imunologia
Pneumonia/imunologia
Pneumonia/prevenção & controle
Fibrose Pulmonar/imunologia
Fibrose Pulmonar/prevenção & controle
[Mh] Termos MeSH secundário: Animais
Anti-Inflamatórios/administração & dosagem
Bleomicina
Citocinas/imunologia
Relação Dose-Resposta a Droga
Fatores Imunológicos/imunologia
Pulmão/efeitos dos fármacos
Masculino
Camundongos
Pneumonia/induzido quimicamente
Fibrose Pulmonar/induzido quimicamente
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Cytokines); 0 (Immunologic Factors); 0 (Iridoid Glucosides); 0WE09Z21RC (gentiopicroside); 11056-06-7 (Bleomycin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171227
[St] Status:MEDLINE


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[PMID]:29388835
[Au] Autor:Durmus N; Grunig G
[Ad] Endereço:1 Department of Medicine, Division of Pulmonary Medicine New York University School of Medicine New York, New York and.
[Ti] Título:Polymorphonuclear Leukocytes in Pulmonary Hypertension and Fibrosis: Not Always What They Appear to Be.
[So] Source:Am J Respir Cell Mol Biol;58(2):135-137, 2018 02.
[Is] ISSN:1535-4989
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Hipertensão Pulmonar/metabolismo
Leucócitos/metabolismo
Fibrose Pulmonar/metabolismo
[Mh] Termos MeSH secundário: Seres Humanos
Hipertensão Pulmonar/patologia
Leucócitos/patologia
Fibrose Pulmonar/patologia
[Pt] Tipo de publicação:EDITORIAL
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180202
[St] Status:MEDLINE
[do] DOI:10.1165/rcmb.2017-0336ED


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[PMID]:29286855
[Au] Autor:McQuattie-Pimentel AC; Budinger GRS; Ballinger MN
[Ad] Endereço:1 Division of Pulmonary and Critical Care Northwestern University Chicago, Illinois and.
[Ti] Título:Monocyte-derived Alveolar Macrophages: The Dark Side of Lung Repair?
[So] Source:Am J Respir Cell Mol Biol;58(1):5-6, 2018 01.
[Is] ISSN:1535-4989
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Lesão Pulmonar/metabolismo
Pulmão/metabolismo
Macrófagos Alveolares/metabolismo
Monócitos/metabolismo
Fibrose Pulmonar/metabolismo
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Pulmão/patologia
Lesão Pulmonar/patologia
Lesão Pulmonar/fisiopatologia
Macrófagos Alveolares/patologia
Monócitos/patologia
Fibrose Pulmonar/patologia
Fibrose Pulmonar/fisiopatologia
[Pt] Tipo de publicação:EDITORIAL
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171230
[St] Status:MEDLINE
[do] DOI:10.1165/rcmb.2017-0328ED


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[PMID]:29411024
[Au] Autor:Blackley DJ; Reynolds LE; Short C; Carson R; Storey E; Halldin CN; Laney AS
[Ad] Endereço:Respiratory Health Division, National Institute for Occupational Safety and Health, Morgantown, West Virginia.
[Ti] Título:Progressive Massive Fibrosis in Coal Miners From 3 Clinics in Virginia.
[So] Source:JAMA;319(5):500-501, 2018 Feb 06.
[Is] ISSN:1538-3598
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Minas de Carvão
Doenças Profissionais/epidemiologia
Fibrose Pulmonar/epidemiologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Antracose/diagnóstico por imagem
Antracose/epidemiologia
Seres Humanos
Meia-Idade
Fibrose Pulmonar/diagnóstico por imagem
Virginia/epidemiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180208
[St] Status:MEDLINE
[do] DOI:10.1001/jama.2017.18444


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[PMID]:28459387
[Au] Autor:Jenkins RG; Moore BB; Chambers RC; Eickelberg O; Königshoff M; Kolb M; Laurent GJ; Nanthakumar CB; Olman MA; Pardo A; Selman M; Sheppard D; Sime PJ; Tager AM; Tatler AL; Thannickal VJ; White ES; ATS Assembly on Respiratory Cell and Molecular Biology
[Ti] Título:An Official American Thoracic Society Workshop Report: Use of Animal Models for the Preclinical Assessment of Potential Therapies for Pulmonary Fibrosis.
[So] Source:Am J Respir Cell Mol Biol;56(5):667-679, 2017 05.
[Is] ISSN:1535-4989
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Numerous compounds have shown efficacy in limiting development of pulmonary fibrosis using animal models, yet few of these compounds have replicated these beneficial effects in clinical trials. Given the challenges associated with performing clinical trials in patients with idiopathic pulmonary fibrosis (IPF), it is imperative that preclinical data packages be robust in their analyses and interpretations to have the best chance of selecting promising drug candidates to advance to clinical trials. The American Thoracic Society has convened a group of experts in lung fibrosis to discuss and formalize recommendations for preclinical assessment of antifibrotic compounds. The panel considered three major themes (choice of animal, practical considerations of fibrosis modeling, and fibrotic endpoints for evaluation). Recognizing the need for practical considerations, we have taken a pragmatic approach. The consensus view is that use of the murine intratracheal bleomycin model in animals of both genders, using hydroxyproline measurements for collagen accumulation along with histologic assessments, is the best-characterized animal model available for preclinical testing. Testing of antifibrotic compounds in this model is recommended to occur after the acute inflammatory phase has subsided (generally after Day 7). Robust analyses may also include confirmatory studies in human IPF specimens and validation of results in a second system using in vivo or in vitro approaches. The panel also strongly encourages the publication of negative results to inform the lung fibrosis community. These recommendations are for preclinical therapeutic evaluation only and are not intended to dissuade development of emerging technologies to better understand IPF pathogenesis.
[Mh] Termos MeSH primário: Congressos como Assunto
Modelos Animais de Doenças
Fibrose Pulmonar/terapia
Sociedades Médicas
[Mh] Termos MeSH secundário: Animais
Determinação de Ponto Final
Feminino
Seres Humanos
Masculino
Organismos Geneticamente Modificados
Reprodutibilidade dos Testes
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1707
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.1165/rcmb.2017-0096ST



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