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  1 / 3897 MEDLINE  
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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


  2 / 3897 MEDLINE  
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[PMID]:29480834
[Au] Autor:Zhang R; Ma G; Xu X; Liang L
[Ad] Endereço:Department of Respiratory Medicine, Sir Run Run Shaw Hospital, Medical School of Zhejiang University, Hangzhou, Zhejiang, China.
[Ti] Título:Percutaneous treatment for silicosis-induced pulmonary artery stenosis: A case report and review of the literature.
[So] Source:Medicine (Baltimore);97(2):e9469, 2018 Jan.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Exposure to crystalline silica results in silicosis with initiation and progression of pulmonary fibrosis. The impaired lung parenchyma leads to pulmonary arterial hypertension and increased pressure in the right ventricle of the heart. Usually, the silicosis may be followed by enlargement of hilar lymphnodes, but silicosis-induced pulmonary artery stenosis with severe pulmonary hypertension is rare. Percutaneous pulmonary artery stenting and balloon angioplasty were performed to relieve stenosis and pulmonary hypertension. METHODS: We report the case of a 52-year-old man who was admitted for persistent dyspnea for 2 years and progressive dyspnea for half a month. He had been a stonemason for 20 years. The computer tomography pulmonary angiography scan images showed partially fibrotic lungs with a disseminated nodular pattern and enlarged bilateral hilar and mediastinal lymphnodes. The echocardiogram and right heart catheterization confirmed the diagnosis of severe pulmonary arterial hypertension. RESULTS: Pulmonary angiograms showed severe stenosis of the proximal upper right and lower left pulmonary artery. Moderate stenosis occured in a branch of the lower right pulmonary artery and a branch of the upper left pulmonary artery. A total of 2 stents and 4 balloons were used to relieve lesions. The final angiograms showed a significantly increased pulmonary artery caliber. The clinical symptom and 6-minute walk distance of the patient were much improved. CONCLUSION: To our knowledge, this is the first reported case of percutaneous treatment for silicosis-induced pulmonary artery stenosis and pulmonary hypertension. The clinical symptom, 6-minute walking test, and vessel caliber at areas of stenosis improved significantly following stent implantation and balloon dilatation. However, the patient was followed up for a short period and long-term outcomes have not yet been sufficiently evaluated.
[Mh] Termos MeSH primário: Silicose/complicações
Estenose de Artéria Pulmonar/etiologia
Estenose de Artéria Pulmonar/terapia
[Mh] Termos MeSH secundário: Angioplastia com Balão
Seres Humanos
Masculino
Meia-Idade
Silicose/diagnóstico por imagem
Estenose de Artéria Pulmonar/diagnóstico por imagem
Stents
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180227
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009469


  3 / 3897 MEDLINE  
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[PMID]:28916165
[Au] Autor:Kato K; Zemskova MA; Hanss AD; Kim MM; Summer R; Kim KC
[Ad] Endereço:Department of Otolaryngology, University of Arizona College of Medicine, Tucson, AZ 85724, United States. Electronic address: kosukekato@email.arizona.edu.
[Ti] Título:Muc1 deficiency exacerbates pulmonary fibrosis in a mouse model of silicosis.
[So] Source:Biochem Biophys Res Commun;493(3):1230-1235, 2017 Nov 25.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: MUC1 (MUC in human and Muc in animals) is a membrane-tethered mucin expressed on the apical surface of lung epithelial cells. However, in the lungs of patients with interstitial lung disease, MUC1 is aberrantly expressed in hyperplastic alveolar type II epithelial (ATII) cells and alveolar macrophages (AM), and elevated levels of extracellular MUC1 are found in bronchoalveolar lavage (BAL) fluid and the serum of these patients. While pro-fibrotic effects of extracellular MUC1 have recently been described in cultured fibroblasts, the contribution of MUC1 to the pathobiology of pulmonary fibrosis is unknown. In this study, we hypothesized that MUC1 deficiency would reduce susceptibility to pulmonary fibrosis in a mouse model of silicosis. METHODS: We employed human MUC1 transgenic mice, Muc1 deficient mice and wild-type mice on C57BL/6 background in these studies. Some mice received a one-time dose of crystalline silica instilled into their oropharynx in order to induce pulmonary fibrosis and assess the effects of Muc1 deficiency on fibrotic and inflammatory responses in the lung. RESULTS: As previously described in other mouse models of pulmonary fibrosis, we found that extracellular MUC1 levels were markedly increased in whole lung tissues, BALF and serum of human MUC1 transgenic mice after silica. We also detected an increase in total MUC1 levels in the lungs of these mice, indicating that production as well as release contributed to elevated levels after lung injury. Immunohistochemical staining revealed that increased MUC1 expression was mostly confined to ATII cells and AMs in areas of fibrotic remodeling, illustrating a pattern similar to the expression of MUC1 in human fibrotic lung tissues. However, contrary to our hypothesis, we found that Muc1 deficiency resulted in a worsening of fibrotic remodeling in the mouse lung as judged by an increase in number of silicotic nodules, an increase in lung collagen deposition and an increase in the severity of pulmonary inflammation. CONCLUSIONS: Altogether, our results indicate that Muc1 has anti-fibrotic properties in the mouse lung and suggest that elevated levels of MUC1 in patients with interstitial lung disease may serve a protective role, which aims to limit the severity of tissue remodeling in the lung.
[Mh] Termos MeSH primário: Mucina-1/metabolismo
Fibrose Pulmonar/fisiopatologia
Silicose/fisiopatologia
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Seres Humanos
Pulmão/efeitos dos fármacos
Pulmão/metabolismo
Pulmão/patologia
Camundongos Endogâmicos C57BL
Camundongos Knockout
Camundongos Transgênicos
Mucina-1/genética
Pneumonia/genética
Pneumonia/patologia
Fibrose Pulmonar/induzido quimicamente
Dióxido de Silício/toxicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MUC1 protein, human); 0 (Mucin-1); 7631-86-9 (Silicon Dioxide)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171027
[Lr] Data última revisão:
171027
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170917
[St] Status:MEDLINE


  4 / 3897 MEDLINE  
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[PMID]:28727677
[Au] Autor:Mazurek JM; Wood JM; Schleiff PL; Weissman DN
[Ad] Endereço:Respiratory Health Division, National Institute for Occupational Safety and Health, CDC.
[Ti] Título:Surveillance for Silicosis Deaths Among Persons Aged 15-44 Years - United States, 1999-2015.
[So] Source:MMWR Morb Mortal Wkly Rep;66(28):747-752, 2017 Jul 21.
[Is] ISSN:1545-861X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Silicosis is usually a disease of long latency affecting mostly older workers; therefore, silicosis deaths in young adults (aged 15-44 years) suggests acute or accelerated disease.* To understand the circumstances surrounding silicosis deaths among young persons, CDC analyzed the underlying and contributing causes of death using multiple cause-of-death data (1999-2015) and industry and occupation information abstracted from death certificates (1999-2013). During 1999-2015, among 55 pneumoconiosis deaths of young adults with International Classification of Diseases, Tenth Revision (ICD-10) code J62 (pneumoconiosis due to dust containing silica), 38 (69%) had code J62.8 (pneumoconiosis due to other dust containing silica), and 17 (31%) had code J62.0 (pneumoconiosis due to talc dust) listed on their death certificate. Decedents whose cause of death code was J62.8 most frequently worked in the manufacturing and construction industries and production occupations where silica exposure is known to occur. Among the 17 decedents who had death certificates listing code J62.0 as cause of death, 13 had certificates with an underlying or a contributing cause of death code listed that indicated multiple drug use or drug overdose. In addition, 13 of the 17 death certificates listing code J62.0 as cause of death had information on decedent's industry and occupation; among the 13 decedents, none worked in talc exposure-associated jobs, suggesting that their talc exposure was nonoccupational. Examining detailed information on causes of death (including external causes) and industry and occupation of decedents is essential for identifying silicosis deaths associated with occupational exposures and reducing misclassification of silicosis mortality.
[Mh] Termos MeSH primário: Vigilância da População
Silicose/mortalidade
[Mh] Termos MeSH secundário: Adolescente
Adulto
Feminino
Seres Humanos
Masculino
Estados Unidos/epidemiologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170724
[Lr] Data última revisão:
170724
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170721
[St] Status:MEDLINE
[do] DOI:10.15585/mmwr.mm6628a2


  5 / 3897 MEDLINE  
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[PMID]:28524802
[Au] Autor:Anlar HG; Bacanli M; Iritas S; Bal C; Kurt T; Tutkun E; Hinc Yilmaz O; Basaran N
[Ad] Endereço:a Department of Pharmaceutical Toxicology , Faculty of Pharmacy, Hacettepe University , Ankara , Turkey.
[Ti] Título:Effects of Occupational Silica Exposure on OXIDATIVE Stress and Immune System Parameters in Ceramic Workers in TURKEY.
[So] Source:J Toxicol Environ Health A;80(13-15):688-696, 2017.
[Is] ISSN:1528-7394
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Silica is the second most common element after oxygen, and therefore, exposures to crystalline silica dust occur in a large variety of occupations such as metal foundries, constructions, and ceramic, quarry, and pottery industries. Since crystalline silica exposure has been linked with silicosis, lung cancer, and other pulmonary diseases, adverse effect attributed to this element has be a cause for concern worldwide. Silica dust exposure in workers is still considered to be important health problem especially in developing countries. The aim of the study was to investigate the effects of occupational silica exposure on oxidative stress parameters including the activities of superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR), glutathione peroxidase (GPx), and levels of total glutathione (GSH) and thiobarbituric acid reactive substance (TBARS) as well as immune system parameters such as interleukin (IL)-1α, IL-1ß, IL-2, IL-4, IL-6, and IL-10 and tumor necrosis factor (TNF)-α in Turkish ceramic workers. In this study, nearly 50% of Turkish ceramic workers were diagnosed with silicosis. Eighty-four percent of these silicotic workers were found to present with profusion category 1 silicosis, whereas controls (n = 81) all displayed normal chest radiographs. Data demonstrated a significant decrease in levels of GSH and activities of CAT, SOD, and GPx, but a significant increase in MDA levels and activity of GR in all workers. Further, workers possessed significantly higher levels of IL-1α, IL-1ß, IL-2, IL-4, IL-6, IL-10, and TNF-α. These observations suggest that ceramic workers may have impaired antioxidant/oxidant status and activated immune system indicative of inflammatory responses.
[Mh] Termos MeSH primário: Cerâmica/efeitos adversos
Sistema Imunitário/efeitos dos fármacos
Exposição Ocupacional/efeitos adversos
Estresse Oxidativo/efeitos dos fármacos
Dióxido de Silício/efeitos adversos
[Mh] Termos MeSH secundário: Adolescente
Adulto
Catalase/sangue
Glutationa/sangue
Glutationa Peroxidase/sangue
Glutationa Redutase/sangue
Seres Humanos
Interleucina-10/sangue
Interleucina-1alfa/sangue
Interleucina-1beta/sangue
Interleucina-2/sangue
Interleucina-4/sangue
Interleucina-6/sangue
Masculino
Exposição Ocupacional/estatística & dados numéricos
Silicose/epidemiologia
Silicose/etiologia
Superóxido Dismutase/sangue
Substâncias Reativas com Ácido Tiobarbitúrico/análise
Turquia/epidemiologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-1alpha); 0 (Interleukin-1beta); 0 (Interleukin-2); 0 (Interleukin-6); 0 (Thiobarbituric Acid Reactive Substances); 130068-27-8 (Interleukin-10); 207137-56-2 (Interleukin-4); 7631-86-9 (Silicon Dioxide); EC 1.11.1.6 (Catalase); EC 1.11.1.9 (Glutathione Peroxidase); EC 1.15.1.1 (Superoxide Dismutase); EC 1.8.1.7 (Glutathione Reductase); GAN16C9B8O (Glutathione)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170520
[St] Status:MEDLINE
[do] DOI:10.1080/15287394.2017.1286923


  6 / 3897 MEDLINE  
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[PMID]:28513256
[Au] Autor:Hoet P; Desvallées L; Lison D
[Ad] Endereço:a Louvain Center for Toxicology and Applied Pharmacology (LTAP), Institute of Experimental and Clinical Research (IREC), Université Catholique de Louvain , Bruxelles , Belgium.
[Ti] Título:Do current OELs for silica protect from obstructive lung impairment? A critical review of epidemiological data.
[So] Source:Crit Rev Toxicol;47(8):650-677, 2017 Sep.
[Is] ISSN:1547-6898
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Inhalation of respirable crystalline silica (RCS) can lead to serious health effects such as silicosis and lung cancer. There also seems to be a general consensus to consider that RCS exposure is associated with obstructive lung impairment or chronic obstructive pulmonary disease (COPD), a leading cause of mortality, morbidity, and disability worldwide. It is, however, not clear whether occupational exposure levels (OELs), generally set to prevent silicosis, also protect workers from developing an obstructive impairment. This review aims at clarifying the potential relationship between RCS exposure and obstructive lung impairment as defined by spirometry. Eleven studies that reported both silica exposure levels and spirometry results were identified. We systematically extracted data pertaining to (a) the population studied, (b) level of exposure to RCS and other pollutants, (c) spirometry procedure and interpretation, and (d) methodology used to investigate the relationship between RCS exposure and spirometry. These studies add supporting evidence in favor of a qualitative association between occupational activities exposing to RCS and obstructive lung dysfunction. However, no well-founded quantitative estimate can be drawn from these investigations; the available relevant literature does not allow defining a RCS exposure threshold associated with an increased risk of obstructive lung dysfunction, as defined by spirometry, in workers without silicosis. Further research is needed, but, as highlighted in this review, conducting epidemiological studies with both valid exposure and outcome measurements is a real challenge.
[Mh] Termos MeSH primário: Exposição Ocupacional/prevenção & controle
Doença Pulmonar Obstrutiva Crônica/epidemiologia
Dióxido de Silício/toxicidade
[Mh] Termos MeSH secundário: Estudos Epidemiológicos
Seres Humanos
Neoplasias Pulmonares/epidemiologia
Neoplasias Pulmonares/prevenção & controle
Doença Pulmonar Obstrutiva Crônica/prevenção & controle
Silicose/epidemiologia
Silicose/prevenção & controle
Espirometria
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
7631-86-9 (Silicon Dioxide)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170518
[St] Status:MEDLINE
[do] DOI:10.1080/10408444.2017.1315363


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[PMID]:28355417
[Au] Autor:Ziemann C; Escrig A; Bonvicini G; Ibáñez MJ; Monfort E; Salomoni A; Creutzenberg O
[Ad] Endereço:Fraunhofer Institute for Toxicology and Experimental Medicine ITEM, Nikolai-Fuchs-Str. 1, 30625 Hannover, Germany.
[Ti] Título:Organosilane-Based Coating of Quartz Species from the Traditional Ceramics Industry: Evidence of Hazard Reduction Using In Vitro and In Vivo Tests.
[So] Source:Ann Work Expo Health;61(4):468-480, 2017 May 01.
[Is] ISSN:2398-7316
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The exposure to respirable crystalline silica (RCS), e.g. quartz, in industrial settings can induce silicosis and may cause tumours in chronic periods. Consequently, RCS in the form of quartz and cristobalite has been classified as human lung carcinogen category 1 by the International Agency for Research on Cancer in 1997, acknowledging differences in hazardous potential depending on source as well as chemical, thermal, and mechanical history. The physico-chemical determinants of quartz toxicity are well understood and are linked to density and abundance of surface silanol groups/radicals. Hence, poly-2-vinylpyridine-N-oxide and aluminium lactate, which effectively block highly reactive silanol groups at the quartz surface, have formerly been introduced as therapeutic approaches in the occupational field. In the traditional ceramics industry, quartz-containing raw materials are indispensable for the manufacturing process, and workers are potentially at risk of developing quartz-related lung diseases. Therefore, in the present study, two organosilanes, i.e. Dynasylan® PTMO and Dynasylan® SIVO 160, were tested as preventive, covalent quartz-coating agents to render ceramics production safer without loss in product quality. Coating effectiveness and coating stability (up to 1 week) in artificial alveolar and lysosomal fluids were first analysed in vitro, using the industrially relevant quartz Q1 as RCS model, quartz DQ12 as a positive control, primary rat alveolar macrophages as cellular model system (75 µg cm-2; 4 h of incubation ± aluminium lactate to verify quartz-related effects), and lactate dehydrogenase release and DNA strand break induction (alkaline comet assay) as biological endpoints. In vitro results with coated quartz were confirmed in a 90-day intratracheal instillation study in rats with inflammatory parameters as most relevant readouts. The results of the present study indicate that in particular Dynasylan® SIVO 160 (0.2% w/w of quartz) was able to effectively and stably block toxicity of biologically active quartz species without interfering with technical process quality of certain ceramic products. In conclusion, covalent organosilane coatings of quartz might represent a promising strategy to increase workers' safety in the traditional ceramics industry.
[Mh] Termos MeSH primário: Poluentes Ocupacionais do Ar/toxicidade
Exposição Ocupacional
Quartzo/toxicidade
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Seres Humanos
Indústrias
Pulmão/efeitos dos fármacos
Macrófagos Alveolares/efeitos dos fármacos
Tamanho da Partícula
Quartzo/administração & dosagem
Ratos
Dióxido de Silício/toxicidade
Silicose/patologia
Propriedades de Superfície
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Air Pollutants, Occupational); 14808-60-7 (Quartz); 7631-86-9 (Silicon Dioxide)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170330
[St] Status:MEDLINE
[do] DOI:10.1093/annweh/wxx014


  8 / 3897 MEDLINE  
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[PMID]:28350071
[Au] Autor:Peng HB; Wang RX; Deng HJ; Wang YH; Tang JD; Cao FY; Wang JH
[Ad] Endereço:Medical Experimental Center of Jitang College, North China University of Science and Technology, Tangshan, Hebei 063210, P.R. China.
[Ti] Título:Protective effects of oleanolic acid on oxidative stress and the expression of cytokines and collagen by the AKT/NF­κB pathway in silicotic rats.
[So] Source:Mol Med Rep;15(5):3121-3128, 2017 May.
[Is] ISSN:1791-3004
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:Oleanolic acid (OA), a natural pentacyclic triterpenoid, has been reported to have several benefits and medicinal properties. However, its protective effects against silica­induced lung injury and fibrosis remain to be elucidated. The aim of the present study was to investigate the effects of OA on oxidative stress, and the expression of cytokines and collagen in silicotic rats. Male rats were induced by intratracheal instillation of silicosis (250 mg/kg), with the exception of the control group (NS). The rats in the OA group were intragastrically administered with OA (60 mg/kg/d). The rats in the solvent control group were gavaged daily with 0.6% sodium carboxymethyl cellulose (10 ml/kg) solution for 56 consecutive days. The data showed that OA significantly attenuated the extent of silicosis fibrosis by histopathologic analysis of the lung tissues. In addition, oxidative stress activated by silica exposure, as evidenced by increasing of malondialdehyde content, and activities of superoxide dismutase and glutathione peroxidase in the lung, was regulated by treatment with OA. Furthermore, enzyme­linked immunosorbent assay analysis showed that OA significantly decreased the levels of tumor necrosis factor­α and transforming growth factor­ß1. Immunohistochemistry analysis showed that OA significantly decreased collagen types I and III. In investigating the mechanisms underlying the action of OA, it was found that OA decreased the level of phosphorylated AKT1, which in turn inactivated the transcriptional of nuclear factor (NF)­κB in the development and progress of silicosis. In conclusion, these results suggested that the protective effects of OA were due, at least in part, to its anti­oxidant activity and its ability to decrease the expression of cytokines and collagen by modulating the AKT/NF­κB pathway.
[Mh] Termos MeSH primário: Colágeno/metabolismo
Citocinas/metabolismo
NF-kappa B/metabolismo
Estresse Oxidativo/efeitos dos fármacos
Proteínas Proto-Oncogênicas c-akt/metabolismo
Silicose/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Fibrose
Glutationa Peroxidase/metabolismo
Pulmão/efeitos dos fármacos
Pulmão/patologia
Masculino
Malondialdeído/metabolismo
Ácido Oleanólico/administração & dosagem
Ratos
Ratos Wistar
Silicose/metabolismo
Silicose/patologia
Superóxido Dismutase/metabolismo
Fator de Crescimento Transformador beta1/metabolismo
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (NF-kappa B); 0 (Transforming Growth Factor beta1); 0 (Tumor Necrosis Factor-alpha); 4Y8F71G49Q (Malondialdehyde); 6SMK8R7TGJ (Oleanolic Acid); 9007-34-5 (Collagen); EC 1.11.1.9 (Glutathione Peroxidase); EC 1.15.1.1 (Superoxide Dismutase); EC 2.7.11.1 (Akt1 protein, rat); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170329
[St] Status:MEDLINE
[do] DOI:10.3892/mmr.2017.6402


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[PMID]:28277537
[Au] Autor:Liu H; Cheng Y; Yang J; Wang W; Fang S; Zhang W; Han B; Zhou Z; Yao H; Chao J; Liao H
[Ad] Endereço:Neurobiology Laboratory, New Drug Screening Centre, China Pharmaceutical University, Nanjing, China.
[Ti] Título:BBC3 in macrophages promoted pulmonary fibrosis development through inducing autophagy during silicosis.
[So] Source:Cell Death Dis;8(3):e2657, 2017 Mar 09.
[Is] ISSN:2041-4889
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Following inhalation into the lungs, silica particles are engulfed by alveolar macrophages, which triggers endogenous or exogenous apoptosis signaling pathways. As an inducer of apoptosis, the role of BBC3/PUMA (BCL2-binding component 3) in macrophages during silicosis remains unknown. Here, we exposed U937 cell-derived macrophages (UDMs) to SiO in vitro to explore the function of BBC3 in SiO -induced disease. We found that SiO induced increased BBC3 expression, as well as macrophage activation and apoptosis. Knockdown of Bbc3 with specific siRNA significantly mitigated the SiO -induced effects. In addition, our results clearly showed increased levels of autophagy in macrophages exposed to SiO . However, inhibition of BBC3 decreased the occurrence of autophagy. Furthermore, we observed that the blockade of autophagy with 3-MA, an autophagy inhibitor, inhibited SiO -induced macrophage activation and apoptosis. In contrast, rapamycin, an autophagy inducer, further enhanced the effects induced by SiO . The conditioned medium from macrophages exposed to SiO promoted the proliferation and migration of fibroblasts, and the inhibition of BBC3/autophagy reduced the effects of the conditioned medium on fibroblasts. In the mouse model of silicosis, Bbc3 knockout mice clearly exhibited decreased levels of autophagy and fibrosis progression. These results suggest that downregulation of BBC3 expression may become a novel therapeutic strategy for the treatment of silicosis.
[Mh] Termos MeSH primário: Proteínas Reguladoras de Apoptose/genética
Autofagia/efeitos dos fármacos
Proteínas Proto-Oncogênicas/genética
Fibrose Pulmonar/genética
Silicose/genética
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Proteínas Reguladoras de Apoptose/antagonistas & inibidores
Autofagia/genética
Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Seres Humanos
Macrófagos/efeitos dos fármacos
Macrófagos/patologia
Macrófagos Alveolares/efeitos dos fármacos
Macrófagos Alveolares/patologia
Camundongos
Camundongos Knockout
Proteínas Proto-Oncogênicas/antagonistas & inibidores
Fibrose Pulmonar/tratamento farmacológico
Fibrose Pulmonar/patologia
Dióxido de Silício/toxicidade
Silicose/complicações
Silicose/tratamento farmacológico
Silicose/patologia
Sirolimo/administração & dosagem
Células U937
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apoptosis Regulatory Proteins); 0 (BBC3 protein, human); 0 (Proto-Oncogene Proteins); 7631-86-9 (Silicon Dioxide); W36ZG6FT64 (Sirolimus)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171103
[Lr] Data última revisão:
171103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170310
[St] Status:MEDLINE
[do] DOI:10.1038/cddis.2017.78


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[PMID]:28251247
[Au] Autor:Jones BA
[Ad] Endereço:University of New Mexico, 1 UNM Drive, MSC 05 3060, Albuquerque, NM, 87131, USA. bajones@unm.edu.
[Ti] Título:The social costs of uranium mining in the US Colorado Plateau cohort, 1960-2005.
[So] Source:Int J Public Health;62(4):471-478, 2017 May.
[Is] ISSN:1661-8564
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Long-term social costs associated with underground uranium mining are largely unknown. This study estimated health costs of Native American and white (Hispanic and non-Hispanic origin) uranium miners in the US Public Health Service Colorado Plateau cohort study. METHODS: Elevated uranium miner person-years of life lost (PYLL) were calculated from the most recent study of the Colorado Plateau cohort over 1960-2005. Nine causes of death categories were included. Costs to society of miner PYLL were monetized using the value of a statistical life-year approach. RESULTS: Costs over 1960-2005 totaled $2 billion USD [95% CI: $1.8, $2.2], or $2.9 million per elevated miner death. This corresponds to $43.1 million [95%: $38.7, $48.7] in annual costs. Lung cancer was the most costly cause of death at $1.4 billion [95%: $1.3, $1.5]. Absolute health costs were largest for white miners, but Native Americans had larger costs per elevated death. Annual excess mortality over 1960-2005 averaged 366.4 per 100,000 miners; 404.6 (white) and 201.5 per 100,000 (Native American). CONCLUSIONS: This research advances our understanding of uranium extraction legacy impacts, particularly among indigenous populations.
[Mh] Termos MeSH primário: Custos de Cuidados de Saúde/estatística & dados numéricos
Mineração/economia
Urânio/efeitos adversos
[Mh] Termos MeSH secundário: Estudos de Coortes
Colorado/epidemiologia
Grupo com Ancestrais do Continente Europeu/estatística & dados numéricos
Seres Humanos
Índios Norte-Americanos/estatística & dados numéricos
Neoplasias Pulmonares/economia
Neoplasias Pulmonares/etnologia
Neoplasias Pulmonares/etiologia
Neoplasias Pulmonares/mortalidade
Doenças Profissionais/economia
Doenças Profissionais/etiologia
Doenças Profissionais/mortalidade
Exposição Ocupacional
Radônio/efeitos adversos
Fatores de Risco
Silicose/economia
Silicose/etnologia
Silicose/etiologia
Silicose/mortalidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
4OC371KSTK (Uranium); Q74S4N8N1G (Radon)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170303
[St] Status:MEDLINE
[do] DOI:10.1007/s00038-017-0943-z



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