Base de dados : MEDLINE
Pesquisa : C08.381.520.500 [Categoria DeCS]
Referências encontradas : 4851 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 486 ir para página                         

  1 / 4851 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29366758
[Au] Autor:Yuhong L; Tana W; Zhengzhong B; Feng T; Qin G; Yingzhong Y; Wei G; Yaping W; Langelier C; Rondina MT; Ge RL
[Ad] Endereço:Research Center for High Altitude Medicine, Qinghai University, Xining 810001, China; Department of Respiratory Medicine, The Affiliated Hospital of Qinghai University, Xining 810001, China.
[Ti] Título:Transcriptomic profiling reveals gene expression kinetics in patients with hypoxia and high altitude pulmonary edema.
[So] Source:Gene;651:200-205, 2018 Apr 20.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: High altitude pulmonary edema (HAPE) is a life threatening condition occurring in otherwise healthy individuals who rapidly ascend to high altitude. However, the molecular mechanisms of its pathophysiology are not well understood. The objective of this study is to evaluate differential gene expression in patients with HAPE during acute illness and subsequent recovery. METHODS: Twenty-one individuals who ascended to an altitude of 3780 m were studied, including 12 patients who developed HAPE and 9 matched controls without HAPE. Whole-blood samples were collected during acute illness and subsequent recovery for analysis of the expression of hypoxia-related genes, and physiologic and laboratory parameters, including mean pulmonary arterial pressure (mPAP), heart rate, blood pressure, and arterial oxygen saturation (SpO ), were also measured. RESULTS: Compared with control subjects, numerous hypoxia-related genes were up-regulated in patients with acute HAPE. Gene network analyses suggested that HIF-1α played a central role in acute HAPE by affecting a variety of hypoxia-related genes, including BNIP3L, VEGFA, ANGPTL4 and EGLN1. Transcriptomic profiling revealed the expression of most HAPE-induced genes was restored to a normal level during the recovery phase except some key hypoxia response factors, such asBNIP3L, EGR1, MMP9 and VEGF, which remained persistently elevated. CONCLUSIONS: Differential expression analysis of hypoxia-related genes revealed distinct molecular signatures of HAPE during acute and recovery phases. This study may help us to better understand HAPE pathogenesis and putative targets for further investigation and therapeutic intervention.
[Mh] Termos MeSH primário: Doença da Altitude/genética
Hipertensão Pulmonar/genética
Edema Pulmonar/genética
[Mh] Termos MeSH secundário: Lesão Pulmonar Aguda/etiologia
Lesão Pulmonar Aguda/genética
Adulto
Estudos de Casos e Controles
Estudos de Coortes
Perfilação da Expressão Gênica
Seres Humanos
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180126
[St] Status:MEDLINE


  2 / 4851 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29374925
[Au] Autor:Liu W; Chai JK
[Ad] Endereço:Burn Institute, the First Affiliated Hospital of PLA General Hospital, Beijing 100048, China.
[Ti] Título:[Influences of ulinastatin on acute lung injury and time phase changes of coagulation parameters in rats with burn-blast combined injuries].
[So] Source:Zhonghua Shao Shang Za Zhi;34(1):32-39, 2018 Jan 20.
[Is] ISSN:1009-2587
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To explore the influences of ulinastatin on acute lung injury and time phase changes of coagulation parameters in rats with severe burn-blast combined injuries. One hundred and ninety-two Sprague-Dawley rats were divided into pure burn-blast combined injury group, ulinastatin+ burn-blast combined injury group, and sham injury group according to the random number table, with 64 rats in each group. Two groups of rats with combined burn-blast injuries were inflicted with moderate blast injuries with the newly self-made explosive device. Then the rats were inflicted with 25% total body surface area full-thickness scald (hereinafter referred to as burn) on the back by immersing in 94 ℃ hot water for 12 s. Rats in sham injury group were sham injured on the back by immersing in 37 ℃ warm water for 12 s. Immediately after injury, rats in the three groups were intraperitoneally injected with Ringer's lactate solution (40 mL/kg), meanwhile rats in ulinastatin+ burn-blast combined injury group were intraperitoneally injected with ulinastatin (4×10(4)U/kg), once every 12 hours, until post injury hour (PIH) 72. Before injury, at PIH 3, 6, 12, 24, 48, 72, and on post injury day (PID) 7, 8 rats in each group were selected to harvest abdominal aortic blood samples to detect plasma levels of activated partial thromboplastin time (APTT), prothrombin time (PT), fibrinogen, D-dimer, antithrombin â…¢ (AT-â…¢), and α2-antiplasmin (α2-AP). At PIH 24, three rats in each group which were used in detection of coagulation parameters were sacrificed to observe lung injury. At PIH 72, three rats in each group were sacrificed for histopathological observation of lung. Data were processed with analysis of variance of factorial design and least-significant difference test. (1) Compared with those of rats in sham injury group, APTT of rats in pure burn-blast combined injury group significantly prolonged at PIH 72 and on PID 7 ( <0.05 or <0.01). PT significantly prolonged at PIH 3 and 72 and significantly shortened at PIH 6 ( <0.05 or <0.01) . Fibrinogen level significantly increased from PIH 12 to PID 7 ( <0.01). AT-â…¢ level significantly decreased at PIH 6 and 12 ( <0.01), and α2-AP level significantly decreased at PIH 6 and significantly increased from PIH 24 to 72 ( <0.01). Compared with those of rats in pure burn-blast combined injury group, APTT of rats in ulinastatin+ burn-blast combined injury group significantly prolonged at PIH 3 and 6 ( <0.01) while PT significantly shortened at PIH 3, 12, and 72 ( <0.05 or <0.01). Fibrinogen level significantly decreased at PIH 6 and 12 and significantly increased at PIH 72 ( <0.05 or <0.01). AT-â…¢ level significantly increased at PIH 3, 12, 48, and 72 ( <0.05 or <0.01), and α2-AP level significantly decreased from PIH 12 to 72 ( <0.05 or <0.01). D-dimer level of rats in sham injury group, pure burn-blast combined injury group, and ulinastatin+ burn-blast combined injury group were respectively (0.084±0.013), (0.115±0.015), (0.158±0.022), (0.099±0.011), (0.099±0.012), (0.089±0.011), (0.124±0.014), and (0.116±0.018) µg/mL, (0.064±0.033), (0.114±0.016), (0.135±0.009), (0.060±0.008), (0.104±0.010), (0.124±0.020), (0.180±0.036), and (0.201±0.032) µg/mL, (0.074±0.013), (0.084±0.035), (0.101±0.050), (0.091±0.046), (0.096±0.034), (0.044±0.019), (0.106±0.049), and (0.118±0.047) µg/mL. Compared with that of rats in sham injury group, D-dimer level significantly decreased at PIH 6 and 12 and significantly increased from PIH 48 to PID 7 ( <0.05 or <0.01). Compared with that of rats in pure burn-blast combined injury group, D-dimer level of rats in ulinastatin+ burn-blast combined injury group significantly decreased at PIH 3, 48, and 72, and on PID 7 ( <0.05 or <0.01). (2) At PIH 24, there was a large amount of light red effusion in the thoracic cavity, and both lung lobes were hyperemic and edematous with a small amount of blood clots in the left and middle lobe of rats in pure burn-blast combined injury group. There was a small amount of yellowish effusion in the thoracic cavity of rats in ulinastatin+ burn-blast combined injury group, and the degree of hyperemic and edematous of bilateral lobes was lighter compared with rats in pure burn-blast combined injury group with no clot in the left lobe. No congestion, edema, or bleeding was observed in lungs of rats in sham injury group. (3) At PIH 72, disorganized alveolar structure, collapsed alveolar cavity, edematous and thickening pulmonary interstitium, infiltration of a large amount of inflammatory cells, obvious rupture of alveolar septum, and hyaline thrombus were observed in lungs of rats in pure burn-blast combined injury group. Significantly improved alveolar structure, less collapsed alveolar cavity, improved edematous pulmonary interstitium, less infiltration of inflammatory cells, rupture of alveolar septum, and no thrombus were observed in lungs of rats in ulinastatin+ burn-blast combined injury group. The lung tissue had a well-filled alveolar cavity with no interstitial edema or infiltration of inflammatory cells and no thrombosis in lungs of rats in sham injury group. Ulinastatin has positive therapeutic effects on acute lung injury in rats with severe burn-blast combined injuries through its good regulating effects on coagulation and fibrinolytic disorders caused by burn-blast combined injuries.
[Mh] Termos MeSH primário: Lesão Pulmonar Aguda/tratamento farmacológico
Traumatismos por Explosões/complicações
Queimaduras/complicações
Glicoproteínas/farmacologia
Inibidores da Tripsina/farmacologia
[Mh] Termos MeSH secundário: Lesão Pulmonar Aguda/complicações
Animais
Traumatismos por Explosões/sangue
Traumatismos por Explosões/patologia
Queimaduras/sangue
Queimaduras/patologia
Edema
Produtos de Degradação da Fibrina e do Fibrinogênio
Edema Pulmonar
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fibrin Fibrinogen Degradation Products); 0 (Glycoproteins); 0 (Trypsin Inhibitors); 0 (fibrin fragment D); OR3S9IF86U (urinastatin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180129
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.1009-2587.2018.01.007


  3 / 4851 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28460454
[Au] Autor:Shan X; Zhang Y; Chen H; Dong L; Wu B; Xu T; Hu J; Liu Z; Wang W; Wu L; Feng Z; Liang G
[Ad] Endereço:Chemical Biology Research Center at School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, China.
[Ti] Título:Inhibition of epidermal growth factor receptor attenuates LPS-induced inflammation and acute lung injury in rats.
[So] Source:Oncotarget;8(16):26648-26661, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Acute lung injury (ALI) and its severe form acute respiratory distress syndrome remain the leading cause of morbidity and mortality in intensive care units. Inhibition of epidermal growth factor receptor (EGFR) has been found to be able to reduce inflammatory response. However, it is still unclear whether EGFR inhibition can prevent ALI. This study aimed to validate the EGFR's role in ALI and investigated the effects of EGFR inhibition on lipopolysaccharides (LPS)-induced ALI in rats. In vitro, both pharmacological inhibitors (AG1478 and 451) and si-RNA silencing of EGFR significantly inhibited LPS-induced EGFR signaling activation and inflammatory response in human lung epithelial cells or macrophages. Mechanistically, LPS induced EGFR activation via TLR4 and c-Src signaling. In vivo, rat model with ALI induced by intratracheal instillation of LPS was treated by oral administration of AG1478 and 451. It was observed that AG1478 and 451 blocked the activation of EGFR signaling in lung tissue and reduced the LPS-induced infiltration of inflammatory cells, inflammatory gene expression, and lung injuries. This study demonstrates that TLR4/c-Src-dependent EGFR signaling plays an important role in LPS-induced ALI, and that EGFR may be a potential target in treating ALI.
[Mh] Termos MeSH primário: Lesão Pulmonar Aguda/etiologia
Lesão Pulmonar Aguda/metabolismo
Lipopolissacarídeos/efeitos adversos
Receptor do Fator de Crescimento Epidérmico/metabolismo
[Mh] Termos MeSH secundário: Lesão Pulmonar Aguda/tratamento farmacológico
Lesão Pulmonar Aguda/patologia
Animais
Linhagem Celular
Citocinas/genética
Citocinas/metabolismo
Mediadores da Inflamação/metabolismo
Macrófagos/imunologia
Macrófagos/metabolismo
Inibidores de Proteínas Quinases/farmacologia
Quinazolinas/farmacologia
Ratos
Receptor do Fator de Crescimento Epidérmico/antagonistas & inibidores
Transdução de Sinais/efeitos dos fármacos
Receptor 4 Toll-Like/metabolismo
Tirfostinas/farmacologia
Quinases da Família src/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Inflammation Mediators); 0 (Lipopolysaccharides); 0 (Protein Kinase Inhibitors); 0 (Quinazolines); 0 (Toll-Like Receptor 4); 0 (Tyrphostins); 170449-18-0 (tyrphostin AG 1478); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); EC 2.7.10.2 (CSK tyrosine-protein kinase); EC 2.7.10.2 (src-Family Kinases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15790


  4 / 4851 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28470756
[Au] Autor:Roubinian NH; Looney MR; Keating S; Kor DJ; Lowell CA; Gajic O; Hubmayr R; Gropper M; Koenigsberg M; Wilson GA; A Matthay M; Toy P; Murphy EL; TRALI Study Group
[Ad] Endereço:Blood Systems Research Institute.
[Ti] Título:Differentiating pulmonary transfusion reactions using recipient and transfusion factors.
[So] Source:Transfusion;57(7):1684-1690, 2017 07.
[Is] ISSN:1537-2995
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: It is increasingly recognized that recipient risk factors play a prominent role in possible transfusion-related acute lung injury (pTRALI) and transfusion-associated circulatory overload (TACO). We hypothesized that both transfusion and recipient factors including natriuretic peptides could be used to distinguish TRALI from TACO and pTRALI. STUDY DESIGN AND METHODS: We performed a post hoc analysis of a case-control study of pulmonary transfusion reactions conducted at the University of California at San Francisco and Mayo Clinic, Rochester. We evaluated clinical data and brain natriuretic peptides (BNP) levels drawn after transfusion in patients with TRALI (n = 21), pTRALI (n = 26), TACO (n = 22), and controls (n = 24). Logistic regression and receiver operating characteristics curve analyses were used to determine the accuracy of clinical and biomarker predictors in differentiating TRALI from TACO and pTRALI. RESULTS: We found that pTRALI and TACO were associated with older age, higher fluid balance, and elevated BNP levels relative to those of controls and TRALI. The following variables were useful in distinguishing cases of pTRALI and TACO from TRALI: age more than 70 years, BNP levels more than 1000 pg/mL, 24-hour fluid balance of more than 3 L, and a lower number of transfused blood components. Using the above variables, our logistic model had a 91% negative predictive value in the differential diagnosis of TRALI. CONCLUSIONS: Models incorporating readily available clinical and biomarker data can be used to differentiate transfusion-related respiratory complications. Additional studies examining recipient risk factors and the likelihood of TRALI may be useful in decision making regarding donor white blood cell antibody testing.
[Mh] Termos MeSH primário: Lesão Pulmonar Aguda/etiologia
Reação Transfusional/etiologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Feminino
Seres Humanos
Modelos Logísticos
Masculino
Meia-Idade
Peptídeo Natriurético Encefálico/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
114471-18-0 (Natriuretic Peptide, Brain)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1111/trf.14118


  5 / 4851 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27774621
[Au] Autor:Schulz U; Reil A; Kiefel V; Bux J; Moog R
[Ad] Endereço:DRK Blood Service North-East, Cottbus, Germany.
[Ti] Título:Evaluation of a new microbeads assay for granulocyte antibody detection.
[So] Source:Transfusion;57(1):70-81, 2017 01.
[Is] ISSN:1537-2995
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: To reduce the risk of transfusion-associated acute lung injury (TRALI), a high number of plasma donors were tested for human leukocyte antigen (HLA) and human neutrophil antigen (HNA) antibodies. For HNA antibody detection, the gold standard is a combination of the granulocyte immunofluorescence test (GIFT) and the granulocyte agglutination test (GAT). However, these tests are not suitable for a high-throughput of samples. STUDY DESIGN AND METHODS: To evaluate the new generation of the LABScreen MULTI assay (One Lambda, Inc.), which has special new beads for all the known HNA specificities, including HNA-3a, 97 sera samples containing well-defined HNA antibodies were used. For background testing, we used 91 samples from plasma donors previously identified by GAT, GIFT, and the monoclonal antibody-specific immobilization of granulocyte antigens (MAIGA) assay. RESULTS: Compared with previous tests, the new LABScreen MULTI assay was highly specific for the HNA-1a, HNA-1b, HNA-2, and HNA-3a antibody specificities required to prevent TRALI. Ninety-eight percent of the HNA-1a, HNA-1b, and HNA-2 antibodies could be detected as true positive; and 90% of the HNA-3a antibodies were recognized correctly as positive. False-positive reactions were identified in 5.5% of samples that previously tested negative. CONCLUSION: The detection of HNA-3a antibody specificities could be integrated into the new LABScreen MULTI assay; however, we detected only 90%. In addition, we detected further HNA antibodies, such as HNA-1c, HNA-1d, and some HNA-3b and HNA-4a antibodies. The new generation of LABScreen MULTI is a great step toward feasible high-throughput testing for HNA antibodies. Nevertheless, GIFT and GAT remain the gold-standard methods for the differentiation of rare and currently unknown HNA specificities.
[Mh] Termos MeSH primário: Autoanticorpos/sangue
Isoantígenos/sangue
Microesferas
[Mh] Termos MeSH secundário: Lesão Pulmonar Aguda/sangue
Lesão Pulmonar Aguda/etiologia
Lesão Pulmonar Aguda/prevenção & controle
Testes de Aglutinação/métodos
Anticorpos Monoclonais/química
Feminino
Técnica Direta de Fluorescência para Anticorpo/métodos
Seres Humanos
Masculino
Reação Transfusional
[Pt] Tipo de publicação:EVALUATION STUDIES; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Autoantibodies); 0 (Isoantigens)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE
[do] DOI:10.1111/trf.13878


  6 / 4851 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29173362
[Au] Autor:Liu W; Zhu H; Fang H
[Ad] Endereço:Department of Anesthesiology, Jinshan Hospital Affiliated to Fudan University, Shanghai, China.
[Ti] Título:Propofol Potentiates Sevoflurane-Induced Inhibition of Nuclear Factor--κB-Mediated Inflammatory Responses and Regulation of Mitogen-Activated Protein Kinases Pathways via Toll-like Receptor 4 Signaling in Lipopolysaccharide-Induced Acute Lung Injury in Mice.
[So] Source:Am J Med Sci;354(5):493-505, 2017 11.
[Is] ISSN:1538-2990
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Toll-like receptor 4 (TLR4)-induced initiation of mitogen-activated protein kinases and the nuclear factor-kappa B signaling cascade is reportedly involved in inflammatory responses during lung injury. Studies have found that volatile anesthetics, such as isoflurane and sevoflurane, inhibit inflammation. This investigation explored the protective effects of propofol and whether propofol potentiates the protective effects of sevoflurane against lipopolysaccharide (LPS)-induced acute lung injury. MATERIALS AND METHODS: Male BALB/c mice were treated with LPS (10µg/mouse; intranasal instillation) to induce acute lung injury. Mice were exposed to sevoflurane (3%; 6 hours) alone or combined with propofol (10 or 20mg/kg body weight; subcutaneously) followed by sevoflurane for 1 hour before the LPS challenge. RESULTS: Sevoflurane with or without propofol attenuated pulmonary edema, restored altered lung architecture and reduced influx of inflammatory cells into bronchoalveolar lavage fluid after the LPS challenge. LPS-mediated overproduction of the proinflammatory cytokines tumor necrosis factor-α, interleukin-1ß, and interleukin-6 as well as nitric oxide, were reduced. Sevoflurane either alone or with propofol downregulated TLR4 and TLR4-mediated mitogen-activated protein kinase and nuclear factor-kappa B signaling. CONCLUSIONS: Combined exposure to propofol and sevoflurane was more effective than sevoflurane administered alone, suggesting the positive effects of propofol on sevoflurane-mediated anti-inflammatory effects.
[Mh] Termos MeSH primário: Lesão Pulmonar Aguda/induzido quimicamente
Lipopolissacarídeos
Éteres Metílicos/farmacologia
Propofol/farmacologia
Transdução de Sinais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Lesão Pulmonar Aguda/tratamento farmacológico
Lesão Pulmonar Aguda/imunologia
Anestésicos Inalatórios/farmacologia
Anestésicos Intravenosos/farmacologia
Animais
Sinergismo Farmacológico
Masculino
Camundongos
Camundongos Endogâmicos BALB C
NF-kappa B/metabolismo
Substâncias Protetoras/farmacologia
Receptor 4 Toll-Like/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anesthetics, Inhalation); 0 (Anesthetics, Intravenous); 0 (Lipopolysaccharides); 0 (Methyl Ethers); 0 (NF-kappa B); 0 (Protective Agents); 0 (Tlr4 protein, mouse); 0 (Toll-Like Receptor 4); 38LVP0K73A (sevoflurane); YI7VU623SF (Propofol)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE


  7 / 4851 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28459384
[Au] Autor:Southern BD; Scheraga RG; Olman MA
[Ad] Endereço:1 Cleveland Clinic Respiratory Institute Lerner Research Institute Department of Pathobiology Cleveland, Ohio.
[Ti] Título:Impaired AMPK Activity Drives Age-Associated Acute Lung Injury after Hemorrhage.
[So] Source:Am J Respir Cell Mol Biol;56(5):553-555, 2017 05.
[Is] ISSN:1535-4989
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Proteínas Quinases Ativadas por AMP/imunologia
Lesão Pulmonar Aguda/imunologia
Envelhecimento/imunologia
Imunidade Inata
Choque Hemorrágico/imunologia
[Mh] Termos MeSH secundário: Lesão Pulmonar Aguda/enzimologia
Lesão Pulmonar Aguda/patologia
Animais
Seres Humanos
Choque Hemorrágico/enzimologia
Choque Hemorrágico/patologia
[Pt] Tipo de publicação:EDITORIAL
[Nm] Nome de substância:
EC 2.7.11.31 (AMP-Activated Protein Kinases)
[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:170502
[St] Status:MEDLINE
[do] DOI:10.1165/rcmb.2017-0023ED


  8 / 4851 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29198702
[Au] Autor:Wu D; Liang M; Dang H; Fang F; Xu F; Liu C
[Ad] Endereço:Department of Pediatric Intensive Care Unit, Children's Hospital of Chongqing Medical University, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing, China; China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Chongq
[Ti] Título:Hydrogen protects against hyperoxia-induced apoptosis in type II alveolar epithelial cells via activation of PI3K/Akt/Foxo3a signaling pathway.
[So] Source:Biochem Biophys Res Commun;495(2):1620-1627, 2018 01 08.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Oxidative stress is regarded as a key regulator in the pathogenesis of prolonged hyperoxia-induced lung injury, which causes injury to alveolar epithelial cells and eventually leads to development of bronchopulmonary dysplasia (BPD). Many studies have shown that hydrogen has a protective effect in a variety of cells. However, the mechanisms by which hydrogen rescues cells from damage due to oxidative stress in BPD remains to be fully elucidated. This study sought to evaluate the effects of hydrogen on hyperoxia-induced lung injury and to investigate the underlying mechanism. Primary type II alveolar epithelial cells (AECIIs) were divided into four groups: control (21% oxygen), hyperoxia (95% oxygen), hyperoxia + hydrogen, and hyperoxia + hydrogen + LY294002 (a PI3K/Akt inhibitor). Proliferation and apoptosis of AECIIs were assessed using MTS assay and flow cytometry (FCM), respectively. Gene and protein expression were detected by quantitative polymerase chain reaction (q-PCR) and western blot analysis. Stimulation with hyperoxia decreased the expression of P-Akt, P- FoxO3a, cyclinD1 and Bcl-2. Hyperoxic conditions increased levels of Bim, Bax, and Foxo3a, which induced proliferation restriction and apoptosis of AECIIs. These effects of hyperoxia were reversed with hydrogen pretreatment. Furthermore, the protective effects of hydrogen were abrogated by PI3K/Akt inhibitor LY294002. The results indicate that hydrogen protects AECIIs from hyperoxia-induced apoptosis by inhibiting apoptosis factors and promoting the expression of anti-apoptosis factors. These effects were associated with activation of the PI3K/Akt/FoxO3a pathway.
[Mh] Termos MeSH primário: Células Epiteliais Alveolares/efeitos dos fármacos
Células Epiteliais Alveolares/metabolismo
Hidrogênio/farmacologia
Hiperóxia/tratamento farmacológico
Hiperóxia/metabolismo
[Mh] Termos MeSH secundário: Lesão Pulmonar Aguda/tratamento farmacológico
Lesão Pulmonar Aguda/metabolismo
Lesão Pulmonar Aguda/patologia
Células Epiteliais Alveolares/patologia
Animais
Apoptose/efeitos dos fármacos
Proteína 11 Semelhante a Bcl-2/genética
Células Cultivadas
Ciclina D1/genética
Feminino
Proteína Forkhead Box O3/genética
Proteína Forkhead Box O3/metabolismo
Expressão Gênica/efeitos dos fármacos
Genes bcl-2/efeitos dos fármacos
Hidrogênio/metabolismo
Hiperóxia/patologia
Estresse Oxidativo/efeitos dos fármacos
Fosfatidilinositol 3-Quinases/metabolismo
Gravidez
Proteínas Proto-Oncogênicas c-akt/metabolismo
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Ratos
Ratos Sprague-Dawley
Transdução de Sinais/efeitos dos fármacos
Proteína X Associada a bcl-2/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Bax protein, rat); 0 (Bcl-2-Like Protein 11); 0 (Bcl2l11 protein, rat); 0 (Ccnd1 protein, rat); 0 (Forkhead Box Protein O3); 0 (Foxo3a protein, rat); 0 (RNA, Messenger); 0 (bcl-2-Associated X Protein); 136601-57-5 (Cyclin D1); 7YNJ3PO35Z (Hydrogen); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171205
[St] Status:MEDLINE


  9 / 4851 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:28456774
[Au] Autor:Salameh A; Greimann W; Vollroth M; Dhein S; Bahramsoltani M; Dahnert I
[Ad] Endereço:Clinic for Peadiatric Cardiology, University of Leipzig, Heart Centre, Leipzig, Germany. aida.salameh@medizin.uni-leipzig.de.
[Ti] Título:Lung protection in cardio-pulmonary bypass.
[So] Source:J Physiol Pharmacol;68(1):99-116, 2017 Feb.
[Is] ISSN:1899-1505
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:Since the invention of the heart-lung machine paediatric cardiac surgery developed rapidly. For correction of complex cardiac malformations the application of a cardio-pulmonary bypass (CPB) has become indispensable but possible negative effects of this technique should not be neglected. Especially, both bypassed organs i.e. heart and lung are not perfused during the procedure and therefore are threatened by ischemia and reperfusion injury. Additionally, CPB was developed with a non-pulsatile flow but there are clinical observations that pulsatile flow might be superior with improved patient outcomes. Thus, the aim of our study was to evaluate the effect of CPB on lung structure and to assess whether different flow modalities (pulsatile vs. non-pulsatile flow) or application of the antibiotic minocycline might be advantageous. Thirty five piglets of four weeks age were examined and divided into five experimental groups: control (no CPB) without or with minocycline, CPB (non-pulsatile flow) without or with minocycline and CPB with pulsatile flow. CPB was performed for 90 min followed by a 120 min reperfusion and recovery phase. Thereafter, adenosine triphosphate-content of lung biopsies and histology was carried out. We found that CPB was associated with a significant thickening of alveolar wall accompanied by an infiltration of neutrophil leucocytes. Moreover, markers for hypoxia, apoptosis, nitrosative stress, inflammation and DNA damage were significantly elevated after CPB. These cellular damages could be partially inhibited by minocycline or pulsatile flow. Both, minocycline and pulsatile flow attenuate lung damage after CPB.
[Mh] Termos MeSH primário: Lesão Pulmonar Aguda/prevenção & controle
Antibacterianos/uso terapêutico
Ponte Cardiopulmonar
Minociclina/uso terapêutico
Fluxo Pulsátil
[Mh] Termos MeSH secundário: Lesão Pulmonar Aguda/metabolismo
Lesão Pulmonar Aguda/patologia
Lesão Pulmonar Aguda/fisiopatologia
Trifosfato de Adenosina/metabolismo
Animais
Antibacterianos/farmacologia
Pulmão/efeitos dos fármacos
Pulmão/metabolismo
Pulmão/patologia
Pulmão/fisiopatologia
Minociclina/farmacologia
Infiltração de Neutrófilos
Suínos
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Tumor Necrosis Factor-alpha); 8L70Q75FXE (Adenosine Triphosphate); FYY3R43WGO (Minocycline)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170501
[St] Status:MEDLINE


  10 / 4851 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
[PMID]:27771726
[Au] Autor:Obi AT; Andraska E; Kanthi Y; Luke CE; Elfline M; Madathilparambil S; Siahaan TJ; Jaffer FA; Wakefield TW; Raghavendran K; Henke PK
[Ad] Endereço:Conrad Jobst Vascular Research Laboratory, University of Michigan Medical School, Ann Arbor, Mich., USA.
[Ti] Título:Gram-Negative Pneumonia Alters Large-Vein Cell-Adhesion Molecule Profile and Potentiates Experimental Stasis Venous Thrombosis.
[So] Source:J Vasc Res;53(3-4):186-195, 2016.
[Is] ISSN:1423-0135
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Pneumonia is a significant risk factor for the development of venous thrombosis (VT). Cell-adhesion molecules (CAMs) are linked to the pathogenesis of both pneumonia and VT. We hypothesized that remote infection would confer a prothrombogenic milieu via systemic elevation of CAMs. METHODS: Lung injury was induced in wild-type (C57BL/6) mice by lung contusion or intratracheal inoculation with Klebsiella pneumoniae or saline controls. K. pneumoniae-treated mice and controls additionally underwent inferior vena cava (IVC) ligation to generate VT. RESULTS: Lung-contusion mice demonstrated no increase in E-selectin or P-selectin whereas mice infected with K. pneumoniae demonstrated increased circulating P-selectin, ICAM-1, VCAM-1 and thrombin-antithrombin (TAT) complexes. Mice with pneumonia formed VT 3 times larger than controls, demonstrated significantly more upregulation of vein-wall and systemic CAMs, and formed erythrocyte-rich thrombi. CONCLUSION: Elevated CAM expression was identified in mice with pneumonia, but not lung contusion, indicating that the type of inflammatory stimulus and the presence of infection drive the vein-wall response. Elevation of CAMs was associated with amplified VT and may represent an alternate mechanism by which to target the prevention of VT.
[Mh] Termos MeSH primário: Moléculas de Adesão Celular/sangue
Infecções por Klebsiella/complicações
Klebsiella pneumoniae/patogenicidade
Pneumonia Bacteriana/complicações
Veia Cava Inferior/metabolismo
Trombose Venosa/etiologia
[Mh] Termos MeSH secundário: Lesão Pulmonar Aguda/sangue
Lesão Pulmonar Aguda/complicações
Animais
Antitrombina III
Moléculas de Adesão Celular/antagonistas & inibidores
Modelos Animais de Doenças
Fibrinolíticos/farmacologia
Molécula 1 de Adesão Intercelular/sangue
Infecções por Klebsiella/sangue
Infecções por Klebsiella/tratamento farmacológico
Infecções por Klebsiella/microbiologia
Ligadura
Masculino
Camundongos Endogâmicos C57BL
Selectina-P/sangue
Peptídeo Hidrolases/sangue
Pneumonia Bacteriana/sangue
Pneumonia Bacteriana/tratamento farmacológico
Pneumonia Bacteriana/microbiologia
Regulação para Cima
Molécula 1 de Adesão de Célula Vascular/sangue
Veia Cava Inferior/cirurgia
Trombose Venosa/sangue
Trombose Venosa/microbiologia
Trombose Venosa/prevenção & controle
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cell Adhesion Molecules); 0 (Fibrinolytic Agents); 0 (Icam1 protein, mouse); 0 (P-Selectin); 0 (Vascular Cell Adhesion Molecule-1); 0 (antithrombin III-protease complex); 126547-89-5 (Intercellular Adhesion Molecule-1); 9000-94-6 (Antithrombin III); EC 3.4.- (Peptide Hydrolases)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE



página 1 de 486 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde