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[PMID]:28460568
[Au] Autor:Akhter MS; Biswas A; Abdullah SM; Behari M; Saxena R
[Ad] Endereço:1 Department of Genetics, College of Applied Medical Sciences, Jazan University, Jizan, Saudi Arabia.
[Ti] Título:The Role of PAI-1 4G/5G Promoter Polymorphism and Its Levels in the Development of Ischemic Stroke in Young Indian Population.
[So] Source:Clin Appl Thromb Hemost;23(8):1071-1076, 2017 Nov.
[Is] ISSN:1938-2723
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The plasminogen activator inhibitor-1 (PAI-1) gene has been found to be associated with the pathogenesis and progression of vascular diseases including stroke. A 4G/5G, PAI-1 gene polymorphism has been found to be associated with the plasma PAI-1 levels in different ethnic populations but results are still controversial. The aim of this study was to determine the potential association of 4G/5G polymorphism and plasma PAI-1 levels in the development of ischemic stroke (IS) in young Asian Indians. One hundred patients with IS and an equal number of age- and sex-matched controls were studied. The 4G/5G polymorphism was genotyped in the study population through allele-specific polymerase chain reaction. Plasma PAI-1 levels were evaluated using a commercial kit. The PAI-1 levels were significantly higher in patients when compared to the controls ( P = .03). The variant 4G allele for the PAI-I 4G/5G polymorphism showed both genotypic ( P = .0013, χ = 10.303; odds ratio [OR] = 3.75) as well as allelic association ( P = .0004, χ = 12.273; OR = 1.99) with IS. The homozygous variant 4G/4G also was found to be associated with the higher PAI-1 levels (0.005). The variant allele 4G of PAI-1 4G/5G polymorphism and higher plasma PAI-1 levels were found to be significantly associated with IS in young Asian Indians.
[Mh] Termos MeSH primário: Isquemia Encefálica/genética
Inibidor 1 de Ativador de Plasminogênio/genética
Polimorfismo Genético
Regiões Promotoras Genéticas
Acidente Vascular Cerebral/genética
[Mh] Termos MeSH secundário: Adolescente
Adulto
Isquemia Encefálica/sangue
Isquemia Encefálica/epidemiologia
Isquemia Encefálica/etnologia
Feminino
Seres Humanos
Índia/epidemiologia
Índia/etnologia
Masculino
Meia-Idade
Inibidor 1 de Ativador de Plasminogênio/sangue
Acidente Vascular Cerebral/sangue
Acidente Vascular Cerebral/epidemiologia
Acidente Vascular Cerebral/etnologia
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Plasminogen Activator Inhibitor 1); 0 (SERPINE1 protein, human)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1177/1076029617705728


  2 / 8174 MEDLINE  
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[PMID]:28450529
[Au] Autor:Bos LD; Schouten LR; van Vught LA; Wiewel MA; Ong DSY; Cremer O; Artigas A; Martin-Loeches I; Hoogendijk AJ; van der Poll T; Horn J; Juffermans N; Calfee CS; Schultz MJ; MARS consortium
[Ad] Endereço:Department of Intensive Care, Academic Medical Center, Amsterdam, The Netherlands.
[Ti] Título:Identification and validation of distinct biological phenotypes in patients with acute respiratory distress syndrome by cluster analysis.
[So] Source:Thorax;72(10):876-883, 2017 10.
[Is] ISSN:1468-3296
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:RATIONALE: We hypothesised that patients with acute respiratory distress syndrome (ARDS) can be clustered based on concentrations of plasma biomarkers and that the thereby identified biological phenotypes are associated with mortality. METHODS: Consecutive patients with ARDS were included in this prospective observational cohort study. Cluster analysis of 20 biomarkers of inflammation, coagulation and endothelial activation provided the phenotypes in a training cohort, not taking any outcome data into account. Logistic regression with backward selection was used to select the most predictive biomarkers, and these predicted phenotypes were validated in a separate cohort. Multivariable logistic regression was used to quantify the independent association with mortality. RESULTS: Two phenotypes were identified in 454 patients, which we named 'uninflamed' (N=218) and 'reactive' (N=236). A selection of four biomarkers (interleukin-6, interferon gamma, angiopoietin 1/2 and plasminogen activator inhibitor-1) could be used to accurately predict the phenotype in the training cohort (area under the receiver operating characteristics curve: 0.98, 95% CI 0.97 to 0.99). Mortality rates were 15.6% and 36.4% (p<0.001) in the training cohort and 13.6% and 37.5% (p<0.001) in the validation cohort (N=207). The 'reactive phenotype' was independent from confounders associated with intensive care unit mortality (training cohort: OR 1.13, 95% CI 1.04 to 1.23; validation cohort: OR 1.18, 95% CI 1.06 to 1.31). CONCLUSIONS: Patients with ARDS can be clustered into two biological phenotypes, with different mortality rates. Four biomarkers can be used to predict the phenotype with high accuracy. The phenotypes were very similar to those found in cohorts derived from randomised controlled trials, and these results may improve patient selection for future clinical trials targeting host response in patients with ARDS.
[Mh] Termos MeSH primário: Biomarcadores/sangue
Síndrome do Desconforto Respiratório do Adulto/sangue
Síndrome do Desconforto Respiratório do Adulto/mortalidade
[Mh] Termos MeSH secundário: Idoso
Angiopoietina-1/sangue
Angiopoietina-2/sangue
Análise por Conglomerados
Feminino
Seres Humanos
Unidades de Terapia Intensiva
Interferon gama/sangue
Interleucina-6/sangue
Masculino
Meia-Idade
Fenótipo
Inibidor 1 de Ativador de Plasminogênio/sangue
Valor Preditivo dos Testes
Estudos Prospectivos
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (ANGPT1 protein, human); 0 (ANGPT2 protein, human); 0 (Angiopoietin-1); 0 (Angiopoietin-2); 0 (Biomarkers); 0 (Interleukin-6); 0 (Plasminogen Activator Inhibitor 1); 82115-62-6 (Interferon-gamma)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1136/thoraxjnl-2016-209719


  3 / 8174 MEDLINE  
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[PMID]:29190254
[Au] Autor:Moore HB; Moore EE; Huebner BR; Dzieciatkowska M; Stettler GR; Nunns GR; Lawson PJ; Ghasabyan A; Chandler J; Banerjee A; Silliman C; Sauaia A; Hansen KC
[Ad] Endereço:From the Department of Surgery (H.B.M., E.E.M., B.R.H., M.D., G.R.S., G.R.N., P.J.L., A.B., C.S., A.S., K.C.H.), University of Colorado; Denver Health Medical Center (E.E.M., A.G., J.C.); and University of Colorado School of Public Health (A.S.), Denver, Colorado.
[Ti] Título:Fibrinolysis shutdown is associated with a fivefold increase in mortality in trauma patients lacking hypersensitivity to tissue plasminogen activator.
[So] Source:J Trauma Acute Care Surg;83(6):1014-1022, 2017 Dec.
[Is] ISSN:2163-0763
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Fibrinolysis shutdown (SD) is an independent risk factor for increased mortality in trauma. High levels of plasminogen activator inhibitor-1 (PAI-1) directly binding tissue plasminogen activator (t-PA) is a proposed mechanism for SD; however, patients with low PAI-1 levels present to the hospital with a rapid TEG (r-TEG) LY30 suggestive SD. We therefore hypothesized that two distinct phenotypes of SD exist, one, which is driven by t-PA inhibition, whereas another is due to an inadequate t-PA release in response to injury. METHODS: Trauma activations from our Level I center between 2014 and 2016 with blood collected within an hour of injury were analyzed with r-TEG and a modified TEG assay to quantify fibrinolysis sensitivity using exogenous t-PA (t-TEG). Using the existing r-TEG thresholds for SD (<0.9%), physiologic (LY30 0.9-2.9%), and hyperfibrinolysis (LY30 > 2.9%) patients were stratified into phenotypes. A t-TEG LY30 greater than 95th percentile of healthy volunteers (n = 140) was classified as t-PA hypersensitive and used to subdivide phenotypes. A nested cohort had t-PA and PAI-1 activity levels measured in addition to proteomic analysis of additional fibrinolytic regulators. RESULTS: This study included 398 patients (median New Injury Severity Score, 18), t-PA-Sen was present in 27% of patients. Shutdown had the highest mortality rate (20%) followed by hyperfibinolysis (16%) and physiologic (9% p = 0.020). In the non-t-PA hypersensitive cohort, SD had a fivefold increase in mortality (15%) compared with non-SD patients (3%; p = 0.003) which remained significant after adjusting for Injury Severity Score and age (p = 0.033). Overall t-PA activity (p = 0.002), PAI-1 (p < 0.001), and t-PA/PAI-1 complex levels (p = 0.006) differed between the six phenotypes, and 54% of fibrinolytic regulator proteins analyzed (n = 19) were significantly different. CONCLUSION: In conclusion, acute fibrinolysis SD is not caused by a single etiology, and is clearly associated with PAI-1 activity. The differential phenotypes require an ongoing investigation to identify the optimal resuscitation strategy for these patients. LEVEL OF EVIDENCE: Prognostic, level III.
[Mh] Termos MeSH primário: Transtornos da Coagulação Sanguínea/sangue
Fibrinólise/fisiologia
Inibidor 1 de Ativador de Plasminogênio/sangue
Ferimentos e Lesões/complicações
[Mh] Termos MeSH secundário: Adulto
Biomarcadores/sangue
Transtornos da Coagulação Sanguínea/etiologia
Transtornos da Coagulação Sanguínea/mortalidade
Ensaio de Imunoadsorção Enzimática
Feminino
Seguimentos
Seres Humanos
Escala de Gravidade do Ferimento
Masculino
Meia-Idade
Fenótipo
Prognóstico
Estudos Prospectivos
Proteômica
Tromboelastografia
Ferimentos e Lesões/sangue
Ferimentos e Lesões/diagnóstico
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Nm] Nome de substância:
0 (Biomarkers); 0 (Plasminogen Activator Inhibitor 1)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171219
[Lr] Data última revisão:
171219
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171201
[St] Status:MEDLINE
[do] DOI:10.1097/TA.0000000000001718


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[PMID]:29049169
[Au] Autor:Li Y; Liu FX; Yuan C; Meng L
[Ad] Endereço:aDepartment of Joint Surgery, Shandong Provincial Hospital Affiliated to Shandong University, Jinan bClinical Laboratory, Juye County Hospital of Traditional Chinese Medicine, Juye cShandong Province Shouguang People's Hospital, Shouguang dAffiliated Hospital of Taishan Medical University, Taian, Shandong, China.
[Ti] Título:Association between plasminogen activator inhibitor gene polymorphisms and osteonecrosis of the femoral head susceptibility: A case-control study.
[So] Source:Medicine (Baltimore);96(42):e7047, 2017 Oct.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:This study aimed to analyze the correlation of the plasminogen activator inhibitor (PAI-1) gene polymorphisms (rs6092 and rs7242) with susceptibility of osteonecrosis of the femoral head (ONFH).This case-control study included 106 ONFH patients and 151 healthy controls. PAI-1 polymorphisms were genotyped by polymerase chain reaction (PCR) with direct sequencing. The genotype distribution of polymorphism in the control group was checked with the status of Hardy-Weinberg equilibrium (HWE). The χ test was applied to compare the genotypes of polymorphisms between the case and control groups. The association intensity between PAI-1 polymorphisms and ONFH risk was estimated by odds ratios (ORs) and 95% confidence intervals (95% CI). The linkage disequilibrium of PAI-1 polymorphisms was analyzed by Haploview.We found that the genotypes and alleles of PAI-1 rs6092 and rs7242 polymorphisms had no obvious association with the risk of ONFH (P >.05). But the strong linkage disequilibrium existed between rs6092 and rs7242 polymorphisms and haplotype G-T was significantly associated with the decreased risk of ONFH occurrence (OR = 0.666, 95%CI = 0.445-0.998).PAI-1 rs6092 and rs7242 polymorphisms are not associated with ONFH development, but haplotype G-T may be a protective factor of ONFH.
[Mh] Termos MeSH primário: Grupo com Ancestrais do Continente Asiático/genética
Necrose da Cabeça do Fêmur/genética
Predisposição Genética para Doença/genética
Inibidor 1 de Ativador de Plasminogênio/genética
Polimorfismo de Nucleotídeo Único
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Alelos
Estudos de Casos e Controles
Feminino
Genótipo
Haplótipos
Seres Humanos
Desequilíbrio de Ligação
Masculino
Meia-Idade
Razão de Chances
Inibidor 1 de Ativador de Plasminogênio/sangue
Fatores de Risco
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Plasminogen Activator Inhibitor 1); 0 (SERPINE1 protein, human)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171122
[Lr] Data última revisão:
171122
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171020
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000007047


  5 / 8174 MEDLINE  
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[PMID]:28988111
[Au] Autor:Lin X; Lin BW; Chen XL; Zhang BL; Xiao XJ; Shi JS; Lin JD; Chen X
[Ad] Endereço:Cancer Center, Traditional Chinese Medicine-Integrated Hospital of Southern Medical University, Guangzhou 510315, Guangdong, PR China.
[Ti] Título:PAI-1/PIAS3/Stat3/miR-34a forms a positive feedback loop to promote EMT-mediated metastasis through Stat3 signaling in Non-small cell lung cancer.
[So] Source:Biochem Biophys Res Commun;493(4):1464-1470, 2017 Dec 02.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:AIM: This study intented to clarify the intracellular effect of PAI-1 on Non-small cell lung cancer (NSCLC) metastasis and the precise mechanism involved. METHODS: The metastatic properties of NSCLC cells were determined by transwell assays and wound-healing assay in vitro. The mRNA and protein expressions of genes were analyzed by Real-time qPCR and western blot, respectively. Pulmonary metastasis model of NSCLC cells was established to evaluate the pro-metastasis effect of PAI-1 and anti-metastatic effect of miR-34a in vivo. The gene targets of miR-34a were confirmed by luciferase reporter assays. Chromatin immunoprecipitation assay was employed to detect the transcriptional regulation of miR-34a. Co-immunoprecipitation assay was performed to observe the interaction of proteins. RESULTS: PAI-1, which was elevated in NSCLC patients with recurrence and metastasis, augmented NSCLC metastasis and was negatively related to the prognosis of NSCLC. miR-34a, which was decreased in NSCLC patients with metastasis, attenuated NSCLC metastasis and was positively correlated with the prognosis of NSCLC. Moreover, PAI-1 was identified as the target gene of miR-34a and activated the Stat3 signaling pathway to promote epithelial-mesenchymal transition (EMT) in NSCLC cells. PAI-1 interacted with PIAS3 to regulate Stat3-dependent gene expression and miR-34a was transcriptionally suppressed by Stat3 to form a positive regulatory loop through Stat3 signaling. CONCLUSION: Our findings suggest that PAI-1 and miR-34a, which can be clinically utilized as biomarkers for the clinical prognosis or diagnosis of NSCLC, are potential targets for the treatment of NSCLC.
[Mh] Termos MeSH primário: Carcinoma Pulmonar de Células não Pequenas/metabolismo
Carcinoma Pulmonar de Células não Pequenas/secundário
Neoplasias Pulmonares/metabolismo
MicroRNAs/metabolismo
Chaperonas Moleculares/metabolismo
Inibidor 1 de Ativador de Plasminogênio/metabolismo
Proteínas Inibidoras de STAT Ativados/metabolismo
Fator de Transcrição STAT3/metabolismo
[Mh] Termos MeSH secundário: Animais
Biomarcadores Tumorais/metabolismo
Carcinoma Pulmonar de Células não Pequenas/genética
Linhagem Celular Tumoral
Transição Epitelial-Mesenquimal/genética
Transição Epitelial-Mesenquimal/fisiologia
Retroalimentação Fisiológica
Técnicas de Silenciamento de Genes
Xenoenxertos
Seres Humanos
Neoplasias Pulmonares/genética
Neoplasias Pulmonares/patologia
Masculino
Camundongos
Camundongos Nus
MicroRNAs/genética
Chaperonas Moleculares/genética
Inibidor 1 de Ativador de Plasminogênio/genética
Prognóstico
Proteínas Inibidoras de STAT Ativados/genética
Fator de Transcrição STAT3/genética
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (MIRN34 microRNA, human); 0 (MicroRNAs); 0 (Molecular Chaperones); 0 (PIAS3 protein, human); 0 (Plasminogen Activator Inhibitor 1); 0 (Protein Inhibitors of Activated STAT); 0 (SERPINE1 protein, human); 0 (STAT3 Transcription Factor); 0 (STAT3 protein, human)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171009
[St] Status:MEDLINE


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[PMID]:28877230
[Au] Autor:Ettl J; Klein E; Hapfelmeier A; Grosse Lackmann K; Paepke S; Petry C; Specht K; Wolff L; Höfler H; Kiechle M
[Ad] Endereço:Klinik und Poliklinik für Frauenheilkunde, Klinikum rechts der Isar, Technische Universität München, Munich, Germany.
[Ti] Título:Decision impact and feasibility of different ASCO-recommended biomarkers in early breast cancer: Prospective comparison of molecular marker EndoPredict and protein marker uPA/PAI-1.
[So] Source:PLoS One;12(9):e0183917, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Adjuvant therapy decisions in early breast cancer are based on accurate risk assessment. Urokinase plasminogen activator (uPA) and plaminogen activator inhibitor-1 (PAI-1) have been the first biomarkers in hormone receptor (HR) positive breast cancer to reach highest level of evidence. The EndoPredict test (EPclin) combines gene expression information with nodal status and tumor size. The aim of this prospective study was to compare uPA/PAI-1 and EPclin as prognostic biomarkers with regard to feasibility, risk stratification and impact on adjuvant therapy recommendation. MATERIALS AND METHOD: 395 patients with HR positive, HER2 negative, intermediate risk breast cancer were enrolled. Relations and concordance of histologic grading as well as EPclin and uPA/PAI-1 values were assessed by Spearman's rank correlation coefficient and Cohen's Kappa. To compare decision impact of EPclin and uPA/PAI-1 three independent case discussions were held: One with known uPA/PAI-1 and EPclin results, one blinded to EPclin alone and another one blinded to both EPclin and uPA/PAI-1. RESULTS: EPclin could be determined in all 395 (100%), uPA/PAI-1 in 190 (48%) of the tumor samples. EPclin allocated 250 patients (63%) to the low-risk group and 145 patients (37%) to the high-risk group, whereas uPA/PAI-1 allocated 88 patients (46%) to the low-risk group and 102 patients (54%) to the high-risk group. In 59% of cases, both tests showed concordant results. EPclin resulted more frequently in a change of therapy recommendation than the uPA/PAI-1 test (46% vs 24%). Recommendation of adjuvant chemotherapy (CTX) was abandoned twice as often by EPclin (45%) compared to uPA/PAI-1 (22%). CONCLUSION: In this first prospective comparison of EPclin and uPA/PAI-1 we found, that EPclin is superior to uPA/PAI-1 with respect to feasibility and decision impact. This leads to substantial avoidance of adjuvant CTX in endocrine-sensitive, HER2-negative breast cancer. Data collection for patients´ clinical outcome is ongoing.
[Mh] Termos MeSH primário: Neoplasias da Mama/diagnóstico
Inibidor 1 de Ativador de Plasminogênio/análise
Ativador de Plasminogênio Tipo Uroquinase/análise
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Biomarcadores/análise
Neoplasias da Mama/química
Neoplasias da Mama/patologia
Neoplasias da Mama/terapia
Quimioterapia Adjuvante
Estudos de Viabilidade
Feminino
Seres Humanos
Meia-Idade
Guias de Prática Clínica como Assunto
Prognóstico
Estudos Prospectivos
Medição de Risco
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Plasminogen Activator Inhibitor 1); 0 (SERPINE1 protein, human); EC 3.4.21.73 (Urokinase-Type Plasminogen Activator)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171003
[Lr] Data última revisão:
171003
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170907
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0183917


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[PMID]:28870787
[Au] Autor:Lavigne J; Soysouvanh F; Buard V; Tarlet G; Guipaud O; Paget V; Milliat F; François A
[Ad] Endereço:Radiobiology and Radiopathology Research Laboratory, Department of Radiobiology and Epidemiology, Institute for Radiological Protection and Nuclear Safety, Fontenay-aux-Roses, France.
[Ti] Título:Conditional Plasminogen Activator Inhibitor Type 1 Deletion in the Endothelial Compartment Has No Beneficial Effect on Radiation-Induced Whole-Lung Damage in Mice.
[So] Source:Int J Radiat Oncol Biol Phys;99(4):972-982, 2017 Nov 15.
[Is] ISSN:1879-355X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: To investigate whether the endothelial pool of plasminogen activator inhibitor type 1 (PAI-1) plays a role in the development of radiation-induced lung damage, as previously demonstrated in the intestine. METHODS AND MATERIALS: Human lung microvascular endothelial cells were exposed to 10 Gy irradiation so as to study their ability to acquire an "activated" phenotype. Mice in which the Cre-Lox strategy was used to produce PAI-1 deletion specifically in the endothelial compartment were exposed to 17 Gy whole-thorax irradiation and followed up for 2, 13, and 23 weeks after irradiation. RESULTS: Human lung microvascular endothelial cells had an activated phenotype after radiation exposure, overexpressed PAI-1, and underwent endothelial-to-mesenchymal transition. In mice, knockout of PAI-1 in the endothelium had no beneficial effect on radiation-induced lung damage and showed a tendency to worsen acute lesions. CONCLUSIONS: As opposed to the intestine, the endothelial pool of PAI-1 does not play a determinant role in the development of radiation-induced lung damage. The therapeutic value of PAI-1 inhibition in lung radiation injury may be associated with other types of cells.
[Mh] Termos MeSH primário: Endotélio Vascular/metabolismo
Transição Epitelial-Mesenquimal
Pulmão/metabolismo
Pulmão/efeitos da radiação
Inibidor 1 de Ativador de Plasminogênio/metabolismo
Lesões Experimentais por Radiação/etiologia
Lesões Experimentais por Radiação/metabolismo
[Mh] Termos MeSH secundário: Animais
Movimento Celular
Endotélio Vascular/efeitos da radiação
Técnicas de Inativação de Genes/métodos
Seres Humanos
Pulmão/citologia
Macrófagos
Camundongos
Camundongos Knockout
Neutrófilos
Inibidor 1 de Ativador de Plasminogênio/deficiência
Inibidor 1 de Ativador de Plasminogênio/genética
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Plasminogen Activator Inhibitor 1)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170906
[St] Status:MEDLINE


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[PMID]:28863189
[Au] Autor:Gindele JA; Mang S; Pairet N; Christ I; Gantner F; Schymeinsky J; Lamb DJ
[Ad] Endereço:Immunology & Respiratory Diseases Research, Boehringer Ingelheim Pharma GmbH & Co. KG, Biberach an der Riß, Germany.
[Ti] Título:Opposing effects of in vitro differentiated macrophages sub-type on epithelial wound healing.
[So] Source:PLoS One;12(9):e0184386, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Inappropriate repair responses to pulmonary epithelial injury have been linked to perturbation of epithelial barrier function and airway remodelling in a number of respiratory diseases, including chronic obstructive pulmonary disease and idiopathic pulmonary fibrosis. We developed an in vitro mechanical scratch injury model in air-liquid interface differentiated primary human small airway epithelial cells that recapitulates many of the characteristics observed during epithelial wound injury in both human tissue and small animal models. Wound closure was initially associated with de-differentiation of the differentiated apical cells and rapid migration into the wound site, followed by proliferation of apical cells behind the wound edge, together with increases in FAK expression, fibronectin and reduction in PAI-1 which collectively facilitate cell motility and extracellular matrix deposition. Macrophages are intimately involved in wound repair so we sought to investigate the role of macrophage sub-types on this process in a novel primary human co-culture model. M1 macrophages promoted FAK expression and both M1 and M2 macrophages promoted epithelial de-differentiation. Interestingly, M2a macrophages inhibited both proliferation and fibronectin expression, possibly via the retinoic acid pathway, whereas M2b and M2c macrophages prevented fibronectin deposition, possibly via MMP expression. Collectively these data highlight the complex nature of epithelial wound closure, the differential impact of macrophage sub-types on this process, and the heterogenic and non-delineated function of these macrophages.
[Mh] Termos MeSH primário: Epitélio/metabolismo
Macrófagos/citologia
Cicatrização/fisiologia
[Mh] Termos MeSH secundário: Remodelação das Vias Aéreas
Brônquios/citologia
Diferenciação Celular
Movimento Celular
Proliferação Celular
Técnicas de Cocultura
Matriz Extracelular
Feminino
Proteína-Tirosina Quinases de Adesão Focal/metabolismo
Seres Humanos
Meia-Idade
Monócitos/citologia
Fenótipo
Inibidor 1 de Ativador de Plasminogênio/genética
Inibidor 1 de Ativador de Plasminogênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Plasminogen Activator Inhibitor 1); 0 (SERPINE1 protein, human); EC 2.7.10.2 (Focal Adhesion Protein-Tyrosine Kinases)
[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:170902
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184386


  9 / 8174 MEDLINE  
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[PMID]:28858863
[Au] Autor:Bubalo P; Buterin I; Salek Z; Ðogic V; Zupancic-Salek S
[Ad] Endereço:Zagreb County Institute of Emergency Medicine, University Hospital Centre Zagreb, Zagreb, Croatia.
[Ti] Título:Association of Plasminogen Activator Inhibitor-1 Gene Polymorphisms and Methylene Tetrahydrofolate Reductase Polymorphisms with Spontaneous Miscarriages.
[So] Source:Acta Haematol;138(2):111-115, 2017.
[Is] ISSN:1421-9662
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:AIM: The objective of this study was to investigate a possible correlation between the plasminogen activator inhibitor-1 (PAI-1) and methylene tetrahydrofolate reductase (MTHFR) polymorphisms and unexplained spontaneous miscarriages (SM). MATERIALS AND METHODS: PAI-1 polymorphisms were evaluated in 150 women with pregnancy in their history. One hundred women with a history of SM formed the study group and 50 women with normal pregnancies served as the control group. Also, the combination of PAI-1 and MTHFR polymorphisms were evaluated in 138 women out of a total of 150, which included 92 women with SM in their history compared to 46 women in the control group. For statistical analysis, χ2 test, Phi, and Cramer V tests were used; p < 0.05 was taken as a statistically significant result. RESULTS: Our findings show: (a) the correlation between SM and PAI-1 mutations reaches statistical significance (p = 0.026); (b) there was a statistically significant difference between heterozygous PAI-1 in women with only 1 SM compared to the control group (p = 0.047); (c) the comparison of combinations of both mutations, PAI-1 and MTHFR, with the control group demonstrates statistical significance in favor of women with SM and both mutations (p = 0.022). CONCLUSION: PAI-1 and MTHFR polymorphisms may play an important role in pregnancy complications because heterozygous PAI-1 mutations and a combination of both PAI-1 and MTHFR mutations might contribute to SM.
[Mh] Termos MeSH primário: Aborto Espontâneo/genética
Predisposição Genética para Doença
Metilenotetra-Hidrofolato Redutase (NADPH2)/genética
Inibidor 1 de Ativador de Plasminogênio/genética
Polimorfismo Genético
[Mh] Termos MeSH secundário: Aborto Espontâneo/enzimologia
Adulto
Estudos de Casos e Controles
Feminino
Genótipo
Heterozigoto
Seres Humanos
Razão de Chances
Gravidez
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Plasminogen Activator Inhibitor 1); 0 (SERPINE1 protein, human); EC 1.5.1.20 (Methylenetetrahydrofolate Reductase (NADPH2))
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170901
[St] Status:MEDLINE
[do] DOI:10.1159/000478084


  10 / 8174 MEDLINE  
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[PMID]:28857040
[Au] Autor:Yang CH; Li HC; Ku TS; Wu PC; Yeh YJ; Cheng JC; Lin TY; Lo SY
[Ad] Endereço:1​Institute of medical Sciences, Tzu Chi University, Hualien, Taiwan, ROC.
[Ti] Título:Hepatitis C virus down-regulates SERPINE1/PAI-1 expression to facilitate its replication.
[So] Source:J Gen Virol;98(9):2274-2286, 2017 Sep.
[Is] ISSN:1465-2099
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Identification of host factors involved in viral replication is critical for understanding the molecular mechanism of viral replication and pathogenesis. Genes differentially expressed in HuH-7 cells with or without a hepatitis C virus (HCV) sub-genomic replicon were screened by microarray analysis. SERPINE1/PAI-1 was found to be down-regulated after HCV infection in this analysis. Down-regulation of SERPINE1/PAI-1 expression at the transcriptional level was verified by the real-time reverse transcriptase (RT)-PCR assay. Reduced SERPINE1/PAI-1 protein secretion was detected in the supernatant of HCV replicon cells and in sera from HCV-infected patients. SERPINE1 gene expression was down-regulated by HCV NS3/4A and NS5A proteins through the transforming growth factor-ß (TGF-ß) signalling pathway at the transcriptional level. Down-regulated genes in HCV replicon cells could be the factors supressing HCV replication. Indeed, over-expressed PAI-1 inhibited HCV replication but the mechanism is unknown. It has been demonstrated that HCV induces the expression of TGF-ß, and TGF-ß enhances HCV replication by a not-yet-defined mechanism. SERPINE1/PAI-1 is also known to be potently induced by TGF-ß at the transcriptional level through both Smad-dependent and Smad-independent pathways. The exogenously expressed SERPINE1/PAI-1 suppressed the expression of the endogenous SERPINE1 gene at the transcriptional level through the TGF-ß signalling but not the Smad pathway. Thus, SERPINE1/PAI-1 could suppress HCV replication possibly by negatively regulating TGF-ß signalling. A model is proposed for the interplay betweenthe TGF-ß signalling pathway, HCV and SERPINE1/PAI-1 to keep the homeostasis of the cells.
[Mh] Termos MeSH primário: Hepacivirus/fisiologia
Hepatite C/genética
Inibidor 1 de Ativador de Plasminogênio/genética
Replicação Viral
[Mh] Termos MeSH secundário: Regulação para Baixo
Hepacivirus/genética
Hepatite C/metabolismo
Hepatite C/virologia
Interações Hospedeiro-Patógeno
Seres Humanos
Inibidor 1 de Ativador de Plasminogênio/metabolismo
Transdução de Sinais
Fator de Crescimento Transformador beta/genética
Fator de Crescimento Transformador beta/metabolismo
Proteínas não Estruturais Virais/genética
Proteínas não Estruturais Virais/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Plasminogen Activator Inhibitor 1); 0 (SERPINE1 protein, human); 0 (Transforming Growth Factor beta); 0 (Viral Nonstructural Proteins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170919
[Lr] Data última revisão:
170919
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170901
[St] Status:MEDLINE
[do] DOI:10.1099/jgv.0.000901



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