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  1 / 1980 MEDLINE  
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[PMID]:29023605
[Au] Autor:Kobayashi H; Otsubo T; Teraoka F; Ikeda K; Seike S; Takahashi E; Okamoto K; Yoshida T; Tsuge H; Yamanaka H
[Ad] Endereço:Laboratory of Molecular Microbiological Science, Faculty of Pharmaceutical Sciences, Hiroshima International University, Hiroshima, Japan.
[Ti] Título:Involvement of the Arg566 residue of Aeromonas sobria serine protease in substrate specificity.
[So] Source:PLoS One;12(10):e0186392, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Aeromonas sobria serine protease (ASP) is an extracellular serine protease secreted by the organism. Here, we identified the amino acid residue of ASP that contributes to substrate specificity by using both synthetic peptides and biological protein components. The results showed that the arginine residue at position 566 (Arg-566) of ASP, which is located in the extra occluding region of ASP close to an entrance of the catalytic cavity, is involved in the substrate specificity. A substitutional point mutation of the Arg-566 residue of ASP to Ala residue (ASP[R566A]) caused a decrease of the proteolytic efficiency for a certain substrate. In addition, ASP lost the ability to recognize the primary substrate by such a point mutation, and ASP[R566A] reacted to a wide range of synthetic substrates. It is likely that Arg-566 causes an interaction with the amino acid residue at position P3 of the substrate, which is the third amino acid residue upstream from the cleavage site. Another study using ORF2 protein, a chaperone protein of ASP, further suggested that Arg-566 could also play an important role in interaction with ORF2. We therefore conclude that the Arg-566 residue of ASP is likely responsible for the selection of substrates.
[Mh] Termos MeSH primário: Aeromonas/enzimologia
Arginina/metabolismo
Proteínas de Bactérias/metabolismo
Serina Proteases/metabolismo
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Arginina/química
Proteínas de Bactérias/química
Proteínas de Bactérias/genética
Fibrinogênio/metabolismo
Seres Humanos
Cininogênios/metabolismo
Chaperonas Moleculares/metabolismo
Mutagênese Sítio-Dirigida
Proteólise
Serina Proteases/química
Serina Proteases/genética
Especificidade por Substrato
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bacterial Proteins); 0 (Kininogens); 0 (Molecular Chaperones); 9001-32-5 (Fibrinogen); 94ZLA3W45F (Arginine); EC 3.4.- (Serine Proteases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171013
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0186392


  2 / 1980 MEDLINE  
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[PMID]:28707730
[Au] Autor:Suffritti C; Tobaldini E; Schiavon R; Strada S; Maggioni L; Mehta S; Sandrone G; Toschi-Dias E; Cicardi M; Montano N
[Ad] Endereço:Departments of Biomedical and Clinical Sciences 'L. Sacco', University of Milan, Milan, Italy.
[Ti] Título:Complement and contact system activation in acute congestive heart failure patients.
[So] Source:Clin Exp Immunol;190(2):251-257, 2017 Nov.
[Is] ISSN:1365-2249
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Recent experimental data indicate a pathogenic role of complement activation in congestive heart failure (CHF). The aim of this study was to evaluate contact and complement systems activation in patients hospitalized for an acute episode of CHF. Forty-two of 80 consecutive patients admitted at our hospital with confirmed diagnosis of acute CHF were enrolled. They underwent blood sampling within 24 h from admission (T0) and at clinical stability (T1). Patients were stratified for ejection fraction (EF) based on echocardiographic test. We measured plasma levels of C3, C4, sC5b-9 and cleaved high molecular weight kininogen (contact activation marker). At T1, C3 levels increased significantly compared to T0 (97 ± 2 versus 104 ± 3% of total pooled plasma, P < 0·01). Classifying patients according to EF, only patients with preserved EF presented a significant increase of C3 from T0 to T1 (99 ± 3 versus 108 ± 4%, P = 0·03). When the sample was stratified according to clinical outcome, C3 (98 ± 3 versus 104 ± 4%, P = 0·03) and sC5b-9 levels (204 ± 10 versus 230 ± 11 ng/ml, P = 0·03) were increased in patients who had positive outcome after hospitalization. CHF patients with preserved EF and positive outcome after hospitalization showed higher levels of sC5b-9 in the T1 period compared with T0 (211 ± 14 versus 243 ± 14 ng/ml, P = 0·04). Our results suggest that the complement system reacts differently if CHF occurs with preserved or reduced EF. This finding is interesting if we consider the difference in epidemiology, pathogenesis and possible therapeutic approaches of these two clinical entities.
[Mh] Termos MeSH primário: Ativação do Complemento
Insuficiência Cardíaca/imunologia
Insuficiência Cardíaca/fisiopatologia
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Complemento C3/análise
Complemento C4/análise
Complexo de Ataque à Membrana do Sistema Complemento/análise
Feminino
Insuficiência Cardíaca/diagnóstico
Hospitalização
Seres Humanos
Cininogênios/sangue
Masculino
Volume Sistólico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Complement C3); 0 (Complement C4); 0 (Complement Membrane Attack Complex); 0 (Kininogens)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171025
[Lr] Data última revisão:
171025
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170715
[St] Status:MEDLINE
[do] DOI:10.1111/cei.13011


  3 / 1980 MEDLINE  
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[PMID]:28628609
[Au] Autor:Gao B; Yu T; Xue D; Sun B; Shao Q; Choudhry H; Marcus V; Ragoussis J; Zhang Y; Zhang W; Gao ZH
[Ad] Endereço:Department of General Surgery, the First Affiliated Hospital of Harbin Medical University, Harbin, China.
[Ti] Título:A multidimensional integration analysis reveals potential bridging targets in the process of colorectal cancer liver metastasis.
[So] Source:PLoS One;12(6):e0178760, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Approximately 9% of cancer-related deaths are caused by colorectal cancer. Liver metastasis is a major factor for the high colorectal cancer mortality rate. However, the molecular mechanism underlying colorectal cancer liver metastasis remains unclear. Using a global and multidimensional integration approach, we studied sequencing data, protein-protein interactions, and regulation of transcription factor and non-coding RNAs in primary tumor samples and liver metastasis samples to unveil the potential bridging molecules and the regulators that functionally link different stages of colorectal cancer liver metastasis. Primary tumor samples and liver metastasis samples had modules with significant overlap and crosstalk from which we identified several bridging genes (e.g. KNG1 and COX5B), transcription factors (e.g. E2F4 and CDX2), microRNAs (e.g. miR-590-3p and miR-203) and lncRNAs (e.g. lincIRX5 and lincFOXF1) that may play an important role in the process of colorectal cancer liver metastasis. This study enhances our understanding of the genetic alterations and transcriptional regulation that drive the metastatic process, but also provides the methodology to guide the studies on other metastatic cancers.
[Mh] Termos MeSH primário: Neoplasias Colorretais/patologia
Neoplasias Hepáticas/secundário
[Mh] Termos MeSH secundário: Fator de Transcrição CDX2/genética
Fator de Transcrição CDX2/metabolismo
Neoplasias Colorretais/genética
Neoplasias Colorretais/mortalidade
Bases de Dados Genéticas
Fator de Transcrição E2F4/genética
Fator de Transcrição E2F4/metabolismo
Complexo IV da Cadeia de Transporte de Elétrons/genética
Complexo IV da Cadeia de Transporte de Elétrons/metabolismo
Regulação Neoplásica da Expressão Gênica
Redes Reguladoras de Genes
Seres Humanos
Cininogênios/genética
Cininogênios/metabolismo
Neoplasias Hepáticas/genética
Neoplasias Hepáticas/metabolismo
MicroRNAs/metabolismo
Mapas de Interação de Proteínas/genética
RNA Longo não Codificante/metabolismo
Taxa de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CDX2 Transcription Factor); 0 (CDX2 protein, human); 0 (E2F4 Transcription Factor); 0 (E2F4 protein, human); 0 (Kininogens); 0 (MicroRNAs); 0 (RNA, Long Noncoding); 0 (kininogen 1, human); EC 1.9.3.1 (COX5B protein, human); EC 1.9.3.1 (Electron Transport Complex IV)
[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:170620
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0178760


  4 / 1980 MEDLINE  
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[PMID]:28367083
[Au] Autor:Lin CH; Liao CC; Huang CH; Tung YT; Chang HC; Hsu MC; Huang CC
[Ad] Endereço:Physical Education Office, Yuan Ze University, Taoyuan 32003, Taiwan.
[Ti] Título:Proteomics Analysis to Identify and Characterize the Biomarkers and Physical Activities of Non-Frail and Frail Older Adults.
[So] Source:Int J Med Sci;14(3):231-239, 2017.
[Is] ISSN:1449-1907
[Cp] País de publicação:Australia
[La] Idioma:eng
[Ab] Resumo:Globally, the proportion of older adults is increasing. Older people face chronic conditions such as sarcopenia and functional decline, which are often associated with disability and frailty. Proteomics assay of potential serum biomarkers of frailty in older adults. Older adults were divided into non-frail and frail groups ( = 6 each; 3 males in each group) in accordance with the Chinese-Canadian Study of Health and Aging Clinical Frailty Scale. Adults were measured for grip power and the 6-min walk test for physical activity, and venous blood was sampled after adults fasted for 8 h. Ultra-high-performance liquid chromatography-tandem mass spectrometry was used for proteomics assay. The groups were compared for levels of biomarkers by test and Pearson correlation analysis. Non-frail and frail subjects had mean age 77.5±0.4 and 77.7±1.6 years, mean height 160.5±1.3 and 156.6±2.9 cm and mean weight 62.5±1.2 and 62.8±2.9 kg, respectively. Physical activity level was lower for frail than non-frail subjects (grip power: 13.8±0.4 26.1±1.2 kg; 6-min walk test: 215.2±17.2 438.3±17.2 m). Among 226 proteins detected, for 31, serum levels were significantly higher for frail than non-frail subjects; serum levels of Ig kappa chain V-III region WOL, COX7A2, and albumin were lower. The serum levels of ANGT, KG and AT were 2.05-, 1.76- and 2.22-fold lower (all < 0.05; Figure 1A, 2A and 3A) for non-frail than frail subjects and were highly correlated with grip power (Figure 1B, 2B and 3B). Our study found that ANGT, KG and AT levels are known to increase with aging, so degenerated vascular function might be associated with frailty. In total, 226 proteins were revealed proteomics assay; levels of angiotensinogen (ANGT), kininogen-1 (KG) and antithrombin III (AT) were higher in frail than non-frail subjects (11.26±2.21 5.09±0.74; 18.42±1.36 11.64±1.36; 22.23±1.64 9.52±0.95, respectively, < 0.05). These 3 factors were highly correlated with grip power ( < 0.05), with higher correlations between grip power and serum levels of ANGT (r = -0.89), KG (r = -0.90), and AT (r = -0.84). In conclusion, this is the first study to demonstrate a serum proteomic profile characteristic of frailty in older adults. Serum ANGT, KG and AT levels could be potential biomarkers for monitoring the development and progression of frailty in older adults.
[Mh] Termos MeSH primário: Envelhecimento/sangue
Biomarcadores/sangue
Idoso Fragilizado
Proteômica
Sarcopenia/sangue
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Envelhecimento/patologia
Angiotensinogênio/sangue
Antitrombina III/metabolismo
Exercício
Feminino
Força da Mão/fisiologia
Seres Humanos
Cininogênios/sangue
Masculino
Sarcopenia/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Kininogens); 11002-13-4 (Angiotensinogen); 9000-94-6 (Antithrombin III)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170717
[Lr] Data última revisão:
170717
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170404
[St] Status:MEDLINE
[do] DOI:10.7150/ijms.17627


  5 / 1980 MEDLINE  
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[PMID]:28272695
[Au] Autor:Luan SX; Chen XH
[Ad] Endereço:Department of Reproductive Medicine, Weifang People's Hospital, Weifang, Shandong, China. zhenyunyin123@sina.com.
[Ti] Título:The glucocorticoid inhibits neutrophils formed extracellular traps (NETs) and suppresses the inflammation caused by fallopian tube staphylococcal infection.
[So] Source:Eur Rev Med Pharmacol Sci;21(4):855-860, 2017 Feb.
[Is] ISSN:2284-0729
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Fallopian tube can transport zygote into the uterine cavity, while inflammation may cause certain influences on the fallopian tube's function. Neutrophils formed extracellular traps (NET) can kill pathogenic microorganisms. This study intends to analyze the role of glucocorticoid in the regulation of NETs sterilization during the fallopian tube staphylococcal infection. MATERIALS AND METHODS: Rat fallopian tube staphylococcal infection model was established. Group A was the control group, group B was the model group, and group C was the dexamethasone intervention group. ELISA was applied to test inflammatory factors, including citrullinated histone H3 (CitH3) and high molecular weight kininogen (HK) content in serum. RT-PCR was performed to test the mRNA expression of glucocorticoid receptor α, ß (GR-α, GR-ß). Western blot was used to detect the protein levels of GR-α and GR-ß. RESULTS: Microscopically, group A showed clear fallopian tube wall and unobstructed lumen. Group B presented obscured tube wall, blocked lumen, and inflammatory cells infiltration. Group C demonstrated unclear tube wall and a few inflammatory cells infiltration. Serum CitH3 level was increased, while HK was down-regulated in group B compared with group A. CitH3 was declined, whereas HK was enhanced in group C compared with group B (p<0.05). The mRNA expression of GR-ß was reduced, while GR-α expression was elevated in group C compared with group A and B. Group B showed upregulated GR-ß expression and reduced GR-α mRNA and protein expression compared with group A (p<0.05). CONCLUSIONS: Rat fallopian tube Staphylococcus aureus infection activates NETs, elevates CitH3, and decreases HK. Glucocorticoid can inhibit inflammation through down-regulate GR-ß and up-regulate GR-α expression.
[Mh] Termos MeSH primário: Dexametasona/farmacologia
Armadilhas Extracelulares
Tubas Uterinas/microbiologia
Glucocorticoides/farmacologia
Infecções Estafilocócicas/imunologia
[Mh] Termos MeSH secundário: Animais
Feminino
Histonas/metabolismo
Inflamação
Cininogênios/metabolismo
Neutrófilos/citologia
RNA Mensageiro/genética
Ratos
Receptores de Glucocorticoides/genética
Receptores de Glucocorticoides/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glucocorticoids); 0 (Histones); 0 (Kininogens); 0 (RNA, Messenger); 0 (Receptors, Glucocorticoid); 7S5I7G3JQL (Dexamethasone)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170727
[Lr] Data última revisão:
170727
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170309
[St] Status:MEDLINE


  6 / 1980 MEDLINE  
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[PMID]:28265106
[Au] Autor:Tang Z; Zhai W; Wang Z; Hu Z; Zhang M
[Ad] Endereço:Department of Cardiovascular Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei, China (mainland).
[Ti] Título:Profiling Proteinic Changes Induced by Vildagliptin Treatment in a Mouse Lung Transplantation Model: The Role of Kininogen-1.
[So] Source:Ann Transplant;22:128-137, 2017 Mar 07.
[Is] ISSN:2329-0358
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND This study investigated the protective effects of pharmaceutical CD26/dipeptidylpeptidase-4 (CD26/DPP-4) inhibitor in lung transplantation (LTx). Changes in protein expression associated with the treatment were screened and identified to evaluate the role of kininogen-1 in early-term ischemia/reperfusion (I/R) injury after LTx. MATERIAL AND METHODS Orthotopic single LTx was performed in syngeneic C57BL/6 mice, with a pharmaceutical CD26/DPP-4 inhibitor (vildagliptin, subcutaneous injection, 10 mg/kg, every 12 h) administered to the investigational group. All donors were perfused and preserved with low potassium dextran (LPD). Grafts were harvested at 60 h post-transplantation after 8 h of cold ischemia. Myeloperoxidase activity and wet/dry weight ratio were measured, followed by histopathological examination. Proteins were separated, analyzed, and identified using proteomics and database searches. The target proteins were validated by Western blot. Immunohistochemical studies were performed in the same lung specimen locus. RESULTS Investigational group (IN) versus control group (CON) comparison showed decreased myeloperoxidase enzymatic activity, as well as decreased edema and interstitial-alveolar inflammation. Proteomics results revealed 78 spots with significant differences in abundance between the 2 groups. Fifteen proteins were identified. Kininogen-1 was up-regulated in CON and down-regulated in IN, with contrasting results for the heat shock protein 70. Immunohistochemical results revealed significantly different staining with kininogen-1 in alveolar macrophages and inflammatory cells. CONCLUSIONS Combined vildagliptin and LPD significantly ameliorated I/R injury after LTx. This treatment may change local pulmonary protein levels. Moreover, proper application of proteins such as kininogen-1 may enhance the protective effects against I/R injury during transplantation.
[Mh] Termos MeSH primário: Adamantano/análogos & derivados
Inibidores da Dipeptidil Peptidase IV/uso terapêutico
Cininogênios/metabolismo
Transplante de Pulmão/métodos
Pulmão/metabolismo
Nitrilos/uso terapêutico
Pirrolidinas/uso terapêutico
[Mh] Termos MeSH secundário: Adamantano/farmacologia
Adamantano/uso terapêutico
Animais
Inibidores da Dipeptidil Peptidase IV/farmacologia
Modelos Animais de Doenças
Regulação para Baixo
Imuno-Histoquímica
Masculino
Camundongos
Nitrilos/farmacologia
Peroxidase/metabolismo
Pirrolidinas/farmacologia
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dipeptidyl-Peptidase IV Inhibitors); 0 (Kininogens); 0 (Nitriles); 0 (Pyrrolidines); EC 1.11.1.7 (Peroxidase); I6B4B2U96P (vildagliptin); PJY633525U (Adamantane)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170323
[Lr] Data última revisão:
170323
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170308
[St] Status:MEDLINE


  7 / 1980 MEDLINE  
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[PMID]:28053049
[Au] Autor:Sennblad B; Basu S; Mazur J; Suchon P; Martinez-Perez A; van Hylckama Vlieg A; Truong V; Li Y; Gådin JR; Tang W; Grossman V; de Haan HG; Handin N; Silveira A; Souto JC; Franco-Cereceda A; Morange PE; Gagnon F; Soria JM; Eriksson P; Hamsten A; Maegdefessel L; Rosendaal FR; Wild P; Folsom AR; Trégouët DA; Sabater-Lleal M
[Ad] Endereço:Cardiovascular Medicine Unit, Department of Medicine, Karolinska Institutet, Stockholm, Sweden.
[Ti] Título:Genome-wide association study with additional genetic and post-transcriptional analyses reveals novel regulators of plasma factor XI levels.
[So] Source:Hum Mol Genet;26(3):637-649, 2017 Feb 01.
[Is] ISSN:1460-2083
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Coagulation factor XI (FXI) has become increasingly interesting for its role in pathogenesis of thrombosis. While elevated plasma levels of FXI have been associated with venous thromboembolism and ischemic stroke, its deficiency is associated with mild bleeding. We aimed to determine novel genetic and post-transcriptional plasma FXI regulators.We performed a genome-wide association study (GWAS) for plasma FXI levels, using novel data imputed to the 1000 Genomes reference panel. Individual GWAS analyses, including a total of 16,169 European individuals from the ARIC, GHS, MARTHA and PROCARDIS studies, were meta-analysed and further replicated in 2,045 individuals from the F5L family, GAIT2 and MEGA studies. Additional association with activated partial thromboplastin time (aPTT) was tested for the top SNPs. In addition, a study on the effect of miRNA on FXI regulation was performed using in silico prediction tools and in vitro luciferase assays.Three loci showed robust, replicating association with circulating FXI levels: KNG1 (rs710446, P-value = 2.07 × 10-302), F11 (rs4253417, P-value = 2.86 × 10-193), and a novel association in GCKR (rs780094, P-value = 3.56 ×10-09), here for the first time implicated in FXI regulation. The two first SNPs (rs710446 and rs4253417) also associated with aPTT. Conditional and haplotype analyses demonstrated a complex association signal, with additional novel SNPs modulating plasma FXI levels in both the F11 and KNG1 loci. Finally, eight miRNAs were predicted to bind F11 mRNA. Over-expression of either miR-145 or miR-181 significantly reduced the luciferase activity in cells transfected with a plasmid containing FXI-3'UTR.These results should open the door to new therapeutic targets for thrombosis prevention.
[Mh] Termos MeSH primário: Proteínas Adaptadoras de Transdução de Sinal/genética
Moléculas de Adesão Celular/sangue
Cininogênios/genética
Receptores de Superfície Celular/sangue
Trombose/genética
[Mh] Termos MeSH secundário: Moléculas de Adesão Celular/genética
Simulação por Computador
Feminino
Regulação da Expressão Gênica/genética
Redes Reguladoras de Genes/genética
Predisposição Genética para Doença
Estudo de Associação Genômica Ampla
Seres Humanos
Masculino
Tempo de Tromboplastina Parcial
Polimorfismo de Nucleotídeo Único
Processamento de Proteína Pós-Traducional/genética
Receptores de Superfície Celular/genética
Trombose/sangue
Trombose/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (Cell Adhesion Molecules); 0 (F11R protein, human); 0 (GCKR protein, human); 0 (Kininogens); 0 (Receptors, Cell Surface); 0 (kininogen 1, human)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170915
[Lr] Data última revisão:
170915
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170106
[St] Status:MEDLINE
[do] DOI:10.1093/hmg/ddw401


  8 / 1980 MEDLINE  
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[PMID]:28044105
[Au] Autor:Cruz-Silva I; Nunes VA; Gozzo AJ; Praxedes-Garcia P; Tanaka AS; Shimamoto K; Araujo MS
[Ad] Endereço:Department of Biochemistry, Universidade Federal de São Paulo, Rua Três de Maio, No. 100, 04044-020 São Paulo, SP, Brazil.
[Ti] Título:Protease Inhibitors Extracted from Lam. Affect Kinin Release during Lung Inflammation.
[So] Source:Pulm Med;2016:9425807, 2016.
[Is] ISSN:2090-1844
[Cp] País de publicação:Egypt
[La] Idioma:eng
[Ab] Resumo:Inflammation is an essential process in many pulmonary diseases in which kinins are generated by protease action on kininogen, a phenomenon that is blocked by protease inhibitors. We evaluated kinin release in an lung inflammation model in rats, in the presence or absence of CeKI ( kallikrein inhibitor), a plasma kallikrein, cathepsin G, and proteinase-3 inhibitor, and rCeEI (recombinant elastase inhibitor), which inhibits these proteases and also neutrophil elastase. Wistar rats were intravenously treated with buffer (negative control) or inhibitors and, subsequently, lipopolysaccharide was injected into their lungs. Blood, bronchoalveolar lavage fluid (BALF), and lung tissue were collected. In plasma, kinin release was higher in the LPS-treated animals in comparison to CeKI or rCeEI groups. rCeEI-treated animals presented less kinin than CeKI-treated group. Our data suggest that kinins play a pivotal role in lung inflammation and may be generated by different enzymes; however, neutrophil elastase seems to be the most important in the lung tissue context. These results open perspectives for a better understanding of biological process where neutrophil enzymes participate and indicate these plant inhibitors and their recombinant correlates for therapeutic trials involving pulmonary diseases.
[Mh] Termos MeSH primário: Caesalpinia
Neutrófilos
Pneumonia
[Mh] Termos MeSH secundário: Animais
Catepsina G/metabolismo
Modelos Animais de Doenças
Cininogênios/metabolismo
Modelos Biológicos
Neutrófilos/efeitos dos fármacos
Neutrófilos/enzimologia
Compostos Fitoquímicos/farmacologia
Calicreína Plasmática/metabolismo
Pneumonia/tratamento farmacológico
Pneumonia/enzimologia
Inibidores de Proteases/farmacologia
Ratos
Sementes
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Kininogens); 0 (Phytochemicals); 0 (Protease Inhibitors); EC 3.4.21.20 (Cathepsin G); EC 3.4.21.34 (Plasma Kallikrein)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170306
[Lr] Data última revisão:
170306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170104
[St] Status:MEDLINE
[do] DOI:10.1155/2016/9425807


  9 / 1980 MEDLINE  
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[PMID]:28005926
[Au] Autor:Brunel H; Massanet R; Martinez-Perez A; Ziyatdinov A; Martin-Fernandez L; Souto JC; Perera A; Soria JM
[Ad] Endereço:Unit of Genomics of Complex Diseases, Sant Pau Institute of Biomedical Research (IIB-Sant Pau), Barcelona, Spain.
[Ti] Título:The Central Role of KNG1 Gene as a Genetic Determinant of Coagulation Pathway-Related Traits: Exploring Metaphenotypes.
[So] Source:PLoS One;11(12):e0167187, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Traditional genetic studies of single traits may be unable to detect the pleiotropic effects involved in complex diseases. To detect the correlation that exists between several phenotypes involved in the same biological process, we introduce an original methodology to analyze sets of correlated phenotypes involved in the coagulation cascade in genome-wide association studies. The methodology consists of a two-stage process. First, we define new phenotypic meta-variables (linear combinations of the original phenotypes), named metaphenotypes, by applying Independent Component Analysis for the multivariate analysis of correlated phenotypes (i.e. the levels of coagulation pathway-related proteins). The resulting metaphenotypes integrate the information regarding the underlying biological process (i.e. thrombus/clot formation). Secondly, we take advantage of a family based Genome Wide Association Study to identify genetic elements influencing these metaphenotypes and consequently thrombosis risk. Our study utilized data from the GAIT Project (Genetic Analysis of Idiopathic Thrombophilia). We obtained 15 metaphenotypes, which showed significant heritabilities, ranging from 0.2 to 0.7. These results indicate the importance of genetic factors in the variability of these traits. We found 4 metaphenotypes that showed significant associations with SNPs. The most relevant were those mapped in a region near the HRG, FETUB and KNG1 genes. Our results are provocative since they show that the KNG1 locus plays a central role as a genetic determinant of the entire coagulation pathway and thrombus/clot formation. Integrating data from multiple correlated measurements through metaphenotypes is a promising approach to elucidate the hidden genetic mechanisms underlying complex diseases.
[Mh] Termos MeSH primário: Cininogênios/genética
Trombofilia/genética
[Mh] Termos MeSH secundário: Coagulação Sanguínea
Fetuína-B/genética
Loci Gênicos
Estudo de Associação Genômica Ampla
Genótipo
Seres Humanos
Modelos Teóricos
Fenótipo
Polimorfismo de Nucleotídeo Único
Análise de Componente Principal
Proteínas/genética
Trombofilia/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (FETUB protein, human); 0 (Fetuin-B); 0 (Kininogens); 0 (Proteins); 0 (histidine-rich proteins); 0 (kininogen 1, human)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161223
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0167187


  10 / 1980 MEDLINE  
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[PMID]:27829441
[Au] Autor:Koh YQ; Peiris HN; Vaswani K; Reed S; Rice GE; Salomon C; Mitchell MD
[Ad] Endereço:University of Queensland Centre for Clinical Research, The University of Queensland, Brisbane, Queensland, Australia.
[Ti] Título:Characterization of exosomal release in bovine endometrial intercaruncular stromal cells.
[So] Source:Reprod Biol Endocrinol;14(1):78, 2016 Nov 09.
[Is] ISSN:1477-7827
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Cell-to-cell communication between the blastocyst and endometrium is critical for implantation. In recent years, evidence has emerged from studies in humans and several other animal species that exosomes are secreted from the endometrium and trophoblast cells and may play an important role in cell-to-cell communication maternal-fetal interface during early pregnancy. Exosomes are stable extracellular lipid bilayer vesicles that encapsulate proteins, miRNAs, and mRNAs, with the ability to deliver their cargo to near and distant sites, altering cellular function(s). Furthermore, the exosomal cargo can be altered in response to environmental cues (e.g. hypoxia). The current study aims to develop an in vitro system to evaluate maternal-embryo interactions via exosomes (and exosomal cargo) produced by bovine endometrial stromal cells (ICAR) using hypoxia as a known stimulus associated with the release of exosomes and alterations to biological responses (e.g. cell proliferation). METHODS: ICAR cells cultured under 8 % O or 1 % O for 48 h and changes in cell function (i.e. migration, proliferation and apoptosis) were evaluated. Exosome release was determined following the isolation (via differential centrifugation) and characterization of exosomes from ICAR cell-conditioned media. Exosomal proteomic content was evaluated by mass spectrometry. RESULTS: Under hypoxic conditions (i.e. 1 % O ), ICAR cell migration and proliferation was decreased (~20 and ~32 %, respectively) and apoptotic protein caspase-3 activation was increased (∼1.6 fold). Hypoxia increased exosome number by ~3.6 fold compared with culture at 8 % O . Mass spectrometry analysis identified 128 proteins unique to exosomes of ICAR cultured at 1 % O compared with only 46 proteins unique to those of ICAR cultured at 8 % O . Differential production of proteins associated with specific biological processes and molecular functions were identified, most notably ADAM10, pantetheinase and kininogen 2. CONCLUSIONS: In summary, we have shown that a stimulus such as hypoxia can alter both the cellular function and exosome release of ICAR cells. Alterations to exosome release and exosomal content in response to stimuli may play a crucial role in maternal-fetal crosstalk and could also affect placental development.
[Mh] Termos MeSH primário: Comunicação Celular
Endométrio/metabolismo
Exossomos/metabolismo
Hipóxia/metabolismo
Células Estromais/metabolismo
Trofoblastos/metabolismo
[Mh] Termos MeSH secundário: Proteína ADAM10/metabolismo
Amidoidrolases/metabolismo
Animais
Apoptose
Caspase 3/metabolismo
Bovinos
Hipóxia Celular
Linhagem Celular
Movimento Celular
Proliferação Celular
Sobrevivência Celular
Endométrio/citologia
Feminino
Proteínas Ligadas por GPI/metabolismo
Técnicas In Vitro
Cininogênios/metabolismo
Espectrometria de Massas
Proteômica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (GPI-Linked Proteins); 0 (Kininogens); EC 3.4.22.- (Caspase 3); EC 3.4.24.81 (ADAM10 Protein); EC 3.5.- (Amidohydrolases); EC 3.5.1.- (pantetheinase)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170328
[Lr] Data última revisão:
170328
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161111
[St] Status:MEDLINE



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