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[PMID]:28468272
[Au] Autor:Bobrowska B; Wieczorek-Surdacka E; Kruszelnicka O; Chyrchel B; Surdacki A; Dudek D
[Ad] Endereço:Second Department of Cardiology, Faculty of Medicine, Jagiellonian University Medical College, 17 Kopernika Street, 31-501 Cracow, Poland. bobrowska.beata@gmail.com.
[Ti] Título:Clinical Correlates and Prognostic Value of Plasma Galectin-3 Levels in Degenerative Aortic Stenosis: A Single-Center Prospective Study of Patients Referred for Invasive Treatment.
[So] Source:Int J Mol Sci;18(5), 2017 Apr 29.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Galectin-3 (Gal-3), a ß-galactoside-binding lectin, has been implicated in myocardial fibrosis, development of left ventricular (LV) dysfunction and transition from compensated LV hypertrophy to overt heart failure (HF), being a novel prognostic marker in HF. Risk stratification is crucial for the choice of the optimal therapy in degenerative aortic stenosis (AS), affecting elderly subjects with coexistent diseases. Our aim was to assess correlates and prognostic value of circulating Gal-3 in real-world patients with degenerative AS referred for invasive treatment. Gal-3 levels were measured at admission in 80 consecutive patients with symptomatic degenerative AS (mean age: 79 ± 8 years; aortic valve area (AVA) index: 0.4 ± 0.1 cm²/m²). The therapeutic strategy was chosen following a dedicated multidisciplinary team-oriented approach, including surgical valve replacement ( = 11), transcatheter valve implantation ( = 19), balloon aortic valvuloplasty (BAV) ( = 25) and optimal medical therapy ( = 25). Besides routine echocardiographic indices, valvulo-arterial impedance (Zva), an index of global LV afterload, was computed. There were 22 deaths over a median follow-up of 523 days. Baseline Gal-3 correlated negatively with estimated glomerular filtration rate (eGFR) ( = -0.61, < 0.001) and was unrelated to age, symptomatic status, AVA index, LV ejection fraction, LV mass index or Zva. For the study group as a whole, Gal-3 tended to predict mortality (Gal-3 >17.8 vs. Gal-3 <17.8 ng/mL; hazard ratio (HR): 2.03 (95% confidence interval, 0.88-4.69), = 0.09), which was abolished upon adjustment for eGFR (HR: 1.70 (0.61-4.73), = 0.3). However, in post-BAV patients multivariate-adjusted pre-procedural Gal-3 was associated with worse survival (HR: 7.41 (1.52-36.1), = 0.01) regardless of eGFR. In conclusion, the inverse eGFR-Gal-3 relationship underlies a weak association between Gal-3 and adverse outcome in patients with degenerative AS referred for invasive therapy irrespective of type of treatment employed. In contrast, pre-procedural Gal-3 appears an independent mortality predictor in high-risk AS patients undergoing BAV.
[Mh] Termos MeSH primário: Estenose da Valva Aórtica/sangue
Estenose da Valva Aórtica/diagnóstico
Galectina 3/sangue
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Angioplastia com Balão
Valva Aórtica/cirurgia
Estenose da Valva Aórtica/cirurgia
Estenose da Valva Aórtica/terapia
Feminino
Taxa de Filtração Glomerular
Seres Humanos
Masculino
Prognóstico
Estudos Prospectivos
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Galectin 3); 0 (galectin-3, human)
[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:170505
[St] Status:MEDLINE


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[PMID]:28471381
[Au] Autor:Fort-Gallifa I; Hernández-Aguilera A; García-Heredia A; Cabré N; Luciano-Mateo F; Simó JM; Martín-Paredero V; Camps J; Joven J
[Ad] Endereço:Biochemical Research Unit, Hospital Universitari de Sant Joan, Institut d'Investigació Sanitària Pere Virgili, Universitat Rovira i Virgili, C. Sant Joan s/n, Reus, 43201 Catalonia, Spain. ifort@lrsud.cat.
[Ti] Título:Galectin-3 in Peripheral Artery Disease. Relationships with Markers of Oxidative Stress and Inflammation.
[So] Source:Int J Mol Sci;18(5), 2017 May 04.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Galectin-3 is a modulator of oxidative stress, inflammation, and fibrogenesis involved in the pathogenesis of vascular diseases. The present study sought to characterize, in patients with peripheral artery disease (PAD), the localization of galectin-3 in arterial tissue, and to analyze the relationships between the circulating levels of galectin-3 and oxidative stress and inflammation. It also sought to compare the diagnostic accuracy of galectin-3 with that of other biochemical markers of this disease. We analyzed femoral or popliteal arteries from 50 PAD patients, and four control arteries. Plasma from 86 patients was compared with that from 72 control subjects. We observed differences in the expression of galectin-3 in normal arteries, and arteries from patients with PAD, with a displacement of the expression from the adventitia to the media, and the intima. In addition, plasma galectin-3 concentration was increased in PAD patients, and correlated with serologic markers of oxidative stress (F2-isoprostanes), and inflammation [chemokine (C-C motif) ligand 2, C-reactive protein, ß-2-microglobulin]. We conclude that the determination of galectin-3 has good diagnostic accuracy in the assessment of PAD and compares well with other analytical parameters currently in use.
[Mh] Termos MeSH primário: Galectina 3/metabolismo
Estresse Oxidativo
Doença Arterial Periférica/metabolismo
[Mh] Termos MeSH secundário: Idoso
Biomarcadores/sangue
Biomarcadores/metabolismo
Estudos de Casos e Controles
Endotélio Vascular/metabolismo
Feminino
Artéria Femoral/metabolismo
Galectina 3/sangue
Seres Humanos
Inflamação/sangue
Masculino
Meia-Idade
Doença Arterial Periférica/sangue
Doença Arterial Periférica/patologia
Artéria Poplítea/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Galectin 3)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE


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[PMID]:29293545
[Au] Autor:Begg GA; Karim R; Oesterlein T; Graham LN; Hogarth AJ; Page SP; Pepper CB; Rhode K; Lip GYH; Holden AV; Plein S; Tayebjee MH
[Ad] Endereço:Department of Cardiology, Leeds General Infirmary, Leeds, United Kingdom.
[Ti] Título:Left atrial voltage, circulating biomarkers of fibrosis, and atrial fibrillation ablation. A prospective cohort study.
[So] Source:PLoS One;13(1):e0189936, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:AIMS: To test the ability of four circulating biomarkers of fibrosis, and of low left atrial voltage, to predict recurrence of atrial fibrillation after catheter ablation. BACKGROUND: Circulating biomarkers potentially may be used to improve patient selection for atrial fibrillation ablation. Low voltage areas in the left atrium predict arrhythmia recurrence when mapped in sinus rhythm. This study tested type III procollagen N terminal peptide (PIIINP), galectin-3 (gal-3), fibroblast growth factor 23 (FGF-23), and type I collagen C terminal telopeptide (ICTP), and whether low voltage areas in the left atrium predicted atrial fibrillation recurrence, irrespective of the rhythm during mapping. METHODS: 92 atrial fibrillation ablation patients were studied. Biomarker levels in peripheral and intra-cardiac blood were measured with enzyme-linked immunosorbent assay. Low voltage (<0.5mV) was expressed as a proportion of the mapped left atrial surface area. Follow-up was one year. The primary endpoint was recurrence of arrhythmia. The secondary endpoint was a composite of recurrence despite two procedures, or after one procedure if no second procedure was undertaken. RESULTS: The biomarkers were not predictive of either endpoint. After multivariate Cox regression analysis, high proportion of low voltage area in the left atrium was found to predict the primary endpoint in sinus rhythm mapping (hazard ratio 4.323, 95% confidence interval 1.337-13.982, p = 0.014) and atrial fibrillation mapping (hazard ratio 5.195, 95% confidence interval 1.032-26.141, p = 0.046). This effect was also apparent for the secondary endpoint. CONCLUSION: The studied biomarkers do not predict arrhythmia recurrence after catheter ablation. Left atrial voltage is an independent predictor of recurrence, whether the left atrium is mapped in atrial fibrillation or sinus rhythm.
[Mh] Termos MeSH primário: Fibrilação Atrial/cirurgia
Biomarcadores/sangue
Ablação por Cateter/métodos
Átrios do Coração/fisiopatologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Fibrilação Atrial/fisiopatologia
Colágeno Tipo I/sangue
Feminino
Fatores de Crescimento de Fibroblastos/sangue
Fibrose
Galectina 3/sangue
Seres Humanos
Masculino
Meia-Idade
Fragmentos de Peptídeos/sangue
Peptídeos/sangue
Pró-Colágeno/sangue
Estudos Prospectivos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers); 0 (Collagen Type I); 0 (Galectin 3); 0 (Peptide Fragments); 0 (Peptides); 0 (Procollagen); 0 (collagen type I trimeric cross-linked peptide); 0 (fibroblast growth factor 23); 0 (galectin-3, human); 0 (procollagen Type III-N-terminal peptide); 62031-54-3 (Fibroblast Growth Factors)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180129
[Lr] Data última revisão:
180129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180103
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189936


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[PMID]:27778367
[Au] Autor:Harrison SA; Marri SR; Chalasani N; Kohli R; Aronstein W; Thompson GA; Irish W; Miles MV; Xanthakos SA; Lawitz E; Noureddin M; Schiano TD; Siddiqui M; Sanyal A; Neuschwander-Tetri BA; Traber PG
[Ad] Endereço:Fort Sam Houston, TX, USA.
[Ti] Título:Randomised clinical study: GR-MD-02, a galectin-3 inhibitor, vs. placebo in patients having non-alcoholic steatohepatitis with advanced fibrosis.
[So] Source:Aliment Pharmacol Ther;44(11-12):1183-1198, 2016 12.
[Is] ISSN:1365-2036
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Non-alcoholic steatohepatitis (NASH) and resultant liver fibrosis is a major health problem without approved pharmacotherapy. Pre-clinical results of GR-MD-02, a galectin-3 inhibitor, suggested potential efficacy in NASH with advanced fibrosis/cirrhosis and prompted initiation of a clinical development programme in NASH with advanced fibrosis. AIM: To evaluate the safety, pharmacokinetics and exploratory pharmacodynamic markers of GR-MD-02 in subjects having NASH with bridging fibrosis. METHODS: The GT-020 study was a first-in-human, sequential dose-ranging, placebo controlled, double-blinded study with the primary objective to assess the safety, tolerability and dose limiting toxicity of GR-MD-02, in subjects with biopsy-proven NASH with advanced fibrosis (Brunt stage 3). The secondary objectives were to characterise first-dose and multiple-dose pharmacokinetic profiles and to evaluate changes in potential serum biomarkers and liver stiffness as assessed by FibroScan. RESULTS: GR-MD-02 single and three weekly repeated of 2, 4 and 8 mg/kg revealed no meaningful clinical differences in treatment emergent adverse events, vital signs, electrocardiographic findings or laboratory tests. Pharmokinetic parameters showed a dose-dependent relationship with evidence of drug accumulation following 8 mg/kg (~twofold). CONCLUSIONS: GR-MD-02 doses were in the upper range of the targeted therapeutic dose determined from pre-clinical data and were safe and well tolerated with evidence of a pharmacodynamic effect. These results provide support for a Phase 2 development programme in advanced fibrosis due to NASH.
[Mh] Termos MeSH primário: Galectina 3/antagonistas & inibidores
Cirrose Hepática/tratamento farmacológico
Hepatopatia Gordurosa não Alcoólica/tratamento farmacológico
Pectinas
[Mh] Termos MeSH secundário: Adulto
Idoso
Biomarcadores/sangue
Método Duplo-Cego
Feminino
Galectina 3/sangue
Seres Humanos
Cirrose Hepática/sangue
Masculino
Meia-Idade
Hepatopatia Gordurosa não Alcoólica/sangue
Pectinas/efeitos adversos
Pectinas/sangue
Pectinas/farmacocinética
Pectinas/farmacologia
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE I; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers); 0 (Galectin 3); 0 (Pectins); 0 (galactoarabino-rhamnogalaturonan)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180110
[Lr] Data última revisão:
180110
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE
[do] DOI:10.1111/apt.13816


  5 / 2249 MEDLINE  
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[PMID]:29277781
[Au] Autor:Cioca A; Muntean D; Bungardean C; Raica M; Cimpean AM
[Ad] Endereço:Department of Histology, Angiogenesis Research Center, "Victor Babes" University of Medicine and Pharmacy, Timisoara, Romania cioca_andre@yahoo.com.
[Ti] Título:Expression and Distribution of Galectin-3 in Chromophobe and Papillary Carcinomas.
[So] Source:Anticancer Res;38(1):259-263, 2018 01.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: Probably due to their low occurrence, chromophobe and papillary renal cell carcinomas are less well characterized and, currently, there are no reliable prognostic markers for this group of patients. Moreover, the optimal therapy for patients with non-clear renal cell carcinoma (RCC) is unknown yet. Although elevated levels of Galectin-3 (Gal-3) were associated with poor prognosis in conventional RCC, the impact of this protein on carcinogenesis of chromophobe and papillary entities has not been previously described. MATERIALS AND METHODS: Gal-3 expression was investigated in 34 consecutive cases of RCCs, including 19 papillary carcinomas and 15 chromophobe carcinomas. RESULTS: Immunohistochemical analysis of Gal-3 in tumor cells showed 3 patterns of expression: membranous, cytoplasmic and nuclear staining. Most tumors included in our study showed a cytoplasmic expression and it was almost equally distributed between the histologic subtypes. However, only nuclear staining of Gal-3 was associated with both Fuhrman grade and tumor stage (p=0.016 and p=0.032, respectively) in chromophobe subtype. CONCLUSION: Our results indicate that the nuclear expression of Gal-3 has an essential role in the development of chromophobe carcinoma. The association with advanced tumor stage and nuclear grade suggests that this protein is an indicator of aggressiveness in the chromophobe subtype, thus targeting anti-nuclear transport may prove an effective therapy for this particular group of patients.
[Mh] Termos MeSH primário: Carcinoma Papilar/metabolismo
Carcinoma de Células Renais/metabolismo
Galectina 3/metabolismo
Neoplasias Renais/metabolismo
[Mh] Termos MeSH secundário: Adulto
Idoso
Carcinoma Papilar/patologia
Carcinoma de Células Renais/patologia
Feminino
Seres Humanos
Neoplasias Renais/patologia
Masculino
Meia-Idade
Gradação de Tumores
Estadiamento de Neoplasias
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Galectin 3); 0 (galectin-3, human)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180105
[Lr] Data última revisão:
180105
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171227
[St] Status:MEDLINE


  6 / 2249 MEDLINE  
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[PMID]:29016609
[Au] Autor:Yang EH; Rode J; Howlader MA; Eckermann M; Santos JT; Hernandez Armada D; Zheng R; Zou C; Cairo CW
[Ad] Endereço:Alberta Glycomics Centre, Department of Chemistry, University of Alberta, Edmonton Alberta, Canada.
[Ti] Título:Galectin-3 alters the lateral mobility and clustering of ß1-integrin receptors.
[So] Source:PLoS One;12(10):e0184378, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Glycoprotein receptors are influenced by myriad intermolecular interactions at the cell surface. Specific glycan structures may interact with endogenous lectins that enforce or disrupt receptor-receptor interactions. Glycoproteins bound by multivalent lectins may form extended oligomers or lattices, altering the lateral mobility of the receptor and influencing its function through endocytosis or changes in activation. In this study, we have examined the interaction of Galectin-3 (Gal-3), a human lectin, with adhesion receptors. We measured the effect of recombinant Gal-3 added exogenously on the lateral mobility of the α5ß1 integrin on HeLa cells. Using single-particle tracking (SPT) we detected increased lateral mobility of the integrin in the presence of Gal-3, while its truncated C-terminal domain (Gal-3C) showed only minor reductions in lateral mobility. Treatment of cells with Gal-3 increased ß1-integrin mediated migration with no apparent changes in viability. In contrast, Gal-3C decreased both cell migration and viability. Fluorescence microscopy allowed us to confirm that exogenous Gal-3 resulted in reorganization of the integrin into larger clusters. We used a proteomics analysis to confirm that cells expressed endogenous Gal-3, and found that addition of competitive oligosaccharide ligands for the lectin altered the lateral mobility of the integrin. Together, our results are consistent with a Gal-3-integrin lattice model of binding and confirm that the lateral mobility of integrins is natively regulated, in part, by galectins.
[Mh] Termos MeSH primário: Endocitose/genética
Galectina 3/genética
Integrina alfa5beta1/metabolismo
Proteômica
[Mh] Termos MeSH secundário: Adesão Celular/genética
Movimento Celular/efeitos dos fármacos
Galectina 3/administração & dosagem
Regulação da Expressão Gênica
Glicoproteínas/genética
Glicoproteínas/metabolismo
Células HeLa
Seres Humanos
Integrina alfa5beta1/genética
Oligossacarídeos/metabolismo
Ligação Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Galectin 3); 0 (Glycoproteins); 0 (Integrin alpha5beta1); 0 (Oligosaccharides)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171011
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184378


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[PMID]:28982723
[Au] Autor:Fernandez-García CE; Tarin C; Roldan-Montero R; Martinez-Lopez D; Torres-Fonseca M; Lindhot JS; Vega de Ceniga M; Egido J; Lopez-Andres N; Blanco-Colio LM; Martín-Ventura JL
[Ad] Endereço:Vascular Research Lab, FIIS-Fundación Jiménez Díaz-Autonoma University, Madrid, Spain.
[Ti] Título:Increased galectin-3 levels are associated with abdominal aortic aneurysm progression and inhibition of galectin-3 decreases elastase-induced AAA development.
[So] Source:Clin Sci (Lond);131(22):2707-2719, 2017 Nov 15.
[Is] ISSN:1470-8736
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Abdominal aortic aneurysm (AAA) evolution is unpredictable and no specific treatment exists for AAA, except surgery to prevent aortic rupture. Galectin-3 has been previously associated with CVD, but its potential role in AAA has not been addressed. Galectin-3 levels were increased in the plasma of AAA patients ( =225) compared with the control group ( =100). In addition, galectin-3 concentrations were associated with the need for surgical repair, independently of potential confounding factors. Galectin-3 mRNA and protein expression were increased in human AAA samples compared with healthy aortas. Experimental AAA in mice was induced via aortic elastase perfusion. Mice were treated intravenously with the galectin-3 inhibitor modified citrus pectin (MCP, 10 mg/kg, every other day) or saline. Similar to humans, galectin-3 serum and aortic mRNA levels were also increased in elastase-induced AAA mice compared with control mice. Mice treated with MCP showed decreased aortic dilation, as well as elastin degradation, vascular smooth muscle cell (VSMC) loss, and macrophage content at day 14 postelastase perfusion compared with control mice. The underlying mechanism(s) of the protective effect of MCP was associated with a decrease in galectin-3 and cytokine (mainly CCL5) mRNA and protein expression. Interestingly, galectin-3 induced CCL5 expression by a mechanism involving STAT3 activation in VSMC. Accordingly, MCP treatment decreased STAT3 phosphorylation in elastase-induced AAA. In conclusion, increased galectin-3 levels are associated with AAA progression, while galectin-3 inhibition decreased experimental AAA development. Our data suggest the potential role of galectin-3 as a therapeutic target in AAA.
[Mh] Termos MeSH primário: Aorta Abdominal/efeitos dos fármacos
Aneurisma da Aorta Abdominal/prevenção & controle
Galectina 3/antagonistas & inibidores
Galectina 3/sangue
Elastase Pancreática
Pectinas/farmacologia
[Mh] Termos MeSH secundário: Animais
Aorta Abdominal/enzimologia
Aorta Abdominal/patologia
Aneurisma da Aorta Abdominal/sangue
Aneurisma da Aorta Abdominal/enzimologia
Aneurisma da Aorta Abdominal/patologia
Estudos de Casos e Controles
Células Cultivadas
Quimiocina CCL5/genética
Quimiocina CCL5/metabolismo
Dilatação Patológica
Modelos Animais de Doenças
Progressão da Doença
Galectina 3/genética
Galectina 3/metabolismo
Seres Humanos
Camundongos Endogâmicos C57BL
Músculo Liso Vascular/efeitos dos fármacos
Músculo Liso Vascular/metabolismo
Miócitos de Músculo Liso/efeitos dos fármacos
Miócitos de Músculo Liso/metabolismo
Fosforilação
RNA Mensageiro/sangue
RNA Mensageiro/genética
Fator de Transcrição STAT3/metabolismo
Transdução de Sinais/efeitos dos fármacos
Fatores de Tempo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ccl5 protein, mouse); 0 (Chemokine CCL5); 0 (Galectin 3); 0 (Lgals3 protein, mouse); 0 (Pectins); 0 (RNA, Messenger); 0 (STAT3 Transcription Factor); 0 (Stat3 protein, mouse); 0 (citrus pectin); 0 (galectin-3, human); EC 3.4.21.36 (Pancreatic Elastase)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171007
[St] Status:MEDLINE
[do] DOI:10.1042/CS20171142


  8 / 2249 MEDLINE  
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[PMID]:28938960
[Au] Autor:Fashanu OE; Norby FL; Aguilar D; Ballantyne CM; Hoogeveen RC; Chen LY; Soliman EZ; Alonso A; Folsom AR
[Ad] Endereço:Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, MN.
[Ti] Título:Galectin-3 and incidence of atrial fibrillation: The Atherosclerosis Risk in Communities (ARIC) study.
[So] Source:Am Heart J;192:19-25, 2017 Oct.
[Is] ISSN:1097-6744
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Galectin-3, a ß-galactoside binding lectin involved in important regulatory roles in adhesion, inflammation, immunity, and fibrosis, may be relevant to atrial fibrillation (AF) etiology. METHODS: We included 8,436 participants free of AF at baseline (1996-1998) and with measures of plasma galectin-3 from the Atherosclerosis Risk in Communities study. We ascertained incident AF through 2013 from study visit electrocardiograms, hospitalizations, and death certificates. Multivariable Cox proportional hazards models, adjusted for AF risk factors plus incident heart failure (HF) and coronary heart disease (CHD), were used to estimate hazard ratios for the association between galectin-3 and incident AF. RESULTS: The mean age (SD) of participants was 62.6 (5.6) years, and the sample was comprised of 58.7% women and 21.2% blacks. During a median follow-up of 15.7 years, 1,185 incident cases of AF were observed. After adjusting for AF risk factors, participants with galectin-3 levels ≥90th percentile (19.5 ng/mL) had a significantly higher risk of incident AF when compared with the lowest quartile (4.4-11.9 ng/mL), with hazard ratios (95% CI) of 1.40 (1.04-1.89) for the 90th-<95th percentile and 1.51 (1.11-2.06) for the 95th-100th percentile. This association was attenuated and no longer statistically significant after accounting for incident CHD and HF as time-dependent variables. CONCLUSIONS: Elevated plasma galectin-3 is associated with increased risk of incident AF. Galectin-3 may increase AF risk via pathways involving CHD and HF.
[Mh] Termos MeSH primário: Aterosclerose/sangue
Fibrilação Atrial/epidemiologia
Galectina 3/sangue
Medição de Risco/métodos
[Mh] Termos MeSH secundário: Aterosclerose/complicações
Aterosclerose/epidemiologia
Fibrilação Atrial/sangue
Fibrilação Atrial/complicações
Biomarcadores/sangue
Eletrocardiografia
Feminino
Seres Humanos
Incidência
Masculino
Meia-Idade
Estudos Retrospectivos
Fatores de Risco
Estados Unidos/epidemiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
0 (Biomarkers); 0 (Galectin 3)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171108
[Lr] Data última revisão:
171108
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170924
[St] Status:MEDLINE


  9 / 2249 MEDLINE  
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[PMID]:28917454
[Au] Autor:Ritchie S; Neal D; Shlevin H; Allgood A; Traber P
[Ad] Endereço:San Antonio Military Medical Center, San Antonio, Texas. Electronic address: simonaritchie@hotmail.com.
[Ti] Título:A phase 2a, open-label pilot study of the galectin-3 inhibitor GR-MD-02 for the treatment of moderate-to-severe plaque psoriasis.
[So] Source:J Am Acad Dermatol;77(4):753-755, 2017 10.
[Is] ISSN:1097-6787
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Drogas em Investigação/uso terapêutico
Galectina 3/efeitos dos fármacos
Pectinas/uso terapêutico
Psoríase/diagnóstico
Psoríase/tratamento farmacológico
[Mh] Termos MeSH secundário: Relação Dose-Resposta a Droga
Esquema de Medicação
Feminino
Seguimentos
Seres Humanos
Masculino
Dose Máxima Tolerável
Segurança do Paciente
Projetos Piloto
Resultado do Tratamento
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE II; LETTER; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Drugs, Investigational); 0 (Galectin 3); 0 (Pectins); 0 (galactoarabino-rhamnogalaturonan)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170918
[St] Status:MEDLINE


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[PMID]:28893908
[Au] Autor:Lin YH; Qiu DC; Chang WH; Yeh YQ; Jeng US; Liu FT; Huang JR
[Ad] Endereço:From the Institute of Biochemistry and Molecular Biology and.
[Ti] Título:The intrinsically disordered N-terminal domain of galectin-3 dynamically mediates multisite self-association of the protein through fuzzy interactions.
[So] Source:J Biol Chem;292(43):17845-17856, 2017 Oct 27.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Galectins are a family of lectins that bind ß-galactosides through their conserved carbohydrate recognition domain (CRD) and can induce aggregation with glycoproteins or glycolipids on the cell surface and thereby regulate cell activation, migration, adhesion, and signaling. Galectin-3 has an intrinsically disordered N-terminal domain and a canonical CRD. Unlike the other 14 known galectins in mammalian cells, which have dimeric or tandem-repeated CRDs enabling multivalency for various functions, galectin-3 is monomeric, and its functional multivalency therefore is somewhat of a mystery. Here, we used NMR spectroscopy, mutagenesis, small-angle X-ray scattering, and computational modeling to study the self-association-related multivalency of galectin-3 at the residue-specific level. We show that the disordered N-terminal domain (residues ∼20-100) interacts with itself and with a part of the CRD not involved in carbohydrate recognition (ß-strands 7-9; residues ∼200-220), forming a fuzzy complex via inter- and intramolecular interactions, mainly through hydrophobicity. These fuzzy interactions are characteristic of intrinsically disordered proteins to achieve liquid-liquid phase separation, and we demonstrated that galectin-3 can also undergo liquid-liquid phase separation. We propose that galectin-3 may achieve multivalency through this multisite self-association mechanism facilitated by fuzzy interactions.
[Mh] Termos MeSH primário: Galectina 3/química
Proteínas Intrinsicamente Desordenadas/química
[Mh] Termos MeSH secundário: Galectina 3/genética
Galectina 3/metabolismo
Seres Humanos
Proteínas Intrinsicamente Desordenadas/genética
Proteínas Intrinsicamente Desordenadas/metabolismo
Domínios Proteicos
Difração de Raios X
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Galectin 3); 0 (Intrinsically Disordered Proteins); 0 (galectin-3, human)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171103
[Lr] Data última revisão:
171103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170913
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.802793



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