Base de dados : MEDLINE
Pesquisa : C14.280.123 [Categoria DeCS]
Referências encontradas : 407 [refinar]
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[PMID]:29355681
[Au] Autor:Fan LL; Huang H; Jin JY; Li JJ; Chen YQ; Zhao SP; Xiang R
[Ad] Endereço:Department of Cell Biology, The School of Life Sciences, Central South University, Changsha 410013, China.
[Ti] Título:Whole exome sequencing identifies a novel mutation (c.333 + 2T > C) of TNNI3K in a Chinese family with dilated cardiomyopathy and cardiac conduction disease.
[So] Source:Gene;648:63-67, 2018 Mar 30.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Dilated Cardiomyopathy (DCM) and cardiac conduction disease (CCD) are two kinds if diseases that can induce heart failure, syncope and even sudden cardiac death (SCD). DCM patients can experience CCD at the same time. In recent research, some disease-causing genes and variants have been identified in patients with DCM and CCD, such as Alpha-Actinin-2 and TNNI3 Interacting Kinase (TNNI3K). In this study, we employed whole-exome sequencing (WES) to explore the potential causative genes in a Chinese family with DCM and CCD. A novel splice site mutation (c.333 + 2 T > C) of TNNI3K was identified and co-segregated with the affected family members. This novel mutation was also absent in 200 healthy local controls and predicted to be disease-causing by Mutationtaster. The splice site mutation (c.333 + 2 T > C) may result in a premature stop codon in exon 4 of the TNNI3K gene and can induce nonsense-mediated mRNA decay. Real-time qPCR also confirmed that the level of TNNI3K mRNA expression was decreased significantly compared with the controls, which may lead to myocardial structural disorder and arrhythmia. In this study we reported the third novel mutation of TNNI3K in DCM and CCD patients which further supported the important role of TNNI3K in heart development and expanded the spectrum of TNNI3K mutations. The results may contribute to the genetic diagnosis and counseling of families with DCM and CCD.
[Mh] Termos MeSH primário: Doença do Sistema de Condução Cardíaco/genética
Cardiomiopatia Dilatada/genética
MAP Quinase Quinase Quinases/genética
Mutação
Sequenciamento Completo do Exoma/métodos
[Mh] Termos MeSH secundário: Grupo com Ancestrais do Continente Asiático/genética
Sequência de Bases
Doença do Sistema de Condução Cardíaco/etnologia
Cardiomiopatia Dilatada/etnologia
China
Saúde da Família
Feminino
Seres Humanos
Masculino
Degradação do RNAm Mediada por Códon sem Sentido/genética
Linhagem
Sítios de Splice de RNA/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA Splice Sites); EC 2.7.11.1 (TNNI3K protein, human); EC 2.7.11.25 (MAP Kinase Kinase Kinases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180123
[St] Status:MEDLINE


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[PMID]:29197877
[Au] Autor:Gerbino A; Bottillo I; Milano S; Lipari M; Zio R; Morlino S; Mola MG; Procino G; Re F; Zachara E; Grammatico P; Svelto M; Carmosino M
[Ad] Endereço:Department of Biosciences, Biotechnologies and Biopharmaceutics, University of Bari, Bari, Italy.
[Ti] Título:Functional Characterization of a Novel Truncating Mutation in Lamin A/C Gene in a Family with a Severe Cardiomyopathy with Conduction Defects.
[So] Source:Cell Physiol Biochem;44(4):1559-1577, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Truncating LMNA gene mutations occur in many inherited cardiomyopathy cases, but the molecular mechanisms involved in the disease they cause have not yet been systematically investigated. Here, we studied a novel frameshift LMNA variant (p.D243Gfs*4) identified in three members of an Italian family co-segregating with a severe form of cardiomyopathy with conduction defects. METHODS: HEK293 cells and HL-1 cardiomyocytes were transiently transfected with either Lamin A or D243Gfs*4 tagged with GFP (or mCherry). D243Gfs*4 expression, cellular localization and its effects on diverse cellular mechanisms were evaluated with western blotting, laser-scanning confocal microscopy and video-imaging analysis in single cells. RESULTS: When expressed in HEK293 cells, GFP- (or mCherry)-tagged LMNA D243Gfs*4 colocalized with calnexin within the ER. ER mislocalization of LMNA D243Gfs*4 did not significantly induce ER stress response, abnormal Ca2+ handling and apoptosis when compared with HEK293 cells expressing another truncated mutant of LMNA (R321X) which similarly accumulates within the ER. Of note, HEK293-LMNA D243Gfs*4 cells showed a significant reduction of connexin 43 (CX43) expression level, which was completely rescued by activation of the WNT/ß-catenin signaling pathway. When expressed in HL-1 cardiomyocytes, D243Gfs*4 significantly impaired the spontaneous Ca2+ oscillations recorded in these cells as result of propagation of the depolarizing waves through the gap junctions between non-transfected cells surrounding a cell harboring the mutation. Furthermore, mCh-D243Gfs*4 HL-1 cardiomyocytes showed reduced CX43-dependent Lucifer Yellow (LY) loading and propagation. Of note, activation of ß-catenin rescued both LY loading and LMNA D243Gfs*4 -HL-1 cells spontaneous activity propagation. CONCLUSION: Overall, the present results clearly indicate the involvement of the aberrant CX43 expression/activity as a pathogenic mechanism for the conduction defects associated to this LMNA truncating alteration.
[Mh] Termos MeSH primário: Doença do Sistema de Condução Cardíaco/genética
Cardiomiopatias/genética
Lamina Tipo A/genética
[Mh] Termos MeSH secundário: Apoptose
Sequência de Bases
Cálcio/metabolismo
Calnexina/metabolismo
Doença do Sistema de Condução Cardíaco/complicações
Doença do Sistema de Condução Cardíaco/patologia
Cardiomiopatias/complicações
Cardiomiopatias/patologia
Linhagem Celular
Conexina 43
Retículo Endoplasmático/metabolismo
Feminino
Junções Comunicantes/metabolismo
Células HEK293
Seres Humanos
Lamina Tipo A/metabolismo
Repetições de Microssatélites/genética
Microscopia Confocal
Meia-Idade
Mutagênese Sítio-Dirigida
Miócitos Cardíacos/citologia
Miócitos Cardíacos/metabolismo
Linhagem
Polimorfismo de Nucleotídeo Único
Imagem com Lapso de Tempo
Via de Sinalização Wnt
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Connexin 43); 0 (LMNA protein, human); 0 (Lamin Type A); 139873-08-8 (Calnexin); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171204
[St] Status:MEDLINE
[do] DOI:10.1159/000485651


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[PMID]:29261713
[Au] Autor:Coll M; Striano P; Ferrer-Costa C; Campuzano O; Matés J; Del Olmo B; Iglesias A; Pérez-Serra A; Mademont I; Picó F; Oliva A; Brugada R
[Ad] Endereço:Cardiovascular Genetics Center, IDIBGI, Dr. Trueta University Hospital, Parc Hospitalari Martí i Julià, Edifici, Salt (Spain).
[Ti] Título:Targeted next-generation sequencing provides novel clues for associated epilepsy and cardiac conduction disorder/SUDEP.
[So] Source:PLoS One;12(12):e0189618, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sudden unexpected death in epilepsy is an unpredicted condition in patients with a diagnosis of epilepsy, and autopsy does not conclusively identify cause of death. Although the pathophysiological mechanisms that underlie this entity remain unknown, the fact that epilepsy can affect cardiac function is not surprising. The genetic factors involving ion channels co-expressed in the heart and brain and other candidate genes have been previously described. In the present study, 20 epilepsy patients with personal or family history of heart rhythm disturbance/cardiac arrhythmias/sudden death were sequenced using a custom re-sequencing panel. Twenty-six relatives were genetically analysed to ascertain the family segregation in ten individuals. Four subjects revealed variants with positive genotype-phenotype segregation: four missense variants in the CDKL5, CNTNAP2, GRIN2A and ADGRV1 genes and one copy number variant in KCNQ1. The potential pathogenic role of variants in new candidate genes will need further studies in larger cohorts, and the evaluation of the potential pathogenic role in the cardio-cerebral mechanisms requires in vivo/in vitro studies. In addition to family segregation, evaluation of the potential pathogenic roles of these variants in cardio-cerebral mechanisms by in vivo/in vitro studies should also be performed. The potential pathogenic role of variants in new candidate genes will need further studies in larger cohorts.
[Mh] Termos MeSH primário: Doença do Sistema de Condução Cardíaco/complicações
Doença do Sistema de Condução Cardíaco/genética
Morte Súbita/etiologia
Epilepsia/complicações
Epilepsia/genética
Sequenciamento de Nucleotídeos em Larga Escala/métodos
[Mh] Termos MeSH secundário: Adolescente
Adulto
Criança
Segregação de Cromossomos
Estudos de Coortes
Éxons/genética
Feminino
Variação Genética
Seres Humanos
Padrões de Herança/genética
Masculino
Meia-Idade
Linhagem
Deleção de Sequência/genética
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171221
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189618


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[PMID]:29049164
[Au] Autor:Li Q; Wang DZ; Chen BX
[Ad] Endereço:Department of Cardiology, Beijing Tiantan Hospital, Capital Medical University, Beijing, China.
[Ti] Título:Electrocardiogram in patients with acute inferior myocardial infarction due to occlusion of circumflex artery.
[So] Source:Medicine (Baltimore);96(42):e6095, 2017 Oct.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:To investigate the diagnostic value of electrocardiographic (ECG) ST-segment in acute inferior myocardial infarction (AIMI) caused by the left circumflex branch (LCX).A total of 240 clinical cases with AIMI in our hospital were retrospectively analyzed. All of them had received percutaneous coronary intervention (PCI) within 12 hours after symptom onset. The clinical features, ECG manifestations, and coronary artery lesion characteristics of the patients were collected.The right coronary artery (RCA) was shown to be the infarct-related artery (IRA) in 177 patients, while LCX was responsible for AIMI in 63 cases. There was no significant difference in the risk factors of coronary heart disease (CHD) (P > .05 for all) between the 2 groups. ST-segment elevation in lead II, III, and AVF could be found in all patients. Moreover, ST-segment depression in lead I (STD I), ST-segment elevation in lead III (STE III), STE III-STE II, STE AVF, STD AVL, STD AVL-STD I and STE v6 lead ST-segment deviation exhibited significant difference in 2 groups (P < .05 for all). The changes of STD I, STE III < STEII, STD AVL < STD I could discriminate between LCX and RCA in AIMI patients with high sensitivity and specificity.ECG may be an effective tool to predict the IRA in patient with AIMI.
[Mh] Termos MeSH primário: Bloqueio de Ramo/diagnóstico por imagem
Oclusão Coronária/diagnóstico por imagem
Eletrocardiografia/métodos
Infarto Miocárdico de Parede Inferior/diagnóstico por imagem
Infarto do Miocárdio com Supradesnível do Segmento ST/diagnóstico por imagem
[Mh] Termos MeSH secundário: Idoso
Síndrome de Brugada/complicações
Síndrome de Brugada/diagnóstico por imagem
Bloqueio de Ramo/complicações
Doença do Sistema de Condução Cardíaco
Doença das Coronárias/complicações
Doença das Coronárias/diagnóstico por imagem
Oclusão Coronária/complicações
Vasos Coronários/diagnóstico por imagem
Feminino
Sistema de Condução Cardíaco/diagnóstico por imagem
Seres Humanos
Infarto Miocárdico de Parede Inferior/etiologia
Masculino
Meia-Idade
Valor Preditivo dos Testes
Estudos Retrospectivos
Fatores de Risco
Infarto do Miocárdio com Supradesnível do Segmento ST/etiologia
Sensibilidade e Especificidade
[Pt] Tipo de publicação:EVALUATION STUDIES; JOURNAL ARTICLE
[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.0000000000006095


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[PMID]:28827800
[Au] Autor:Liao WC; Juo LY; Shih YL; Chen YH; Yan YT
[Ad] Endereço:Institute of Biochemistry and Molecular Biology, National Yang-Ming University, Taipei, Taiwan.
[Ti] Título:HSPB7 prevents cardiac conduction system defect through maintaining intercalated disc integrity.
[So] Source:PLoS Genet;13(8):e1006984, 2017 Aug.
[Is] ISSN:1553-7404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:HSPB7 is a member of the small heat-shock protein (HSPB) family and is expressed in the cardiomyocytes from cardiogenesis onwards. A dramatic increase in HSPB7 is detected in the heart and blood plasma immediately after myocardial infarction. Additionally, several single-nucleotide polymorphisms of HSPB7 have been identified to be associated with heart failure caused by cardiomyopathy in human patients. Although a recent study has shown that HSPB7 is required for maintaining myofiber structure in skeletal muscle, its molecular and physiological functions in the heart remain unclear. In the present study, we generated a cardiac-specific inducible HSPB7 knockout mouse and demonstrated that the loss of HSPB7 in cardiomyocytes results in rapid heart failure and sudden death. The electrocardiogram showed cardiac arrhythmia with abnormal conduction in the HSPB7 mutant mice before death. In HSPB7 CKO cardiomyocytes, no significant defect was detected in the organization of contractile proteins in sarcomeres, but a severe structural disruption was observed in the intercalated discs. The expression of connexin 43, a gap-junction protein located at the intercalated discs, was downregulated in HSPB7 knockout cardiomyocytes. Mislocalization of desmoplakin, and N-cadherin, the intercalated disc proteins, was also observed in the HSPB7 CKO hearts. Furthermore, filamin C, the interaction protein of HSPB7, was upregulated and aggregated in HSPB7 mutant cardiomyocytes. In conclusion, our findings characterize HSPB7 as an intercalated disc protein and suggest it has an essential role in maintaining intercalated disc integrity and conduction function in the adult heart.
[Mh] Termos MeSH primário: Cardiomiopatias/genética
Proteínas de Choque Térmico HSP27/genética
Insuficiência Cardíaca/genética
Miócitos Cardíacos/metabolismo
[Mh] Termos MeSH secundário: Animais
Síndrome de Brugada/genética
Síndrome de Brugada/patologia
Caderinas/genética
Doença do Sistema de Condução Cardíaco
Cardiomiopatias/fisiopatologia
Conexina 43/genética
Modelos Animais de Doenças
Eletrocardiografia
Sistema de Condução Cardíaco/metabolismo
Sistema de Condução Cardíaco/patologia
Insuficiência Cardíaca/fisiopatologia
Seres Humanos
Camundongos
Camundongos Knockout
Músculo Esquelético/metabolismo
Músculo Esquelético/patologia
Miocárdio/metabolismo
Miocárdio/patologia
Miócitos Cardíacos/patologia
Sarcômeros/metabolismo
Sarcômeros/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cadherins); 0 (Connexin 43); 0 (GJA1 protein, human); 0 (HSP27 Heat-Shock Proteins); 0 (HSPB7 protein, human)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170823
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pgen.1006984


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[PMID]:28822650
[Au] Autor:Reddy N; Moudgil R; Lopez-Mattei JC; Karimzad K; Mouhayar EN; Somaiah N; Conley AP; Patel S; Giza DE; Iliescu C
[Ad] Endereço:Department of Cardiology, Division of Internal Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
[Ti] Título:Progressive and Reversible Conduction Disease With Checkpoint Inhibitors.
[So] Source:Can J Cardiol;33(10):1335.e13-1335.e15, 2017 Oct.
[Is] ISSN:1916-7075
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Novel antineoplastic therapies are focused on harnessing our own immune system to fight cancer. To that end, cytotoxic T-lymphocyte-associated antigen 4 and programmed death ligand 1 are 2 coinhibitory signals that play central roles in decreasing T-cell response and represent a class of medications termed "checkpoint inhibitors." We present an unusual case of progressive conduction abnormalities induced by checkpoint inhibitors. Prompt medical intervention resulted in full recovery. Despite the anticancer efficacy, the newer antineoplastic agents pose a significant and often life-threatening risk of cardiotoxicity.
[Mh] Termos MeSH primário: Síndrome de Brugada/induzido quimicamente
Eletrocardiografia
Imunoterapia/efeitos adversos
[Mh] Termos MeSH secundário: Idoso
Antineoplásicos/efeitos adversos
Síndrome de Brugada/diagnóstico
Síndrome de Brugada/fisiopatologia
Doença do Sistema de Condução Cardíaco
Progressão da Doença
Seres Humanos
Masculino
Sarcoma/terapia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170821
[St] Status:MEDLINE


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[PMID]:28625016
[Au] Autor:Mascia G; Arbelo E; Ojeda JH; Solimene F; Brugada R; Brugada J
[Ad] Endereço:Department of Medical and Surgical Critical Care, University of Florence, Florence, Italy.
[Ti] Título:Brugada Syndrome and Exercise Practice: Current Knowledge, Shortcomings and Open Questions.
[So] Source:Int J Sports Med;38(8):573-581, 2017 Jul.
[Is] ISSN:1439-3964
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Since its recognition as a clinical entity in 1992, the Brugada Syndrome (BrS), a hereditary disease characterized by a typical electrocardiogram (ECG) pattern potentially predisposing to sudden cardiac death (SCD), has attracted the attention of many physicians for its circadian pattern of ventricular arrhythmias (VA), mostly occurring at rest. Exercise may potentially worsen the ECG abnormalities in BrS patients, resulting in higher peak J-point amplitudes during the vasovagal reaction of the recovery period, possibly leading to an increased risk of cardiac events. Moreover, the enhanced vagal tone in athletes could be both a BrS risk factor and an exercise effect. Therefore, the true risk of a BrS patient during exercise is still unclear. This review summarizes current knowledge, shortcomings and open questions on BrS and exercise. The paper, in particular, underlines specific considerations including BrS diagnostic criteria and differential diagnosis in athletes, the genetic basis, the autonomic imbalance during exercise practice and the recommendations for athletic participation in this patient group.
[Mh] Termos MeSH primário: Síndrome de Brugada/diagnóstico
Síndrome de Brugada/fisiopatologia
Exercício
[Mh] Termos MeSH secundário: Atletas
Síndrome de Brugada/complicações
Síndrome de Brugada/etiologia
Síndrome de Brugada/genética
Doença do Sistema de Condução Cardíaco
Morte Súbita Cardíaca/etiologia
Diagnóstico Diferencial
Eletrocardiografia
Teste de Esforço
Seres Humanos
Fatores de Risco
Medicina Esportiva
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170619
[St] Status:MEDLINE
[do] DOI:10.1055/s-0043-107240


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[PMID]:28358866
[Au] Autor:Bhattacharyya S; Bhakta M; Munshi NV
[Ad] Endereço:Department of Internal Medicine (Cardiology Division), UT Southwestern Medical Center, Dallas, TX, United States of America.
[Ti] Título:Phenotypically silent Cre recombination within the postnatal ventricular conduction system.
[So] Source:PLoS One;12(3):e0174517, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The cardiac conduction system (CCS) is composed of specialized cardiomyocytes that initiate and maintain cardiac rhythm. Any perturbation to the normal sequence of electrical events within the heart can result in cardiac arrhythmias. To understand how cardiac rhythm is established at the molecular level, several genetically modified mouse lines expressing Cre recombinase within specific CCS compartments have been created. In general, Cre driver lines have been generated either by homologous recombination of Cre into an endogenous locus or Cre expression driven by a randomly inserted transgene. However, haploinsufficiency of the endogenous gene compromises the former approach, while position effects negatively impact the latter. To address these limitations, we generated a Cre driver line for the ventricular conduction system (VCS) that preserves endogenous gene expression by targeting the Contactin2 (Cntn2) 3' untranslated region (3'UTR). Here we show that Cntn23'UTR-IRES-Cre-EGFP/+ mice recombine floxed alleles within the VCS and that Cre expression faithfully recapitulates the spatial distribution of Cntn2 within the heart. We further demonstrate that Cre expression initiates after birth with preservation of native Cntn2 protein. Finally, we show that Cntn23'UTR-IRES-Cre-EGFP/+ mice maintain normal cardiac mechanical and electrical function. Taken together, our results establish a novel VCS-specific Cre driver line without the adverse consequences of haploinsufficiency or position effects. We expect that our new mouse line will add to the accumulating toolkit of CCS-specific mouse reagents and aid characterization of the cell-autonomous molecular circuitry that drives VCS maintenance and function.
[Mh] Termos MeSH primário: Arritmias Cardíacas/genética
Síndrome de Brugada/genética
Contactina 2/genética
Sistema de Condução Cardíaco
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas
Animais
Arritmias Cardíacas/fisiopatologia
Síndrome de Brugada/fisiopatologia
Doença do Sistema de Condução Cardíaco
Contactina 2/biossíntese
Modelos Animais de Doenças
Marcação de Genes
Haploinsuficiência/genética
Ventrículos do Coração/metabolismo
Ventrículos do Coração/fisiopatologia
Recombinação Homóloga/genética
Seres Humanos
Integrases/genética
Camundongos
Camundongos Transgênicos
Miócitos Cardíacos/metabolismo
Fenótipo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (Cntn2 protein, mouse); 0 (Contactin 2); EC 2.7.7.- (Cre recombinase); EC 2.7.7.- (Integrases)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170331
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0174517


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[PMID]:28296544
[Au] Autor:Wen Y; Li B
[Ad] Endereço:a Department of Histology and Embryology , College of Basic Medical Sciences.
[Ti] Título:The conduction system and expressions of hyperpolarization-activated cyclic nucleotide-gated cation channel 4 and connexin43 expressions in the hearts of fetal day 13 mice.
[So] Source:Biotech Histochem;92(2):86-91, 2017.
[Is] ISSN:1473-7760
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:We investigated the development of the sinus node of the heart conduction system by localizing hyperpolarization-activated cyclic nucleotide-gated cation channel 4 (HCN4) and connexin43 (Cx43) in the hearts of fetal day 13 mice. Horizontal serial sections of day 13 whole fetuses were stained by hematoxylin and eosin and immunofluorescence to identify myocardial cells that express HCN4, hyperpolarization-activated cyclic nucleotide-gated cation channel 2 (HCN2) and Cx43. Expression levels of HCN4 and Cx43 were determined by quantitative RT-PCR in both fetal day 13 and adult mice. We found that both Cx43 and HCN4 expressions were located on the cell membranes in the hearts of fetal day 13 mice, but Cx43 was distributed throughout the myocardial cells. HCN4 expression was concentrated mainly in the left dorsal epicardium of the right atrium where Cx43 expression was low or absent. Quantitative RT-PCR demonstrated that HCN4 expression was significantly higher and HCN2 expression was significantly lower in fetal day 13 mice than in adults. We found no statistically significant difference in Cx43 expression between fetal day 13 mice and adults. HCN4 stained myocardial cells in the left dorsal epicardium of the right atrium are the origin of the sinus node and the remainder of the heart conduction system.
[Mh] Termos MeSH primário: Conexina 43/metabolismo
Canais Disparados por Nucleotídeos Cíclicos Ativados por Hiperpolarização/metabolismo
Miocárdio/metabolismo
Nó Sinoatrial/metabolismo
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Síndrome de Brugada/metabolismo
Doença do Sistema de Condução Cardíaco
Canais de Cátion Regulados por Nucleotídeos Cíclicos/metabolismo
Feminino
Coração/embriologia
Camundongos
RNA Mensageiro/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Connexin 43); 0 (Cyclic Nucleotide-Gated Cation Channels); 0 (Hcn4 protein, mouse); 0 (Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels); 0 (RNA, Messenger)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170316
[St] Status:MEDLINE
[do] DOI:10.1080/10520295.2016.1255994


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[PMID]:28267962
[Au] Autor:Maheshwari A; Norby FL; Soliman EZ; Alraies MC; Adabag S; O'Neal WT; Alonso A; Chen LY
[Ad] Endereço:Cardiovascular Division, Department of Medicine, University of Minnesota, Minneapolis, Minnesota. Electronic address: mahes046@umn.edu.
[Ti] Título:Relation of Prolonged P-Wave Duration to Risk of Sudden Cardiac Death in the General Population (from the Atherosclerosis Risk in Communities Study).
[So] Source:Am J Cardiol;119(9):1302-1306, 2017 May 01.
[Is] ISSN:1879-1913
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Prolonged P-wave duration, a marker of left atrial abnormality, is associated with myocardial fibrosis, atrial fibrillation, and all-cause death. It is not known if prolonged P-wave duration is associated with sudden cardiac death (SCD) in the general population. We aimed to evaluate whether prolonged P-wave duration is independently associated with SCD risk in the Atherosclerosis Risk in Communities Study, a community-based prospective cohort study. We included 15,321 participants in our analysis (age 54.2 ± 5.7 years, 55.2% women, 26.4% black). Prolonged P-wave duration was defined as maximum P-wave duration >120 ms and was determined from 12-lead electrocardiograms obtained during 4 exams (1987 to 1999). SCD was physician adjudicated and defined as a sudden, pulseless condition in a previously stable patient without evidence for noncardiac cause of death. We used Cox proportional hazard models to assess the association between prolonged P-wave duration and SCD, adjusting for cardiovascular risk factors and conditions including atrial fibrillation. During a mean follow-up of 12.5 years (1987 to 2001), 268 SCDs were identified. The multivariable hazard ratio (95% confidence interval) of prolonged P-wave duration for SCD was 1.70 (1.31 to 2.20). This association was attenuated but remained significant after updating covariates to the end of follow-up with a hazard ratio of 1.35 (1.04 to 1.76). In conclusion, prolonged P-wave duration is independently associated with an increased risk of SCD in the general population. This association is independent of atrial fibrillation and is only partially mediated by shared cardiovascular risk factors.
[Mh] Termos MeSH primário: Síndrome de Brugada/epidemiologia
Morte Súbita Cardíaca/epidemiologia
[Mh] Termos MeSH secundário: Afroamericanos
Fibrilação Atrial/epidemiologia
Doença do Sistema de Condução Cardíaco
Causas de Morte
Estudos de Coortes
Doença das Coronárias/complicações
Morte Súbita Cardíaca/etiologia
Eletrocardiografia
Grupo com Ancestrais do Continente Europeu
Feminino
Seres Humanos
Vida Independente
Masculino
Meia-Idade
Modelos de Riscos Proporcionais
Estudos Prospectivos
Fatores de Risco
Taquicardia Ventricular/complicações
Estados Unidos/epidemiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1704
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170308
[St] Status:MEDLINE



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