检索结果-南通市图书馆

胎盘血管生成因子和子宫动脉多普勒检查定性不同类型的先兆子痫和孤立的胎儿宫内生长受限

世界核心医学期刊文摘（妇产科学分册） 2006年第10期2卷 9-9页

作者： crispi f. Domnguez C. Llurba E. 张新艳 Biochemistry and Molecular Biology Center Hospital Vall d'Hebron Universitat Autònoma de Barcelona Barcelona Spain Dr.

Objective: The purpose of.this study was to evaluate possible relationships between placental markers and endothelial dysf.nction in preeclampsia and intrauterine growth restriction. Study design: A prospective study was conducted in 76 patients with preeclampsia and 37 patients with intrauterine growth restriction that were classif.ed as early onset( f.gestational age) or late onset, and 40 control subjects. Plasma levels of.placental growth f.ctor, soluble f.s-like tyrosine kinase-1, vascular cell adhesion molecule-1, and uterine artery Doppler indices were measured. Results: In early-onset preeclampsia and intrauterine growth restriction, placental growth f.ctor was lower and soluble f.s-like tyrosine kinase-1 and vascular cell adhesion molecule-1 higher than in control subjects, although all changes were more pronounced in preeclampsia. In late onset preeclampsia, those patients with abnormal uterine artery Doppler indices had higher soluble f.s-like tyrosine kinase-1 and vascular cell adhesion molecule-1 levels. Conclusion: Biochemical changes in early-onset preeclampsia and intrauterine growth restriction point to a common placental disorder and a state of.endothelial dysf.nction, which may require interaction with other f.ctors to explain the maternal disease in preeclampsia. Data in late-onset preeclampsia suggest that a proportion of.them may occur with minimal placental involvement.

关键词：胎儿宫内生长血管生成因子先兆子痫子宫动脉多普勒检查内皮功能失调生化改变研究设计内皮功

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

SIRT3-mediated inhibition of.f.S through histone H3 deacetylation prevents cardiac f.brosis and inf.ammation

引用

Signal Transduction and Targeted Therapy 2020年第1期5卷 2322-2331页

作者： Xavier Palomer MSilvia Román-Azcona Javier Pizarro-Delgado Ana Planavila f.ancesc Villarroya Brenda Valenzuela-Alcaraz f.tima crispi Álvaro Sepúlveda-Martínez Irene Miguel-Escalada Jorge f.rrer Jf.ancisco Nistal Raquel García Mercy MDavidson Emma Barroso Manuel Vázquez-Carrera Department of.Pharmacology Toxicology and Therapeutic ChemistryIBUB(Institut de Biomedicina de la Universitat de Barcelona)Research Institute-Pediatric Research InstituteHospital Sant Joan de Déuand CIBER de Diabetes y Enfermedades Metabólicas Asociadas(CIBERDEM)Faculty of Pharmacy and Food SciencesUniversity of BarcelonaBarcelonaSpain Department of.Biochemistry and Molecular Biomedicine IBUB and CIBER Fisiopatología de la Obesidad y Nutrición(CIBEROBN)Faculty of BiologyUniversity of BarcelonaBarcelonaSpain aBCNatal-Barcelona Center f.r Maternal–f.tal and Neonatal Medicine(Hospital Clínic and Hospital Sant Joan de Deu) Institut d’Investigacions Biomèdiques August Pi i SunyerUniversitat de Barcelonaand Center for Biomedical Research on Rare Diseases(CIBER-ER)BarcelonaSpain Genomic Programming of.Betacells Laboratory Institut d’Investigacions August Pi i Sunyer(IDIBAPS)and CIBERDEMBarcelonaSpain Section of.Epigenomics and Disease Department of Medicineand National Institute for Health Research(NIHR)Imperial Biomedical Research CentreImperial College LondonLondonUK Servicio de Cirugía Cardiovascular Hospital Universitario Marqués de ValdecillaDepartamento de Ciencias Médicas y QuirúrgicasFacultad de MedicinaUniversidad de CantabriaInstituto de Investigación Marqués de Valdecilla(IDIVAL)Centro de Investigación Biomédica en Red Cardiovascular(CIBERCV)Instituto de Salud Carlos IIISantanderSpain Departamento de f.siología y f.rmacología Facultad de MedicinaUniversidad de CantabriaInstituto de Investigación Marqués de Valdecilla(IDIVAL)SantanderSpain Department of.Radiation Oncology Columbia UniversityNew YorkNYUSA

Sirtuin 3(SIRT3)is a deacetylase that modulates proteins that control metabolism and protects against oxidative stress.Modulation of.SIRT3 activity has been proposed as a promising therapeutic target f.r ameliorating metabolic diseases and associated cardiac disturbances.In this study,we investigated the role of.SIRT3 in inf.ammation and f.brosis in the heart using male mice with constitutive and systemic deletion of.SIRT3 and human cardiac AC16 cells.SIRT3 knockout mice showed cardiac f.brosis and inf.ammation that was characterized by augmented transcriptional activity of.AP-1.Consistent with this,SIRT3 overexpression in human and neonatal rat cardiomyocytes partially prevented the inf.ammatory and prof.brotic response induced by TNf.α.Notably,these ef.ects were associated with a decrease in the mRNA and protein levels of.f.S and the DNA-binding activity of.AP-1.f.nally,we demonstrated that SIRT3 inhibits f.S transcription through specif.c histone H3 lysine K27 deacetylation at its promoter.These f.ndings highlight an important f.nction of.SIRT3 in mediating the of.en intricate prof.brotic and proinf.ammatory responses of.cardiac cells through the modulation of.the f.S/AP-1 pathway.Since f.brosis and inf.ammation are crucial in the progression of.cardiac hypertrophy,heart f.ilure,and diabetic cardiomyopathy,our results point to SIRT3 as a potential target f.r treating these diseases.

关键词： SIRT3 inf.ammation cardiac

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

欢迎您,

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

请选择保存的检索档案：

请选择收藏分类：

通借通还

欢迎您,

建议与咨询 留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

请选择保存的检索档案： 新增检索档案 确定 取消

请选择收藏分类： 新增自定义分类 确定 取消

通借通还

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

请选择保存的检索档案：

请选择收藏分类：