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Exercise stress echocardiography:Where are we now?

World Journal of Cardiology 2022年第2期14卷 64-82页

作者： carlos alberto cotrim Hugo Café Isabel João Nuno cotrim Jorge Guardado Pedro Cordeiro Hortense cotrim Luis Baquero Heart Center Hospital da Cruz Vermelha PortuguesaLisboa 1549-008Portugal Faculdade de Medicina Algarve UniversityFaro 8005-139Portugal Department of Cardiology Garcia de Orta HospitalAlmada 2805-267Portugal Department of Medicine Garcia de Orta HospitalAlmada 2805-267Portugal Cardiovascular Unit UCARDIOCentro ClinicoRiachos 2350-325Portugal Department of Cardiology Hospital Particular do AlgarveFaro 8005-226Portugal

Exercise stress echocardiography(ESE)is a widely used diagnostic test in cardiology *** is mainly used to study patients with coronary artery disease;however,it has increasingly been used in other clinical scenarios including valve pathology,congenital heart disease,hypertrophic and dilated cardiomyopathies,athlete evaluations,diastolic function evaluation,and pulmonary circulation *** our laboratories,we use an established methodology in which cardiac function is evaluated while exercising on a *** completing the exercise regimen,patients remain in a standing position or lie down on the left lateral decubitus,depending on the clinical questions to be answered for further *** method increases the quality and quantity of information ***,we present the various methods of exercise stress echocardiography and our experience in many clinical arenas in *** also present alternatives to ESE that may be used and their advantages and *** review recent advances in ESE and future directions for this established method in the study of cardiac patients and underline the advantage of using a diagnostic tool that is radiation-free.

关键词： Exercise stress echocardiography Coronary artery disease Valve disease Athletes Intraventricular gradients Children

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Leptin Signaling Modulates Expression of Polycomb and Trithorax Complexes in the Brain of Fat Tissue Implanted Polycystic Ovarian Sindrome Mice

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American Journal of Molecular Biology 2014年第4期4卷 177-192页

作者： Eduardo Henrique da Silva Freitas Samuel Marcos Ribeiro de Noronha Maria Nazareth Gamboa Ritto carlos Fernandes Baptista Ismael Dale cotrim Guerreiro da Silva Silvana Aparecida Alves Correa-Noronha Ivaldo da Silva Gynecology Department Federal University of Sao Paulo Paulista School of Medicine (UNIFESP-EPM) Sao Paulo Brazil General Medicine Department Federal University of Rio de Janeiro State (UNIRIO) Rio de Janeiro Brazil Translacional Surgery Division Surgery Department Federal University of Sao Paulo Paulista School of Medicine (UNIFESP-EPM) Sao Paulo Brazil General and Specialized Surgery Department Federal University of Rio de Janeiro State (UNIRIO) Rio de Janeiro Brazil

The Polycystic Ovary Syndrome (PCOS) is the most common androgenic disorder in women during reproductive life. PCOS may also be accompanied by metabolic syndrome and recent studies point to leptin as playing a role in disrupting infertility and in changing the energy balance in obese mice through its action on the hypothalamus. The aim is to assess the expression of the Polycomb & Trithorax Complexes genes in brain of mice transplanted with fat tissue from normal mice, in order to better understand the neuronal mechanisms underlying the reversion of PCOS. Three B6 V-Lepob/J mouse groups: Normal weight, obese and seven-day-treatment obese had their brain RNA extracted and submitted to an 84 Polycomb & Trithorax Complexes genes PCR Array plate and MetacoreTM pathways localization. Genomic profiles obtained were compared to the ones of the normal-weight-mice group. Differentially expressed genes were 13% and 26% respectively to control and treatment. Major changes were in genes: Snai1/31;Smarca1/?17;Dnmt3b/4.7;Ezh1/ 15. Altered genes were associated to canonical pathways and provided 3 networks related to epigenetics. Underlying neuronal changes caused by leptin in obese mice brain, there is an important role being played by the histone code. Here there is evidence that leptin drives the chromatin packing to a more condensed pattern. Upregulation of methyltransferase genes, like Ezh1, favors this thought. In summary the Polycomb & Trithorax complexes might answer for the silencing of some downregulated genes in the obese mice brain when exposed to leptin.

关键词： Polycistic Ovarian Sindrome Obesity Polycomb and Trithorax Complexes Leptin Fat Mouse

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Leptin Causes the Early Inhibition of Glycolysis-and TCA Cycle-Related Genes in the Brain of Ob/Ob Mice to Restore Fertility

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American Journal of Molecular Biology 2014年第3期4卷 105-113页

作者： carlos Fernandes Baptista Samuel Marcos Ribeiro de Noronha Maria de Nazareth Gamboa Ritto Eduardo Henrique da Silva Freitas Melquíades Pereira Júnior Mauro Abi Haidar Ismael Dale cotrim Guerreiro da Silva Silvana Aparecida Alves Corrêa de Noronha Marisa Teresinha Patriarca Gynecology Department Escola Paulista de Medicina/Universidade Federal de Sao Paulo(EPM-UNIFESP)São PauloBrazil Departmento de Cirurgia Geral e Especializada Universidade Federal do Rio de Janeiro(UNIRIO)Rio de JaneiroBrazil Surgery Department Escola Paulista de Medicina/Universidade Federal de Sao Paulo(EPM-UNIFESP)Sao PauloBrazil Departmento de Medicina Geral Universidade Federal do Rio de Janeiro(UNIRIO)Rio de JaneiroBrazil

Introduction: Polycystic ovarian syndrome (PCOS) is undoubtedly the commonest androgen disorder in woman’s fertile period and certainly one of the most prevalent causes of anovulation. The syndrome has an estimated prevalence of 4% - 10% among women of childbearing age. Previously, our group demonstrated the effect of gonadal white adipose tissue transplantation from wild-type lean and fertile female mice to isogenic obese anovulatory ob/ob mice. These complex metabolic interrelationships between obesity and PCOS have yet to be fully understood. The aim of this study was to evaluate the effect of gonadal white adipose tissue (WAT) transplantation from the wild-type lean and fertile female mice to isogenic obese, anovulatory mice (Lep ob/Lep ob) on the expression of glycolysis- and TCA cycle-related genes and obtain a general view of the glucose metabolism in the brain of these animals. Methods: Fifteen ob/ob mice ranging from 2 to 3 months of age were divided into 3 experimental groups: control normal weight (n = 5), obese control (n = 5) and obese 7 days leptin treated (n = 5). The whole brains of the mice were processed for RNA extraction. The samples from each group were used to perform PCR assays using an array plate containing 84 primers to study the glucose metabolism-related genes. Results: The glycolysis- and TCA cycle-related genes were significantly downregulated. The most significantly affected genes were as follows: for glycolysis (fold regulation with p < 0.05):Pgm1,Bpgm,Aldob, andEno3 (119, 45, 18, and 28 times less, respectively);and for the TCA cycle (fold regulation with p < 0.05):Cs,Idh3b, andMdh2 (84, 27, and 37 times less, respectively).Conclusion: The seven-day leptin treated mice show a decrease in the glucose metabolism. These results confirm the ability of the adipose tissue-derived hormone leptin to regulate early crucial genes that are related to glycolysis mechanisms and to the TCA cycle. This hormone seems to revert early the central phys

关键词： PCOS Obesity Leptin Glycolysis TCA Cycle Gene Expression

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