WordNet

an abnormal enlargement of the heart; "mild cardiomegaly is common in athletes" (同)megalocardia, megacardia, enlarged_heart
a plane figure with rounded sides curving inward at the top and intersecting at the bottom; conventionally used on playing cards and valentines; "he drew a heart and called it a valentine"
the courage to carry on; "he kept fighting on pure spunk"; "you havent got the heart for baseball" (同)mettle, nerve, spunk
an inclination or tendency of a certain kind; "he had a change of heart" (同)spirit
a playing card in the major suit that has one or more red hearts on it; "he led the queen of hearts"; "hearts were trumps"
the locus of feelings and intuitions; "in your heart you know it is true"; "her story would melt your bosom" (同)bosom
the hollow muscular organ located behind the sternum and between the lungs; its rhythmic contractions move the blood through the body; "he stood still, his heart thumping wildly" (同)pump, ticker
a firm rather dry variety meat (usually beef or veal); "a five-pound beef heart will serve six"
able to perceive sound
an opportunity to state your case and be heard; "they condemned him without a hearing"; "he saw that he had lost his audience" (同)audience
(law) a proceeding (usually by a court) where evidence is taken for the purpose of determining an issue of fact and reaching a decision based on that evidence
the ability to hear; the auditory faculty; "his hearing was impaired" (同)audition, auditory sense, sense of hearing, auditory modality
a session (of a committee or grand jury) in which witnesses are called and testimony is taken; "the investigative committee will hold hearings in Chicago"
receive a communication from someone; "We heard nothing from our son for five years"
examine or hear (evidence or a case) by judicial process; "The jury had heard all the evidence"; "The case will be tried in California" (同)try
perceive (sound) via the auditory sense
abnormal enlargement of a body part or organ
undergo hypertrophy; "muscles can hypertrophy when people take steroids"
a form of whist in which players avoid winning tricks containing hearts or the queen of spades (同)Black_Maria

PrepTutorEJDIC

〈C〉『心臓』;胸 / 〈C〉(感情の中心をなす)『心』,気持ち / 〈U〉愛情,同情 / 〈U〉『勇気』,元気,熱意 / 《the ~》『中心』,内部,(物事の)本質,核心 / 〈C〉ハート形の物;(カードの)ハートの札
〈U〉『聴力』,聴覚〈U〉〈C〉(…を)『聞くこと』,(…の)聞き取り《+『of』+『名』》・〈C〉聞いてもらう機会,聞いてやること・聴取・聴聞会〈C〉(法廷などでの)尋問,審問,;(刑罰の減免を求める)釈明,意見陳述 / 〈U〉聞こえる距離(範囲)
〈音〉‘が'『聞こえる』,‘を'聞く(進行形にできない) / 〈人の言うこと〉‘に'『耳を傾ける』,‘を'注意深く聞く(listen);(裁判官などが)…の申し立てを聞く / 〈うわさ・ニュースなど〉‘を'『耳にしている』,聞いている / 『耳が聞こえる』 / 《しばしば命令形で》耳を傾ける,注意を向ける / 『うわさ』(『消息』)『を聞く』
(生物体の部分・器官の)異常肥大,異常発達

UpToDate Contents

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1. 左室肥大の心電図による診断 electrocardiographic diagnosis of left ventricular hypertrophy
2. 高血圧における左室肥大の臨床的意義および治療 clinical implications and treatment of left ventricular hypertrophy in hypertension
3. 左室肥大および不整脈 left ventricular hypertrophy and arrhythmia
4. 高血圧における左室肥大の定義および病因 definition and pathogenesis of left ventricular hypertrophy in hypertension
5. 慢性腎疾患における貧血および左室肥大 anemia and left ventricular hypertrophy in chronic kidney disease

English Journal

Cardiac-specific Traf2 overexpression enhances cardiac hypertrophy through activating AKT/GSK3β signaling.

Huang Y1, Wu D2, Zhang X1, Jiang M1, Hu C3, Lin J1, Tang J1, Wu L4.Author information 1Department of Cardiology, The Second Affiliated Hospital of Wenzhou Medical University, 109 Xueyuan Road, Wenzhou 25035, Zhejiang, China.2Medical College of Zhejiang University City College, 51 Huzhou Road, Hangzhou 310000, China.3Department of Cardiology, The Tongji Hospital of Tongji University, 309 Xincun Road, Putuo District, Shanghai 200065, China.4Department of Cardiology, The Second Affiliated Hospital of Wenzhou Medical University, 109 Xueyuan Road, Wenzhou 25035, Zhejiang, China. Electronic address: wulianpin@gmail.com.AbstractTumor necrosis factor superfamily ligands provoke a dilated cardiac phenotype signal through a common scaffolding protein termed tumor necrosis factor receptor-associated factor 2 (Traf2); however, Traf2 signaling in the adult mammalian cardiac hypertrophy is not fully understood. This study was aimed to identify the effect of Traf2 on cardiac hypertrophy and the underlying mechanisms. A significant up-regulation of Traf2 expression was observed in mice failing hearts. To further investigate the role of Traf2 in cardiac hypertrophy, we used cultured neonatal rat cardiomyocytes with gain and loss of Traf2 function and cardiac-specific Traf2-overexpressing transgenic (TG) mice. In cultured cardiomyocytes, Traf2 positively regulated angiotensin II (Ang II)-mediated hypertrophic growth, as detected by [(3)H]-Leucine incorporation, cardiac myocyte area, and hypertrophic marker protein levels. Cardiac hypertrophy in vivo was produced by constriction of transverse aortic (TAC) in TG mice and their wild-type controls. The extent of cardiac hypertrophy was evaluated by echocardiography as well as by pathological and molecular analyses of heart samples. Traf2 overexpression in the heart remarkably enhanced cardiac hypertrophy, left ventricular dysfunction in mice in response to TAC. Further analysis of the signaling pathway in vitro and in vivo suggested that these adverse effects of Traf2 were associated with the activation of AKT/glycogen synthase kinase 3β (GSK3β). The present study demonstrates that Traf2 serves as a novel mediator that enhanced cardiac hypertrophy by activating AKT/GSK3β signaling.
Gene.Gene.2014 Feb 25;536(2):225-31. doi: 10.1016/j.gene.2013.12.052. Epub 2013 Dec 27.
Tumor necrosis factor superfamily ligands provoke a dilated cardiac phenotype signal through a common scaffolding protein termed tumor necrosis factor receptor-associated factor 2 (Traf2); however, Traf2 signaling in the adult mammalian cardiac hypertrophy is not fully understood. This study was aim
PMID 24378234

COX-2 is involved in ET-1-induced hypertrophy of neonatal rat cardiomyocytes: Role of NFATc3.

Li H1, Gao S1, Ye J1, Feng X1, Cai Y2, Liu Z1, Lu J1, Li Q1, Huang X1, Chen S3, Liu P4.Author information 1Department of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-sen University, Higher Education Mega Center, Guangzhou 510006, Guangdong, PR China.2Guangzhou Research Institute of Snake Venom, Guangzhou Medical College, Guangzhou 510182, Guangdong, PR China.3Department of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-sen University, Higher Education Mega Center, Guangzhou 510006, Guangdong, PR China. Electronic address: chshaor@mail.sysu.edu.cn.4Department of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-sen University, Higher Education Mega Center, Guangzhou 510006, Guangdong, PR China. Electronic address: liupq@mail.sysu.edu.cn.AbstractEndothelin-1 (ET-1) is a critical molecule that involved in heart failure. It has been proved that ET-1 stimulation results in cardiac hypertrophy both in vitro and in vivo, but the mechanisms underlying remain largely unknown. In this study, we reported that cyclooxygenase-2 (COX-2) might be an important mediator of hypertrophic responses to ET-1 stimulation. In the cultured rat neonatal cardiomyocytes, ET-1 significantly upregulated the expression and activity of COX-2, which was accompanied by increase in cell surface area and BNP mRNA level. In contrast, ET-1-dependent cardiomyocyte hypertrophy was abolished by COX-2 selective inhibitors, NS-398 and celecoxib, or by COX-2 RNA interference, but the inhibitory effects could be diminished by pretreatment with PGE2. Furthermore, cyclosporin A (CsA) and knockdown of nuclear factor of activated T-cells c3 (NFATc3) inhibited the expression of COX-2 induced by ET-1, and NFATc3 could also bound to the -GGAAA- sequence in the promoter region of rat COX-2 gene, indicating that calcineurin/NFATc3 signaling participated in the transcriptional regulation of COX-2 following ET-1 treatment. These findings provided further insight into the roles of ET-1 in cardiac hypertrophy and suggested a potential therapeutic strategy against cardiac hypertrophy by inhibiting COX-2.
Molecular and cellular endocrinology.Mol Cell Endocrinol.2014 Feb 15;382(2):998-1006. doi: 10.1016/j.mce.2013.11.012. Epub 2013 Nov 26.
Endothelin-1 (ET-1) is a critical molecule that involved in heart failure. It has been proved that ET-1 stimulation results in cardiac hypertrophy both in vitro and in vivo, but the mechanisms underlying remain largely unknown. In this study, we reported that cyclooxygenase-2 (COX-2) might be an imp
PMID 24291639

Effect of genetic polymorphisms of vascular endothelial growth factor on left ventricular hypertrophy in patients with systemic hypertension.

Lacchini R1, Luizon MR1, Gasparini S2, Ferreira-Sae MC2, Schreiber R2, Nadruz W Jr2, Tanus-Santos JE3.Author information 1Department of Pharmacology, Faculty of Medicine of Ribeirao Preto, University of Sao Paulo, Ribeirao Preto, Brazil.2Department of Internal Medicine, Faculty of Medical Sciences, State University of Campinas, Campinas, Brazil.3Department of Pharmacology, Faculty of Medicine of Ribeirao Preto, University of Sao Paulo, Ribeirao Preto, Brazil. Electronic address: tanussantos@yahoo.com.AbstractVascular endothelial growth factor (VEGF) is a cytokine involved in angiogenesis and upregulated during adaptive heart hypertrophy. Downregulation of VEGF seems to trigger the transition from adaptive to dilated cardiac hypertrophy. We investigated for the first time whether 3 clinically relevant polymorphisms in the VEGFA gene are associated with altered echocardiographic parameters in hypertensive patients. We determined genotypes for 3 polymorphisms in VEGFA promoter in 179 hypertensive patients and 169 healthy controls: g.-2578C>A (rs699947), g.-1154G>A (rs1570360), and g.-634G>C (rs2010963). Although the variant genotypes of the g.-634G>C (GC + CC) were associated with reduced left ventricular mass index (p = 0.030), the variant genotypes for the g.-1154G>A (GA + AA) were associated with reduced ejection fraction (p = 0.008). In addition, we found that VEGFA haplotypes were associated with altered ejection fraction (p = 0.024). The AAG haplotype was associated with reduced ejection fraction (p = 0.006), whereas the AGG haplotype was associated with increased ejection fraction (p = 0.010). Our results suggest that VEGF polymorphisms affect cardiac remodeling. Genotypes for VEGFA polymorphisms can be useful to help to identify hypertensive patients at greater intrinsic risk for heart failure.
The American journal of cardiology.Am J Cardiol.2014 Feb 1;113(3):491-6. doi: 10.1016/j.amjcard.2013.10.034. Epub 2013 Nov 9.
Vascular endothelial growth factor (VEGF) is a cytokine involved in angiogenesis and upregulated during adaptive heart hypertrophy. Downregulation of VEGF seems to trigger the transition from adaptive to dilated cardiac hypertrophy. We investigated for the first time whether 3 clinically relevant po
PMID 24321896

Japanese Journal

Subendocardial Systolic Dysfunction in Asymptomatic Normotensive Diabetic Patients

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Circulation Journal advpub(0), 2015
… Background:It remains uncertain whether diabetes itself causes specific echocardiographic features of myocardial morphology and function in the absence of hypertension or ischemic heart disease. … Patients with coronary artery stenosis or structural heart disease were excluded. …
NAID 130005073170

Delivery of Imatinib-Incorporated Nanoparticles into Lungs Suppresses the Development of Monocrotaline-Induced Pulmonary Arterial Hypertension

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International Heart
… Three weeks after monocrotaline injection, intratracheal administration of Ima-NPs suppressed the development of pulmonary hypertension, small pulmonary artery remodeling, and right ventricular hypertrophy in the rat model of monocrotaline-induced PAH. …
NAID 130005070013

Delivery of Imatinib-Incorporated Nanoparticles into Lungs Suppresses the Development of Monocrotaline-Induced Pulmonary Arterial Hypertension

, , , , , , , ,
International Heart
… Three weeks after monocrotaline injection, intratracheal administration of Ima-NPs suppressed the development of pulmonary hypertension, small pulmonary artery remodeling, and right ventricular hypertrophy in the rat model of monocrotaline-induced PAH. …
NAID 130005066384