WordNet
- (medicine) any disturbance in the functioning of an organ or body part or a disturbance in the functioning of a social group; "erectile dysfunction"; "sexual relationship dysfunction" (同)disfunction
- of or relating to a ventricle (of the heart or brain)
PrepTutorEJDIC
- 機能障害,機能不全
UpToDate Contents
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- 1. 無症候性左室収縮機能障害の評価および管理 evaluation and management of asymptomatic left ventricular systolic dysfunction
- 2. 心不全の疫学および原因 epidemiology and causes of heart failure
- 3. 拡張期心不全の病態生理 pathophysiology of diastolic heart failure
- 4. 心臓リモデリング：臨床的評価および治療 cardiac remodeling clinical assessment and therapy
- 5. 心不全の病態生理：左心室の圧-容積関係 pathophysiology of heart failure left ventricular pressure volume relationships
English Journal
- MDMA induces cardiac contractile dysfunction through autophagy upregulation and lysosome destabilization in rats.
- Shintani-Ishida K1, Saka K2, Yamaguchi K3, Hayashida M3, Nagai H2, Takemura G4, Yoshida K2.Author information 1Department of Forensic Medicine, Graduate School of Medicine, the University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan. Electronic address: kaori@m.u-tokyo.ac.jp.2Department of Forensic Medicine, Graduate School of Medicine, the University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan.3Department of Legal Medicine, Graduate School of Medicine, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo 113-8602, Japan.4Department of Cardiology, Gifu University Graduate School of Medicine, 1-1 Yanagido, Gifu 501-1194, Japan.AbstractThe underlying mechanisms of cardiotoxicity of 3,4-methylenedioxymethylamphetamine (MDMA, "ecstasy") abuse are unclear. Autophagy exerts either adaptive or maladaptive effects on cardiac function in various pathological settings, but nothing is known on the role of autophagy in the MDMA cardiotoxicity. Here, we investigated the mechanism through which autophagy may be involved in MDMA-induced cardiac contractile dysfunction. Rats were injected intraperitoneally with MDMA (20mg/kg) or saline. Left ventricular (LV) echocardiography and LV pressure measurement demonstrated reduction of LV systolic contractility 24h after MDMA administration. Western blot analysis showed a time-dependent increase in the levels of microtubule-associated protein light chain 3-II (LC3-II) and cathepsin-D after MDMA administration. Electron microscopy showed the presence of autophagic vacuoles in cardiomyocytes. MDMA upregulated phosphorylation of adenosine monophosphate-activated protein kinase (AMPK) at Thr172, mammalian target of rapamycin (mTOR) at Thr2446, Raptor at Ser792, and Unc51-like kinase (ULK1) at Ser555, suggesting activation of autophagy through the AMPK-mTOR pathway. The effects of autophagic inhibitors 3-methyladenine (3-MA) and chloroquine (CQ) on LC3-II levels indicated that MDMA enhanced autophagosome formation, but attenuated autophagosome clearance. MDMA also induced release of cathepsins into cytosol, and western blotting and electron microscopy showed cardiac troponin I (cTnI) degradation and myofibril damage, respectively. 3-MA, CQ, and a lysosomal inhibitor, E64c, inhibited cTnI proteolysis and improved contractile dysfunction after MDMA administration. In conclusion, MDMA causes lysosome destabilization following activation of the autophagy-lysosomal pathway, through which released lysosomal proteases damage myofibrils and induce LV systolic dysfunction in rat heart.
- Biochimica et biophysica acta.Biochim Biophys Acta.2014 May;1842(5):691-700. doi: 10.1016/j.bbadis.2014.01.013. Epub 2014 Jan 31.
- The underlying mechanisms of cardiotoxicity of 3,4-methylenedioxymethylamphetamine (MDMA, "ecstasy") abuse are unclear. Autophagy exerts either adaptive or maladaptive effects on cardiac function in various pathological settings, but nothing is known on the role of autophagy in the MDMA cardiotoxici
- PMID 24491919
- Angiotensin-(1-12): A Chymase-Mediated Cellular Angiotensin II Substrate.
- Ahmad S1, Varagic J, Groban L, Dell'italia LJ, Nagata S, Kon ND, Ferrario CM.Author information 1Division of Surgical Sciences, Wake Forest School of Medicine, Winston Salem, NC, USA.AbstractThe classical view of biochemical pathways for the formation of biologically active angiotensins continues to undergo significant revision as new data uncovers the existence of important species differences between humans and rodents. The discovery of two novel substrates that, cleaved from angiotensinogen, can lead to direct tissue angiotensin II formation has the potential of radically altering our understanding of how tissues source angiotensin II production and explain the relative lack of efficacy that characterizes the use of angiotensin converting enzyme inhibitors in cardiovascular disease. This review addresses the discovery of angiotensin-(1-12) as an endogenous substrate for the production of biologically active angiotensin peptides by a non-renin dependent mechanism and the revealing role of cardiac chymase as the angiotensin II convertase in the human heart. This new information provides a renewed argument for exploring the role of chymase inhibitors in the correction of cardiac arrhythmias and left ventricular systolic and diastolic dysfunction.
- Current hypertension reports.Curr Hypertens Rep.2014 May;16(5):429. doi: 10.1007/s11906-014-0429-9.
- The classical view of biochemical pathways for the formation of biologically active angiotensins continues to undergo significant revision as new data uncovers the existence of important species differences between humans and rodents. The discovery of two novel substrates that, cleaved from angioten
- PMID 24633843
- Regulator of g protein signaling 3 protects against cardiac hypertrophy in mice.
- Liu Y1, Huang H, Zhang Y, Zhu XY, Zhang R, Guan LH, Tang Q, Jiang H, Huang C.Author information 1Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, 430060, China; Cardiovascular Research Institute of Wuhan University, Wuhan, 430060, China.AbstractRegulator of G protein signaling 3 (RGS3) is a negative regulator of G protein-mediated signaling. RGS3 has previously been shown to be expressed among various cell types within the mature heart. Basic and clinical studies have reported abnormal expressions of RGS3 in hypertrophic hearts and in the failing myocardium. However, the role of RGS3 in cardiac remodeling remains unclear. In this study, we investigated the effect of cardiac overexpression of human RGS3 on cardiac hypertrophy induced by aortic banding (AB) in RGS3 transgenic mice and wild-type littermates. The extent of cardiac hypertrophy was evaluated by echocardiography as well as pathological and molecular analyses of heart samples. RGS3 overexpression in the heart markedly reduced the extent of cardiac hypertrophy, fibrosis, and left ventricular dysfunction in response to AB. These beneficial effects were associated with the inhibition of MEK-ERK1/2 signaling. In vitro studies performed in cultured neonatal rat cardiomyocytes confirmed that RGS3 overexpression inhibits hypertrophic growth induced by angiotensin II, which was associated with the attenuation of MEK-ERK1/2 signaling. Therefore, cardiac overexpression of RGS3 inhibits maladaptive hypertrophy and fibrosis and improves cardiac function by blocking MEK-ERK1/2 signaling. J. Cell. Biochem. 115: 977-986, 2014. © 2013 Wiley Periodicals, Inc.
- Journal of cellular biochemistry.J Cell Biochem.2014 May;115(5):977-86. doi: 10.1002/jcb.24741.
- Regulator of G protein signaling 3 (RGS3) is a negative regulator of G protein-mediated signaling. RGS3 has previously been shown to be expressed among various cell types within the mature heart. Basic and clinical studies have reported abnormal expressions of RGS3 in hypertrophic hearts and in the
- PMID 24375609
Japanese Journal
- 急性心不全を契機に診断された心サルコイドーシスの1例
- 田中 絢子,鈴木 敦,新井 光太郎,鈴木 豪,志賀 剛,萩原 誠久
- 東京女子医科大学雑誌 83(4), 261-266, 2013-08-25
- 症例は54歳男性で、2011年某月に、急性発症した高度呼吸困難により救急搬送された。胸部レントゲンで心拡大を認め、BNP値は2000pg/mLと高値を認め、急性心不全と診断された。カルベジロール3.75mg/日、エナラプリル1.25mg/日、フロセミド20mg/日とアミオダロン100mg/日を投与され退院した。冠動脈CT検査で、冠状動脈に有意狭窄は認めなかった。心臓超音波検査では、左室駆出率21% …
- NAID 110009610664
- 心不全患者の日常生活動作に対する左室収縮不全や心腎貧血症候群の影響
- 齊藤 正和,小澤 哲也,塩谷 洋平,岡村 大介,馬淵 美也子,中澤 麻理子,青柳 真理恵,坂本 純子,秋保 光利
- 理学療法学 40(1), 10-15, 2013-02-20
- 【目的】心不全患者の日常生活動作に対する左室収縮不全ならびに心腎貧血症候群に(CRAS)の影響を検討する。【方法】2011年8月から2012年2月の間に入院加療中より理学療法を施行した心不全患者256例(女性49%,年齢79±11歳)を対象とした。入院時の左室駆出率(LVEF)によりHFrEF群(LVEF≦40%)119例とHFpEF群(LVEF > 40%)137例に分類した。また,Hb& …
- NAID 110009594478
- 片側性の脳室上衣下嚢胞と脳室内隔壁を呈したピルビン酸脱水素酵素複合体欠損症の一女児例
- 伊藤 進,小國 弘量,大谷 ゆい,島田 姿野,石垣 景子,舟塚 真,大澤 眞木子
- 東京女子医科大学雑誌 83(E1), E296-E300, 2013-01-31
- ピルビン酸脱水素酵素複合体(PDHC)欠損症は、小児の一次性乳酸アシドーシスと神経学的異常の主原因となる先天性代謝異常症である。我々は、特異な片側性の脳室上衣下嚢胞と脳室内隔壁を呈したPDHA1遺伝子変異を伴うPDHC欠損症の一女児例を経験した。本症例では、精神運動発達遅滞、てんかん、小頭症を呈した。また、高乳酸血症は伴わなかったが、乳酸/ピルビン酸比正常の高乳酸髄液症を認めた。片側性の脳室周囲白 …
- NAID 110009559412
Related Links
- Tachycardia induced cardiomyopathy (TIC) is defined as atrial or ventricular dysfunction as a result of prolonged elevated heart rate that is reversible upon control of the arrhythmia. There may be no underlying structural ...
- ventricular dysfunction, an abnormality in the contraction of the ventricles or the motion of the cells. ventricular dysfunction, n an abnormality in contraction and wall motion within the ventricles. ven·tric·u·lar dys·func·tion (ven-trikyū-lăr ...
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★リンクテーブル★
| リンク元 | 「心室機能不全」「心室機能障害」 |
| 関連記事 | 「dysfunction」「ventricular」 |
「心室機能不全」
「心室機能障害」
「dysfunction」
- n.
- vi
- 機能不全に陥る
- 関
- barrier、damage、difficulty、disorder、disturbance、foe、functional disorder、functional impairment、hindrance、hypofunction、impair、impairment、impediment、incompetence、insufficiency、lesion、malfunction、obstacle、stun
「ventricular」
- adj.
- 室の、心室の、脳室の、心室性の
- 関
- cardiac ventricle、cerebral ventricle、cerebroventricle、cerebroventricular、heart ventricle、ventricle、ventriculi、ventriculus