WordNet
- a cellular structure that is postulated to exist in order to mediate between a chemical agent that acts on nervous tissue and the physiological response
- of or relating to the heart; "cardiac arrest"
- the opening into the stomach and that part of the stomach connected to the esophagus
PrepTutorEJDIC
- =sense organ / 受信装置
- 心臓の
UpToDate Contents
全文を閲覧するには購読必要です。 To read the full text you will need to subscribe.
- 1. カテコラミン誘発多形性心室頻拍および他のQT間隔正常の多形性心室頻拍 catecholaminergic polymorphic ventricular tachycardia and other polymorphic ventricular tachycardias with a normal qt interval
- 2. 不整脈原性右室心筋症：解剖学、組織学、病因、および遺伝学 arrhythmogenic right ventricular cardiomyopathy anatomy histology pathogenesis and genetics
- 3. 明らかな器質的心疾患のない患者における突然の心停止 sudden cardiac arrest in the absence of apparent structural heart disease
- 4. 小児におけるQRS幅の広い頻脈の原因 causes of wide qrs complex tachycardia in children
- 5. 溺死（水没事故） drowning submersion injuries
English Journal
- Dantrolene Improves Survival Following Ventricular Fibrillation by Mitigating Impaired Calcium Handling in Animal Models.
- Zamiri N, Massé S, Ramadeen A, Kusha M, Hu X, Azam MA, Liu J, Lai PF, Vigmond EJ, Boyle PM, Behradfar E, Al-Hesayen A, Waxman MB, Backx P, Dorian P, Nanthakumar K.Author information University of Toronto, Toronto, Canada.AbstractBACKGROUND: Resistant ventricular fibrillation, re-fibrillation and diminished myocardial contractility are important factors leading to poor survival following cardiac arrest. We hypothesized dantrolene improves survival following VF by rectifying calcium dysregulation caused by VF.
- Circulation.Circulation.2014 Jan 8. [Epub ahead of print]
- BACKGROUND: Resistant ventricular fibrillation, re-fibrillation and diminished myocardial contractility are important factors leading to poor survival following cardiac arrest. We hypothesized dantrolene improves survival following VF by rectifying calcium dysregulation caused by VF.METHODS AND RESU
- PMID 24403563
- Exon 3 deletion of RYR2 encoding cardiac ryanodine receptor is associated with left ventricular non-compaction.
- Ohno S, Omura M, Kawamura M, Kimura H, Itoh H, Makiyama T, Ushinohama H, Makita N, Horie M.Author information Department of Cardiovascular and Respiratory Medicine, Shiga University of Medical Science, Seta-Tsukinowa-cho, Otsu, Shiga 520-2192, Japan.AbstractAIMS: Ryanodine receptor gene (RYR2) mutations are well known to cause catecholaminergic polymorphic ventricular tachycardia (CPVT). Recently, RYR2 exon 3 deletion has been identified in patients with dilated cardiomyopathy (DCM) and/or CPVT. This study aimed to screen for the RYR2 exon 3 deletion in CPVT probands, characterize its clinical pathology, and confirm the genomic rearrangement.METHODS AND RESULTS: Our cohort consisted of 24 CPVT probands. Polymerase chain reaction (PCR)-based conventional genetic analysis did not identify any mutations in coding exons of RYR2 in these probands. They were screened using multiplex ligation-dependent probe amplification (MLPA). In probands identified with RYR2 exon 3 deletion, the precise location of the deletion was identified by quantitative PCR and direct sequencing methods. We identified two CPVT probands from unrelated families who harboured a large deletion including exon 3. The probands were 9- and 17-year-old girls. Both probands had a history of syncope related to emotional stress or exercise, exhibited bradycardia, and were diagnosed with left ventricular non-compaction (LVNC). We examined 10 family members and identified six more RYR2 exon 3 deletion carriers. In total, there were eight carriers, of which seven were diagnosed with LVNC (87.5%). Two carriers under the age of 4 years remained asymptomatic, although they were diagnosed with LVNC. Using quantitative PCR and direct sequencing, we confirmed that the deletions were 1.1 and 37.7 kb in length.CONCLUSION: RYR2 exon 3 deletion is frequently associated with LVNC. Therefore, detection of the deletion offers a new modality for predicting the prognosis of patients with LVNC with ventricular/atrial arrhythmias, particularly in children.
- Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology.Europace.2014 Jan 6. [Epub ahead of print]
- AIMS: Ryanodine receptor gene (RYR2) mutations are well known to cause catecholaminergic polymorphic ventricular tachycardia (CPVT). Recently, RYR2 exon 3 deletion has been identified in patients with dilated cardiomyopathy (DCM) and/or CPVT. This study aimed to screen for the RYR2 exon 3 deletion i
- PMID 24394973
- Mechanical Stretch-Induced Activation of ROS/RNS Signaling in Striated Muscle.
- Ward CW, Prosser BL, Lederer WJ.Author information 1 School of Nursing, University of Maryland , Baltimore, Maryland.AbstractSignificance: Mechanical activation of reactive oxygen species (ROS) and reactive nitrogen species (RNS) occurs in striated muscle and affects Ca2+ signaling and contractile function. ROS/RNS signaling is tightly controlled, spatially compartmentalized, and source specific. Recent Advances: Here, we review the evidence that within the contracting myocyte, the trans-membrane protein NADPH oxidase 2 (Nox2) is the primary source of ROS generated during contraction. We also review a newly characterized signaling cascade in cardiac and skeletal muscle in which the microtubule network acts as a mechanotransduction element that activates Nox2-dependent ROS generation during mechanical stretch, a pathway termed X-ROS signaling. Critical Issues: In the heart, X-ROS acts locally and affects the sarcoplasmic reticulum (SR) Ca2+ release channels (ryanodine receptors) and tunes Ca2+ signaling during physiological behavior, but excessive X-ROS can promote Ca2+-dependent arrhythmias in pathology. In skeletal muscle, X-ROS sensitizes Ca2+-permeable sarcolemmal "transient receptor potential" channels, a pathway that is critical for sustaining SR load during repetitive contractions, but when in excess, it is maladaptive in diseases such as Duchenne Musclar dystrophy. Future directions: New advances in ROS/RNS detection as well as molecular manipulation of signaling pathways will provide critical new mechanistic insights into the details of X-ROS signaling. These efforts will undoubtedly reveal new avenues for therapeutic intervention in the numerous diseases of striated muscle in which altered mechanoactivation of ROS/RNS production has been identified. Antioxid. Redox Signal. 00, 000-000.
- Antioxidants & redox signaling.Antioxid Redox Signal.2014 Jan 3. [Epub ahead of print]
- Significance: Mechanical activation of reactive oxygen species (ROS) and reactive nitrogen species (RNS) occurs in striated muscle and affects Ca2+ signaling and contractile function. ROS/RNS signaling is tightly controlled, spatially compartmentalized, and source specific. Recent Advances: Here, we
- PMID 23971496
Japanese Journal
- 建築物における構造体コンクリートの強度に関する基準の変遷 (特集 コンクリート技術者の挑戦 : 不易流行の観点から) -- (コンクリートに関わる不易流行 : 継承,改変と今後)
- 桝田 佳寛
- コンクリート工学 51(1), 16-19, 2013-01-00
- … モデルやCPVT型knock-inマウスにおいてもダントンは,RyR2に結合し,RyR2からのCa^{2+}漏出を抑制し,心不全の進展やCPVTを抑制する.このように,ダントロレンはRyR2を分子標的とした新しい心不全･不整脈治療薬となることが期待される.The inter-domain interaction between N-terminal(1-600)and central domains(2000-2500)of the ryanodine receptor(RyR)plays a critical role in channel gating in both skeletal(RyR1)and cardiac(RyR2)muscle …
- NAID 120005246291
- フレカイニドによる治療を行った心臓リアノジン受容体遺伝子変異を有する カテコラミン誘発多形性心室頻拍の1例
- 福岡 正隆,吉田 葉子,岸本 慎太郎,鈴木 嗣敏,藤野 光洋,平野 恭悠,小澤 有希,江原 英治,村上 洋介,中村 好秀
- Pediatric Cardiology and Cardiac
- 患者は特記すべき既往歴・家族歴のない10歳男児で，運動時の失神を主訴に受診した．トレッドミル運動負荷心電図検査では上室頻拍と多形性心室期外収縮が誘発され，ホルター心電図検査では多形性心室頻拍が記録され，カテコラミン誘発多形性心室頻拍（CPVT）と診断．遺伝子検査で筋小胞体カルシウム放出チャネルの心臓リアノジン受容体遺伝子（RyR2）に既報のミスセンス変異が同定された．運動制限の後，プロプラノロール …
- NAID 130003380036
- Genetic Background of Catecholaminergic Polymorphic Ventricular Tachycardia in Japan
- Kawamura Mihoko,Ohno Seiko,Naiki Nobu,Nagaoka Iori,Dochi Kenichi,Wang Qi,Hasegawa Kanae,Kimura Hiromi,Miyamoto Akashi,Mizusawa Yuka,Itoh Hideki,Makiyama Takeru,Sumitomo Naokata,Ushinohama Hiroya,Oyama Kotaro,Murakoshi Nobuyuki,Aonuma Kazutaka,Horigome Hitoshi,Honda Takafumi,Yoshinaga Masao,Ito Makoto,Horie Minoru
- Circulation Journal, 2013
- … Methods and Results: In 50 Japanese probands from unrelated families who satisfied clinical criteria for CPVT, genetic testing was conducted in all exons on 3 CPVT-related genes: cardiac ryanodine receptor 2 (RYR2), calsequestrin 2 (CASQ2) and inward rectifier potassium channel 2 (KCNJ2), and the clinical features between RYR2-genotyped and -non-genotyped patient groups were compared. …
- NAID 130003361749
Related Links
- Cardiac ryanodine receptors Alterations in the expression and/or function of several key proteins involved in regulating and maintaining ionic homeostasis can cause cardiac disturbances. One such group of proteins is ...
- The cardiac type 2 ryanodine receptor (RYR2) is activated by Ca 2+-induced Ca 2+ release (CICR). The inherent positive feedback of CICR is well controlled in cells, but the nature of this control is debated. Here, we explore how 2+ ...
Related Pictures
★リンクテーブル★
| リンク元 | 「リアノジン受容体2型」「RyR2」「ryanodine receptor 2」「type 2 ryanodine receptor」「心筋リアノジン受容体」 |
| 関連記事 | 「cardiac」 |
「リアノジン受容体2型」
- 英
- type 2 ryanodine receptor、ryanodine receptor 2、cardiac ryanodine receptor、RyR2
- 関
- リアノジン受容体、リアノジン受容体カルシウム放出チャネル、リアノジン受容体1型、心筋リアノジン受容体、リアノジン受容体3型
「RyR2」
- 関
- cardiac ryanodine receptor、ryanodine receptor、ryanodine receptor 2、ryanodine receptor calcium release channel、RyR1、RyR3、type 2 ryanodine receptor
「ryanodine receptor 2」
「type 2 ryanodine receptor」
「心筋リアノジン受容体」
「cardiac」
- adj.
- 心臓の、心の、心臓性、強心の