WordNet
- abnormal enlargement of a body part or organ
- undergo hypertrophy; "muscles can hypertrophy when people take steroids"
- increase in size, magnitude, number, or intensity; "The music swelled to a crescendo"
- expand abnormally; "The bellies of the starving children are swelling" (同)swell up, intumesce, tumefy, tumesce
- cause to become swollen; "The water swells the wood"
- a crescendo followed by a decrescendo
- the undulating movement of the surface of the open sea (同)crestless wave
- a rounded elevation (especially one on an ocean floor)
- become filled with pride, arrogance, or anger; "The mother was swelling with importance when she spoke of her son" (同)puff_up
- make viscous or dense; "thicken the sauce by adding flour" (同)inspissate
- become thick or thicker; "The sauce thickened"; "The egg yolk will inspissate" (同)inspissate
- make thick or thicker; "Thicken the sauce"; "inspissate the tar so that it becomes pitch" (同)inspissate
- becoming more intricate or complex; "a thickening plot"
- any material used to thicken; "starch is used in cooking as a thickening" (同)thickener
- the act of thickening (同)inspissation
PrepTutorEJDIC
- (生物体の部分・器官の)異常肥大,異常発達
- 〈物が〉『大きくなる』,ふくれる,はれる《+up》 / 〈帆などが〉『張り出る』,ふくらむ《+out》 / 〈数量・程度・力などが〉『増大する』,増える,強まる / 〈川などが〉増水する,〈海が〉うねる,〈土地が〉高まる / 《話》〈感情が〉高まる;(感情で)〈胸が〉いっぱいになる《+with+名》 / …‘を'『ふくらます』,‘の'かさを大きくする / 〈帆など〉‘を'『張り出させる』,ふくらませる《+out+名,+名+out》 / …‘を'『増大させる』,増やす,強める / 〈心・胸など〉‘を'いっぱいにする / 〈U〉《時にa ~》ふくれる(増大する)こと;ふくれている状態 / 〈C〉土地の隆起部,なだらかな丘 / 〈U〉《単数形で》大波,うねり / 〈C〉音の高まり,音量の増減 / 〈C〉《古》《話》名士;(特に)流行の服を着た人 / 《米話》すばらしい,すてきな / 《古》《俗》いきな,しゃれた
- …‘を'厚くする;…‘を'濃くする / 厚くなる;濃くなる / 〈話の筋などが〉複雑になる
- 厚くする(なる)こと / 厚くなった部分 / 濃縮材料
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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/04/28 18:11:21」(JST)
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- 1. 心電図チュートリアル：心室拡大および心室肥大 ecg tutorial chamber enlargement and 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. 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
- 4. 左室肥大および不整脈 left ventricular hypertrophy and arrhythmia
- 5. 肥大型心筋症の臨床症状、診断、および評価 clinical manifestations diagnosis and evaluation of hypertrophic cardiomyopathy
English Journal
- Efficacy and safety of incobotulinum toxin A in periocular rhytides and masseteric hypertrophy: side-by-side comparison with onabotulinum toxin A.
- Lee JH, Park JH, Lee SK, Han KH, Kim SD, Yoon CS, Park JY, Lee JH, Yang JM, Lee JH.Author information Department of Dermatology, Samsung Medical Center, Sungkyunkwan University School of Medicine , Seoul , Republic of Korea.AbstractBACKGROUND: Incobotulinum is a newly developed botulinum toxin A in which the complexing proteins had been removed.
- The Journal of dermatological treatment.J Dermatolog Treat.2014 Aug;25(4):326-30. doi: 10.3109/09546634.2013.769041. Epub 2013 Jun 2.
- BACKGROUND: Incobotulinum is a newly developed botulinum toxin A in which the complexing proteins had been removed.OBJECTIVE: The aim was to compare the efficacy and safety of incobotulinum with onabotulinum in treating periocular rhytides and masseteric hypertrophy.METHODS: A randomized, double-bli
- PMID 23356833
- The Many Lives of CTIP2: From AIDS to Cancer and Cardiac Hypertrophy.
- Le Douce V, Cherrier T, Riclet R, Rohr O, Schwartz C.Author information Institut de Parasitologie et de Pathologie Tropicale, EA7292, Université de Strasbourg, Strasbourg, France; IUT de Schiltigheim, 1 Allée d'Athènes, Schiltigheim, France.AbstractCTIP2 is a key transcriptional regulator involved in numerous physiological functions. Initial works have shown the importance of CTIP2 in the establishment and persistence of HIV latency in microglial cells, the main latent/quiescent viral reservoir in the brain. Recent studies have highlighted the importance of CTIP2 in several other pathologies, such as cardiac hypertrophy and various types of human malignancies. Targeting CTIP2 may therefore constitute a new approach in the treatment of these pathologies. J. Cell. Physiol. 229: 533-537, 2014. © 2013 Wiley Periodicals, Inc.
- Journal of cellular physiology.J Cell Physiol.2014 May;229(5):533-7. doi: 10.1002/jcp.24490.
- CTIP2 is a key transcriptional regulator involved in numerous physiological functions. Initial works have shown the importance of CTIP2 in the establishment and persistence of HIV latency in microglial cells, the main latent/quiescent viral reservoir in the brain. Recent studies have highlighted the
- PMID 24122342
- Angiotensin II and the ERK pathway mediate the induction of leptin by mechanical cyclic stretch in cultured rat neonatal cardiomyocytes.
- Chiu CZ, Wang BW, Shyu KG.AbstractMechanical cyclic stretch of cardiomyocytes causes cardiac hypertrophy through cardiac-restricted gene expression. Leptin induces cardiomyocyte hypertrophy in response to myocardial stress. In the present study, we evaluated the expression of leptin under cyclic stretch and its role in regulating genetic transcription in cardiomyocytes. Cultured rat neonatal cardiomyocytes were subjected to cyclic stretch, and the expression levels of leptin, ROS (reactive oxygen species) and AngII (angiotensin II) were evaluated. Signal transduction inhibitors were used to identify the pathway of leptin expression. EMSAs were used to identify the binding of leptin/STAT3 (signal transducer and activator of transcription 3) and luciferase assays were used to identify the transcription of leptin in cardiomyocytes. The study also used an in vivo model of AV (aortocaval) shunt in rats to investigate leptin, ROS and AngII expression. Leptin and leptin receptor levels increased after cyclic stretch with the earlier expression of AngII and ROS. Leptin expression was suppressed by AngII receptor blockers, an ROS scavenger [NAC (N-acetylcysteine)], an ERK (extracellular-signal-regulated kinase) pathway inhibitor (PD98059) and ERK siRNA. Binding of leptin/STAT3 was identified by EMSAs, and luciferase assays confirmed the transcription of leptin in neonatal cardiomyocytes after cyclic stretch. Increased MHC (myosin heavy chain) expression and [3H]-proline incorporation in cardiomyocytes was detected after cyclic stretch, which were inhibited by leptin siRNA and NAC. The in vivo model of AV shunt also demonstrated increased levels of plasma and myocardial leptin, ROS and AngII expression after cyclic stretch. Mechanical cyclic stretch in cardiomyocytes increased leptin expression mediated by the induction of AngII, ROS and the ERK pathway to cause cardiomyocyte hypertrophy. Myocardial hypertrophy can be identified by increased transcriptional activity and an enhanced hypertrophic phenotype of cardiomyocytes.
- Clinical science (London, England : 1979).Clin Sci (Lond).2014 Apr;126(7):483-95. doi: 10.1042/CS20130235.
- Mechanical cyclic stretch of cardiomyocytes causes cardiac hypertrophy through cardiac-restricted gene expression. Leptin induces cardiomyocyte hypertrophy in response to myocardial stress. In the present study, we evaluated the expression of leptin under cyclic stretch and its role in regulating ge
- PMID 24063596
- Role of Heterotrimeric G Protein and Calcium in Cardiomyocyte Hypertrophy Induced by IGF-1.
- Carrasco L, Cea P, Rocco P, Peña-Oyarzún D, Rivera-Mejias P, Sotomayor-Flores C, Quiroga C, Criollo A, Ibarra C, Chiong M, Lavandero S.Author information Advanced Center for Chronic Diseases, Universidad de Chile, Santiago, Chile; Centro Estudios Moleculares de la Celula, Facultad de Ciencias y Farmacéuticas, Universidad de Chile, Santiago, Chile.AbstractIn the heart, insulin-like growth factor-1 (IGF-1) is a peptide with pro-hypertrophic and anti-apoptotic actions. The pro-hypertrophic properties of IGF-1 have been attributed to the extracellular regulated kinase (ERK) pathway. Recently, we reported that IGF-1 also increases intracellular Ca(2+) levels through a pertussis toxin (PTX)-sensitive G protein. Here we investigate whether this Ca(2+) signal is involved in IGF-1-induced cardiomyocyte hypertrophy. Our results show that the IGF-1-induced increase in Ca(2+) level is abolished by the IGF-1 receptor tyrosine kinase inhibitor AG538, PTX and the peptide inhibitor of Gβγ signaling, βARKct. Increases in the activities of Ca(2+) -dependent enzymes calcineurin, calmodulin kinase II (CaMKII), and protein kinase Cα (PKCα) were observed at 5 min after IGF-1 exposure. AG538, PTX, βARKct, and the dominant negative PKCα prevented the IGF-1-dependent phosphorylation of ERK1/2. Participation of calcineurin and CaMKII in ERK phosphorylation was discounted. IGF-1-induced cardiomyocyte hypertrophy, determined by cell size and β-myosin heavy chain (β-MHC), was prevented by AG538, PTX, βARKct, dominant negative PKCα, and the MEK1/2 inhibitor PD98059. Inhibition of calcineurin with CAIN did not abolish IGF-1-induced cardiac hypertrophy. We conclude that IGF-1 induces hypertrophy in cultured cardiomyocytes by activation of the receptor tyrosine kinase activity/βγ-subunits of a PTX-sensitive G protein/Ca(2+) /PKCα/ERK pathway without the participation of calcineurin. J. Cell. Biochem. 115: 712-720, 2014. © 2013 Wiley Periodicals, Inc.
- Journal of cellular biochemistry.J Cell Biochem.2014 Apr;115(4):712-20. doi: 10.1002/jcb.24712.
- In the heart, insulin-like growth factor-1 (IGF-1) is a peptide with pro-hypertrophic and anti-apoptotic actions. The pro-hypertrophic properties of IGF-1 have been attributed to the extracellular regulated kinase (ERK) pathway. Recently, we reported that IGF-1 also increases intracellular Ca(2+) le
- PMID 24243530
Japanese Journal
- Personal Training Quarterly PTQ レジスタンストレーニングによる筋肥大のための高ホルモン状態 : 思い込み : ストレングス&コンディショニングにおける根拠に基づかない実践
- Strength & conditioning journal : 日本ストレングス&コンディショニング協会機関誌 23(8), 12-15, 2016-10
- NAID 40020971163
- CASE REPORT : Laparoscopic long myotomy and Dor fundoplication guided by perioperative endoscopic ultrasound
- Esophagus : official journal of the Japan Esophageal Society 13(4), 391-394, 2016-10
- NAID 40020963350
- Suppressive Effects of Glucose-Dependent Insulinotropic Polypeptide on Cardiac Hypertrophy and Fibrosis in Angiotensin Ⅱ-Infused Mouse Models
- Circulation journal : official journal of the Japanese Circulation Society 80(9), 1988-1997, 2016-09
- NAID 40020916012
- Erythroblastosis of the Donor Twin of Twin Anemia-Polycythemia Sequence
- Acta Medica Okayama 70(4), 269-272, 2016-08
- NAID 120005828914
Related Links
- Hypertrophy results from an increase in cell size, while hyperplasia is from an increase in cell number. Hypertrophy (from Greek ὑπέρ "excess" + τροφή " nourishment") is the increase in the volume of an organ or tissue due to the enlargement ...
- Muscle hypertrophy is an increase in the size of muscle cells. It differs from muscle hyperplasia, which is the formation of new muscle cells. Contents. 1 Hypertrophy stimuli. 1.1 Strength training; 1.2 Anaerobic training. 2 Factors affecting ...
Related Pictures
★リンクテーブル★
| リンク元 | 「拡大」「swell」「肥厚」「肥大」「thicken」 |
「拡大」
胸部X線写真上での拡大
- 胸郭に大して心陰影が大きくなった状態、つまり心胸郭比 CTRが上昇した状態
- 組織的には拡張 dilatationか肥大 hypertrophyが起こっていることが考えられるが、X線写真上では両者は区別できない。
「swell」
- v.
- 膨潤する、肥大する、膨張する
「肥厚」
- 英
- hyperplasia、hypertrophy、hyperplasy、thickening、thicken、pachismus
- 関
- 過形成、増生、肥厚化、肥大、肥厚部、肥大化
「肥大」
- 英
- hypertrophy
- ラ
- hypertrophia
- 関
- 過形成、増殖
- 組織や臓器が反応性に一定以上に容積を増すこと。
「thicken」
- adj.
- 肥厚する