出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2014/02/13 06:45:20」(JST)[Wiki en表示]
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- 1. 小児におけるチアノーゼの病因および評価 etiology and evaluation of cyanosis in children
- 2. 新生児におけるチアノーゼの概要 overview of cyanosis in the newborn
- 3. 新生児におけるチアノーゼ性心疾患の診断および初期マネージメント diagnosis and initial management of cyanotic heart disease in the newborn
- 4. 成人におけるチアノーゼ性先天性心疾患の内科的マネージメント medical management of cyanotic congenital heart disease in adults
- 5. 新生児におけるチアノーゼの心臓の原因 cardiac causes of cyanosis in the newborn
- Erythropoietin enhances mitochondrial biogenesis in cardiomyocytes exposed to chronic hypoxia through Akt/eNOS signalling pathway.
- Qin C, Zhou S, Xiao Y, Chen L.Author information Department of Cardiovascular Surgery, Xinqiao Hospital, The Third Military Medical University, Chongqing, China.AbstractAdaptation of cardiomyocytes to chronic hypoxia in cyanotic patients remains unclear. Mitochondrial biogenesis is enhanced in myocardium from cyanotic patients, which is possibly an adaptive response. Erythropoietin (EPO) in blood and its receptor (EPOR) on cardiomyocytes are upregulated by chronic hypoxia, suggesting that EPO-EPOR interaction is increased, which is inferred to positively regulate mitochondrial biogenesis through protein kinase B (Akt)/endothelial nitric oxide synthase (eNOS) signalling pathway. H9c2 cardiomyocytes were exposed to hypoxia (1% O2 ) for 1 week and treated with different doses of recombinant human erythropoietin (rhEPO). Mitochondrial number, mitochondrial DNA (mtDNA) copy number and peroxisome proliferator activated receptor gamma coactivator alpha (PGC-1α) mRNA expression increased in a dose-dependent manner induced by rhEPO. Akt and eNOS were significantly phosphorylated by rhEPO. Both blocking Akt with Wortmannin and silencing eNOS expression with shRNA plasmid decreased the mtDNA copy number and PGC-1α mRNA expression induced by rhEPO. Blocking Akt was associated with the decreased phosphorylation of Akt and eNOS. RNA interference led to a reduction in the total and phosphorylated proteins of eNOS. Thus EPO enhances mitochondrial biogenesis in cardiomyocytes exposed to chronic hypoxia, at least partly through Akt/eNOS signalling, which might be an adaptive mechanism of cardiomyocytes associated with the increased EPO-EPOR interaction in patients with cyanotic congenital heart disease (CCHD).
- Cell biology international.Cell Biol Int.2014 Mar;38(3):335-42. doi: 10.1002/cbin.10205. Epub 2014 Jan 16.
- Adaptation of cardiomyocytes to chronic hypoxia in cyanotic patients remains unclear. Mitochondrial biogenesis is enhanced in myocardium from cyanotic patients, which is possibly an adaptive response. Erythropoietin (EPO) in blood and its receptor (EPOR) on cardiomyocytes are upregulated by chronic
- PMID 24436050
- Successful hybrid method to occlude a narrowed persistent left superior vena cava after cardiac surgery.
- Chen Y, Feng Y, Luo S, An Q.Author information Department of Cardiovascular Surgery, West China Hospital, Sichuan University, Chengdu, Sichuan, China.AbstractA 25-year old woman with complicated cyanotic heart disease and a large persistent left superior vena cava (PLSVC) with dysplasia of the innominate vein draining into the left atrium underwent cardiac surgery. Six months later, the narrowed PLSVC was successfully occluded using a muscular ventricular septal occluder (nitinol wire mesh). No complications occurred during or immediately following the catheterization. This case report is the first to describe the utilization of a hybrid method to occlude a narrowed PLSVC after cardiac surgery.
- Interactive cardiovascular and thoracic surgery.Interact Cardiovasc Thorac Surg.2014 Feb 13. [Epub ahead of print]
- A 25-year old woman with complicated cyanotic heart disease and a large persistent left superior vena cava (PLSVC) with dysplasia of the innominate vein draining into the left atrium underwent cardiac surgery. Six months later, the narrowed PLSVC was successfully occluded using a muscular ventricula
- PMID 24532311
- Rare and private variations in neural crest, apoptosis and sarcomere genes define the polygenic background of isolated Tetralogy of Fallot.
- Grunert M, Dorn C, Schueler M, Dunkel I, Schlesinger J, Mebus S, Alexi-Meskishvili V, Perrot A, Wassilew K, Timmermann B, Hetzer R, Berger F, Sperling SR.Author information Group of Cardiovascular Genetics, Department of Vertebrate Genomics and.AbstractTetralogy of Fallot (TOF) is the most common cyanotic congenital heart disease. Its genetic basis is demonstrated by an increased recurrence risk in siblings and familial cases. However, the majority of TOF are sporadic, isolated cases of undefined origin and it had been postulated that rare and private autosomal variations in concert define its genetic basis. To elucidate this hypothesis, we performed a multilevel study using targeted re-sequencing and whole-transcriptome profiling. We developed a novel concept based on a gene's mutation frequency to unravel the polygenic origin of TOF. We show that isolated TOF is caused by a combination of deleterious private and rare mutations in genes essential for apoptosis and cell growth, the assembly of the sarcomere as well as for the neural crest and secondary heart field, the cellular basis of the right ventricle and its outflow tract. Affected genes coincide in an interaction network with significant disturbances in expression shared by cases with a mutually affected TOF gene. The majority of genes show continuous expression during adulthood, which opens a new route to understand the diversity in the long-term clinical outcome of TOF cases. Our findings demonstrate that TOF has a polygenic origin and that understanding the genetic basis can lead to novel diagnostic and therapeutic routes. Moreover, the novel concept of the gene mutation frequency is a versatile measure and can be applied to other open genetic disorders.
- Human molecular genetics.Hum Mol Genet.2014 Feb 11. [Epub ahead of print]
- Tetralogy of Fallot (TOF) is the most common cyanotic congenital heart disease. Its genetic basis is demonstrated by an increased recurrence risk in siblings and familial cases. However, the majority of TOF are sporadic, isolated cases of undefined origin and it had been postulated that rare and pri
- PMID 24459294
- 本田 一穂,小田 秀明,西川 俊郎,HONDA Kazuho,ODA Hideaki,NISHIKAWA Toshio
- 東京女子医科大学雑誌 84(臨時増刊2(西川俊郎教授退任記念特別)), E237-E243, 2014-03-31
- NAID 120005430907
- 本田 一穂,小田 秀明,西川 俊郎
- 東京女子医科大学雑誌 84(E2), E237-E243, 2014-03-31
- … チアノーゼ腎症(cyanotic nephropathy: CN)は、チアノーゼ型先天性心疾患(cyanotic congenital heart disease: CCHD)に合併する腎障害である。 …
- NAID 110009770490
- チアノーゼ腎症の病理 (病理診断科 西川俊郎教授退任記念特別号)
- 本田 一穂,小田 秀明,西川 俊郎
- 東京女子医科大学雑誌 84(臨増2), E237-243, 2014-03
- NAID 40020099021
- British Dictionary definitions for cyanotic Expand cyanosis / ˌsaɪəˈnəʊsɪs / noun 1. (pathol) a bluish-purple discoloration of skin and mucous membranes usually resulting from a deficiency of oxygen in the blood Derived Forms () ...
- cy·a·not·ic (sī'ă-not'ik), Avoid substituting the substandard cyanosed for this word. Relating to or marked by cyanosis. Synonym(s): cyanochroic, cyanochrous, cyanosed cyanotic See cyanosed. cy·a·not·ic (sī'ă-not'ik) Relating to or ...
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