WordNet
- fasten or secure with chains; "Chain the chairs together"
- a unit of length
- a necklace made by a stringing objects together; "a string of beads"; "a strand of pearls"; (同)string, strand
- a linked or connected series of objects; "a chain of daisies"
- a series of (usually metal) rings or links fitted into one another to make a flexible ligament
- anything that acts as a restraint
- (chemistry) a series of linked atoms (generally in an organic molecule) (同)chemical chain
- a series of things depending on each other as if linked together; "the chain of command"; "a complicated concatenation of circumstances" (同)concatenation
- (business) a number of similar establishments (stores or restaurants or banks or hotels or theaters) under one ownership
- connect or arrange into a chain by linking
- (meat) cooked until there is just a little pink meat inside
- (biology) a substance in which specimens are preserved or displayed
- a liquid with which pigment is mixed by a painter
- a state that is intermediate between extremes; a middle position; "a happy medium"
- an intervening substance through which something is achieved; "the dissolving medium is called a solvent"
- (usually plural) transmissions that are disseminated widely to the public (同)mass medium
- someone who serves as an intermediary between the living and the dead; "he consulted several mediums" (同)spiritualist, sensitive
- a means or instrumentality for storing or communicating information
- an intervening substance through which signals can travel as a means for communication
- the surrounding environment; "fish require an aqueous medium"
- the 3rd letter of the Roman alphabet (同)c
- (music) the keynote of the scale of C major
- a general-purpose programing language closely associated with the UNIX operating system
- British biochemist (born in Germany) who isolated and purified penicillin, which had been discovered in 1928 by Sir Alexander Fleming (1906-1979) (同)Ernst Boris Chain, Sir Ernst Boris Chain
- any group or radical of the form RCO- where R is an organic group; "an example of the acyl group is the acetyl group" (同)acyl_group
PrepTutorEJDIC
- 『鎖』;(装飾用の)鎖 / 《複数形で》『束縛』,拘束;囚人をつなぐ鎖 / (物事の)『連続』,つながり《+『of』+『名』》 / (商店・銀行・ホテルなどの)チェーン(一連の店が同一資本のもとで連携して経営される方式;その店) / チェーン(測量で用いられる単位;約21.7m) / …'を'『鎖でつなぐ』《+『up』(『together』)+『名,』+『名』+『up』(『together』)》
- 中間(中程度)にあるもの,中庸(mean) / 媒介物,媒体 / 《複数形mediaで》=mass media / 『手段』,方法(means) / (芸術の)表現手段,手法 / (動植物がそこで生存し機能を発揮する)環境;(細菌の)培地,培養基 / 霊媒者 / 『中間の』,並みの
- carbonの化学記号
Wikipedia preview
出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2014/05/13 10:19:12」(JST)
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- 1. 先天性代謝異常：分類 inborn errors of metabolism classification
- 2. 先天性代謝異常：代謝性救急疾患 inborn errors of metabolism metabolic emergencies
- 3. 幼児および小児における低血糖症の病因 etiology of hypoglycemia in infants and children
- 4. 新生児スクリーニング newborn screening
- 5. 代謝性アシドーシスを有する小児に対するアプローチ approach to the child with metabolic acidosis
English Journal
- Development and pathomechanisms of cardiomyopathy in very long-chain acyl-CoA dehydrogenase deficient (VLCAD(-/-)) mice.
- Tucci S1, Flögel U2, Hermann S3, Sturm M4, Schäfers M3, Spiekerkoetter U5.Author information 1Department of General Pediatrics, Center for Pediatrics and Adolescent Medicine, University Hospital Freiburg, 79106 Freiburg, Germany; Department of General Pediatrics, University Children's Hospital Duesseldorf, 40225 Duesseldorf, Germany. Electronic address: sara.tucci@uniklinik-freiburg.de.2Department of Molecular Cardiology, Heinrich Heine University Duesseldorf, 40225 Duesseldorf, Germany.3European Institute for Molecular Imaging - EIMI, University of Muenster, 48149 Muenster, Germany.4Department of General Pediatrics, University Children's Hospital Duesseldorf, 40225 Duesseldorf, Germany.5Department of General Pediatrics, Center for Pediatrics and Adolescent Medicine, University Hospital Freiburg, 79106 Freiburg, Germany.AbstractHypertrophic cardiomyopathy is a typical manifestation of very long-chain acyl-CoA dehydrogenase deficiency (VLCADD), the most common long-chain β-oxidation defects in humans; however in some patients cardiac function is fully compensated. Cardiomyopathy may also be reversed by supplementation of medium-chain triglycerides (MCT). We here characterize cardiac function of VLCAD-deficient (VLCAD(-/-)) mice over one year. Furthermore, we investigate the long-term effect of a continuous MCT diet on the cardiac phenotype. We assessed cardiac morphology and function in VLCAD(-/-) mice by in vivo MRI. Cardiac energetics were measured by (31)P-MRS and myocardial glucose uptake was quantified by positron-emission-tomography (PET). Metabolic adaptations were identified by the expression of genes regulating glucose and lipid metabolism using real-time-PCR. VLCAD(-/-) mice showed a progressive decrease in heart function over 12months accompanied by a reduced phosphocreatine-to-ATP-ratio indicative of chronic energy deficiency. Long-term MCT supplementation aggravated the cardiac phenotype into dilated cardiomyopathy with features similar to diabetic heart disease. Cardiac energy production and function in mice with a β-oxidation defect cannot be maintained with age. Compensatory mechanisms are insufficient to preserve the cardiac energy state over time. However, energy deficiency by impaired β-oxidation and long-term MCT induce cardiomyopathy by different mechanisms. Cardiac MRI and MRS may be excellent tools to assess minor changes in cardiac function and energetics in patients with β-oxidation defects for preventive therapy.
- Biochimica et biophysica acta.Biochim Biophys Acta.2014 May;1842(5):677-85. doi: 10.1016/j.bbadis.2014.02.001. Epub 2014 Feb 12.
- Hypertrophic cardiomyopathy is a typical manifestation of very long-chain acyl-CoA dehydrogenase deficiency (VLCADD), the most common long-chain β-oxidation defects in humans; however in some patients cardiac function is fully compensated. Cardiomyopathy may also be reversed by supplementation of m
- PMID 24530811
- Phosphoproteome mapping of cardiomyocyte mitochondria in a rat model of heart failure.
- Giorgianni F1, Usman Khan M, Weber KT, Gerling IC, Beranova-Giorgianni S.Author information 1Department of Pharmaceutical Sciences, University of Tennessee Health Science Center, 881 Madison Avenue, Room 445, Memphis, TN, 38163, USA.AbstractMitochondria are complex organelles essential to cardiomyocyte survival. Protein phosphorylation is emerging as a key regulator of mitochondrial function. In the study reported here, we analyzed subsarcolemmal (SSM) mitochondria harvested from rats who have received 4 weeks of aldosterone/salt treatment to simulate the neurohormonal profile of human congestive heart failure. Our objective was to obtain an initial qualitative inventory of the phosphoproteins in this biologic system. SSM mitochondria were harvested, and the phosphoproteome was analyzed with a gel-free bioanalytical platform. Mitochondrial proteins were digested with trypsin, and the digests were enriched for phosphopeptides with immobilized metal ion affinity chromatography. The phosphopeptides were analyzed by ion trap liquid chromatography-tandem mass spectrometry, and the phosphoproteins identified via database searches. Based on MS/MS and MS(3) data, we characterized a set of 42 phosphopeptides that encompassed 39 phosphorylation sites. These peptides mapped to 26 proteins, for example, long-chain specific acyl-CoA dehydrogenase, Complex III subunit 6, and mitochondrial import receptor TOM70. Collectively, the characterized phosphoproteins belong to diverse functional modules, including bioenergetic pathways, protein import machinery, and calcium handling. The phosphoprotein panel discovered in this study provides a foundation for future differential phosphoproteome profiling toward an integrated understanding of the role of mitochondrial phosphorylation in heart failure.
- Molecular and cellular biochemistry.Mol Cell Biochem.2014 Apr;389(1-2):159-67. doi: 10.1007/s11010-013-1937-7. Epub 2014 Jan 7.
- Mitochondria are complex organelles essential to cardiomyocyte survival. Protein phosphorylation is emerging as a key regulator of mitochondrial function. In the study reported here, we analyzed subsarcolemmal (SSM) mitochondria harvested from rats who have received 4 weeks of aldosterone/salt trea
- PMID 24395194
- Opening of the mitochondrial permeability transition pore links mitochondrial dysfunction to insulin resistance in skeletal muscle.
- Taddeo EP1, Laker RC2, Breen DS1, Akhtar YN2, Kenwood BM1, Liao JA1, Zhang M2, Fazakerley DJ3, Tomsig JL1, Harris TE1, Keller SR1, Chow JD1, Lynch KR4, Chokki M5, Molkentin JD6, Turner N7, James DE8, Yan Z9, Hoehn KL10.Author information 1Department of Pharmacology, University of Virginia, Charlottesville, VA 22908, USA.2Department of Medicine, University of Virginia, Charlottesville, VA 22908, USA ; Robert M. Berne Cardiovascular Research Center, University of Virginia, Charlottesville, VA 22908, USA.3Diabetes and Obesity Program, Garvan Institute of Medical Research, 384 Victoria St., Darlinghurst, NSW 2010, Australia.4Department of Pharmacology, University of Virginia, Charlottesville, VA 22908, USA ; Emily Couric Clinical Cancer Center, University of Virginia, Charlottesville, VA 22908, USA.5Teijin Pharma Limited, 4-3-2, Asahigaoka, Hino, Tokyo 191-8512, Japan.6Department of Pediatrics, University of Cincinnati, Cincinnati Children's Hospital Medical Center, Howard Hughes Medical Institute, Cincinnati, OH, USA.7Department of Pharmacology, University of New South Wales, Sydney, NSW, Australia.8Diabetes and Obesity Program, Garvan Institute of Medical Research, 384 Victoria St., Darlinghurst, NSW 2010, Australia ; School of Medical Sciences, University of New South Wales, Sydney, NSW, Australia ; School of Biotechnology and Biomolecular Sciences, University of New South Wales, Sydney, NSW, Australia.9Department of Pharmacology, University of Virginia, Charlottesville, VA 22908, USA ; Department of Medicine, University of Virginia, Charlottesville, VA 22908, USA ; Robert M. Berne Cardiovascular Research Center, University of Virginia, Charlottesville, VA 22908, USA.10Department of Pharmacology, University of Virginia, Charlottesville, VA 22908, USA ; Department of Medicine, University of Virginia, Charlottesville, VA 22908, USA ; Robert M. Berne Cardiovascular Research Center, University of Virginia, Charlottesville, VA 22908, USA ; Emily Couric Clinical Cancer Center, University of Virginia, Charlottesville, VA 22908, USA.AbstractInsulin resistance is associated with mitochondrial dysfunction, but the mechanism by which mitochondria inhibit insulin-stimulated glucose uptake into the cytoplasm is unclear. The mitochondrial permeability transition pore (mPTP) is a protein complex that facilitates the exchange of molecules between the mitochondrial matrix and cytoplasm, and opening of the mPTP occurs in response to physiological stressors that are associated with insulin resistance. In this study, we investigated whether mPTP opening provides a link between mitochondrial dysfunction and insulin resistance by inhibiting the mPTP gatekeeper protein cyclophilin D (CypD) in vivo and in vitro. Mice lacking CypD were protected from high fat diet-induced glucose intolerance due to increased glucose uptake in skeletal muscle. The mitochondria in CypD knockout muscle were resistant to diet-induced swelling and had improved calcium retention capacity compared to controls; however, no changes were observed in muscle oxidative damage, insulin signaling, lipotoxic lipid accumulation or mitochondrial bioenergetics. In vitro, we tested 4 models of insulin resistance that are linked to mitochondrial dysfunction in cultured skeletal muscle cells including antimycin A, C2-ceramide, ferutinin, and palmitate. In all models, we observed that pharmacological inhibition of mPTP opening with the CypD inhibitor cyclosporin A was sufficient to prevent insulin resistance at the level of insulin-stimulated GLUT4 translocation to the plasma membrane. The protective effects of mPTP inhibition on insulin sensitivity were associated with improved mitochondrial calcium retention capacity but did not involve changes in insulin signaling both in vitro and in vivo. In sum, these data place the mPTP at a critical intersection between alterations in mitochondrial function and insulin resistance in skeletal muscle.
- Molecular metabolism.Mol Metab.2013 Nov 26;3(2):124-34. doi: 10.1016/j.molmet.2013.11.003. eCollection 2014.
- Insulin resistance is associated with mitochondrial dysfunction, but the mechanism by which mitochondria inhibit insulin-stimulated glucose uptake into the cytoplasm is unclear. The mitochondrial permeability transition pore (mPTP) is a protein complex that facilitates the exchange of molecules betw
- PMID 24634818
Japanese Journal
- Inhibitory Effect of a Cirsium setidens Extract on Hepatic Fat Accumulation in Mice Fed a High-Fat Diet via the Induction of Fatty Acid β-Oxidation
- NOH Hwayoung,LEE Heejin,KIM Eunhye [他],MU Ling,RHEE Young Kyoung,CHO Chang-Won,CHUNG Jayong
- Bioscience, Biotechnology, and Biochemistry 77(7), 1424-1429, 2013
- … CSE strongly increased the hepatic mRNA levels of carnitine palmitoyltransferase (CPT1) and medium-chain acyl-CoA dehydrogenase (MCAD), the fatty acid β-oxidation enzymes. …
- NAID 130003361135
- Angelica keiskei Extract Improves Insulin Resistance and Hypertriglyceridemia in Rats Fed a High-Fructose Drink
- OHNOGI Hiromu,HAYAMI Shoko,KUDO Yoko [他],DEGUCHI Suzu,MIZUTANI Shigetoshi,ENOKI Tatsuji,TANIMURA Yuko,AOI Wataru,NAITO Yuji,KATO Ikunoshin,YOSHIKAWA Toshikazu
- Bioscience, biotechnology, and biochemistry 76(5), 928-932, 2012-05-23
- … Treatment with AE enhanced the expression of the acyl-CoA oxidase 1 (ACO1), medium-chain acyl-CoA dehydrogenase (MCAD), ATP-binding membrane cassette transporter A1 (ABCA1) and apolipoprotein A1 (Apo-A1) genes. …
- NAID 10030752696
- 新生児タンデムマススクリーニングで発見された超低出生体重児の中鎖アシルCoA脱水素酵素(MCAD)欠損症
- 長尾 雅悦,野町 祥介,田中 藤樹
- 日本マス・スクリーニング学会誌 = Journal of Japanese Society for Mass-screening 21(3), 247-252, 2011-12-01
- NAID 10030204890
Related Links
- Derks TG, Reijngoud DJ, Waterham HR, Gerver WJ, van den Berg MP, Sauer PJ, Smit GP. The natural history of medium-chain acyl CoA dehydrogenase deficiency in the Netherlands: clinical presentation and outcome. J Pediatr ...
- Medium-chain acyl-coenzyme A dehydrogenase (MCAD) deficiency belongs to the acyl-CoA dehydrogenase (ACAD ...
Related Pictures
★リンクテーブル★
| リンク元 | 「中鎖アシルCoAデヒドロゲナーゼ」「MCAD」 |
| 関連記事 | 「C」「medium」「chain」「CoA」「dehydrogenase」 |
「中鎖アシルCoAデヒドロゲナーゼ」
臨床関連
「MCAD」
「C」
- 炭素 carbon
- シトシン cytosine
- システイン cysteine
- シチジン
- セルシウス度 摂氏 degrees Celsius degree C
- 産婦人科領域で「子宮外頚 子宮外頚部 exocervix」を表現するための略語
「medium」
「chain」
- n.
- adj.
- 鎖状の、鎖式の