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the 9th letter of the Roman alphabet (同)i

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iodineの化学記号

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2016/04/06 01:53:42」(JST)

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Troponin

Troponin I is a part of the troponin complex. It binds to actin in thin myofilaments to hold the actin-tropomyosin complex in place. Because of it, myosin cannot bind actin in relaxed muscle. When calcium binds to the Troponin C it causes conformational changes which lead to dislocation of troponin I and finally tropomyosin leaves the binding site for myosin on actin leading to contraction of muscle. The letter I is given due to its inhibitory character.

The tissue specific subtypes are:

Slow-twitch skeletal muscle isoform troponin I, TNNI1 (1q31.3, 191042)
Fast-twitch skeletal muscle isoform troponin I, TNNI2 (11p15.5, 191043)
Cardiac troponin I, TNNI3 (19q13.4, 191044)

cTnI

Cardiac troponin I, often denoted as cTnI, is presented in cardiac muscle tissue by a single isoform with molecular weight 23876 Da and it consists of 209 amino acid residues. The theoretical pI of cTnI is 9.87. cTnI differs from other troponins due to its N-terminal extension of 26 amino acids. This extension contains two serines, residues 23 and 24, which are phosphorylated by protein kinase A in response to beta-adrenergic stimulation and important in increasing the inotropic response.^[1] Phosphorylation of cTnI changes the conformation of the protein and modifies its interaction with other troponins as well as the interaction with anti-TnI antibodies. These changes alter the myofilament response to calcium, and are of interest in targeting heart failure. Multiple reaction monitoring of human cTnI has revealed that there are 14 phosphorylation sites and the pattern of phosphorylation observed these sites is changed in response to disease.^[2] cTnI has been shown to be phosphorylated by protein kinase A, protein kinase C, protein kinase G, and p21-activated kinase 3.^[3] A significant part of cTnI released into the patient’s blood stream is phosphorylated.^[4] For more than 15 years cTnI has been known as a reliable marker of cardiac muscle tissue injury. It is considered to be more sensitive and significantly more specific in diagnosis of the myocardial infarction than the "golden marker" of last decades – CK-MB, as well as total creatine kinase, myoglobin and lactate dehydrogenase isoenzymes.

Problems

Troponin I is not entirely specific for myocardial damage secondary to infarction. Other causes of raised Troponin I include chronic renal failure, heart failure, subarachnoid haemorrhage and pulmonary embolus.^[5]^[6]

External links

Troponin I at the US National Library of Medicine Medical Subject Headings (MeSH)

References

^ Solaro RJ, Moir AJG, Perry SV (1976). "Phosphorylation of troponin I and the inotropic effect of adrenaline in the perfused rabbit heart". Nature 262: 615–616. doi:10.1038/262615a0.
^ Zhang P, Kirk, JA, Ji W, dos Remedios CG, Kass DA, Van Eyk JE, Murphy AM (2012). "Multiple Reaction Monitoring to Identify Site-Specific Troponin I Phosphorylated Residues in the Failing Human Heart". Circulation 126: 1828–1837. doi:10.1161/circulationaha.112.096388.
^ Layland J, Solaro RJ, Shah AM (2005). "Regulation of cardiac contractile function by troponin I phosphorylation". Cardiovascular Research 66: 12–21. doi:10.1016/j.cardiores.2004.12.022.
^ Labugger R, Organ L, Collier C, Atar D, Van Eyk JE (2000). "Extensive troponin I and T modification detected in serum from patients with acute myocardial infarction". Circulation. 102 (11): 1221–1226. doi:10.1161/01.cir.102.11.1221.
^ Mannu GS, The non-cardiac use and significance of cardiac troponins. Scott Med J, 2014. 59(3): p. 172-8.
^ Tanindi, Asil; Cemri, Mustafa. "Troponin elevation in conditions other than acute coronary syndromes". National Center for Biotechnology Information. Vascular Health and Risk Management. Retrieved 21 October 2014.

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UpToDate Contents

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1. Troponins as biomarkers of cardiac injury
2. 急性冠症候群がない患者にでの心筋トロポニン濃度の上昇 elevated cardiac troponin concentration in the absence of an acute coronary syndrome
3. Biomarkers suggesting cardiac injury other than troponins
4. 腎不全患者における血清心臓バイオマーカー serum cardiac biomarkers in patients with renal failure
5. 周産期心筋症：治療および予後 peripartum cardiomyopathy treatment and prognosis

English Journal

A fluorescent immunosensor for high-sensitivity cardiac troponin I using a spatially-controlled polymeric, nano-scale tracer to prevent quenching.

Seo SM1, Kim SW1, Park JN1, Cho JH2, Kim HS2, Paek SH3.
Biosensors & bioelectronics.Biosens Bioelectron.2016 Sep 15;83:19-26. doi: 10.1016/j.bios.2016.04.027. Epub 2016 Apr 11.
For detection of high-sensitivity cardiac troponin I (hs-cTnI<0.01ng/mL), signal amplification was attained using a rapid immunosensor with a fluorescently-labeled, polymeric detection antibody. As fluorescent molecules tend to quench when they are less than 10nm apart, a synthetic scheme for the
PMID 27093486

Rapid electrical immunoassay of the cardiac biomarker troponin I through dielectrophoretic concentration using imbedded electrodes.

Sharma A1, Han CH1, Jang J2.
Biosensors & bioelectronics.Biosens Bioelectron.2016 Aug 15;82:78-84. doi: 10.1016/j.bios.2016.03.056. Epub 2016 Mar 26.
Rapidity and high sensitivity are critical factors for the diagnoses of heart attacks, and cardiac troponin I (cTnI) is at present a clinical standard for its diagnosis. Here we report a rapid, label-free, and highly sensitive single-walled carbon nanotube (SWCNT) electrical immunosensor, featuring
PMID 27043478

ST-elevation myocardial infarction with reduced left ventricular ejection fraction: Insights into persisting left ventricular dysfunction. A pPCI-registry analysis.

Stolfo D1, Cinquetti M2, Merlo M2, Santangelo S2, Barbati G2, Alonge M2, Vitrella G2, Rakar S2, Salvi A2, Perkan A2, Sinagra G2.
International journal of cardiology.Int J Cardiol.2016 Jul 15;215:340-5. doi: 10.1016/j.ijcard.2016.04.097. Epub 2016 Apr 14.
Primary percutaneous coronary intervention (pPCI) largely reduced the rate of left ventricular (LV) dysfunction after ST-segment elevation acute myocardial infarction (STEMI). Though LV recovery begins early following revascularization, the optimal timing for re-assessment of LV function is still un
PMID 27128558

Japanese Journal

救急現場で知っておきたい循環器疾患の基礎知識 (特集救急医療の最前線)

成瀬寛之,北川文彦,久野貴弘 [他]
生物試料分析 = Journal of analytical bio-science 38(3), 163-172, 2015
NAID 40020515342

High Sensitive CRP Level Is Associated With Intermediate and High Syntax Score in Patients With Acute Coronary Syndrome

Karadeniz Muhammed,Duran Mustafa,Akyel Ahmet,Yarlıoğlueş Mikail,Öcek Adil Hakan,Çelik İbrahim Etem,Kılıç Alparslan,Yalcin Ahmet Arif,Ergün Gökhan,Murat Sani Namık
International Heart Journal 56(4), 377-380, 2015
… Multivariate logistic regression analysis showed that the strongest predictors of high SXScore were increased serum hs-CRP levels (OR: 1.14) together with multivessel disease (OR: 0.23), left ventricular ejection fraction (LVEF) (OR: 0.90), and troponin levels (OR: 1.12).Serum hs-CRP levels on admission in patients with ACS could predict the severity and complexity of coronary atherosclerosis together with multivessel disease, LVEF, and troponin levels. …
NAID 130005087578

High Sensitive CRP Level Is Associated With Intermediate and High Syntax Score in Patients With Acute Coronary Syndrome

Karadeniz Muhammed,Duran Mustafa,Akyel Ahmet,Yarlıoğlueş Mikail,Öcek Adil Hakan,Çelik İbrahim Etem,Kılıç Alparslan,Yalcin Ahmet Arif,Ergün Gökhan,Murat Sani Namık
International Heart Journal advpub(0), 2015
… Multivariate logistic regression analysis showed that the strongest predictors of high SXScore were increased serum hs-CRP levels (OR: 1.14) together with multivessel disease (OR: 0.23), left ventricular ejection fraction (LVEF) (OR: 0.90), and troponin levels (OR: 1.12).Serum hs-CRP levels on admission in patients with ACS could predict the severity and complexity of coronary atherosclerosis together with multivessel disease, LVEF, and troponin levels. …
NAID 130005084049