Evaluations of the Analytical Performance of the Singulex Cardiac Troponin I Assay Used on its
SAN DIEGO, Aug. 1, 2017 /PRNewswire/ -- Evaluations of the Analytical Performance of the Singulex Cardiac Troponin I Assay Used on its Single Molecule...https://www.prnewswire.com/news-releases/evaluations-of-the-analytical-performance-of-the-singulex-cardiac-troponin-i-assay-used-on-its-single-molecule-counting-technology-platform-demonstrates-ability-to-improve-cardiovascular-disease-rule-out-300497454.html
Cardiac troponin I levels in patients with non-ST-elevation acute coronary syndrome : the importance of gender
BACKGROUND: Measurement of high-sensitivity cardiac troponin levels is increasingly used in non-ST-elevation acute coronary syndrome (NSTE-ACS). However, studies investigating the distribution and prognostic implications of high-sensitivity troponin levels in men and women separately are currently lacking.. METHODS: Cardiac troponin I (cTnI) levels were determined using a high-sensitivity assay (Abbott Laboratories, Abbott Park, IL) in 1,677 male and 1,073 female NSTE-ACS patients participating in the GUSTO IV study. The prognostic associations of cTnI to outcome (30-day composite end point of recurrent myocardial infarction and 1-year mortality) were assessed in multivariable models, using cTnI both as a continuous variable and dichotomized at different sets of single and gender-specific 99th percentiles.. RESULTS: Median cTnI levels were 947 and 175 ng/L in men and women, respectively (P , .001). The adjusted odds ratios for cTnI (ln) were similar in men ...http://uu.diva-portal.org/smash/record.jsf?pid=diva2:758980
Evaluation of cardiac troponin I (cTnI), electrocardiography, creatine kinase (CK) and aspartate aminotransferase (AST) in...
BACKGROUND: Cardiac Troponin I (cTnI) is known as a cardiac biomarker in determining the myocardial damage of diseases which affect the heart muscle. OBJECTIVES: This study aims to evaluate the serum cTnI concentration in Markhoz Breed goats suffering selenium (Se) deficiency and its correlation with electrocardiographic parameters, and activity of creatine kinase (CK) and aspartate aminotransferase (AST) enzymes, as well as to determine the diagnostic value of troponin in that disease. METHODS: Blood samples of 94 goat kids of Markhoz breed with the age less than one month were taken, serum analyzed for the assessment of cTnI, CK and AST, 2 ml blood was used for determination of selenium concentration. Electrocardiography was recorded from all kids by using base-apex lead. Kids were divided into two groups based on serum selenium concentration. RESULTS: The concentration of cTnI was significantly higher in deficient kids compared with the control group. Results indicated ...https://ijvm.ut.ac.ir/article_62192.html
Cardiac Troponin I Predicts Short-Term Mortality in Vascular Surgery Patients | Circulation
Elevated cTnI levels after major vascular surgery are associated with an increased risk of short-term mortality and morbidity. Patients with postoperative cTnI ,1.5 ng/mL are 6 times more likely to die within 6 months of surgery compared with patients with levels ≤1.5 ng/mL, after adjusting for age, congestive heart failure, surgical procedure, and perioperative β-blockade. Moreover, we observed a dose-response relation between cTnI concentration and death. The strong association between cTnI and short-term mortality suggests that clinically meaningful postoperative ischemia may have been missed in a significant number of vascular surgery patients. More importantly, the survival analysis demonstrates that the difference in mortality associated with an elevated cTnI does not emerge until 5 weeks after surgery. Thus, routine postoperative surveillance for cTnI may alert clinicians to patients at high risk for cardiovascular complications and death before the occurrence of a morbid event. ...http://circ.ahajournals.org/content/106/18/2366
Protein Kinase D Is a Novel Mediator of Cardiac Troponin I Phosphorylation and Regulates Myofilament Function | Circulation...
Covalent modification of cTnI by kinase-mediated phosphorylation is an important mechanism in the regulation of thin filament function and thereby the cardiac contractile phenotype.26 Furthermore, altered phosphorylation of cTnI and other myofilament proteins may contribute causally to cardiac dysfunction in the transition from compensated hypertrophy to heart failure.30 In this context, the present work shows, for the first time to our knowledge, that PKD interacts with and directly phosphorylates a number of myofilament proteins, including cTnI at Ser22 and Ser23, and that PKD-mediated phosphorylation of cardiac myofilaments has a functional impact on both the Ca2+ sensitivity of tension development and the crossbridge cycling kinetics.. To date, most investigative effort in phosphorylation-mediated regulation of cTnI function has focused on the actions of PKA and PKC. Evidence from studies in a variety of systems, ranging from reconstituted myofilament proteins to cultured myocytes or ...http://circres.ahajournals.org/content/95/11/1091.long
Protein Kinase A (PKA)-Dependent Troponin-I Phosphorylation and PKA Regulatory Subunits Are Decreased in Human Dilated...
The main findings in this study are that baseline TnI phosphorylation is diminished in myocardial samples from patients with end-stage DCM and that PKA-RI and RII protein levels are decreased in these same hearts. Decreased TnI phosphorylation would lead to an increase in the Ca2+ affinity of troponin C (TnC) and subsequent decreased off-rate of Ca2+ from TnC.4 This results in an increased Ca2+ sensitivity of force development. Decreased baseline PKA phosphorylation of TnI in the failing human heart is consistent with our previous observations in spontaneously hypertensive rat (SHR). In the 76-week-old SHR, a model of decompensated cardiac hypertrophy and precursor to heart failure, baseline TnI phosphorylation was significantly reduced versus Wistar-Kyoto (WKY) controls.6 This was associated with increased Ca2+ sensitivity of actomyosin ATPase activity. Although PKA-dependent TnI phosphorylation under baseline conditions in the 76-week old SHR was decreased, the β-adrenergic pathway was not ...http://circ.ahajournals.org/content/99/4/505
Ståle Nygård - Department of Informatics
Lyngbakken, Magnus Nakrem; Skranes, Julia Brox; de Lemos, JA; Nygård, Ståle; Dalen, Håvard; Hveem, Kristian; Røsjø, Helge & Omland, Torbjørn (2016). Impact of Smoking on Circulating Cardiac Troponin I Concentrations and Cardiovascular Events in the General Population: The HUNT Study (Nord-Trøndelag Health Study).. Circulation. ISSN 0009-7322. 134(24), s 1962- 1972 . doi: 10.1161/CIRCULATIONAHA.116.023726 Show summary BACKGROUND: Both tobacco smoking and circulating cardiac troponin I (cTnI) levels are associated with the risk of acute myocardial infarction, heart failure, and cardiovascular death. However, whether cTnI levels differ according to smoking status and whether smoking modifies the prognostic relationship between cTnI and outcomes remain unclear. METHODS: Using data from a large, population-based cohort, we assessed the association between smoking and cTnI and the impact of smoking on the associations between cTnI levels and the incidence of acute myocardial ...http://www.mn.uio.no/ifi/english/people/aca/staaln/
Cardiac Troponin Specific Autoantibodies: Analytical Tools for Exploring Their Impact on Cardiac Troponin I Testing
The extent of cTnAAb interference in different cTnI assay configurations and the molecular characteristics of cTnAAbs were investigated in publications I and II, respectively. The findings showed that cTnI midfragment targeting immunoassays used predominantly in clinical practice are affected by cTnAAb interference which can be circumvented by using a novel 3+1-type assay design with three capture antibodies against the N-terminus, midfragment and C-terminus and one tracer antibody against the C-terminus. The use of this assay configuration was further supported by the epitope specificity study, which showed that although the midfragment is most commonly targeted by cTnAAbs, the interference basically encompasses the whole molecule, and there may be remarkable individual variation at the affected sites. In publications III and IV, all the data obtained in previous studies were utilized to develop an improved version of an existing cTnAAb assay and a sensitive cTnI assay free of this specific ...http://www.doria.fi/handle/10024/99057
Elevated cardiac troponin concentration in the absence of an acute coronary syndrome
Cardiac troponin (cTn) is the standard serologic test to confirm the diagnosis of acute myocardial infarction. (See.)However, troponin is not specific for acute thrombotic occlusion of a coronary artery, the most common precursor to acute myocardialhttps://www.uptodate.com/contents/elevated-cardiac-troponin-concentration-in-the-absence-of-an-acute-coronary-syndrome
Data from: Randomized comparison of sevoflurane versus propofol-remifentanil on the cardioprotective effects in elderly...
Background It is skeptical about cardioprotective property of sevoflurane in patients undergoing noncardiac surgery, especially in the elderly patients with coronary heart disease. We hypothesized that long duration of sevoflurane inhalation in noncardiac surgery could ameliorate myocardial damage in such patients. Methods This was a randomized, prospective study. One hundred twenty-one elderly patients with coronary heart disease were randomly allocated into two groups. Maintenance of anesthesia was achieved by sevoflurane inhalation (Group S) or propofol-remifentanil respectively (Group PR). Serum cardiac troponin I (cTnI) and brain natriuretic peptide (BNP) were measured before anesthesia induction (T0), 8 h (T1) and 24 h (T2) after anesthesia respectively. The perioperative cardiac output, complications and postoperative 3-month follow-up from end of surgery were recorded. Results Between the two groups, there were no statistical differences in the values of cTnI and BNP during the ...http://datadryad.org/resource/doi:10.5061/dryad.2b8s8
Troponins as cardiac markers | HyTest Troponins
Cardiac conditions. Certain subtypes of troponin (cardiac troponin I and T) are very sensitive and specific indicators of damage to the heart muscle (myocardium). They are measured in the blood to differentiate between unstable angina and myocardial infarction (heart attack) in patients with chest pain or acute coronary syndrome. A patient who had suffered from a myocardial infarction would have an area of damaged heart muscle and so would have elevated cardiac troponin levels in the blood. This can also occur in patients with coronary vasospasm.. It is important to note that cardiac troponins are a marker of all heart muscle damage, not just myocardial infarction. Other conditions that directly or indirectly lead to heart muscle damage can also increase troponin levels. Severe tachycardia (for example due to supraventricular tachycardia) in an individual with normal coronary arteries can also lead to increased ...http://troponins.com/general_information/troponins-cardiac-markers-0
VDAC | PI3-kinase inhibitors in lymphoma
nontechnical summary Carrying out a myocardial infarction cardiac muscle becomes irreversibly broken and as time passes this may result in heart failure. which this occurs as well as the degree to which adverse remodelling can be attenuated. Abstract Abstract The goal of this research was to research the part of intramyocardial administration of chimeric ephrinA1-Fc in modulating the degree of damage and swelling in non reperfused myocardial infarction (MI). Our outcomes display that intramyocardial shot of 6 μg ephrinA1-Fc in to the boundary zone soon after long term coronary artery ligation in AG-490 B6129s mice led to 50% reduced amount of infarct size 64 much less necrosis 35 less chamber dilatation and 32% less left ventricular free wall thinning at 4 days post-MI. In the infarct zone Ly6G+ neutrophil density was 57% reduced and CD45+ leukocyte density was 21% reduced. Myocyte damage was also reduced in ephrinA1-Fc-treated hearts as evidenced by 54% reduced serum cardiac troponin I. ...http://mirc-undernet.org/category/vdac/
Number 16-01: A Peculiar Case of Myocarditis in an Adolescent - Society for Cardiovascular Magnetic Resonance
Table 1. The troponin I trend from admission to discharge.. Discussion:. Chest pain is a common complaint in children and adolescents presenting to the emergency room. However, a cardiac etiology for their chest pain is defined in only 0.6% out of all cases [3, 4]. Troponin I is the most cardiac-specific among the three subunits of the troponin complex and has high sensitivity for acute myocardial injury . It has been established as a useful screening tool for the evaluation of acute coronary ischemic disease in adults, but not in acute perimyocarditis in the pediatric population [2, 4]. In children, reports of elevations of Troponin I are rare. According to a study of elevated troponins in adolescents with chest pain, the median peak troponin I level was 17.8 ng/ml . Our case is interesting given the age of the patient as well as the extreme elevation of Troponin I to 54 ng/ml and his ...http://scmr.org/page/COW1601
Risk stratification in acute coronary syndrome using cardiac troponin I. - Free Online Library
Free Online Library: Risk stratification in acute coronary syndrome using cardiac troponin I.(Editorial) by 'Clinical Chemistry'; Cardiac patients Coronary heart disease Geology, Stratigraphic Stratigraphy Troponinhttps://www.thefreelibrary.com/Risk+stratification+in+acute+coronary+syndrome+using+cardiac+troponin+...-a0209407226
anti-Cardiac Troponin I antibody [N1C3-3] | GeneTex
Cardiac Troponin I antibody [N1C3-3] (troponin I type 3 (cardiac)) for ICC/IF, IHC, WB. Anti-Cardiac Troponin I pAb (GTX113028) is tested in Human, Mouse, Pig samples. 100% Ab-Assurance.http://www.genetex.com/Cardiac-Troponin-I-antibody-N1C3-3-GTX113028.html
Elimination half-life of intravenously administered equine cardiac troponin I in healthy ponies.
Reasons for performing study: To date, no information is available on the true biological elimination half-life (T(1/2) ) of cardiac troponin I (cTnI) in the equine species. Such data are required to better evaluate the optimal time to acquire the cThttp://www.biomedsearch.com/nih/Elimination-half-life-intravenously-administered/22432543.html
HyTest anti-cTnI antibodies utilized in a novel, highly sensitive cTnI assay | HyTest Troponins
LamdaGen's Optical Enhancement System™ (OES™) based diagnostic platform allows precise quantification of cTnI in human whole blood, plasma and serum samples.. For optimization of the cTnI assay, the company utilized HyTest's monoclonal antibodies and troponin I-T-C complex.. For more information, please see the application note below.. Download Application Note. ...http://troponins.com/news/hytest-anti-ctni-antibodies-utilized-novel-highly-sensitive-ctni-assay-0
To the Editor:. The interpretation of cardiac troponin concentrations at presentation and their dynamics over time is a key aspect in the diagnostic workup of acute myocardial infarction in the absence of characteristic electrocardiogram abnormalities. The present biological variation study sought to examine and compare the hour-to-hour biological variation in cardiac troponin I (cTnI) over 24 h in individuals with and without chronic kidney disease (CKD).1 This study was carried out according to the principles of the Declaration of Helsinki and approved by the Institutional Review Board and Ethics Committee of Maastricht University Medical Center (clinicaltrials.gov: NCT02091427 and NCT02210897). All participants provided written informed consent.. From 8:30 AM until 9:30 AM the next day, 20 individuals with clinically stable CKD stage 3 or higher (estimated glomerular filtration rate (eGFR) ,59 mL · min−1 · 1.73 m−2) and 20 individuals without CKD were restricted to the ...http://clinchem.aaccjnls.org/content/63/10/1655
TNNI1 - Wikipedia
Troponin I, slow skeletal muscle is a protein that in humans is encoded by the TNNI1 gene. It is a tissue-specific subtype of troponin I, which in turn is a part of the troponin complex. Gene TNNI1, troponin I type 1 (skeletal muscle, slow), also known as TNN1 and SSTNI, is located at 1q31.3 in the human chromosomal genome, encoding the slow twitch skeletal muscle isoform of troponin I (ssTnI), the inhibitory subunit of the troponin complex in striated muscle myofilaments. Human TNNI1 spans 12.5 kilobases in the genomic DNA and contains 9 exons and 8 introns. Exon 2 to exon 8 contain the coding sequences, encoding a protein of 21.7 kDa consisting of 187 amino acids including the first methionine with an isoelectric point (pI) of 9.59. Three homologous genes have evolved in vertebrates, encoding three muscle type-specific isoforms of TnI. In mammals, the amino acid sequence of ssTnI is highly conserved. Mouse ...https://en.wikipedia.org/wiki/TNNI1
Myocardial injury and cardiac troponin I release after off-pump versus on-pump coronary surgery - Response - Radcliffe...
TNNI3 - Wikipedia
Troponin I, cardiac muscle is a protein that in humans is encoded by the TNNI3 gene. It is a tissue-specific subtype of troponin I, which in turn is a part of the troponin complex. The TNNI3 gene encoding cardiac troponin I (cTnI) is located at 19q13.4 in the human chromosomal genome. Human cTnI is a 24 kDa protein consisting of 210 amino acids with isoelectric point (pI) of 9.87. cTnI is exclusively expressed in adult cardiac muscle. cTnI has diverged from the skeletal muscle isoforms of TnI (slow TnI and fast TnI) mainly with a unique N-terminal extension. The amino acid sequence of cTnI is strongly conserved among mammalian species (Fig. 1). On the other hand, the N-terminal extension of cTnI has significantly different structures among mammal, amphibian and fish. TNNI3 is expressed as a heart specific gene. Early embryonic heart expresses solely slow skeletal muscle TnI. cTnI begins to express in mouse heart at approximately embryonic ...https://en.wikipedia.org/wiki/TNNI3
Troponin I - CTK Biotech
Troponin I is a protein normally not found in serum, released only when myocardial damage occurs which makes it a sensitive and specific marker of acute coronary syndrome (ACS) including myocardial infarction. Early accurate diagnosis of ACS may influence the patient's prognosis, however, symptoms may be atypical or nonexistent and electrocardiogram changes may be absent or nonspecific. Troponin I tests, therefore, present an effective tool to aid in the diagnosis of myocardial infarction rapidly to allow prompt care. ...http://ctkbiotech.com/products/disease-category/troponin-i/
Troponin I type 2 (fast skeletal) Antibodies: Novus Biologicals
Troponin I type 2 (fast skeletal) Antibodies available through Novus Biologicals. Browse our Troponin I type 2 (fast skeletal) Antibody catalog backed by our Guarantee+.https://www.novusbio.com/primary-antibodies/troponin-i-type-2-
Anti-Cardiac Troponin I 抗体 [19C7] (ab92408)
マウス・モノクローナル抗体 ab92408 交差種: Hu 適用: WB,sELISA…Cardiac Troponin I抗体一覧…画像、プロトコール、文献などWeb上の情報が満載のアブカムの Antibody 製品。国内在庫と品質保証制度も充実。http://www.abcam.co.jp/cardiac-troponin-i-antibody-19c7-ab92408.html
Troponin I, Stunning, Hypertrophy, and Failure of the Heart | Circulation Research
From all that we know concerning the complexity of myofilament control mechanisms and the role of cTnI in contraction and relaxation (see Solaro and Rarick7 for review), it is not surprising that a mouse cannot live without cTnI and that alterations in cTnI affect myofilament function. cTnI occupies a central position at the crossroads of the signaling pathways between Ca2+ binding to cTnC and crossbridge binding to actin. An N-terminal region of cTnI anchors cTnC to the thin filament by a strong interaction with its C-terminus. When Ca2+ is not bound to the regulatory site on cTnC, a C-terminal region of cTnI and a highly basic inhibitory region (Ip) tether cTnI to actin. When Ca2+ is bound to the cTnC regulatory site, these regions of cTnI move away from actin and bind to the N-terminus of cTnC. As shown by the data of Huang et al1 and by in vitro experiments,8 removal of cTnI from myofilaments induces activation of the myofilaments independent of the Ca2+ concentration. Current concepts7 ...http://circres.ahajournals.org/content/84/1/122