ライフサイエンスコーパス: cTnT

1 cTnT is frequently elevated in PAD patients and is assoc

2 cTnT levels correlated with CK levels in all 3 subgroups

3 cTnT levels were elevated in 82% of patients (median 27

4 cTnT mRNA expression in skeletal muscle was not detectab

5 cTnT protein was identified by mass spectrometry in pati

6 cTnT was measured for 3 days after surgery and considere

7 s) : HR = 5.575, CI 3.207-9.692, p < 0.0001; cTnT(1year) : 3.664, 2.129-6.305, p < 0.0001) independen

8 ABC-bleeding score (age, biomarkers [GDF-15, cTnT-hs, and haemoglobin], and clinical history [previou

9 3D/S24D Ca(2+)-bound cTnC(1-161)-cTnI(1-172)-cTnT(236-285), and cTnI-R145G/PS23/PS24 Ca(2+)-bound cTn

10 I-R145G Ca(2+)-bound cTnC(1-161)-cTnI(1-172)-cTnT(236-285), cTnI-R145G/S23D/S24D Ca(2+)-bound cTnC(1-

11 23/PS24 Ca(2+)-bound cTnC(1-161)-cTnI(1-172)-cTnT(236-285), respectively.

12 Nine percent of participants were LVH+, 25% cTnT+, and 24% NT-proBNP+.

13 ted hazard ratios for death with an abnormal cTnT concentration were 4.37 (95% confidence intervals [

14 Redefining abnormal cTnT concentration as >/=0.03 ng/ml or a change of >/=0.

15 cluding residues cTnC 1-161, cTnI 1-172, and cTnT 236-285) with the N-terminus of cTnI.

16 n human serum was achieved for both cTnI and cTnT.

17 U/l), CK-MB (18 mug/l; 11 to 28 mug/l), and cTnT (0.03 mug/l; 0.02 to 0.05 mug/l) in 21, 22, and 18

18 The interactions between LVH and cTnT (p(interaction) = 0.0005) and LVH and NT-proBNP (p(

19 Those LVH+ and cTnT+ and/or NT-proBNP+ (n = 144) were older and more li

20 Covalently bonded PNIPAAm on an anti-cTnT bioelectrode showed on/off-switchability, regenerat

21 onalised cardiac troponin T (cTnT) with anti-cTnT.

22 minent in subjects with the highest baseline cTnT values (Pearson's R 0.93).

23 herefore, evaluated the relationship between cTnT concentration and kidney function on the outcome of

24 with Pompe disease, the relationship between cTnT, cardiac troponin I, creatine kinase (CK), CK-myoca

25 studies were conducted to assess biological cTnT variation and to investigate the presence of a diur

26 ent concentrations of Troponin T biomarkers (cTnT) through antibody-functionalized nanowire FETs.

27 The commercial cTnT assay is claimed to be cardiac specific.

28 tratified according to LVH and by detectable cTnT (>/=3 pg/ml) and increased NT-proBNP (>75th age- an

29 analysis showed the selectivity of detecting cTnT and cTnI in human serum with wide dynamic range.

30 A diurnal cTnT rhythm substantiates the recommendation that all dy

31 In study 2, the presence of a diurnal cTnT rhythm was investigated by hourly sampling of 7 sub

32 Individuals who were LVH+ and either cTnT+ or NT-proBNP+ remained at >4-fold higher risk for

33 Elevated cTnT(pre) declined rapidly posttransplant and was normal

34 3 weeks were more likely to have an elevated cTnT(3wks) and remained at high risk.

35 cle appears to be the source of the elevated cTnT detected in the circulation of these patients.

36 Variables related to elevated cTnT posttransplant included pretransplant diabetes, old

37 No patients with elevated cTnT, but with normal cTnI, had any cardiovascular event

38 Re-expressed cTnT in diseased skeletal muscle appears to be the sourc

39 principles whereby monoclonal antibodies for cTnT were immobilized on the sensor electrodes using thi

40 timal threshold of 25x ULN (0.25, ng/mL) for cTnT, which provided similar early outcome information a

41 ty and temperature triggered sensitivity for cTnT.

42 surface, making available binding space for cTnT, and facilitating analyte recognition.

43 eshold for 3-month mortality was 25x ULN for cTnT (hazard ratio, 4.53; 99% confidence interval, 1.59-

44 /mL) at 7% CV (coefficient of variation) for cTnT in HS was demonstrated on nanostructured ZnO electr

45 llografts restore sufficient kidney function cTnT normalizes and patient survival improves.

46 diabetes, older age, time on dialysis, high cTnT(pre) and lower graft function.

47 Negative/positive predictive values for high cTnT(3wks) were 91.4%/50% respectively.

48 Higher cTnT(pre) was associated with increased risk of posttran

49 Hs-cTnT as a risk factor for the primary end point (cardiov

50 hs-cTnT levels are associated with replacement fibrosis and

51 Hs-cTnT results at 1 h and the ED physician's assessments o

52 -cTnI) and 0.61 for ATRIA scores (P=0.005 hs-cTnT and P=0.034 for hs-cTnI).

53 tention for chest pain and had at least 1 hs-cTnT analyzed during 2 years at the Karolinska Universit

54 was detectable in 80.0% (hs-cTnI: 82.6%; hs-cTnT: 69.7%).

55 C), was comparable for cMyC (AUC, 0.924), hs-cTnT (AUC, 0.927), and hs-cTnI (AUC, 0.922) and superior

56 Over 4 to 14 hours, 661 patients had a hs-cTnT<14 ng/L.

57 itivity (hs) cTn assays (hs-cTnI, Abbott; hs-cTnT, Roche) among 2300 consecutive patients with suspec

58 The absolute hs-cTnT levels above the 99th percentile of a healthy refer

59 h acute conditions that may have affected hs-cTnT, or MI associated with the visit, or insufficient i

60 HR, 1.5; 95% CI, 1.3-1.7), relative to an hs-cTnT level less than 0.005 ng/mL at both visits.

61 usted mortality started to increase at an hs-cTnT level of 14 ng/l.

62 high-sensitivity C-reactive protein, and hs-cTnT (both dichotomized according to the 99th percentile

63 = 0.61), SYNTAX score II (r = 0.62), and hs-cTnT (r = 0.29).

64 -proBNP (RR, 3.16; 95% CI, 2.33-4.27) and hs-cTnT (RR, 2.17; 95% CI, 1.00-4.74) were found in partici

65 -proBNP (RR, 3.19; 95% CI, 2.62-3.90) and hs-cTnT (RR, 4.86; 95% CI, 3.03-7.08) were associated with

66 589) >25 years of age with chest pain and hs-cTnT analyzed concurrently in the emergency department o

67 In Communities) cohort, analyzing DBP and hs-cTnT associations as well as prospective associations be

68 oprotein cholesterol, where NT-proBNP and hs-cTnT had greater prognostic value than any other biomark

69 risk patients (no new ischemia on ECG and hs-cTnT measurements <0.005 microg/L) and the number who ha

70 cute coronary syndrome in whom an ECG and hs-cTnT measurements were obtained and AMI outcomes adjudic

71 rdized mental stress tests (exposure) and hs-cTnT plasma concentration using a high-sensitivity assay

72 n independent association between SES and hs-cTnT.

73 troponin T with a highly sensitive assay (hs-cTnT) at 2 time points, 6 years apart, among 9051 partic

74 igh-sensitivity cardiac troponin T assay (hs-cTnT) in 3 large independent cohorts.

75 T, measured by a highly sensitive assay (hs-cTnT), are strongly associated with incident coronary he

76 study, hs-cTn was measured with 3 assays (hs-cTnT, Roche Diagnostics; hs-cTnI, Beckman-Coulter; hs-cT

77 D association was strongest with baseline hs-cTnT >/=14 ng/l (p value for interaction <0.001).

78 39 patients (7.7%) with elevated baseline hs-cTnT (P<0.001).

79 tion was observed between higher baseline hs-cTnT categories and late gadolinium enhancement (>/=7.42

80 We examined the association of baseline hs-cTnT categories with incident diagnosed hypertension (de

81 according to SES, stratified by baseline hs-cTnT concentration.

82 Having elevated baseline hs-cTnT doubled the risk of heart failure and death.

83 o-brain natriuretic peptide, and baseline hs-cTnT level.

84 In contrast, the baseline hs-cTnT levels on admission were not related to lesion loca

85 Baseline hs-cTnT was also strongly associated with incident left ven

86 of log-linear shape were observed between hs-cTnT and CVD outcomes.

87 core achieved C indices of 0.65 with both hs-cTnT and hs-cTnI, in comparison with 0.60 for CHA2DS2VAS

88 linical myocardial damage, as assessed by hs-cTnT, and those persons with evidence of subclinical dam

89 hs-CRP, hs-cTnT, Cyst-C, and NT-proBNP were independent predictors

90 ntify cardiac troponins I and T (hs-cTnI, hs-cTnT) in individuals with no clinically manifest myocard

91 re measured with a high-sensitivity cTnT (hs-cTnT) assay, and 37 clinical parameters were evaluated i

92 Incident detectable hs-cTnT (baseline, <0.005 ng/mL; follow-up, >/=0.005 ng/mL)

93 between cortisol response and detectable hs-cTnT (odds ratio [OR]: 3.98; 95% confidence interval [CI

94 ith no history of cardiovascular disease, hs-cTnT was associated with incident hypertension and risk

95 k patients had an m-HS</=3 and had either hs-cTnT<14 ng/L over serial testing or had AMI excluded by

96 st, we examined the incidence of elevated hs-cTnT (>/=14 ng/L) at 6 years of follow-up.

97 6.5%) and our primary outcome of elevated hs-cTnT (>/=14 ng/l).

98 Cumulative probabilities of elevated hs-cTnT at 6 years among persons with no diabetes mellitus,

99 Persons with low SES and elevated hs-cTnT concentrations have the greatest risk of cardiovasc

100 Patients with elevated hs-cTnT had increased risks of all-cause (hazard ratio 5.73

101 Elevated hs-cTnT levels provide strong and independent prognostic in

102 e adjusted prevalence ratios for elevated hs-cTnT were 1.36 (95% confidence interval: 1.05, 1.75) ove

103 sted relative risks for incident elevated hs-cTnT were 1.40 (95% CI, 1.08-1.80) for prediabetes and 2

104 iac injury biomarkers (NT-proBNP, H-FABP, hs-cTnT, and cTnI) strongly associated with the primary out

105 ers of cardiac injury (NT-proBNP, H-FABP, hs-cTnT, cTnI, and CK-MB).

106 (95% confidence interval, 1.07-1.61) for hs-cTnT >/=14 ng/L (P for trend <0.001).

107 [95% confidence interval, 1.49-18.08] for hs-cTnT >/=14 versus <5 ng/L).

108 erating characteristics curve of 0.94 for hs-cTnT (0.92 for both hs-cTnI assays).

109 ents for traditional risk factors and for hs-cTnT (OR: 2.05; 95% confidence interval: 1.45 to 2.90; p

110 on with 0.60 for CHA2DS2VASc (P=0.004 for hs-cTnT and P=0.022 hs-cTnI) and 0.61 for ATRIA scores (P=0

111 (95% confidence interval, 1.14-1.47) for hs-cTnT of 9 to 13 ng/L, and 1.31 (95% confidence interval,

112 sex-specific vs uniform cutoff levels for hs-cTnT.

113 initially free of CHD and HF and who had hs-cTnT measured twice, 6 years apart.

114 sit 2), the adjusted odds ratio of having hs-cTnT >/=14 ng/l at that visit was 2.2 and 1.5 in those w

115 isk of incident HF was greater for higher hs-cTnT (>/=8.81 ng/L versus <limit of detection; adjusted

116 Higher hs-cTnT was also associated with a greater probability of a

117 als with adjudicated HF hospitalizations, hs-cTnT change appeared to be similarly associated with HF

118 association between changes over time in hs-cTnT and outcome in patients with chronic HF.

119 n the basis of estimated annual change in hs-cTnT over the 6 years between ARIC visits 2 and 4.

120 data linking long-term temporal change in hs-cTnT to outcomes are limited, particularly in primary pr

121 betes mellitus and incident elevations in hs-cTnT were at a substantially higher risk of heart failur

122 Temporal increases in hs-cTnT, suggestive of progressive myocardial damage, are i

123 tes mellitus and no incident elevation in hs-cTnT.

124 s with and without incident elevations in hs-cTnT.

125 as high as patients with large changes in hs-cTnT.

126 ients with chest pain who have an initial hs-cTnT level of <5 ng/l and no signs of ischemia on an ECG

127 ients, of whom 8,907 (61%) had an initial hs-cTnT of <5 ng/l; 21% had 5 to 14 ng/l, and 18% had >14 n

128 Introducing hs-cTnT into clinical practice has led to the recognition o

129 ed among individuals with the most marked hs-cTnT increases (eg, baseline, < 0.005 ng/mL; follow-up,

130 We measured hs-cTnT at baseline among 4986 participants in MESA (Multi-

131 n studies (p = 0.010) and those measuring hs-cTnT rather than hs-cTnI (p = 0.027).

132 Median hs-cTnT on day 4 was 2,160 (Q1 to Q3: 1,087 to 3,274) ng/l

133 Among participants with nonelevated hs-cTnT concentrations, when comparing those in the lowest

134 ccurred in 20 patients (1.4%) with normal hs-cTnT versus 39 patients (7.7%) with elevated baseline hs

135 Measurements of hs-cTnT (99th percentile, 14 ng/L) were performed at 0, 1,

136 ted with the relative temporal changes of hs-cTnT (p < 0.01, corrected for multiple comparisons).

137 ng sex-specific 99th percentile levels of hs-cTnT (women, 9 ng/L; men, 15.5 ng/L).

138 ociation between all detectable levels of hs-cTnT and risk for MI, heart failure, and cardiovascular

139 egression, we examined the association of hs-cTnT change with subsequent CHD, HF, and death during a

140 ge-scale genome-wide association study of hs-cTnT has been reported.

141 We examined the prognostic value of hs-cTnT in a subgroup of patients from the Controlled Rosuv

142 troponin levels, any detectable level of hs-cTnT is associated with an increased risk of death and c

143 Preprocedural elevation of hs-cTnT is observed in one fourth of SCAD patients undergoi

144 Minor elevations of hs-cTnT may represent a biochemical signature of early subc

145 Serial testing of hs-cTnT over 1 hour along with application of an m-HS ident

146 Serial determination of hs-cTnT trajectory adds clinically relevant information to

147 rgency department presentation, levels of hs-cTnT were already above the uniform cutoff value in 427

148 he association of preprocedural levels of hs-cTnT with 1-year clinical outcomes among SCAD patients u

149 Associations of hs-cTnT with incident HF, CV-related mortality, and coronar

150 Evaluating the association of hs-cTnT with replacement fibrosis and progression of struct

151 Furthermore, information on hs-cTnT change improved discrimination for HF and death whe

152 had no effect on ST-segment resolution or hs-cTnT, and did not improve clinical outcomes or LV remode

153 B-type natriuretic peptide plus hs-cTnT together performed best.

154 29), 527 (26%) had elevated preprocedural hs-cTnT above the upper reference limit of 14 ng/L.

155 Increased levels of preprocedural hs-cTnT are proportionally related to the risk of death and

156 higher tertiles of elevated preprocedural hs-cTnT, but not among patients with hs-cTnT below the uppe

157 Associations of low DBP with prevalent hs-cTnT and incident CHD were most pronounced among patient

158 luded age (A), biomarkers (B) (NT-proBNP, hs-cTnT, and low-density lipoprotein cholesterol), and clin

159 A relative hs-cTnT change <20% was linked to higher long-term mortalit

160 was similar across quartiles of relative hs-cTnT change.

161 comes was lower among those with relative hs-cTnT reductions greater than 50% from baseline.

162 rmation, including measurements of serial hs-cTnT blood concentrations twice: once using the uniform

163 To estimate the ability of a single hs-cTnT concentration below the limit of detection (<0.005

164 A single hs-cTnT concentration below the limit of detection in combi

165 gnosis of NSTEMI in our hospital, a small hs-cTnT change may not be useful to exclude NSTEMI, particu

166 nd a high-sensitivity cardiac troponin T (hs-cTnT) acquired on the day of admission.

167 ons of high-sensitive cardiac troponin T (hs-cTnT) are associated with incident heart failure (HF) in

168 ensitivity assays for cardiac troponin T (hs-cTnT) are sometimes used to rapidly rule out acute myoca

169 ated high-sensitivity cardiac troponin T (hs-cTnT) concentrations (>/=14 ng/L) using Poisson and mult

170 and high-sensitivity cardiac troponin T (hs-cTnT) concentrations were measured by electrochemilumine

171 line high-sensitivity cardiac troponin T (hs-cTnT) elevation in SCAD patients undergoing elective per

172 ated high-sensitivity cardiac troponin-T (hs-cTnT) in a 1-hour acute myocardial infarction (AMI) excl

173 and high-sensitivity cardiac troponin T (hs-cTnT) in healthy older individuals without history of ca

174 ostic value of high-sensitive troponin T (hs-cTnT) in heart failure (HF) beyond that of high-sensitiv

175 cing high-sensitivity cardiac troponin T (hs-cTnT) into clinical practice and to define at what hs-cT

176 High-sensitivity cardiac troponin T (hs-cTnT) is a biomarker of cardiovascular risk and could be

177 g/l) high-sensitivity cardiac troponin T (hs-cTnT) level and an electrocardiogram (ECG) without signs

178 able high-sensitivity cardiac troponin T (hs-cTnT) level is associated with adverse outcomes.

179 sing high-sensitivity cardiac troponin T (hs-cTnT) levels in the diagnosis of acute myocardial infarc

180 heir high-sensitivity cardiac troponin T (hs-cTnT) levels were measured.

181 uded high-sensitivity cardiac troponin T (hs-cTnT) on day 4, left ventricular (LV) remodeling, and cl

182 d on high-sensitivity cardiac troponin T (hs-cTnT) testing at presentation and again 1 h thereafter h

183 ther high-sensitivity cardiac troponin T (hs-cTnT), a marker of subclinical myocardial damage, can id

184 ide, high-sensitivity cardiac troponin T (hs-cTnT), and high-sensitivity cardiac troponin I (hs-cTnI)

185 NP), high-sensitivity cardiac troponin T (hs-cTnT), and low-density lipoprotein cholesterol, where NT

186 sing high-sensitivity cardiac troponin-T [hs-cTnT]) and with coronary heart disease (CHD), stroke, or

187 Risk factor and temporal hs-cTnT data were collected.

188 The 99th percentile values for the hs-cTnT assay in DHS, ARIC, and CHS were 18, 22, and 36 ng/

189 Use of a uniform 14 ng/l cutoff for the hs-cTnT assay may lead to over-diagnosis of myocardial infa

190 gnosis of myocardial infarction using the hs-cTnT assay was derived from small studies of presumably

191 f observation, the relative change in the hs-cTnT level remained <20% in 26% and the absolute change

192 The hs-cTnT-associated single-nucleotide polymorphisms were not

193 Relative to hs-cTnT <5 ng/L, adjusted hazard ratios for incident diagno

194 ovides discriminatory power comparable to hs-cTnT and hs-cTnI in the diagnosis of AMI and may perform

195 ity cTnI (P<0.05 for both) and similar to hs-cTnT at predicting death at 3 years.

196 ding patients into 20 groups according to hs-cTnT level, the adjusted mortality started to increase a

197 tive predictive values of an undetectable hs-cTnT and ECG without ischemia for MI and death within 30

198 hin 30 days in patients with undetectable hs-cTnT and no ischemic ECG changes was 99.8% (95% confiden

199 up, 39 (0.44%) patients with undetectable hs-cTnT had a MI, of whom 15 (0.17%) had no ischemic ECG ch

200 nd to compare it with the algorithm using hs-cTnT alone (the troponin algorithm).

201 ty of Cardiology 0/1-hour algorithm using hs-cTnT and hs-cTnI in patients with RD, defined as an esti

202 ld remain the standard of care when using hs-cTnT levels for the diagnosis of AMI.

203 Using hs-cTnT, patients with RD had comparable sensitivity of rul

204 eclassification Improvement +0.149 versus hs-cTnT, +0.235 versus hs-cTnI (P<0.001).

205 o clinical practice and to define at what hs-cTnT level risk starts to increase.

206 r research is needed to determine whether hs-cTnT can identify people who may benefit from ambulatory

207 department (ED) with chest pain, for whom hs-cTnT testing was ordered at presentation.

208 cation with cMyC was larger compared with hs-cTnT (Net Reclassification Improvement +0.256) and hs-cT

209 hs-cTnT 6 to 13 ng/l; Group 3, those with hs-cTnT 14 to 49 ng/l (i.e., a group in which most patients

210 with hs-cTnT<6 ng/l; Group 2, those with hs-cTnT 6 to 13 ng/l; Group 3, those with hs-cTnT 14 to 49

211 ural hs-cTnT, but not among patients with hs-cTnT below the upper reference limit.

212 riation was significantly associated with hs-cTnT levels.

213 genetic variants that are associated with hs-cTnT levels.

214 interval, 1.08-1.25) for individuals with hs-cTnT of 5 to 8 ng/L, 1.29 (95% confidence interval, 1.14

215 The combination of cMyC with hs-cTnT or standard-sensitivity cTnI (but not hs-cTnI) led

216 th older assays); and Group 4, those with hs-cTnT>/=50 ng/l.

217 nts were divided into Group 1, those with hs-cTnT<6 ng/l; Group 2, those with hs-cTnT 6 to 13 ng/l; G

218 risk group for the ABC-stroke score with hs-cTnT.

219 In a clinical setting, where a change in cTnT was not mandatory for the diagnosis of NSTEMI, seri

220 e recommendation that all dynamic changes in cTnT should be interpreted in relation to the clinical p

221 n study 1, we observed a gradual decrease in cTnT concentrations during the day (24 +/- 2%).

222 infarction, and there were no differences in cTnT levels between patients with and without (n=90) abn

223 e interval: 0.16 to 0.55) for an increase in cTnT, after adjusting for comorbidities and baseline lev

224 Increased cTnT levels in Pompe disease and likely other neuromuscu

225 (LVH- cTnT-), 4% (LVH- cTnT+), and 6% (LVH+ cTnT-) (p < 0.0001).

226 ce of HF or CV death over 8 years among LVH+ cTnT+ was 21% versus 1% (LVH- cTnT-), 4% (LVH- cTnT+), a

227 ars among LVH+ cTnT+ was 21% versus 1% (LVH- cTnT-), 4% (LVH- cTnT+), and 6% (LVH+ cTnT-) (p < 0.0001

228 nT+ was 21% versus 1% (LVH- cTnT-), 4% (LVH- cTnT+), and 6% (LVH+ cTnT-) (p < 0.0001).

229 At baseline, measurable cTnT levels (>/=0.01 ng/ml) were detected in 21.3% of in

230 In adjusted Cox regression models, cTnT levels >/=0.01 ng/ml were associated with increased

231 cific regions within the N-terminus of mouse cTnT (McTnT) to create McTnT1-44 and McTnT45-74 proteins

232 LV mass by magnetic resonance imaging (MRI), cTnT by highly sensitive assay, and NT-proBNP analysis (

233 Although cTnI is unique to myocardium, cTnT can be re-expressed in skeletal muscle in response

234 tients with reversible myopathies normalized cTnT, CK, and CK-MB in unison.

235 free energies associated with the binding of cTnT with PNIPAAm at 25 (DeltaGcoil=-6.0 Kcal/mole) and

236 We assessed correlates of cTnT levels pre- and posttransplantation and their relat

237 ur data suggest the following: (1) the CR of cTnT modulates XB recruitment dynamics; (2) the N-termin

238 Detection of cTnT in phosphate buffered saline (PBS) and human serum

239 R92 within the tropomyosin-binding domain of cTnT, despite being distal to the ATP hydrolysis domain

240 hazard models (hazard ratio per doubling of cTnT, 1.24; 95% confidence interval, 1.08-1.43; P=0.003

241 of 2.4 years showed persistent elevation of cTnT (median: 0.08 mug/l; interquartile range: 0.06 to 0

242 seases commonly have persistent elevation of cTnT and CK-MB in the absence of clinical and cTnI evide

243 e modulating effect of the N-terminal end of cTnT on CR-tropomyosin interactions may lead to the emer

244 associated with detectable plasma levels of cTnT using high-sensitivity assays in healthy participan

245 Lack of normalization of cTnT posttransplant identifies a group of individuals wi

246 Normalization of cTnT posttransplant was associated with reduced risk.

247 The analytical performance of cTnT N-MIP performed by differential pulse voltammetry s

248 t dynamics; (2) the N-terminal end region of cTnT has a synergistic effect on the ability of the CR t

249 estigate the presence of a diurnal rhythm of cTnT.

250 r the diagnosis of NSTEMI, serial samples of cTnT were measured with a high-sensitivity cTnT (hs-cTnT

251 R205A, residing in the short helix H1(T2) of cTnT, whereas the mutations to nearby residues exhibited

252 that the interplay between the N terminus of cTnT and the overlapping ends of contiguous Tm effectuat

253 the functional effects of the N-terminus of cTnT are modulated by Tm isoforms, McTnT deletion protei

254 functional regions within the N-terminus of cTnT, but also offer mechanistic insights into the diver

255 isk-stratification protocols with the use of cTnT may benefit from standardized sampling times.

256 Diurnal variation of cTnT, as assessed in study 2, was characterized by peak

257 Coexistence of more than one cTnT variant results in a temporally split myofilament r

258 to determine how to interpret perioperative cTnT values for patients with low kidney function.

259 Elevated plasma cTnT levels in patients with Pompe disease are associate

260 cause the risk associated with postoperative cTnT levels may be different for patients with eGFR<30 m

261 Postprocedural cTnT and creatine kinase-MB mass levels (ULN, 6.7 ng/mL

262 Elevated posttransplant cTnT was associated with reduced patient survival (cTnT(

263 n between 2000 and 2009 with a preprocedural cTnT level below the upper limit of normal (ULN, </=0.01

264 Pretransplant cTnT was elevated (>/=0.01 ng/mL) in 56.4%.

265 f the presence and the level of a prognostic cTnT threshold.

266 eity, we replaced the T1 or T2 domain of rat cTnT (RcT1 or RcT2) with its counterpart from rat fsTnT

267 Practice guidelines regard cTnT and cardiac troponin I (cTnI) as equally sensitive

268 f cTnT were measured with a high-sensitivity cTnT (hs-cTnT) assay, and 37 clinical parameters were ev

269 graphy and serial levels of high-sensitivity cTnT.

270 ac investigations, and measurements of serum cTnT, cTnI, creatine kinase (CK), creatine kinase myocar

271 Even small cTnT elevations predict a markedly increased risk that i

272 as associated with reduced patient survival (cTnT(3wks) : HR = 5.575, CI 3.207-9.692, p < 0.0001; cTn

273 Cardiac troponin T (cTnT) and sensitive cardiac troponin I (s-cTnI) were als

274 Abstract Cardiac troponin T (cTnT) has a highly acidic extended N-terminus, the physi

275 significance of elevated cardiac troponin T (cTnT) in patients with neuromuscular diseases.

276 Changes in cardiac troponin T (cTnT) levels are required for the diagnosis of NSTEMI, a

277 hat chronically elevated cardiac troponin T (cTnT) levels fluctuate randomly around a homeostatic set

278 Elevated plasma cardiac troponin T (cTnT) levels in patients with neuromuscular disorders ma

279 vides the capability for cardiac-troponin T (cTnT) measurements with co-existed 10 microg/ml BSA inte

280 rinted electrode for the cardiac troponin T (cTnT) was developed.

281 valuate whether elevated cardiac troponin T (cTnT) was independently associated with an increased all

282 ac troponin I (cTnI) and cardiac troponin T (cTnT) which have been considered as 'gold standard'.

283 (PNIPAAm) functionalised cardiac troponin T (cTnT) with anti-cTnT.

284 he gene that encodes for cardiac troponin T (cTnT), a biomarker of myocardial injury.

285 LVH, low but detectable cardiac troponin T (cTnT), and elevated N-terminal pro-B-type natriuretic pe

286 Cardiac troponin T (cTnT), even at low concentrations, is a risk factor for

287 tive mechanism is cardiac muscle troponin T (cTnT), the central region (CR) and the T2 region of whic

288 f the myocardial marker, cardiac troponin T (cTnT).

289 pecially with the use of cardiac troponin T (cTnT).

290 DF-15), high-sensitivity cardiac troponin T (cTnT-hs) and haemoglobin, age, and previous bleeding.

291 ac Troponin-I (cTnI) and cardiac-Troponin-T (cTnT) in a point-of-care sensor format.

292 on and quantification of cardiac Troponin-T (cTnT).

293 Pretransplant cardiac troponin T(cTnT(pre) ) is a significant predictor of survival postk

294 achieving surface confinement of the target cTnT and cTnI molecules on to the electrode surface.

295 The cTnT active sites were engineered using pyrrole and carb

296 and pyrrole-3-acid carboxylic to perform the cTnT biomimetic nanosurface was obtained at 1:5 ratio.

297 sulted in a N-MIP with excellent affinity to cTnT binding (KD=7.3 10(-13) molL(-1)).

298 Compared with patients who had undetectable cTnT levels, those with cTnT levels >/=0.01 ng/ml had hi

299 was one-step electropolymerized jointly with cTnT by cyclic voltammetry.

300 who had undetectable cTnT levels, those with cTnT levels >/=0.01 ng/ml had higher rates for mortality