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

8 3D/S24D Ca(2+)-bound cTnC(1-161)-cTnI(1-172)-cTnT(236-285), and cTnI-R145G/PS23/PS24 Ca(2+)-bound cTn

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

10 23/PS24 Ca(2+)-bound cTnC(1-161)-cTnI(1-172)-cTnT(236-285), respectively.

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

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

13 se a significant decrease of MDA, MMP-9, and cTnT levels which were found to be significantly higher

14 c causes of low-grade elevations in cTnI and cTnT appear distinct, and their associations with outcom

15 Both cTnI and cTnT had strong associations with CVD death and heart fa

16 Both cTnI and cTnT were strongly associated with CVD risk in unadjuste

17 1.17-1.32) and 1.11 (1.04-1.19) for cTnI and cTnT, respectively; ratio of hazard ratios 1.12 (1.04-1.

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

19 ultiple cardiac biomarkers - GPBB, CK-MB and cTnT for early diagnosis and prognosis of acute myocardi

20 8, 10, and 1 pg mL(-1), for GPBB, CK-MB and cTnT, respectively, which is well below the clinical cut

21 Serum NT-proBNP and cTnT levels correlated with increasing LGE and extracell

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

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

24 staining for cardiac lineage markers such as cTnT, GATA4, and NKX2.5.

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

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

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

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

29 By contrast, cTnT, but not cTnI, was associated with non-CVD death; r

30 Alterations in cTnC-cTnT binding may compromise contractile performance and

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

32 A diurnal cTnT rhythm substantiates the recommendation that all dy

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

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

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

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

37 loci (4 single-nucleotide polymorphisms) for cTnT.

38 ty and temperature triggered sensitivity for cTnT.

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

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

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

42 hs-cTnT levels are associated with replacement fibrosis and

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

44 : 1.59; 95% CI: 1.17 to 2.16; p = 0.003), hs-cTnT < LoD/CAC > 0: 11.1 per 1,000 person-years (HR: 2.7

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

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

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

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

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

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

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

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

53 alyses were based on measurements with an hs-cTnT assay and an alternative hs-cTnI assay with even hi

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

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

56 ; 95% CI: 1.96 to 3.83; p < 0.00001), and hs-cTnT >= LoD/CAC > 0: 22.6 per 1,000 person-years (HR: 3.

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

58 = 0.61), SYNTAX score II (r = 0.62), and hs-cTnT (r = 0.29).

59 -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

60 -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

61 589) >25 years of age with chest pain and hs-cTnT analyzed concurrently in the emergency department o

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

63 accuracy of BNP, NT-proBNP, hs-cTnI, and hs-cTnT for MACE was moderate-to-good (AUC 0.75-0.79), supe

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

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

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

67 n independent association between SES and hs-cTnT.

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

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

70 ed by 3 high-sensitivity (hs) cTn assays: hs-cTnT (Roche), hs-cTnI (Siemens), and hs-cTnI (Abbott).

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

72 Baseline hs-cTnT (limit of detection [LoD] 3 ng/l) and CAC measureme

73 39 patients (7.7%) with elevated baseline hs-cTnT (P<0.001).

74 se of this study was to evaluate baseline hs-cTnT and CAC in relation to ASCVD.

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

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

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

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

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

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

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

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

83 those with ECG-LVH and normal biomarkers (hs-cTnT (high sensitivity cardiac troponin-T) <6 ng/L and N

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

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

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

87 Among participants without prevalent CVD, hs-cTnT and NT-proBNP were independently associated with in

88 ]: 2.0 to 2.76; p < 0.001) and detectable hs-cTnT (15.4 vs. 5.2 per 1,000 person-years; adjusted HR:

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

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

91 Relationships with ECV, hs-cTnT, and NT-proBNP were examined separately and as a co

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

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

94 rs (e.g., breast, prostate) with elevated hs-cTnT (>=14 ng/L).

95 had significantly higher odds of elevated hs-cTnT (odds ratio [OR] = 1.26, 95% confidence interval [C

96 had significantly higher odds of elevated hs-cTnT (OR = 1.26, 95% CI: 1.03, 1.53).

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

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

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

100 ed to clarify the association of elevated hs-cTnT levels among survivors of specific cancer sites, st

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

102 Persons without CVD but with elevated hs-cTnT or NT-proBNP levels should be recognized to have si

103 ncers may be more likely to have elevated hs-cTnT than patients without prior cancer.

104 ers might be more likely to have elevated hs-cTnT than persons without prior cancer.

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

106 breast and prostate cancers and elevated hs-cTnT.

107 breast and prostate cancers and elevated hs-cTnT.

108 For 30-day MACE + UA, the ESC hs-cTnT 0/1 h algorithm had a higher positive predictive va

109 The ESC hs-cTnT 0/1 h algorithm ruled-in fewer patients (16%; 95% C

110 Among 3,123 patients, the ESC hs-cTnT 0/1 h algorithm triaged significantly more patients

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

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

113 (95% confidence interval, 1.07-1.61) for hs-cTnT >/=14 ng/L (P for trend <0.001).

114 [95% confidence interval, 1.49-18.08] for hs-cTnT >/=14 versus <5 ng/L).

115 (e.g., HR = 1.44 (95% CI: 1.24, 1.69) for hs-cTnT >=14 ng/L and HR = 1.28 (95% CI: 1.14, 1.44) for hs

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

117 /L and HR = 1.28 (95% CI: 1.14, 1.44) for hs-cTnT 9-13 ng/L vs. <3 ng/L; HR = 1.57 (95% CI: 1.35, 1.8

118 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

119 (95% confidence interval, 1.14-1.47) for hs-cTnT of 9 to 13 ng/L, and 1.31 (95% confidence interval,

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

121 ts who did not have prevalent CVD but had hs-cTnT >=14 ng/L or NT-proBNP >=248.1 pg/mL.

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

123 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

124 rt failure outcomes in patients with high hs-cTnT and NT-proBNP levels.

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

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

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

128 ceived care guided either by the 0/1-hour hs-cTnT protocol (n=1646) or the 0/3-hour standard masked h

129 re randomly assigned to either a 0/1-hour hs-cTnT protocol (reported to the limit of detection [<5 ng

130 This in-practice evaluation of a 0/1-hour hs-cTnT protocol embedded in ED care enabled more rapid dis

131 The 0/1-hour hs-cTnT protocol was not inferior to standard care (0/1-hou

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

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

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

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

136 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

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

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

139 (n=1646) or the 0/3-hour standard masked hs-cTnT protocol (n=1642) and were followed for 30 days.

140 ocol in comparison with a 0/3-hour masked hs-cTnT protocol in patients with suspected acute coronary

141 e limit of detection [<5 ng/L]) or masked hs-cTnT reported to <=29 ng/L evaluated at 0/3-hours (stand

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

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

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

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

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

147 outcome for patients with high levels of hs-cTnT (>=14 ng/L; hazard ratio [HR] 2.42 [95% confidence

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

165 ing the alternative assays for hs-cTnI or hs-cTnT, no cutoff achieved the target performance: hs-cTnT

166 terminal pro-B-type natriuretic peptide), hs-cTnT, CRP (C-reactive protein), and circulating oxidativ

167 o cutoff achieved the target performance: hs-cTnT concentrations less than 5 ng/L yielded an NPV of 6

168 tion with infection in relation to plasma hs-cTnT and NT-proBNP concentrations among participants wit

169 29), 527 (26%) had elevated preprocedural hs-cTnT above the upper reference limit of 14 ng/L.

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

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

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

173 BNP, NT-proBNP, hs-cTnT and hs-cTnI concentrations were measured in a blind

174 BNP, NT-proBNP, hs-cTnT, and hs-cTnI concentrations provide useful diagnost

175 nd prognostic accuracy of BNP, NT-proBNP, hs-cTnT, and hs-cTnI concentrations, alone and against the

176 BNP, NT-proBNP, hs-cTnT, and hs-cTnI cut-offs, achieving pre-defined thresh

177 BNP, NT-proBNP, hs-cTnT, and hs-cTnI were significantly higher in cardiac s

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

179 were correlated with levels of NT-proBNP, hs-cTnT, CRP, or oxidative stress biomarkers.

180 ulted in the following ASCVD event rates: hs-cTnT < LoD/CAC = 0: 2.8 per 1,000 person-years (referenc

181 : 2.8 per 1,000 person-years (reference), hs-cTnT >= LoD/CAC = 0: 6.8 per 1,000 person-years (HR: 1.5

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

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

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

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

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

187 High-sensitivity cardiac troponin T (hs-cTnT) and N-terminal B-type natriuretic peptide (NT-proB

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

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

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

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

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

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

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

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

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

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

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

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

200 s of high-sensitivity cardiac troponin T (hs-cTnT) or N-terminal pro-B-type natriuretic peptide (NT-p

201 hour high-sensitivity cardiac troponin T (hs-cTnT) protocol in comparison with a 0/3-hour masked hs-c

202 ated high-sensitivity cardiac troponin T (hs-cTnT) test results.

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

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

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

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

207 ated high-sensitivity cardiac Troponin T (hs-cTnT).

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

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

210 Thus, hs-cTnT and NT-proBNP were independently associated with in

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

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

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

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

215 3 to 0.96) and was at least comparable to hs-cTnT-Elecsys (AUC: 0.94; 95% CI: 0.93 to 0.96; p = 0.213

216 Together, hs-cTnT and CAC (discordance 38%) resulted in the following

217 Individuals with undetectable hs-cTnT (32%) had similar risk for ASCVD as did those with

218 An undetectable hs-cTnT identifies patients with a similar, low risk for AS

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

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

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

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

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

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

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

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

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

228 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

229 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

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

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

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

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

234 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

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

236 Combining BNP/NT-proBNP with hs-cTnT/hs-cTnI further improved diagnostic accuracy to an

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

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

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

240 Increased cTnT levels in Pompe disease and likely other neuromuscu

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

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

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

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

245 cTnI, but not cTnT, was associated with myocardial infarction and coro

246 derm results in not only greater than 90% of cTnT(+) cardiomyocytes but also high cardiomyocytes yiel

247 compare and contrast (1) the association of cTnT and cTnI with CVD and non-CVD outcomes, and (2) the

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

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

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

251 etection of prolonged elevation of levels of cTnT and CK-MB, which are only produced 6 h after the on

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

253 t the intrinsically disordered C terminus of cTnT directly interacts with the regulatory N-domain of

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

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

256 iomarkers including troponin I or T (cTnI or cTnT), creatine kinase-MB (CK-MB), and myoglobin.

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

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

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

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

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

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

263 High-sensitivity cTnT and cTnI were measured in serum from 19 501 individ

264 graphy and serial levels of high-sensitivity cTnT.

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

266 Prestress and stressor cTnT cutpoints of 4.2 pg/mL predicted 24-hour, daytime,

267 iac stress (by measuring cardiac troponin T (cTnT) and N-terminal prohormone of brain natriuretic pep

268 it is not clear whether cardiac troponin T (cTnT) and troponin I (cTnI) are equivalent measures of r

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

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

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

272 c cardiomyopathy-causing cardiac troponin T (cTnT) mutation Delta160Glu (Delta160E) is located in a p

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

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

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

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

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

278 NP) and high-sensitivity cardiac troponin T (cTnT), and genetic analysis.

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

280 first time, we show that cardiac troponin T (cTnT), in part through its intrinsically disordered C te

281 serum albumin (BSA) and cardiac troponin T (cTnT), respectively.

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

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

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

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

286 roteinase-9 (MMP-9), and cardiac Troponin-T (cTnT) were evaluated by appropriate biochemical methods.

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

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

289 We hypothesized that cTnT-Delta160E repositions the flexible linker, altering

290 The cTnT active sites were engineered using pyrrole and carb

291 ere we first defined the WT structure of the cTnT-linker region and then identified Delta160E mutatio

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

293 Using the cTnT, hs-cTnI (Siemens), and hs-cTnI (Abbott) concentrat

294 These cTnT cutpoints were associated with an ethnicity-specifi

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

296 yopathic variant displays tighter binding to cTnT.

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

298 y associated with some CVD outcomes, whereas cTnT is more strongly associated with the risk of non-CV

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