ライフサイエンスコーパス: troponin I

1 ardiac myosin-binding protein C, and cardiac troponin I).

2 in-1), and cardiomyocytes (alpha-actinin and troponin I).

3 igen responses directed against cardiac TnI (troponin I).

4 for troponin T and 2.7 (CI, 1.9 to 4.6) for troponin I.

5 ery and between myocardial tissue and plasma troponin I.

6 ain natriuretic peptide and high-sensitivity troponin I.

7 for troponin T and 4.2 (CI, 2.0 to 9.2) for troponin I.

8 chain 2a, alpha/beta-myosin heavy chain, and troponin I.

9 littermates, which express wild-type cardiac troponin I.

10 oponin I but not when it is bound to cardiac troponin I.

11 of acutely infected mice and serum levels of troponin I.

12 panning the sequence of its natural partner, troponin-I.

13 avy chain 7 (MyH7), succinate dehydrogenase, troponin I 1, troponin C1, troponin T1], capillary densi

14 ed extraordinary sensitivity towards cardiac troponin I [1.7microA/(ng/mL) in phosphate buffer], but

15 CI, 1.76-3.83) for high-sensitivity cardiac troponin I, 1.65 (95% CI, 1.12-2.44) for NT-proBNP, and

16 d significant myocardial injury (median peak troponin I, 138 ng/dL [limits, 58-356 ng/dL]) and sustai

17 312) ng/L, hs-cTnI (high sensitivity cardiac troponin I) 6.3 (3.4-13.0) ng/L, hs-CRP (high sensitivit

18 The level of troponin is a powerful predictor of cardiovascular event

19 The device can detect serum cardiac troponin I, a biomarker of cardiac disease to 100 pg/ml

20 printed biosensor for the early detection of Troponin I, a crucial biomarker for heart failure, by co

21 association of circulating high-sensitivity troponin I (Abbott ARCHITECT), with acute respiratory di

22 d with PAPP-A stratified by baseline cardiac troponin I [Accu-TnI >0.04 mug/l], p interaction = 0.87)

23 analysis of serum biomarkers (e.g., cardiac troponin I) afforded up to 130-fold enhancement of near-

24 uces the incidence of postprocedural cardiac troponin I after elective PCI and confers an MACCE-free

25 ents with an MACCE had a higher mean cardiac troponin I after PCI (+/-SD): 2.07+/-6.99 versus 0.91+/-

26 % (95% CI, 57.5%-68.9%).The high-sensitivity troponin I algorithm ruled out 1205 (54.2%) with a sensi

27 e at baseline, including 44% with detectable troponin I, although in comparison, median levels of bra

28 Cardiac troponin is an independent predictor of cardiovascular m

29 edian age, 79 years): 78.6% (n = 26896) with troponin I and 21.4% (n = 7319) with troponin T measurem

30 recorded during the study (six patients for troponin I and 25 patients for troponin T).

31 mary prevention population, baseline cardiac troponin I and BNP were associated with the risk of vasc

32 K resulted in higher serum levels of cardiac troponin I and elevated amounts of reactive oxygen speci

33 oses a hydrophobic patch that interacts with troponin I and initiates cardiac muscle contraction.

34 rement of the heart attack indicator cardiac troponin I and is shown to successfully combine antigen

35 e was found for long-term cardiac events for troponin I and long-term outcomes for troponin T (insuff

36 lol treatment of mice to reduce the level of troponin I and myosin binding protein C (MyBP-C) phospho

37 ity and hyperphosphorylation of its targets, troponin I and myosin-binding protein C.

38 M detection, were included in this study and troponin I and N terminal fragment of B-type natriuretic

39 High-sensitivity troponin I and N-terminal pro-brain natriuretic peptide

40 t weak association between autoantibodies to troponin I and proinflammatory cytokine IL-18.

41 expression of the maturation marker cardiac troponin I and significantly increased action potential

42 High-sensitivity troponin I and T assays were used to measure troponin co

43 orylation of thin filament proteins, such as troponin I and T, dramatically affects calcium sensitivi

44 creased when troponin C is bound to skeletal troponin I and the pK(a) of His-130 is shifted upward.

45 ls did not increase significantly over time, troponin I and troponin T increased moderately, and no c

46 restat also inhibits DOX-induced increase in troponin-I and various inflammatory markers in the serum

47 High-sensitivity assays can quantify cardiac troponins I and T (hs-cTnI, hs-cTnT) in individuals with

48 red the prognostic value of cardiac markers (troponins I and T, N-terminal prohormone of brain natriu

49 ), injury biomarkers (creatine-kinase-MB and troponin I), and histopathologic evaluations were quanti

50 part of an ongoing study), high-sensitivity troponin I, and B-type natriuretic peptide ( Table 1 ).

51 on fraction, pro-B-type natriuretic peptide, troponin I, and C-reactive protein levels.

52 riuretic peptide, aldosterone, endothelin-1, troponin I, and C-telopeptide for type I collagen levels

53 infarct size as assessed by cardiac enzymes, troponin I, and creatine kinase.

54 soluble fms-like tyrosine kinase receptor-1, troponin I, and creatinine were greater in HF-REF and HF

55 (TpnT-CD70) retains binding of tropomyosin, troponin I, and troponin C, indicating a preserved core

56 ke cardiac myosin heavy chain-alpha, cardiac troponin-I, and adenine nucleotide translocator 1 (ANT1)

57 ition, we established that autoantibodies to troponin I, annexin-A5, and beta 1-adrenegic receptor be

58 ted with an immobilized antibody for cardiac troponin I (anti-cTnI) on a photoresponsive composite ma

59 fGQDs) conjugated with antibody anti-cardiac Troponin I (anti-cTnI) to detect cardiac marker antigen

60 B-type natriuretic peptide (BNP) and cardiac troponin I are associated with adverse outcomes in stabl

61 NP) concentrations at 72 h and 12 weeks, and troponin I area under the curve (AUC) over 72 h.

62 y) measures of troponin level (troponin T or troponin I, as available).

63 udy that investigated the application of the troponin I assay for the diagnosis of AMI in 1040 patien

64 impact of transitioning from a conventional troponin I assay to a high-sensitivity assay with sex-sp

65 o the nearest integer for a high-sensitivity troponin I assay were used in the analysis.

66 five times lower detection limit for cardiac troponin I assay with a high selectivity.

67 t of implementing a high-sensitivity cardiac troponin I assay with sex-specific diagnostic thresholds

68 Use of the high-sensitivity cardiac troponin I assay with sex-specific thresholds increased

69 resentation using a high-sensitivity cardiac troponin I assay.

70 (<5 ng/L) using the Abbott high-sensitivity troponin I assay.

71 reduction; P=0.0026), an effect supported by troponin-I assessment and histopathologic analysis (P=0.

72 Elevated high-sensitivity troponin is associated with increasing disease severity

73 s and still enabled the detection of cardiac troponin I at pg/mL concentrations in 10% serum without

74 Mean troponin I AUC values did not differ.

75 Troponin I blood levels were determined before and 2 to

76 Furthermore, we found that skeletal troponin I bound to troponin C tighter at pH 6.1 than at

77 d Pulmonary Embolism Severity Index, cardiac troponin I, brain natriuretic peptide, and lower limb ul

78 tely 6.7 when it is in complex with skeletal troponin I but not when it is bound to cardiac troponin

79 00 ng/L to 9800 +/- 7900 ng/L, P=0.047), and troponin I by 40% (171 000 +/- 151 000 ng/L to 103 000 +

80 Phosphorylation of troponin I by protein kinase A (PKA) reduces Ca(2+) sens

81 lecular recognition of model analyte cardiac troponin I by two antibody fragments brought the label m

82 linical biomarker of cardiac injury, cardiac troponin-I, by 52+/-17% (P=1.01x10(-2)).

83 elected sarcomere proteins (including TNNI3 [troponin I, cardiac muscle]) and ion channels (including

84 prevented matrix metalloproteinase-2-induced troponin I cleavage in rat hearts and improved contracti

85 s were shown to have elevated phosphorylated troponin I compared to slow-relaxing cells.

86 jury was defined as high-sensitivity cardiac troponin I concentration >99th centile of 16 ng/l in wom

87 oronary syndrome, a high-sensitivity cardiac troponin I concentration of less than 5 ng/L identified

88 Plasma cardiac troponin I concentration was measured with a high-sensit

89 dial injury (high-sensitivity plasma cardiac troponin I concentration, 4.3 ng/L [interquartile range,

90 were associated with higher high-sensitivity troponin I concentration.

91 sessed by serial measurements of the cardiac troponin I concentration.

92 .001), 27% of participants with postexercise troponin I concentrations >0.040 ug/L experienced an end

93 tive patients (n=2122) with elevated cardiac troponin I concentrations (>/=0.05 microg/L) at a tertia

94 ischemia, and an increase in plasma cardiac troponin I concentrations (1.4 [0.8-2.5] versus 3.0 [1.7

95 sted for an association between postexercise troponin I concentrations above the 99(th) percentile (>

96 xamined the association between postexercise troponin I concentrations and clinical outcomes in long-

97 High-sensitivity troponin I concentrations determined at presentation to

98 We measured cardiac troponin I concentrations in 725 participants (61 [54-69

99 e studies measuring high-sensitivity cardiac troponin I concentrations in patients with suspected acu

100 Troponin I concentrations increased after walking (P<.00

101 For example, high-sensitivity troponin I concentrations of less than 6 ng per liter an

102 Baseline troponin I concentrations were >0.040 ug/L in 9 particip

103 Cardiac troponin I concentrations were less than 5 ng/L at prese

104 ge, sex, and paired high-sensitivity cardiac troponin I concentrations, was trained on 3,013 patients

105 ion, stroke, or heart failure), and baseline troponin I concentrations.

106 genes, such as MYH (myosin heavy chain) and troponin I, consistent with its depressive effects on co

107 ease, the relationship between cTnT, cardiac troponin I, creatine kinase (CK), CK-myocardial band lev

108 including age, sex, and admission levels of troponin I, creatine kinase, and N-terminal pro-brain na

109 atriuretic peptide, hs-TnI (high-sensitivity troponin I), CRP (C-reactive protein), GDF-15 (growth di

110 (AMI) when used in combination with cardiac troponin I (cTnI) <99 th percentile and a nondiagnostic

111 cific markers for cardiac injury are cardiac troponin I (cTnI) and cardiac troponin T (cTnT) which ha

112 KA-site dependent phosphorylation of cardiac troponin I (cTnI) and phospholamban (PLN).

113 clear whether cardiac troponin T (cTnT) and troponin I (cTnI) are equivalent measures of risk in thi

114 Practice guidelines regard cTnT and cardiac troponin I (cTnI) as equally sensitive and specific for

115 metrics of a novel high-sensitivity cardiac troponin I (cTnI) assay for this purpose.

116 Ps in the enhancement of LSPR assay, cardiac troponin I (cTnI) for myocardial infarction diagnosis wa

117 Cardiac troponin I (cTnI) geometric mean decreased by 34% in the

118 The cardiac isoform of troponin I (cTnI) has a unique 31-residue N-terminal reg

119 (anti-cTnI) to detect cardiac marker antigen Troponin I (cTnI) in blood based on fluorescence resonan

120 monophosphorylates Ser(23) of human cardiac troponin I (cTnI) in isolation and in the trimeric tropo

121 During beta-adrenergic stimulation, cardiac troponin I (cTnI) is phosphorylated by protein kinase A

122 Both tobacco smoking and circulating cardiac troponin I (cTnI) levels are associated with the risk of

123 pertrophic cardiomyopathy-associated cardiac troponin I (cTnI) mutations, R146G and R21C, are located

124 ns revealed site-specific changes in cardiac Troponin I (cTnI) phosphorylation, as well as a unique d

125 coincided with a similar increase in cardiac troponin I (cTnI) protein, the established marker for he

126 The cardiac troponin I (cTnI) R145W mutation is associated with rest

127 The cardiac troponin I (cTnI) R21C (cTnI-R21C) mutation has been lin

128 rt effluents to demonstrate reduced card-iac troponin I (cTnI) release from ischemic rat hearts perfu

129 Cardiac troponin I (cTnI) was measured by using a novel, high-se

130 competitive binding assay to detect cardiac Troponin I (cTnI) was used as an example to demonstrate

131 ensitive and label-free detection of cardiac troponin I (cTnI), a biomarker for diagnosis of acute my

132 chment and comprehensive analysis of cardiac troponin I (cTnI), a gold-standard cardiac biomarker, di

133 ype natriuretic peptide (NT-proBNP), cardiac troponin I (cTnI), and fibrinogen- were rapidly (5 min)

134 argets the N-terminus (Ser-23/24) of cardiac troponin I (cTnI), cardiac myosin-binding protein C (cMy

135 In myofilaments PKA targets troponin I (cTnI), myosin binding protein-C (cMyBP-C) an

136 titin, myosin-binding protein-C and cardiac troponin I (cTnI), we sought to define if phosphorylatio

137 the ultrasensitive immunosensing of Cardiac Troponin I (cTnI).

138 sensitive detection of the cardiac biomarker troponin I (cTnI).

139 label-free detection of a cardiac biomarker: Troponin I (cTnI).

140 ies of monoclonal antibodies against cardiac troponin I (cTnI).

141 and interacts with the actomyosin inhibitory troponin I (cTnI).

142 rapid and simultaneous screening of cardiac Troponin-I (cTnI) and cardiac-Troponin-T (cTnT) in a poi

143 rdiac myosin binding protein C (cMyBP-C) and troponin-I (cTnI) are prominent myofilament targets of P

144 he detection performance of cardiac-specific troponin-I (cTnI) concentration levels in serum samples.

145 The cardiac Troponin-I (cTnI) is one of the subunits of cardiac trop

146 With application of a low troponin I cutoff value of 6 ng/L, the rule-out algorith

147 tion, matrix metalloproteinase activity, and troponin I degradation after reperfusion.

148 Circulating troponin is detectable in over 90% of patients with acut

149 measurement unit, to carry out quantitative troponin I detection in serum samples with < 2microl sam

150 w concentrations of high-sensitivity cardiac troponin I determined on presentation to the emergency d

151 Exercise-induced troponin I elevations above the 99(th) percentile after

152 olled and serial echocardiograms and cardiac troponin I evaluations were performed.

153 r high-sensitivity (hs-TnI) and conventional troponin I (EXL-LOCI and RXL) assessment.

154 e efficacy data (n = 322), was the change in troponin I from baseline at 16 and 24 h after PCI.

155 We discuss a current concept of cardiac troponin I function in the A-band region of the sarcomer

156 en small amounts of myocardial injury (e.g., troponin I >0.03 to 0.09 ng/ml; n = 455; 16.6%) were sig

157 .24; p < 0.001) while greater amounts (e.g., troponin I >0.09 ng/dl; n = 530; 19.4%) were significant

158 Results Elevated baseline troponin I (> 40 ng/L) and T (> 14 ng/L), occurring in 5

159 Per cryo-electron microscopy, each troponin is highly extended and contacts both tropomyosi

160 inistration-cleared high-sensitivity cardiac troponin I (hs-cTnI) assays.

161 al infarction using high-sensitivity cardiac troponin I (hs-cTnI) have been identified.

162 in T (hs-cTnT), and high-sensitivity cardiac troponin I (hs-cTnI) were determined in plasma samples o

163 uartiles of BNP and high-sensitivity cardiac troponin I (hs-cTnI) were included in adjusted models.

164 seline and 8 weeks: high-sensitivity cardiac troponin I (hs-cTnI), N-terminal pro-B-type natriuretic

165 ctive was to validate a new high-sensitivity troponin I (hs-TnI) assay in a clinical protocol for ass

166 High-sensitivity cardiac troponin I (hs-TnI) levels at baseline were assessed in

167 High-sensitivity troponin-I (hs-TnI) measurement improves risk assessment

168 of single-molecule counting high-sensitivity troponin I (hsTnI) (normal range <6 ng/l) among outpatie

169 between changes in high-sensitivity cardiac troponin I (hsTnI) and cardiovascular outcomes.

170 We measured high-sensitivity cardiac troponin I (hsTnI) in 12 956 and BNP in 11 076 participa

171 uretic peptide (NT-proBNP), high-sensitivity troponin I (hsTnI), soluble (s)ST2, and galectin-3 from

172 sarcomere and potential signaling to cardiac troponin I in a network involving the ends of the thin f

173 ces when electrochemically detecting cardiac troponin I in complex biological samples.

174 ssay for the detection of the cardiac marker troponin I in human serum using sample volumes of ~1 muL

175 the performance of high-sensitivity cardiac troponin I in those with and without renal impairment (e

176 and markedly reduced elaboration of cardiac troponin-I in coronary effluent during ESHP.

177 atures correlated with elevations in cardiac Troponin-I in severely injured hearts during EVHP, and m

178 lectrode arrays for the detection of cardiac troponin-I in the early diagnosis of myocardial infarcti

179 of cardiac biomarkers (myoglobin and cardiac troponin I) in the clinically significant sensing range

180 was positively related (P < .001) to peak of troponin I, inflammatory biomarkers, area at risk, and i

181 The G526D substitution in troponin I interacting kinase, with the most deleterious

182 Investigation of troponin I-interacting kinase (TNNI3K) as a potential ta

183 A series of cardiac troponin I-interacting kinase (TNNI3K) inhibitors arisin

184 enetic loss or pharmacological inhibition of troponin I-interacting kinase.

185 iew how phosphorylation signaling to cardiac troponin I is integrated, with parallel signals controll

186 etween CiMRF and an essential E-box of Ciona Troponin I is required for the expression of this muscle

187 Troponin-I is detected in 98.5% and elevated in 9.2% of

188 ivalent to Ser200 in mouse) of cTnI (cardiac troponin I) is significantly hyperphosphorylated, and in

189 transgenic mouse hearts expressing the fetal troponin I isoform, (ssTnI) to be protected from ischemi

190 lar mechanism(s) of the mutant human cardiac troponin I (K206I), we tested the Ca(2+) dependence of t

191 ion between postoperative myocardial injury (troponin I level >0.06 mug/L) and all-cause 30-day morta

192 y, coupled with reduced infarct size, plasma troponin I level, and apoptosis.

193 mine matrix metalloproteinase-2 activity and troponin I level.

194 d patients, those who died had elevated peak troponin I levels (0.27 versus 0.02 ng/mL) and more prim

195 Circulating troponin I levels after ISO were elevated, further docum

196 doxycycline did not change tissue or plasma troponin I levels at 10 minutes reperfusion.

197 Maternal CRP and cord troponin I levels did not differ between the groups.

198 Elevated donor troponin I levels in the setting of preserved left ventr

199 Similarly, a rule-in algorithm based on troponin I levels provided a high positive predictive va

200 tended to have worse prognoses with elevated troponin I levels than those without them (moderate SOE)

201 Presence of elevated troponin I levels was also significantly associated with

202 Cardiac troponin I levels were normal in all patients, whereas C

203 re to assess the prognostic value of cardiac troponin I levels, measured with a new high-sensitivity

204 y and interleukin-6, C-reactive protein, and troponin I levels.

205 nd was observed for long-term mortality with troponin I (low SOE), but less evidence was found for lo

206 ied HEART score </=3 (which includes cardiac troponin I <0.04 ng/mL at 0 and 3 hours) were randomized

207 Compared with 7% with postexercise troponin I <=0.040 ug/L (log-rank P<.001), 27% of partic

208 ps used to immobilise antibodies for cardiac troponin I marker.

209 -pro-B-type natriuretic peptide (NT-proBNP); troponin I; matrix metalloproteinase (MMP)-2; urokinase

210 rocardiogram determined and high-sensitivity troponin I measured at presentation.

211 We assessed whether plasma troponin I measured by a high-sensitivity assay (hs-TnI)

212 (n=1218) underwent high-sensitivity cardiac troponin I measurement at presentation and 3 and 6 or 12

213 -sensitivity troponin T and high-sensitivity troponin I measurements.

214 Density attributable to the troponin-I mobile regulatory domain was positioned where

215 ured in transgenic mice expressing a cardiac troponin I mutation (R145G).

216 eviously identified that HCM causing cardiac troponin I mutation Gly203Ser (cTnI-G203S) is associated

217 between markers of myocardial injury (plasma troponin I, myocardial lactate) and functional recovery

218 cardial injury (plasma and myocardial tissue troponin I; myocardial lactate) and oxidative stress (li

219 score and clinical outcomes based on cardiac troponin I, N-terminal pro-B-type natriuretic peptide, a

220 Cardiac troponin I, N-terminal pro-B-type natriuretic peptide, a

221 February 27, 2020, and April 12, 2020, with troponin-I (normal value <0.03 ng/ml) measured within 24

222 cholesterol ratio, high-sensitivity cardiac troponin I, NT-proBNP (N-terminal pro-B-type natriuretic

223 mined the concentrations of high-sensitivity troponin I or high-sensitivity troponin T at presentatio

224 ion of specific cardiac biomarkers including troponin I or T (cTnI or cTnT), creatine kinase-MB (CK-M

225 Conclusion Elevated troponin I or T before trastuzumab is associated with in

226 developed to integrate the high-sensitivity troponin I or troponin T concentration at emergency depa

227 Elevated levels of troponin I or troponin T were associated with higher ris

228 as indicated by a positive test for cardiac troponin I or troponin T.

229 nditional cMLCK gene ablation did not affect troponin-I or myosin-binding protein-C phosphorylation i

230 eased base deficit (P = 0.003), (3) elevated Troponin I (P = 0.04), and histological evidence of kidn

231 ulation of thin filament activity by cardiac troponin I phosphorylation as an integral and adaptive m

232 e two groups revealed significantly elevated troponin I phosphorylation in fast-relaxing cells.

233 ACTC E361G myofibrils did not depend on the troponin I phosphorylation level (EC50 P/unP = 0.88 +/-

234 w linear phase, tLIN, was increased when the troponin I phosphorylation level was reduced from 1.02 t

235 Our results confirm that troponin I phosphorylation specifically alters the Ca(2+

236 ardiac myosin binding protein C (MyBP-C) and troponin I phosphorylation to accelerate pressure develo

237 We additionally measured human cardiac troponin I protein in 9 human plasma samples, and showed

238 rom nebulin, titin, myosin heavy chains, and troponin I proteins, those showing the highest number of

239 r zone mass (r=0.84, P<0.0001) and with peak troponin I (r=0.76, P<0.001); it also correlated with se

240 The sensitivity and specificity of troponin I ranged from 43% to 94% and from 48% to 100%,

241 ptoms, ECG ST-segment deviation, and cardiac troponin I release after elective PCI and reduced the ma

242 on was reflected by a 35% reduction of serum troponin I release.

243 to 1.30; P=0.72), nor did the area under the troponin I-release curve (102 ngxhour per milliliter and

244 diac troponin T (cTnT) and sensitive cardiac troponin I (s-cTnI) were also significantly higher in is

245 ce expressing a pseudophosphorylated cardiac troponin I (S23D and S24D; TnI-PP).

246 Periprocedural cardiac troponin I significantly increased (F=3.64; P=0.01334) a

247 Troponin I specific antibody and aptamer are used as rec

248 cein covalently bound to Cys-133 of skeletal troponin I (sTnI).

249 nsically disordered C-terminal domain of the troponin I subunit (TnIC) of the cardiac troponin comple

250 rmational changes in flexible regions of the troponin I subunit.

251 teraction between the Ca(2+) ion and cardiac troponin I subunit.

252 ude but decreased phosphorylation of cardiac troponin I, suggesting direct effects on the contractile

253 domain of cTnC, followed by cTnC binding the troponin I switch peptide (TnISW).

254 ivation of force, perhaps by controlling the troponin I switching mechanism of striated muscle contra

255 SA for the detection of a cardiac biomarker, troponin I-T-C (Tn I-T-C) complex, was developed.

256 periprocedural myocardial infarction (PPMI) (troponin I/T >3x upper limit of normal) was 13.9% and as

257 ated with both CK-MB-defined (p = 0.026) and troponin I/T-defined PPMI (p = 0.036).

258 High-sensitivity cardiac troponin I testing is widely used to evaluate patients w

259 es afforded higher sensitivities for cardiac troponin I than those prepared by the chemisorption of a

260 Cardiac troponin is the preferred biomarker for diagnosing myoca

261 In parallel tests, cardiac myoglobin and troponin I, the AMI biomarkers, were determined in each

262 has been applied to the detection of cardiac Troponin I, the gold standard biomarker for the diagnosi

263 I that could be utilized in combination with troponin-I, the conventional marker of cardiac injury, t

264 To evaluate the performance of a cardiac troponin I threshold of 5 ng/L at presentation as a risk

265 el lacking protein kinase A-phosphorylatable troponin I (TnI) and MyBP-C, we examined in vivo haemody

266 Two key myofilaments proteins, troponin I (TnI) and myosin binding protein-C (MyBP-C),

267 , TTR, B-type natriuretic peptide (BNP), and troponin I (TnI) concentrations and electrocardiographic

268 Autoimmune response to cardiac troponin I (TnI) induces inflammation and fibrosis in th

269 Troponin I (TnI) is the molecular switch of the sarcomer

270 aseline and change in contemporary sensitive troponin I (TnI) levels predicts coronary heart disease

271 ronary CT angiography after single or serial troponin I (TnI) measurement, depending on time of prese

272 ants sharing a previously unknown variant in troponin I (TnI) were identified.

273 onsists of three subunits, troponin C (TnC), troponin I (TnI), and troponin T (TnT).

274 edominant discriminators in serum by LR were troponin I (TnI), B-type natriuretic peptide (BNP), and

275 icin and trastuzumab therapy: ultrasensitive troponin I (TnI), high-sensitivity C-reactive protein (C

276 rogressive increase in expression of cardiac troponin I (TnI), with a concurrent decrease in slow ske

277 POINTS: Mutations in genes encoding cardiac troponin I (TNNI3) and cardiac troponin T (TNNT2) caused

278 Cardiac troponin I (TNNI3) gene mutations account for 3% of hype

279 rcomeric mutations in genes encoding cardiac troponin I (TNNI3p.98truncation ) and cardiac troponin T

280 217del mutation showed reduced expression of troponin I to 39% and 51%, troponin T to 64% and 53%, an

281 he K206I mutation impairs the ability of the troponin I to inhibit ATPase activity in the absence of

282 binding of calcium and the mobile segment of troponin-I to troponin-C were described by a simple kine

283 which were positive for the cardiac markers troponin I, troponin T, myosin heavy chain, and connexin

284 require only changes in myosin affinity and troponin I/troponin C affinity.

285 nsitivity assay for the detection of cardiac troponin I using electrical double layer gated high fiel

286 ac troponins, cardiac troponin T and cardiac troponin I, using sensitive methods, defines a true refe

287 ction fraction (>/=50%) and where peak donor troponin I values were available.

288 e entire cohort into 3 groups based on donor troponin I values: <1 ng/mL (n=7812), 1 to 10 ng/mL (n=2

289 h to the first quintiles of high-sensitivity troponin I was 1.61 (95% CI, 1.11-2.32; p trend = 0.003)

290 The additional effect of microemboli on troponin I was demonstrated at 68-72 hours (3.2 ng/mL +/

291 as decreased, whereas PKA phosphorylation of troponin I was increased, explaining the decoupling betw

292 ry was found in 315 of 1627 patients in whom troponin I was measured (19%).

293 Detectable high-sensitivity troponin I was present in 94% of patients; 38% of patien

294 Peak troponin I was reduced by 23.8% (p = 0.05) and area unde

295 d myocardial blush grade), and serum cardiac troponin I were assessed before and after PCI.

296 d and maternal CRP, cord NT-proBNP, and cord troponin I were evaluated using multiplex assays.

297 e-2, Ser16 in phospholamban, and Ser23/24 in troponin-I were hyperphosphorylated in SA mice, whereas

298 rder transitions in the C-terminal domain of troponin I, which have important implications in cardiac

299 o-adjusted geometric mean percent changes in troponin I with inclacumab 20 mg/kg were -24.4% at 24 h

300 drome outcomes, we measured high-sensitivity troponin I within 24 hours of intubation.