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

3 ery and between myocardial tissue and plasma troponin I.

4 ain natriuretic peptide and high-sensitivity troponin I.

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

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

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

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

9 , which is replaced by an alanine in cardiac troponin I.

10 response element binding protein and cardiac troponin I.

11 area-under-the-curve for creatine kinase or 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 d significant myocardial injury (median peak troponin I, 138 ng/dL [limits, 58-356 ng/dL]) and sustai

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

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

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

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

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

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

22 % (95% CI, 57.5%-68.9%).The high-sensitivity troponin I algorithm ruled out 1205 (54.2%) with a sensi

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

24 Cardiac troponin is an independent predictor of cardiovascular m

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

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

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

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

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

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

31 e TnT (ssTnT) together with cardiac forms of troponin I and myosin as determined using immunoblotting

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

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

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

35 We evaluated the prevalence of elevated troponin I and N-terminal pro-B-type natriuretic peptide

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

37 Elevations of troponin I and NT-proBNP are common in patients with AF

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

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

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

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

42 , or -3 and reconstituted with human cardiac troponin I and troponin C (HCTnI.TnC) complex showed a d

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

44 , along with contractile regulatory proteins troponin I and troponin T, is reduced during the first 3

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

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

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

48 recent coronary occlusion (including cardiac troponin I) and their respective contribution.

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

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

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

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

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

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

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

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

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

60 c MRI (CMRI; day 3+/-1), creatine kinase and troponin I area-under-the-curve, and severity of wall mo

61 rdiography, and 0 + 2 h values of laboratory troponin I as the sole biomarker.

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

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

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

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

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

69 ion for such patients, the dosage of cardiac troponin I at admission could not help in the decision o

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

71 Mean troponin I AUC values did not differ.

72 Troponin I blood levels were determined before and 2 to

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

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

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

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

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

78 evaluate if an early measurement of cardiac troponin I can help to detect a recent coronary occlusio

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

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

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

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

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

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

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

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

87 High-sensitivity troponin I concentrations determined at presentation to

88 Protection was confirmed by reduced serum troponin I concentrations in patients with RIPC versus c

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

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

91 Patients were stratified based on troponin I concentrations: <0.010 mug/L, n=2663; 0.010 t

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

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

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

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

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

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

98 esidues of gamma2 as bait identified cardiac troponin I (cTnI) as a putative interactor.

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

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

101 emonstrated that AMPK phosphorylates cardiac troponin I (cTnI) at Ser-150 in vitro.

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

103 Cardiac troponin I (cTnI) functions as the molecular switch of t

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

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

106 The regulatory function of cardiac troponin I (cTnI) involves three important contiguous re

107 Phosphorylation of cardiac troponin I (cTnI) is critical in modulating contractilit

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

109 The R21C substitution in cardiac troponin I (cTnI) is the only identified mutation within

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

138 in the highest and 0.84%/year in the lowest troponin I group (hazard ratio [HR], 1.99 [95% CI, 1.17-

139 ear in the highest and 1.04%/year the lowest troponin I group (HR, 4.38 [95% CI, 3.05-6.29]; P<0.0001

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

141 s on troponin C and of histidine on skeletal troponin I (His-130).

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

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

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

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

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

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

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

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

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

151 ferentiation factor-15, and high-sensitivity troponin I in 3428 participants (mean age, 59 years; 53%

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

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

154 s occurred on individual residues of cardiac troponin I in heart failure, likely reflecting an imbala

155 ximately 25% reduction in phosphorylation of troponin I in HTN patients (P<0.05).

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

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

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

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

160 ry data, 14 phosphorylation sites on cardiac troponin I, including 6 novel residues (S4, S5, Y25, T50

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

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

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

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

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

166 The isoform-specific response of troponin I is dictated by a single histidine, which is r

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

168 Human cardiac troponin I is known to be phosphorylated at multiple ami

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

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

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

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

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

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

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

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

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

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

179 First, blood cardiac troponin I levels at admission were analyzed to assess t

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

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

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

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

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

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

186 diocirculatory (norepipnehrine requirements, troponin I levels) dysfunction was attenuated in the sim

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

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

189 INF/AAR by 37% (p < 0.001 vs. VEH) and serum troponin-I levels from 41 +/- 4 ng/ml to 25 +/- 4 ng/ml

190 percentage of the area at risk and by serum Troponin-I levels.

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

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

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

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

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

196 tudinal myocardial strain and ultrasensitive troponin I measured at the completion of anthracyclines

197 tudinal myocardial strain and ultrasensitive troponin I measured at the completion of anthracyclines

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

199 diac arrest patients, isolated early cardiac troponin I measurement is modestly predictive of a recen

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

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

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

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

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

205 Ultrasensitive troponin I, N-terminal pro-B-type natriuretic peptide, a

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

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

208 moking and epinephrine initial dose, cardiac troponin I (odds ratio 3.58 [2.03-6.32], p < .001) and S

209 Cardiac troponin (I or T) is the biomarker of choice for the dia

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

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

212 difications representing different proteins (troponin I or troponin T), modifications (missense mutat

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

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

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

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

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

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

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

220 Troponin I phosphorylation was lower in both patient gro

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

222 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

223 gy, the restrictive cardiomyopathy mutation, troponin I R192H, and ischemia-induced truncation of tro

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

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

226 ld and at approximately 30 J causes 58% less troponin I release than the truncated exponential biphas

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

228 firmed by a significant reduction of cardiac troponin-I release and less myocardial apoptosis in mice

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

230 I R192H, and ischemia-induced truncation of troponin I (residues 1-192) increased the Ca(2+) sensiti

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

232 omain novel phosphorylation sites of cardiac troponin I (S165, T180, S198).

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

234 cated in the N-terminal extension of cardiac troponin I (S4, S5, Y25), an increase in phosphorylation

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

236 soluble fms-like tyrosine kinase receptor-1, troponin I, soluble toll-like receptor-2, creatinine, an

237 Troponin I specific antibody and aptamer are used as rec

238 After adjustment for cardiac troponin I, ST-segment deviation, age, sex, diabetes, sm

239 ic properties of MPO compared with sensitive troponin I (sTNI) in patients admitted to the emergency

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

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

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

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

244 s associated with reduced phosphorylation of troponin I, suggesting decreased phosphorylation of prot

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

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

247 c Ca(2)(+) and subsequent recognition of the Troponin I switch peptide.

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

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

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

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

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

253 Cardiac troponin is the preferred biomarker for diagnosing myoca

254 fetal Tn environment, (cTnT1 + slow skeletal troponin I), the single (cTnT1-DeltaN110) and double (cT

255 In the adult Tn environment (cTnT3 + cardiac troponin I), the single cTnT3-DeltaN100 and cTnT3-DeltaE

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

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

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

259 The optimum cardiac troponin I threshold was determined at 4.66 ng.mL(-1) (s

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

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

262 Troponin I (TnI) and myosin heavy chain (MHC) are two co

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

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

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

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

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

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

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

270 urface, to which a helix of another subunit, troponin I (TnI), binds.

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

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

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

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

275 217del mutation showed reduced expression of troponin I to 39% and 51%, troponin T to 64% and 53%, an

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

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

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

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

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

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

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

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

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

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

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

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

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

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

290 Six hours after shock, troponin I was significantly less for the ascending-ramp

291 Serum B-type natriuretic peptide and troponin I were also assessed at the same time points.

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

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

294 We also found that Ser23/24 residues of troponin I were hypophosphorylated in SOCS3 cKO hearts b

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

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

297 roke were independently related to levels of troponin I with 2.09%/year in the highest and 0.84%/year

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

299 c muscle can be reduced by replacing cardiac troponin I with its skeletal or neonatal counterparts.

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