ライフサイエンスコーパス: ST

1 ST Direct was evaluated using 1,084 prospectively collec

2 ST Direct was found to be 93.2% sensitive and 99.3% spec

3 ST progressively disabled a host mechanism of protection

4 ST protein (STP) hydrolysates were generated with differ

5 ST- and LT-IH treated rats exhibited hypertension, irreg

6 ST-elevation myocardial infarction and sinus venous trac

7 STs also exhibit poor attentional performance, relative

8 The increase of type-1 ST-segment elevation correlated with AES expansion (r=0.

9 212-strain validation set that included 109 STs other than STc648, from phylogroups A, B1, B2, C, D,

10 Among 2290 ST-segment-elevation myocardial infarction patients, 36.

11 esistance was associated with NG-STAR ST-26, ST-90, ST-91, ST-97, ST-150, and ST-158 (n = 196; 98.0%)

12 Of 278 ST patients, 179 (64%) were skin test eligible; 43 (24%)

13 All isolates of NG-STAR ST-42, ST-43, ST-63, ST-81, and ST-160 (n = 106) were susceptib

14 All isolates of NG-STAR ST-42, ST-43, ST-63, ST-81, and ST-160 (n = 106) were susceptible to a

15 METHODS AND Hospitals (n=167 with 23 498 ST-segment-elevation myocardial infarction patients) wer

16 thromycin was associated with NG-STAR ST-58, ST-61, ST-64, ST-79, ST-91, and ST-139 (n = 156; 92.3%);

17 in was associated with NG-STAR ST-58, ST-61, ST-64, ST-79, ST-91, and ST-139 (n = 156; 92.3%); decrea

18 mplete Revascularization), we randomized 627 ST-segment-elevation myocardial infarction patients to f

19 All isolates of NG-STAR ST-42, ST-43, ST-63, ST-81, and ST-160 (n = 106) were susceptible to all four

20 associated with NG-STAR ST-58, ST-61, ST-64, ST-79, ST-91, and ST-139 (n = 156; 92.3%); decreased sus

21 Of 7086 patients, 773 ST/LV patients traveled </=6.3 (median 3.2) miles to cen

22 ted with NG-STAR ST-58, ST-61, ST-64, ST-79, ST-91, and ST-139 (n = 156; 92.3%); decreased susceptibi

23 losporins was associated with NG-STAR ST-90, ST-91, and ST-97 (n = 162; 94.2%); and ciprofloxacin res

24 ce was associated with NG-STAR ST-26, ST-90, ST-91, ST-97, ST-150, and ST-158 (n = 196; 98.0%).

25 associated with NG-STAR ST-26, ST-90, ST-91, ST-97, ST-150, and ST-158 (n = 196; 98.0%).

26 ted with NG-STAR ST-26, ST-90, ST-91, ST-97, ST-150, and ST-158 (n = 196; 98.0%).

27 of persistent T2 hyperintensity after acute ST-segment-elevation myocardial infarction (STEMI) is un

28 rognostic utility in patients after an acute ST-segment-elevation myocardial infarction (STEMI).

29 For patients presenting with an acute ST-segment-elevation myocardial infarction, the most eff

30 reatment, 533 sustained ACS (excluding acute ST-segment-elevation myocardial infarction).

31 ommon dominant finding adjudicated for acute ST was uncovered struts (66.7% of cases); for subacute S

32 and very late ST, whereas the risk of acute ST was similar.

33 tionwide registries French Registry of Acute ST-Elevation or Non-ST-Elevation Myocardial Infarction (

34 o determine if timing of cell delivery after ST-segment-elevation myocardial infarction affects recov

35 assessment of myocardial injury early after ST-segment-elevation myocardial infarction.

36 ardiac magnetic resonance (MR) imaging after ST-segment-elevation myocardial infarction (STEMI).

37 ival for overweight and obese patients after ST-segment-elevation myocardial infarction (STEMI) has b

38 stent with uptake/translocation alterations, STs demonstrated a reduced ability to support cortical A

39 Although ST period patients did not have increased odds of penici

40 An ST 90 degrees -X quartz Love wave device with a layer of

41 eme uses sequences of 7 genes to generate an ST, which results in a powerful tool for inferring the p

42 t elevated in patients with RA prescribed an ST (0.96).

43 s highest in patients with PsO prescribed an ST (2.23) and PsA with an ST (2.11).

44 PsO prescribed an ST (2.23) and PsA with an ST (2.11).

45 was highest among patients with PsO with an ST (2.62) and PsA without an ST (3.15).

46 ut ST 1.38; with ST 1.67), and RA without an ST (1.49) but not elevated in patients with RA prescribe

47 ith PsO with an ST (2.62) and PsA without an ST (3.15).

48 elevation acute coronary syndrome (14%) and ST-segment elevation myocardial infarction (11%).

49 STAR ST-26, ST-90, ST-91, ST-97, ST-150, and ST-158 (n = 196; 98.0%).

50 s of NG-STAR ST-42, ST-43, ST-63, ST-81, and ST-160 (n = 106) were susceptible to all four antimicrob

51 -STAR ST-58, ST-61, ST-64, ST-79, ST-91, and ST-139 (n = 156; 92.3%); decreased susceptibility to cep

52 as associated with NG-STAR ST-90, ST-91, and ST-97 (n = 162; 94.2%); and ciprofloxacin resistance was

53 Both APP and ST-when completed-increased the use of penicillin and ce

54 interpretation, appropriate monitoring, and ST-segment monitoring when indicated), the intervention

55 Our new method nala captured NL and ST by combining conditional random fields with word embe

56 ing analyses of patients with large anterior ST-segment-elevation myocardial infarctions, bone marrow

57 A total of 16 patients with anterior ST-segment-elevation MI successfully treated by primary

58 versus placebo in 120 patients with anterior ST-segment-elevation myocardial infarctions resulting in

59 20% of MI cases and presented more often as ST-segment elevation MI versus MI not related to a stent

60 ikely to include high-risk features, such as ST-segment-elevation myocardial infarction, cardiogenic

61 The Shiga Toxin Direct molecular assay (ST Direct) relies on nucleic acid amplification and soli

62 ence in amino acid sequence identity between STs (i.e., 59%-61% median identity), on par with observa

63 ontain a C-terminal KDEL-like sequence, bind ST-FRB in the Golgi, and are transported together back t

64 cells were comparable to levels exhibited by ST-246-treated wild-type cells.

65 during the initial survey; 1 student carried ST-9069 in the second and third surveys.

66 patients with cardiogenic shock complicating ST-segment-elevation myocardial infarction, there may be

67 For comparison, a known antiviral compound, ST-246, was used in our experiments, demonstrating that

68 Using a comprehensive ST-segment-elevation myocardial infarction registry, we

69 ND In this prospective study, 88 consecutive ST-segment-elevation myocardial infarction patients were

70 METHODS AND Consecutive ST-segment-elevation myocardial infarction patients from

71 Contemporary ST-segment-elevation myocardial infarction management in

72 which is correlated with the degree of coved ST-elevation.

73 ace tension (ST, 25.4mN/m) than the critical ST (35.2mN/m) of banana peels, and exhibited good wettab

74 ackground absence of cpsA reduces and delays ST biosynthesis decreasing the expression of ST genes.

75 In the absence of veA (DeltaveA), ST biosynthesis is blocked.

76 O-PCI) in patients with multivessel disease, ST-segment-elevation myocardial infarction, and cardioge

77 The percentage of proteins unique to each ST ranges from 6.2% to 20.5%, greatly exceeding the diff

78 patency, the quantitative intracoronary ECG ST-segment elevation, and angina pectoris during the sam

79 Rats exposed to either ST- or LT-IH exhibited hypertension, irregular breathing

80 ical trial, we enrolled patients with either ST-segment elevation myocardial infarction (STEMI) or no

81 -wave onset to R-peak, R-peak to R-wave end, ST-segment, T-wave onset to T-peak, and T-peak to T-wave

82 ral delivery of the heat-stable enterotoxin (ST), an exogenous GUCY2C ligand, opposed RIGS, a process

83 We found higher F ST using microsatellites, but that RAD-Seq-based estimat

84 t between 0.02-0.07 for MCC, 4.18-21.47% for ST and 0.013-0.131 for AUC.

85 ive sample of patients in China admitted for ST-segment-elevation myocardial infarction in 2001, 2006

86 ent analysis, the associated risk of HPR for ST was similar in both sexes.

87 imary percutaneous coronary intervention for ST-segment elevation myocardial infarction (STEMI).

88 Routine thrombus aspiration during PCI for ST-segment-elevation myocardial infarction did not impro

89 percutaneous coronary intervention (PCI) for ST-segment elevation myocardial infarction (STEMI) may n

90 an alternative to mechanical reperfusion for ST-segment elevation myocardial infarction (STEMI) in se

91 ctive value of ST, resource requirements for ST, and the benefits of early treatment, data do not sup

92 , natural and anthropogenic) responsible for ST variability are studied from Coupled Model Inter-comp

93 The increased risk for ST associated with BVS was concordant across the early (

94 elop and validate a CMR-based risk score for ST-segment-elevation myocardial infarction patients.

95 Findings were similar for ST-segment elevation myocardial infarction (ATE coeffici

96 ses becoming normalized during recovery from ST- but not from LT-IH.

97 effects were normalized after recovery from ST-IH but not from LT-IH.

98 three stereo wave imaging systems to gather ST records of the sea surface elevation, which were coll

99 here were 294 (20%) women, and 846 (57%) had ST-segment elevation MI.

100 All presented with MI; 25.7% had ST-segment elevation MI, 74.3% had non-ST-segment elevat

101 Challenges to improving ST-segment elevation myocardial infarction (STEMI) care

102 antify the edema-based area-at-risk (AAR) in ST-segment elevation myocardial infarction (STEMI).

103 l Infarction], TASTE [Thrombus Aspiration in ST-Elevation Myocardial Infarction in Scandinavia], and

104 ognostic value over clinical risk factors in ST-segment-elevation myocardial infarction patients.

105 jection over India shows a sharp increase in ST under Representative Concentration Pathways (RCP) 8.5

106 on of major adverse cardiac events (MACE) in ST-segment-elevation myocardial infarction.

107 predictor of left ventricular remodeling in ST-segment-elevation myocardial infarction.

108 reserve-guided complete revascularization in ST-segment-elevation myocardial infarction patients with

109 marrow mononuclear cell (BM-MNC) therapy in ST-elevation acute myocardial infarction (STEMI) has no

110 tivation of cortical cholinergic activity in STs degrades top-down executive control over behavior, p

111 uptake nor translocation of CHTs occurred in STs.

112 djusting for multiple comparisons, including ST-elevation myocardial infarction (OR, 0.99; 95% CI, 0.

113 g with an acute coronary syndrome, including ST-segment-elevation myocardial infarction were enrolled

114 in the culprit artery (P=0.020), incomplete ST-segment resolution (P=0.037), and higher troponin (P=

115 emains to be seen to what extent these inter-ST differences persist at the intra-ST level.

116 farction has traditionally been divided into ST elevation or non-ST elevation myocardial infarction;

117 se inter-ST differences persist at the intra-ST level.

118 No correlation was found between J-ST point elevation and activation recovery intervals pro

119 In controls, there was minimal change in J-ST point elevation, conduction delay, or activation reco

120 eft ventricle, correlated to the degree of J-ST point elevation (Pearson R, 0.81; P<0.001).

121 Peak J-ST point elevation was calculated from the surface ECG a

122 (61.7%) and underexpansion (25.5%); for late ST, the most common dominant finding was uncovered strut

123 .4%) presented with early and late/very late ST, respectively.

124 severe restenosis (19.1%); and for very late ST, the most common dominant finding was neoatherosclero

125 In patients presenting very late ST, uncovered stent struts were a common dominant findin

126 higher risk of subacute, late, and very late ST, whereas the risk of acute ST was similar.

127 rosis and uncovered struts in late/very late ST.

128 after nitroglycerin administration with less ST-segment depression (P=0.003) and therefore myocardial

129 To test this, male STs and GTs were trained to self-administer cocaine usin

130 ks, partial NMR assignments, and JM mutants (ST(296)AA or T(304)A) investigated, confirm that the bac

131 ersensitivity reaction to BLs, with negative ST and positive DPT.

132 Non-ST-segment elevation acute coronary syndromes include un

133 (OR, 0.99; 95% CI, 0.96-1.03; P = .65), non-ST-elevation acute coronary syndrome (OR, 0.99; 95% CI,

134 s consisting of patients admitted with a non-ST-segment elevation acute coronary syndrome, we constru

135 0; 95% CI: -0.98 to 1.58; p = 0.637) and non-ST-segment elevation myocardial infarction (ATE coeffici

136 ment elevation myocardial infarction and non-ST-segment elevation myocardial infarction were consider

137 ry syndromes include unstable angina and non-ST-segment elevation myocardial infarction.

138 lder than 18 years with unstable angina, non-ST segment elevation myocardial infarction (NSTEMI) or S

139 syndrome (25%), which consisted of both non-ST-segment elevation acute coronary syndrome (14%) and S

140 cardial infarction (n=5996, 853 deaths), non-ST-segment-elevation myocardial infarction (n=5371, 901

141 by 9254 operators at 1538 hospitals for non-ST-segment-elevation myocardial infarction from 2009 to

142 e analysis of bivalirudin versus UFH for non-ST-segment-elevation myocardial infarction to date, biva

143 Most patients had non-ST-elevation acute coronary syndromes and complex lesion

144 % had ST-segment elevation MI, 74.3% had non-ST-segment elevation MI, and 8.9% had ventricular tachyc

145 orithm for rapid rule-out and rule-in of non-ST-segment elevation myocardial infarction using high-se

146 onally been divided into ST elevation or non-ST elevation myocardial infarction; however, therapies a

147 French Registry of Acute ST-Elevation or Non-ST-Elevation Myocardial Infarction (FAST-MI) 2005 (n=367

148 ected patients presenting with suspected non-ST-segment elevation myocardial infarction to the emerge

149 rkedly, particularly among patients with non-ST elevation myocardial infarction (NSTEMI).

150 tion, and presented more frequently with non-ST segment elevation acute coronary syndrome compared wi

151 ion DESs in randomized participants with non-ST-elevation acute coronary syndromes or stable angina a

152 ctive invasive strategy in patients with non-ST-segment elevation acute coronary syndrome (NSTE-ACS)

153 r the care and outcomes of patients with non-ST-segment elevation myocardial infarction (NSTEMI).

154 dial infarction and 87,915 patients with non-ST-segment elevation myocardial infarction, 88,542 (96.4

155 In patients with non-ST-segment-elevation myocardial infarction (NSTEMI) and

156 nger age categories and in patients with non-ST-segment-elevation myocardial infarction and stable an

157 ) in the United States for patients with non-ST-segment-elevation myocardial infarction and the compa

158 All urethral Nm isolates were nongroupable, ST-11 clonal complex (cc11), ET-15, and clustered togeth

159 r obstruction, which occurs in around 50% of ST-segment-elevation myocardial infarction patients post

160 n on the basis of the presence or absence of ST-segment elevation, a century-old technology.

161 ovalent synthetic oligosaccharide analogs of ST-5 CPS RU induced long-term memory and protective immu

162 After angiographic confirmation of ST, OCT imaging of the culprit vessel was performed with

163 bility of occurrence, also in the context of ST extreme value distributions, and we conclude that rog

164 without PCI or in those with a diagnosis of ST-segment elevation myocardial infarction (group by PCI

165 ST biosynthesis decreasing the expression of ST genes.

166 Magnitude of ST (J point) elevation in the type I BrS pattern is attr

167 (PPV) and negative predictive value (NPV) of ST for anaphylaxis related to HBAT and other botulinum a

168 NTS-CeA neurons received greater numbers of ST-related inputs compared to unlabelled NTS neurons, in

169 n-hospital reperfusion rates and outcomes of ST-segment elevation MI (STEMI) in renal transplant reci

170 of >/=2 years demonstrated a higher risk of ST and of TLF in patients treated with BVS compared with

171 provides better prognostic stratification of ST-segment-elevation myocardial infarction patients trea

172 ely 4% to 5%, a figure comparable to that of ST-segment-elevation myocardial infarction in the era of

173 letion of KDEL receptor prevents trapping of ST-FRB in the ER by rapamycin.

174 nary intervention (PCI) for the treatment of ST-segment-elevation myocardial infarction (STEMI) has b

175 , fatal outcomes, modest predictive value of ST, resource requirements for ST, and the benefits of ea

176 39 (n = 26; 6.8%), with greater diversity of STs in ILTCFs relative to the ACH.

177 The greater diversity of STs in ILTCFs suggests that the ecosystem in such settin

178 scoring model was developed and validated on ST-segment-elevation myocardial infarction cohorts from

179 elevation myocardial infarction (NSTEMI) or ST segment elevation myocardial infarction (STEMI), with

180 ation myocardial infarction (group by PCI or ST-segment elevation myocardial infarction interaction e

181 changes in circulating strains, particularly ST-269 clonal complex strains.

182 port delaying HBAT administration to perform ST in a mass botulinum toxin exposure.

183 Dynamic changes in post-ST-segment-elevation MI edema highlight the need for sta

184 h BVS had a higher risk of definite/probable ST compared with patients treated with EES (odds ratio,

185 ndings support efforts to implement regional ST-segment-elevation myocardial infarction networks focu

186 fusions in the NF-kappaB subunit gene RELA (ST-EPN-RELA), and a smaller number involve fusion of the

187 e-, erythromycin-, and clindamycin-resistant ST first identified in Minnesota, which is considered to

188 eA genetic background cpsA deletion restores ST production, in a veA wild-type background absence of

189 nce similarity searching before an isolate's ST can be determined.

190 non-outbreak-related strains within the same ST.

191 Under RCP2.6 emission scenarios, ST increases up to the year 2050 and decreases afterward

192 lt C57BL/6 mice with S. pneumoniae serotype (ST) 6A or 8 and then coinfected them with mouse-adapted

193 Norovirus GII, Cryptosporidium, Shigella, ST-ETEC, and adenovirus 40/41 were also important.

194 Golgi-specific sialyltransferase (ST) expressed as a chimera with the rapamycin-binding do

195 DAS) and without (CNTL) initialization of SM/ST dataset.

196 A high resolution (3 km foot print) SM/ST dataset prepared from a land data assimilation system

197 s such as soil moisture/soil temperature (SM/ST) can significantly improve the modeling of mesoscale

198 e rats an SPI diet for 30 d [short-term SPI (ST-SPI)], and on PND 55, we switched SPI diet to control

199 esence of genes that encode the heat-stable (ST) and/or heat-labile (LT) enterotoxins, as well as sur

200 xacin resistance was associated with NG-STAR ST-26, ST-90, ST-91, ST-97, ST-150, and ST-158 (n = 196;

201 All isolates of NG-STAR ST-42, ST-43, ST-63, ST-81, and ST-160 (n = 106) were su

202 to azithromycin was associated with NG-STAR ST-58, ST-61, ST-64, ST-79, ST-91, and ST-139 (n = 156;

203 o cephalosporins was associated with NG-STAR ST-90, ST-91, and ST-97 (n = 162; 94.2%); and ciprofloxa

204 of a single-locus variation, and 76 NG-STAR STs (n = 109) were identified as unrelated singletons.

205 l, which leads to a large ground spin state (ST =16) that is confirmed by magnetization studies up to

206 ary metabolites, including sterigmatocystin (ST).

207 The outbreak strain (ST-9069) was not detected during the initial survey; 1 s

208 struts and underexpansion in acute/subacute ST and neoatherosclerosis and uncovered struts in late/v

209 overed struts (66.7% of cases); for subacute ST, the most common dominant finding was uncovered strut

210 jority of tumours in the molecular subgroups ST-EPN-SE and PF-EPN-SE.

211 the genome sequence of Blastocystis subtype (ST) 1 is presented and compared to previously published

212 , phosphatidylinositol (PI), and sulfatides (ST).

213 ntified revertant mutants able to synthesize ST, among them RM1.

214 ogue waves collected within spatio-temporal (ST) records of 3D wave fields.

215 banana surfaces, and lower surface tension (ST, 25.4mN/m) than the critical ST (35.2mN/m) of banana

216 KEY POINTS: The effects of short-term (ST; 10 days) and long-term (LT; 30 days) intermittent hy

217 ue-Dawley rats exposed to either short-term (ST; 10 days) or long-term (LT, 30 days) IH.

218 g-term, LT) or 19 months of age (short-term, ST) and tested memory performance in the Morris water ma

219 nd (2) the predictive value of skin testing (ST) before botulinum antitoxin administration.

220 ate cocaine seeking more readily in GTs than STs and that this would require intact cholinergic neuro

221 eased osteoblastic cell senescence, and that ST-SPI diet early in life has modest but persistent prog

222 We show that ST-FRB is trapped in the ER even without Ii-FKBP upon ra

223 Taken together, these data suggest that ST Direct may provide a cost-effective, rapid molecular

224 in rabbits superior to those elicited by the ST-5 CPS component in multivalent Prevnar13.

225 a stationary voltage profile was used in the ST region, ions are blocked at the TT-ST interface and a

226 eleased by resuming a conventional TW in the ST region.

227 in the TT region into a single TW bin in the ST region.

228 ach is that it captures small changes in the ST segment over time that cannot be detected by visual i

229 The wave with the ST maximum elevation (happening to be larger than the ro

230 The STs also display substantial variation in gene family di

231 patients with PsO (without systemic therapy [ST] 1.37; with ST 1.97), PsA (without ST 1.38; with ST 1

232 e direct immediate intervention and therapy, ST-segment-elevation myocardial infarction (STEMI) victi

233 there is unexpected diversity between these STs in terms of their genome sizes, guanine-cytosine (GC

234 motor threshold (MT) and seizure threshold (ST) in four nonhuman primates (NHPs) to determine the st

235 sis were definite/probable stent thrombosis (ST) and target lesion failure (TLF; device-oriented comp

236 Stent thrombosis (ST) is a serious complication following coronary stentin

237 were definite and probable stent thrombosis (ST), clinically relevant bleeding, all-cause mortality,

238 Thus ST-FRB cycles artificially by binding to FKBP domain-con

239 tion between the measured amplitude-titrated ST and the prediction of the E-field models, supporting

240 ghbouring neurons were directly connected to ST.

241 Some rats [sign-trackers (STs)] are prone to attribute incentive salience to rewar

242 Solitary tract (ST) afferents converged onto NTS-CeA second-order sensor

243 Graded shocks to the solitary tract (ST) always (93%) triggered EPSCs at CeA projecting NTS n

244 Aged rats treated ST or LT with FKBP1b substantially outperformed age-matc

245 recovery of proteins from salmon trimmings (ST), yielding 93% (w/w) protein.

246 RPV1) expressing C-fibres] or only non-TRPV1 ST afferent inputs, and never a combination of both.

247 in the ST region, ions are blocked at the TT-ST interface and accumulated in the TT region and then c

248 ciated strain, L. pneumophila sequence type (ST) 1.

249 lonal group, Escherichia coli sequence type (ST) 131, harbors both MDR and a deadly complement of vir

250 e outbreak of severe invasive sequence type (ST) 283 GBS infections in adults epidemiologically linke

251 The sequence type (ST) composition of 78 serotype 35B isolates obtained fro

252 ccurate identification of the sequence type (ST) of bacterial pathogens is critical for epidemiologic

253 otype IV isolates belonged to sequence type (ST)459, a tetracycline-, erythromycin-, and clindamycin-

254 (multilocus sequence typing) sequence type (ST-1068) regardless of their geographic sources and time

255 206) revealed diverse bacterial strain type (STs).

256 The predominant clones were sequence type [ST] 22 (n = 183; 47.8%), ST45 (n = 129; 33.7%), and ST23

257 rouped 768 isolates into 139 sequence types (STs) (n = 660) consisting of 29 clonal complexes (CCs) h

258 am-negative Salmonella enterica Typhimurium (ST), a major source of human food poisoning, caused infl

259 MCRPEC also included 17 unreported ST clades.

260 up based on unbiased estimates of pairwise V ST .

261 volume established short travel/low-volume (ST/LV) and long travel/high-volume (LT/HV) cohorts.

262 vely enrolled 27 patients with anterior wall ST segment elevation myocardial infarction (STEMI) and 4

263 , and cortical bone mineral density, whereas ST-SPI diet only reduced cortical bone mineral density l

264 The MIs included 28 (19%) with ST-segment elevation.

265 sO (without systemic therapy [ST] 1.37; with ST 1.97), PsA (without ST 1.38; with ST 1.67), and RA wi

266 7; with ST 1.97), PsA (without ST 1.38; with ST 1.67), and RA without an ST (1.49) but not elevated i

267 ar risk of incident MI (0.8% annually), with ST-segment elevation MI constituting one-third of all ca

268 In patients with ST, uncovered and malapposed struts were frequently obse

269 of Optimal Acute Treatment of Patients With ST-elevation Myocardial Infarction [DANAMI-3]; NCT014354

270 PRIMULTI study (Primary PCI in Patients With ST-Elevation Myocardial Infarction and Multivessel Disea

271 of Optimal Acute Treatment of Patients With ST-elevation Myocardial Infarction) did not show any imp

272 ovement in clinical outcome in patients with ST-segment elevation myocardial infarction (STEMI) treat

273 In patients with ST-segment elevation myocardial infarction (STEMI), the

274 prove the clinical outcomes in patients with ST-segment elevation myocardial infarction (STEMI).

275 nts standard care for treating patients with ST-segment elevation myocardial infarction (STEMI).

276 Of 91,895 patients with ST-segment elevation myocardial infarction and 87,915 pa

277 me course of edema reaction in patients with ST-segment-elevation MI by CMR and assessed its implicat

278 ive survival was estimated for patients with ST-segment-elevation myocardial infarction (n=5996, 853

279 iated with adverse outcomes in patients with ST-segment-elevation myocardial infarction (STEMI).

280 1-year cumulative survival for patients with ST-segment-elevation myocardial infarction aged >/=76 ye

281 wn to have prognostic value in patients with ST-segment-elevation myocardial infarction and cardiac a

282 complete revascularization in patients with ST-segment-elevation myocardial infarction and multivess

283 rfusion times and mortality in patients with ST-segment-elevation myocardial infarction are influence

284 ions in time to reperfusion in patients with ST-segment-elevation myocardial infarction as well as in

285 MVO in a cohort of consecutive patients with ST-segment-elevation myocardial infarction treated with

286 ects of NAC on infarct size in patients with ST-segment-elevation myocardial infarction undergoing pe

287 d with reduced infarct size in patients with ST-segment-elevation myocardial infarction undergoing pe

288 Of 112 randomized patients with ST-segment-elevation myocardial infarction, 75 (37 in NA

289 ombus aspiration during PCI in patients with ST-segment-elevation myocardial infarction.

290 thrombectomy and PCI alone in patients with ST-segment-elevation myocardial infarction.

291 approach to emergency care for patients with ST-segment-elevation myocardial infarction.

292 gnosis, particularly for older patients with ST-segment-elevation myocardial infarction.

293 dy to evaluate OCT findings in patients with ST.

294 SCAD patients more frequently presented with ST-segment elevation myocardial infarction (57% vs. 36%;

295 2015 included 120 cases; 75% presented with ST-segment-elevation myocardial infarction, and 80% had

296 hundred thirty-one patients presenting with ST underwent OCT imaging; 14 (6.1%) had image quality pr

297 Consecutive patients presenting with ST were prospectively enrolled in a registry by using a

298 cept for those (n=78, 23.6%) presenting with ST-segment-elevation myocardial infarction who underwent

299 revascularization in clinical scenarios with ST-segment elevation myocardial infarction and non-ST-se

300 riage of survivors of cardiac arrest without ST-segment-elevation myocardial infarction at the point

301 A total of 8,404 patients, with or without ST-segment elevation acute coronary syndrome, were rando

302 nd this was true even among patients without ST exposure.

303 opulmonary resuscitation in patients without ST-segment-elevation myocardial infarction.

304 erapy [ST] 1.37; with ST 1.97), PsA (without ST 1.38; with ST 1.67), and RA without an ST (1.49) but

305 encoding the transcriptional activator YAP1 (ST-EPN-YAP1).

306 ociated with a roughly double risk of 1-year ST in both women and men (women with versus without HPR: