ライフサイエンスコーパス: TIA

1 TIA could be measured in 94% of the eyes, and AOD500 and

2 TIA patients with high estimated ischemic stroke risk ar

3 TIA proteins contain a C-terminal PrLD, and mutations in

4 TIA-1 (T-cell restricted intracellular antigen-1) is an

5 TIA-1 is composed of three RNA recognition motifs (RRMs)

6 TIA/stroke before or after onset of ocular condition occ

7 T-cell intracellular antigen-1 (TIA-1) is a DNA/RNA-binding protein that regulates criti

8 s of transient ischaemic attacks (TIAs; 4.18 TIAs per 100 person-years vs 0.60 TIAs per 100 person-ye

9 Here, we show that the C. elegans TIAR-2/TIA protein functions cell autonomously to inhibit axon

10 ly (0.08 strokes per 100 patient-years; 0.26 TIAs per 100 patient-years).

11 nalysis of a large monocentric cohort of 446 TIA patients, we explored the frequency and determinants

12 TIAs; 4.18 TIAs per 100 person-years vs 0.60 TIAs per 100 person-years; p=0.0005) and all strokes or

13 Total of 661 TIA patients were enrolled, 279 of whom were DWI positiv

14 We linked 67 892 TIA Get With The Guidelines-Stroke patients >65 years (2

15 onfatal MI (RR: 0.82; 95% CI: 0.72 to 0.94), TIA (RR: 0.79; 95% CI: 0.71 to 0.89), and ischemic strok

16 sk of recurrent stroke within 1 year after a TIA or minor stroke.

17 n 30 days, 13 (0.50%) patients experienced a TIA (TF 10 [0.67%]; TA 3 [0.27%]; P>0.17).

18 We recruited patients who had had a TIA or minor stroke within the previous 7 days.

19 gic factors, and outcomes in patients with a TIA or minor ischemic stroke who receive care in health

20 ly well understood, much less is known about TIA membrane transport mechanisms.

21 point mixed models resulted in more accurate TIA estimates for 94% (17/18) and 72% (13/18) of kidneys

22 Time-integrated activities (TIAs) calculated from mixed model fits and other reduced

23 Trypsin inhibitor activity (TIA) was evaluated using a small-scale quantitative assa

24 ed differential trypsin inhibitory activity (TIA) under non-reducing conditions.

25 r event was 27.7% (95% CI = 18.5-37.0) after TIA and 32.8% (95% CI = 26.7-38.9) after ischemic stroke

26 % confidence interval [CI] = 9.5-25.1) after TIA, 19.4% (95% [CI] = 14.6-24.3) after ischemic stroke,

27 A 53% after stroke versus 80%, and 64% after TIA versus 83%).

28 F 47% after stroke versus 82%, and 64% after TIA versus 83%; TA 53% after stroke versus 80%, and 64%

29 very high for only the first few days after TIA and minor ischaemic stroke, and observational studie

30 a lower risk of cardiovascular events after TIA than previously reported.

31 weeks) and late phases (>/= 3 months) after TIA or stroke in this prospective, pilot observational s

32 llowed up from the early to late phase after TIA or stroke (339.7 nM vs 308.6 nM; p = 0.02).

33 versus control in secondary prevention after TIA or ischaemic stroke, we studied the effects of aspir

34 ces the risk of early recurrent stroke after TIA and minor stroke and identify aspirin as the key int

35 et With The Guidelines Ischemic Stroke after TIA Risk Score; performance was examined in the validati

36 in their dimeric terpenoid indole alkaloids (TIAs) vinblastine and vincristine, which are used in can

37 oduces bioactive terpenoid indole alkaloids (TIAs), including the chemotherapeutics, vincristine and

38 uable, bioactive terpenoid indole alkaloids (TIAs).

39 re classified as terpenoid indole alkaloids (TIAs).

40 Overall, 240 (54%) of all TIA patients presented with DWI lesions.

41 Although TIA was not detected in the protein extracts obtained fr

42 rs vindoline and catharanthine and, although TIA biosynthesis is reasonably well understood, much les

43 ; p=0.005), all strokes (1.38; p<0.001), and TIA (1.47; p<0.001).

44 io, 0.20; 95% CI, 0.02 to 1.72; P=0.14), and TIA occurred in 5 patients (2.5%) and 7 patients (3.3%),

45 OD500, AOD750, TISA500, TISA750, ARA750, and TIA significantly increased following LPI by paired Stud

46 IPs content was significantly decreased and TIA as well as lectins content had a reduction higher th

47 e variance in estimates of global stroke and TIA burden of disease.

48 ascular causes), and nondisabling stroke and TIA occurred in 2 and 6 patients, respectively (0.08 str

49 Stroke and TIA were associated with lower 1-year survival than expe

50 Stroke and TIA were identified by protocol and adjudicated by a Cli

51 educe the incidence and burden of stroke and TIA.

52 Trabecular-iris angle (TIA) and angle opening distance 500 mum anterior to the

53 l angle measurements: trabecular-iris angle (TIA), angle opening distance (AOD500) and trabecular-iri

54 Trabecular-iris angle (TIA), angle opening distance 500 mum from the scleral sp

55 the scleral spur; and trabecular-iris angle (TIA).

56 the first atomic resolution structure of any TIA protein RRM in complex with oligonucleotide.

57 eat flour, dough, and bread did not show any TIA.

58 urological attack (TNA), are as prevalent as TIAs.

59 haemic stroke or transient ischaemic attack (TIA) and AF treated with OAC.

60 and ischaemic), transient ischaemic attack (TIA) and subarachnoid haemorrhage (SAH).

61 nts with a young transient ischaemic attack (TIA) or ischaemic stroke and its association with functi

62 prevention after transient ischaemic attack (TIA) or ischaemic stroke on the basis of trials showing

63 with a previous transient ischaemic attack (TIA) or stroke and chronic kidney disease (adjusted OR=3

64 ischaemic stroke/transient ischaemic attack (TIA) referrals.

65 haemic stroke or transient ischaemic attack (TIA) were randomised to pioglitazone (target 45 mg daily

66 haemic stroke or transient ischaemic attack (TIA) within 48 h of onset.

67 irst-ever stroke/transient ischaemic attack (TIA), >/=18 y, with diagnosis between 1 January 2009 and

68 ent stroke after transient ischaemic attack (TIA), but this approach may not be safe in patients with

69 in patients with transient ischaemic attack (TIA)/stroke.

70 e prior stroke or transient ischemic attack (TIA) (HR 1.42, 95% CI 0.96 to 2.10) and ipsilateral arte

71 ies of stroke and transient ischemic attack (TIA) after transcatheter aortic valve replacement (TAVR)

72 schemic stroke or transient ischemic attack (TIA) are at increased risk for future cardiovascular eve

73 Patients with transient ischemic attack (TIA) are at increased risk for ischemic stroke.

74 d previous stroke/transient ischemic attack (TIA) as a marker of increased intracranial bleeding risk

75 Transient ischemic attack (TIA) can be difficult to diagnose.

76 stroke or stroke/transient ischemic attack (TIA) combined.

77 cidence of stroke/transient ischemic attack (TIA) in this population was 18 of 1,086 (1.7%), whereas

78 Transient ischemic attack (TIA) is defined as focal neurological deficit caused by

79 schemic stroke or transient ischemic attack (TIA) may be impacted by undiagnosed atrial fibrillation

80 tory of stroke or transient ischemic attack (TIA) of the Rotterdam Study, a population-based cohort s

81 3 months after a transient ischemic attack (TIA) or minor stroke.

82 risk in high-risk transient ischemic attack (TIA) patients assessed by ABCD2 score.

83 accident (CVA) or transient ischemic attack (TIA), and 30-day mortality.

84 ion (MI), stroke, transient ischemic attack (TIA), and major adverse cardiovascular events.

85 f prognosis after transient ischemic attack (TIA), ischemic stroke, or hemorrhagic stroke in adults a

86 with a first-ever transient ischemic attack (TIA), ischemic stroke, or intracerebral hemorrhage (ICH)

87 site of stroke or transient ischemic attack (TIA), myocardial infarction, acute decompensated HF, or

88 ischemic stroke, transient ischemic attack (TIA), or a peripheral thromboembolic event were randomly

89 schemic stroke or transient ischemic attack (TIA).

90 schemic stroke or transient ischemic attack (TIA).

91 x and a stroke or transient ischemic attack (TIA).

92 ght help diagnose transient ischemic attack (TIA).

93 schemic stroke or transient ischemic attack (TIA).

94 schemic stroke or transient ischemic attack (TIA).

95 schemic stroke or transient ischemic attack (TIA).

96 ts with stroke or transient ischemic attack (TIA).

97 and incidence of transient ischemic attack (TIA)/stroke and myocardial ischemia.

98 ism (stroke: 76%, transient ischemic attack [TIA]: 32%, systemic embolism: 1%).

99 y classified as transient ischaemic attacks (TIAs) and data for prognosis are limited.

100 A third of transient ischaemic attacks (TIAs) and ischaemic strokes are of undetermined cause (i

101 reased rates of transient ischaemic attacks (TIAs; 4.18 TIAs per 100 person-years vs 0.60 TIAs per 10

102 ding strokes and transient ischemic attacks [TIAs]).

103 linked to CD4(+) T cells, whilst Granzyme B/TIA-1 to CD8(+) T cells.

104 h data from the prospective, hospital-based, TIA database of the First Affiliated Hospital of Zhengzh

105 tion whereas blocking the assembly of SGs by TIA-1 depletion resulted in rapid and increased producti

106 Interestingly, the central TIA intermediate strictosidine also accumulates in both

107 patients with definite specialist-confirmed TIA have negative DWI findings.

108 prevalence of UIA in patients with confirmed TIA/minor stroke is likely higher than that in the gener

109 tify the allosteric site for rho-conopeptide TIA, an inverse agonist at this receptor.

110 The clinical burden of cryptogenic TIA and stroke is substantial.

111 tors, and long-term prognosis of cryptogenic TIA and stroke.

112 wn by the appearance of distinct cytoplasmic TIA-1- and DDX3-containing foci.

113 monest DWI finding in patients with definite TIA is a negative scan.

114 All patients with neurologist-diagnosed TIA-S with a National Institutes of Health Stroke Scale

115 stions the accuracy of clinically diagnosing TIA and suggests added value for early magnetic resonanc

116 Other flours displayed TIA.

117 on complex formation with target RNA or DNA, TIA-1 RRM23 adopts a compact structure, showing that bot

118 o determine whether positive or negative DWI TIA patients could get benefits from HST we conducted a

119 A total of 987 eligible TIA patients were analyzed.

120 The study enrolled TIA patients within 72 h of onset from the prospective T

121 f 959 consecutive patients with a first-ever TIA (n = 262), ischemic stroke (n = 606), or intracerebr

122 among 511 stroke survivors with a first-ever TIA or ischaemic stroke, aged 18-50 years.

123 26 of 47 studies (55%); all studies excluded TIA mimics.

124 , protein extract of rye mix flour exhibited TIA.

125 Oxfordshire, UK, among patients with a first TIA or ischaemic stroke from April 1, 2002, to March 31,

126 stenosis, and decreases over time following TIA or stroke associated with carotid stenosis.

127 of death was 24.9% (95% CI, 16.0%-33.7%) for TIA, 26.8% (95% CI, 21.9%-31.8%) for ischemic stroke, an

128 ality ratio [SMR], 2.6 [95% CI, 1.8-3.7] for TIA, 3.9 [95% CI, 3.2-4.7] for ischemic stroke, and 3.9

129 emporal and nasal quadrant was R = 0.902 for TIA.

130 al Disorders and Stroke (NINDS) criteria for TIA.

131 pt of inpatient quality of care measures for TIA, and the presence or absence of stroke at 1 year pos

132 Substitution of the prion domain from TIA-1 or an authentic yeast prion domain from RNQ1 into

133 elements are either resident in cells (e.g., TIA-1) or induced (e.g., tristetraprolin).

134 nslational regulatory mechanisms that govern TIA biosynthesis in C. roseus.

135 ntitumour drugs, much remains unknown on how TIAs are biosynthesised from a central precursor, strict

136 rfering RNAs to deplete Ataxin2, G3BP1, HuR, TIA-1, TIAR, and YB1.

137 nts used monotherapy than those used DAPT in TIA with positive DWI (23.7% vs. 13.4%, p = 0.029).

138 iliary role of the C-terminal RRM3 domain in TIA-1 RNA recognition is poorly understood, and this wor

139 However, the benefit didn't exist in TIA patients with negative DWI (HR = 0.43; 95% CI, 0.14-

140 We assessed DWI positivity in TIA and implications for reclassification as stroke.

141 T was associated with reduced stroke risk in TIA patients with positive DWI (hazard ratio [HR] = 0.54

142 Early use of DAPT reduced stroke risk in TIA patients with positive DWI.

143 ate whether DAPT could reduce stroke risk in TIA with DWI positive.

144 and its regulator, CrMYC2, play key roles in TIA biosynthesis.

145 oints and high-intensity statin treatment in TIA patients with positive and negative DWI.

146 We identified 19 studies of UIA in TIA/stroke cohorts (n=12 781), all with either symptomat

147 upregulated TIA pathways genes and increased TIA accumulation.

148 nd to develop strategies aimed at increasing TIA production.

149 ARF, CrARF16, binds to the promoters of key TIA pathway genes and repress their expression.

150 c acid, IAA) repressed the expression of key TIA pathway genes in C. roseus seedlings.

151 cantly fewer outliers when estimating kidney TIA, compared with popular reduced-time-point methods.

152 the vacuolar transport mechanism of the main TIAs accumulated in C. roseus leaves, vindoline, cathara

153 localised in the epidermal cells, but major TIAs including serpentine and vindoline are localised in

154 These metabolomic studies revealed that most TIA precursors (iridoids) are localised in the epidermal

155 T trial (Platelet-Oriented Inhibition in New TIA and Minor Ischemic Stroke [POINT] Trial), the combin

156 SG scaffold proteins G3BP1 and G3BP2 but not TIA-1.

157 se, patient characteristics, or aetiology of TIA or stroke.

158 k]), findings on brain imaging, and cause of TIA or minor stroke with the risk of recurrent stroke ov

159 The Kaplan-Meier curves of TIA patients with DAPT and monotherapy were plotted.

160 nges due to the protonation/deprotonation of TIA-1 RRM3 histidine residues.

161 ACV emerged as the main determinant of TIA (R(2) = 0.705; p < 0.001).

162 emerging the ACV as the main determinant of TIA.

163 Kaplan-Meier estimate of the incidence of TIA /stroke within 3 months after onset was 6% (95% CI:

164 rexpression resulted in dramatic increase of TIA accumulation in C. roseus hairy roots.

165 Knockdown of TIA-1 and TIAR affected ZIKV protein and RNA levels but

166 of ischemic brain injury in the majority of TIA patients.

167 Together our data support a specific mode of TIA-1 RRM23 interaction with target oligonucleotides con

168 primary outcome was the composite outcome of TIA, stroke (ischaemic stroke or intracranial haemorrhag

169 f thrombin generation in the pathogenesis of TIA or stroke and its relationship with cerebral microem

170 Factors predictive of TIA could serve to identify suitable candidates for ICL

171 x variables were identified as predictors of TIA at 1 month postsurgery (R(2) = .907).

172 The pooled proportion of TIA patients with an acute DWI lesion was 34.3% (95% con

173 Transcriptional regulation of TIA biosynthesis is not fully understood.

174 nor was there evidence of increased risk of TIA in either time period.

175 oligonucleotides consistent with the role of TIA-1 in binding RNA to regulate gene expression.

176 y with ORCA3, modulates an additional set of TIA genes.

177 We also report the crystal structure of TIA-1 RRM2 in complex with DNA to 2.3 A resolution provi

178 nce of acute cerebral ischemia in a third of TIA patients.

179 bosis was associated with increased rates of TIAs and strokes or TIAs.

180 rmentation, baking and in vitro digestion on TIA and CIA were studied.

181 embolic ischemic stroke (NIHSS score <=5) or TIA who were not undergoing intravenous or endovascular

182 ere was no difference in freedom from CVA or TIA for the 2 groups (P = .07).

183 The rate of CVA or TIA in the iBCVI group was 5.1% compared with 15.2% in t

184 assessed using the modified Rankin Scale) or TIA within 90 days, as assessed by central telephone fol

185 E following DRS stratification was stroke or TIA (hazard ratio: 3.94; 95% confidence interval: 1.72 t

186 nificantly higher risk of ischemic stroke or TIA (incidence rate, 18.9 vs 10.0 per 1000 person-years;

187 patients with cryptogenic ischemic stroke or TIA admitted in a comprehensive stroke center during an

188 te of the first recurrent ischemic stroke or TIA after PFO closure.

189 s, early OAC after acute ischaemic stroke or TIA associated with AF was not associated with a differe

190 ant difference in the incidence of stroke or TIA between patients with reduced leaflet motion and tho

191 ncidence and severity of recurrent stroke or TIA did not differ between intensive and guideline thera

192 d who experienced chickenpox and a stroke or TIA during follow-up.

193 patients with a sentinel ischemic stroke or TIA event in the prior 6 months.

194 rt study of patients with an index stroke or TIA event recorded in years 2008 through 2011.

195 antify any increased risk of first stroke or TIA in the 0-6 and 7-12 months following chickenpox comp

196 Risk of stroke or TIA is highest early after TAVR and is associated with i

197 associated with a higher risk for stroke or TIA recurrence (HR, 4.50 [CI, 2.20 to 9.20]; P < 0.001);

198 ociated with an increased risk for stroke or TIA recurrence.

199 ents who had had a recent ischemic stroke or TIA to receive either pioglitazone (target dose, 45 mg d

200 patients with a recent cryptogenic stroke or TIA who were 55 years of age or older, paroxysmal atrial

201 th acute noncardioembolic ischemic stroke or TIA with treatment initiated within 3 days of ictus.

202 who had had a cryptogenic ischemic stroke or TIA within the previous 6 months (cause undetermined aft

203 ncidence and severity of recurrent stroke or TIA, but did significantly increase the risk of major bl

204 th acute noncardioembolic ischemic stroke or TIA, dual therapy was more effective than monotherapy in

205 t patients with a recent ischaemic stroke or TIA, pioglitazone did not affect cognitive function, as

206 with a recent history of ischemic stroke or TIA, the risk of stroke or myocardial infarction was low

207 was the recurrence of an ischemic stroke or TIA.

208 ot prescribed prior to the time of stroke or TIA.

209 viduals were followed for incident stroke or TIA.

210 or aspirin alone in acute ischemic stroke or TIA.

211 airment in patients with ischaemic stroke or TIA.

212 or acute noncardioembolic ischemic stroke or TIA.

213 th a significant increased risk of stroke or TIA.

214 ation after a cryptogenic ischemic stroke or TIA.

215 ing vascular events or death after stroke or TIA.

216 h within 90 days of the qualifying stroke or TIA.

217 ven primarily by increased risk of stroke or TIA.

218 n increased incidence of recurrent stroke or TIA: 2.32 versus 0.75 events per 100 patient-years (haza

219 er scores indicating more severe stroke), or TIA and who were not undergoing thrombolysis or thrombec

220 Of the 15 total CVAs or TIAs, 11 (73.3%) resulted from carotid injury and 4 (26.

221 0 person-years; p=0.0005) and all strokes or TIAs (7.85 vs 2.36 per 100 person-years; p=0.001).

222 the early-OAC group (5 ischaemic strokes or TIAs and 2 deaths).

223 ranial haemorrhages, 18 ischaemic strokes or TIAs and 31 deaths (three deaths were as a result of new

224 The proportions of strokes or TIAs with prevention drugs under-prescribed, when clinic

225 .2 years), there were 71 ischemic strokes or TIAs, 266 subsequent documented AF episodes, and 571 dea

226 During follow-up, 62 strokes or TIAs, 42 myocardial infarctions, 156 HF events, and 38 c

227 with increased rates of TIAs and strokes or TIAs.

228 escent probe showed that vindoline and other TIAs indeed were able to dissipate an H(+) gradient pree

229 ch Program (W81XWH-14-2-0183, W81XWH-12-PCRP-TIA, W81XWH-15-1-0430, and W81XWH-13-2-0070), the Pacifi

230 D103, PD1, CD30, ALK1, CD10, BCL6, perforin, TIA-1, Granzyme B and Epstein-Barr virus-encoded RNA.

231 days' recurrent stroke risk in DWI-positive TIA patients but not in DWI-negative patients.

232 etter understood, reclassifying DWI-positive TIAs as strokes is likely to increase variance in estima

233 ion about self-administration after possible TIA.

234 on rule for 1-year ischemic stroke risk post-TIA, examining estimated risk, receipt of inpatient qual

235 ate for ischemic stroke during the year post-TIA was 5.7%.

236 chemic stroke admission during the year post-TIA, and developed a Get With The Guidelines Ischemic St

237 Preoperative TIA was 48.7 +/- 8.7, 48.2 +/- 8.7, and 48.7 +/- 9.3 deg

238 Preoperative TIAs were 49.5 +/- 8.7, 48.3 +/- 9.6, and 49.1 +/-8.6 de

239 Following in vitro digestion process, TIA of wheat bread was found as 5.91units/mL gastric dia

240 es of 68, 46, 33 and 22 kDa showed prominent TIA.

241 ts within 72 h of onset from the prospective TIA database of the First Affiliated Hospital of Zhengzh

242 logical deterioration only, 11 had recurrent TIA-S only, and 5 had both).

243 bsence of a medical explanation or recurrent TIA-S during hospitalization.

244 apable of activating ORCA3 and co-regulating TIA pathway genes concomitantly with ORCA3.

245 er-bridging hydrogen bonds between Asn-2-rho-TIA and Val-197, Trp-3-rho-TIA and Ser-318, and the posi

246 T-stacking-pi interaction between Trp-3-rho-TIA and Phe-330.

247 between Asn-2-rho-TIA and Val-197, Trp-3-rho-TIA and Ser-318, and the positively charged N terminus a

248 salt bridge and cation-pi between Arg-4-rho-TIA and Asp-327 and Phe-330, respectively, and a T-stack

249 ycle analysis and docking confirmed that rho-TIA binding was dominated by a salt bridge and cation-pi

250 tenosis and plaques, cardiac embolic source, TIA/stroke and myocardial ischemia differ among various

251 e in leaf tissue of C. roseus, cell-specific TIAs localisation and accumulation with 10 mum spatial r

252 troke recurrence in our cryptogenic stroke / TIA cohort.

253 t was a composite of death, nonfatal stroke, TIA, or peripheral embolism.

254 the rate of the composite outcome of stroke, TIA or death at 90 days, compared with late OAC.

255 <0.001) and the composite outcome of stroke, TIA, acute coronary syndrome, and all death (risk ratio,

256 In all, 29,043 stroke/TIA patients met the inclusion criteria; 17,680 had >/=1

257 ared confined to the 1st year after a stroke/TIA (adjusted HR, 3.03; 95% CI, 1.51-6.08 for the first

258 let therapy and in the 1st year after stroke/TIA.

259 onents of the composite endpoint: all-stroke/TIA (sHR: 1.00; 95% CI: 0.40 to 2.51), clinically signif

260 bstantially increased risk of embolic stroke/TIA.

261 comes were recurrent ischaemic event (stroke/TIA/systemic arterial embolism) and delayed symptomatic

262 predictors of early ischaemic events (stroke/TIA/systemic embolism) and d-sICH.

263 re not prescribed them prior to first stroke/TIA.

264 For stroke/TIA combined, prior atrial fibrillation (p = 0.03) and m

265 ion of under-prescribing of drugs for stroke/TIA prevention did not address patients' adherence to me

266 emale), the Kaplan-Meier estimate for stroke/TIA recurrence within 1 year was 10.6%.

267 gulation treatment and a reduction in stroke/TIA recurrence.

268 or of late stroke (p = 0.007) or late stroke/TIA (p = 0.06).

269 The primary end point of stroke/TIA consistent with a cardioembolic etiology and the sec

270 g events associated with a history of stroke/TIA in patients with coronary artery disease.

271 coronary artery disease, a history of stroke/TIA is associated with an independent increase in risk o

272 egory was an independent predictor of stroke/TIA or death, with elevated odds ratios associated with

273 ly indicated in 54% (9,579/17,680) of stroke/TIA patients: 49% (7,836/16,028) were not prescribed lip

274 The primary end point of stroke/TIA was met in 30/364 (8.2%) PFO versus 117/5711 (2.0%)

275 associated with an increased risk of stroke/TIA/death.

276 impact of AF diagnosis and timing on stroke/TIA recurrence rates in a large real-world sample of pat

277 Patients with previous stroke/TIA had a higher rate of recurrent cardiovascular events

278 s (doubled), diabetes mellitus, prior stroke/TIA (doubled), vascular disease, age 65-74 years, sex ca

279 omboembolic or bleeding events (prior stroke/TIA 29%; prior bleeding 54%.

280 was highly associated with recurrent stroke/TIA (hazard ratio, 2.0; 95% confidence interval, 1.9-2.1

281 with transient ischemic attacks and strokes (TIA-S).

282 d data on patients presenting with suspected TIA who underwent MR DWI and reported the proportion wit

283 rd Vascular Study (2011-2020) with suspected TIA/minor stroke and non-invasive angiography were inclu

284 prognosis of UIA in patients with suspected TIA/minor stroke.

285 ltogether, our results strongly support that TIAs are actively taken up by C. roseus mesophyll vacuol

286 both RRM2 and RRM3 and demonstrated that the TIA-1 RRM23 construct preferentially binds the UC-rich R

287 These TIAs are produced in very low levels in the leaves of th

288 In this study trypsin (TIA) and chymotrypsin inhibitory (CIA) activities were d

289 owledge is extremely important to understand TIA metabolic fluxes and to develop strategies aimed at

290 rMAPKK1 in C. roseus hairy roots upregulated TIA pathways genes and increased TIA accumulation.

291 central precursor, strictosidine, to various TIAs in planta.

292 The means recorded were TIA 35.8 +/- 12.2 degrees (range 1.5 to 76.1), AOD500 54

293 of UIA prevalence/prognosis in cohorts with TIA/stroke.

294 surgery, vault measurements correlated with TIA (R = -.309; P = .048).

295 6691 participants in the aspirin group with TIA or minor stroke had a disabling or fatal ischaemic s

296 Reclassification of patients with TIA and a DWI lesion as "stroke" is under consideration.

297 There were 505 patients with TIA-S at Columbia University; 31 (6.1%) had RCVEs (15 pa

298 icated to urgent evaluation of patients with TIA.

299 pooled mean UIA prevalence in patients with TIA/stroke was 5.1% (95% CI 4.8 to 5.5) and the incidenc

300 st benefit noted in patients presenting with TIA or minor stroke (at 0-2 weeks, two of 6691 participa