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

4 TIA-1 and TTP both bind phospho-tau, and TIA-1 overexpre

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

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

7 s T-cell-restricted intracellular antigen 1 (TIA-1), TIA1-related protein (TIAR), and RasGAP-SH3 doma

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

9 positive for T-cell intracellular antigen-1 (TIA-1) or tristetraprolin (TTP) initially do not colocal

10 T-cell intracellular antigen-1 (TIA-1) regulates developmental and stress-responsive pat

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

12 Sixty patients were included (25 stroke, 29 TIA, 6 retinal embolism).

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

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

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

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

17 ring analyses demonstrated a "V" shape for a TIA-1 construct comprising the three RRMs and revealed t

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

19 of 0.66, but 2 of 12 with a zero score had a TIA/stroke.

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

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

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

23 cations for U1-C recruitment by the adjacent TIA-1 binding sites of the fas pre-mRNA and the bent TIA

24 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

25 % confidence interval [CI] = 9.5-25.1) after TIA, 19.4% (95% [CI] = 14.6-24.3) after ischemic stroke,

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

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

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

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

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

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

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

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

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

35 a large array of terpenoid indole alkaloids (TIAs) that are an important source of natural or semisyn

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 Although TIA was not detected in the protein extracts obtained fr

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

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

42 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%),

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

44 e points in the infection and that G3BP1 and TIA-1 are required for intracellular and extracellular i

45 es of binding by MBNL, PTB, RBFOX, STAR, and TIA family splicing factors, implicating them as ancestr

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

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

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

49 educe the incidence and burden of stroke and TIA.

50 TIA-1 and TTP both bind phospho-tau, and TIA-1 overexpression induces formation of inclusions con

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

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

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

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

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

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

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

58 Here we identify stress granule-associated TIA-1 and TIAR proteins as key factors in human 5'TOP mR

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

60 evious stroke or transient ischaemic attack (TIA) have a high risk of stroke.

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

70 ates of stroke or transient ischemic attack (TIA) among patients using rhythm (class Ia, Ic, and III

71 togenic stroke or transient ischemic attack (TIA) and had a patent foramen ovale.

72 Rates of stroke/transient ischemic attack (TIA) and heart failure hospitalizations for up to 3 year

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

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

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

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

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

78 tory of stroke or transient ischemic attack (TIA) have an increased rate of recurrent cardiac events

79 he risk of stroke/transient ischemic attack (TIA) in patients with endocardial leads.

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

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

82 3 months after a transient ischemic attack (TIA) or minor stroke.

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

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

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

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

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

88 nge, 4-8) stroke, transient ischemic attack (TIA), or retinal embolism and ipsilateral carotid stenos

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

90 ght help diagnose transient ischemic attack (TIA).

91 schemic stroke or transient ischemic attack (TIA).

92 chemic stroke and transient ischemic attack (TIA).

93 history of stroke/transient ischemic attack (TIA).

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

95 , previous Stroke/transient ischemic attack [TIA], Vascular disease, Age 65-74 years, and Sex categor

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

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

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

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

100 nding sites of the fas pre-mRNA and the bent TIA-1 shape, which organizes the N- and C-termini on the

101 tion at the initiation step, as evidenced by TIA-1/TIAR-dependent 5'TOP mRNA translation repression,

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

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

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

105 ins at late times postinfection and contains TIA but lacks translation initiation factors, mRNA bindi

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

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

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

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

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

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

112 Other flours displayed TIA.

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

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

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

116 26 of 47 studies (55%); all studies excluded TIA mimics.

117 , protein extract of rye mix flour exhibited TIA.

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

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

120 1% for stroke (P=0.79) and 3.1% and 4.1% for TIA (P=0.44).

121 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

122 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

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

124 sites with indistinguishable affinities for TIA-1.

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

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

127 f cardiac thrombus formation responsible for TIA/stroke in patients with atrial fibrillation (AF).

128 ng adults in the United States searching for TIA/stroke-related keywords.

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

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

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

132 d a medical evaluation yet, and 68 (39%) had TIA/stroke.

133 e with new symptoms were more likely to have TIA/stroke (OR 4.90, 95% CI 2.56-9.09).

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

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

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

137 upregulated TIA pathways genes and increased TIA accumulation.

138 nd to develop strategies aimed at increasing TIA production.

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

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

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

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

143 Analyses of TIA-1 variants established that RRM1 was dispensable for

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

145 ms do not satisfy traditional definitions of TIA.

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

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

148 emerging the ACV as the main determinant of TIA.

149 nteractions of a C-terminal Q-rich domain of TIA-1 with the U1-C splicing factor, despite linear sepa

150 nces in regulating the distinct functions of TIA-1.

151 of the LAA and were screened for history of TIA/stroke.

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

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

154 The sequence-selective involvement of TIA-1 RRM1 in RNA recognition suggests a possible role f

155 ular neurologist to assess the likelihood of TIA/stroke.

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

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

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

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

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

161 Transcriptional regulation of TIA biosynthesis is not fully understood.

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

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

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

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

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

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

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

169 ing individuals searching for information on TIA/stroke symptoms online as a target for future interv

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

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

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

173 had a significantly lower rate of stroke or TIA (3.4% per year) than a group of patients with AF man

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

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

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

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

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

179 e with a prior history of ischemic stroke or TIA had higher rates of clinical outcomes than patients

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

181 ith and without a history of prior stroke or TIA in the PLATelet inhibition and patient Outcomes (PLA

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

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

184 In patients with cryptogenic stroke or TIA who had a patent foramen ovale, closure with a devic

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

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

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

188 s, Diabetes mellitus, and previous stroke or TIA) score and improve the identification of atrial fibr

189 s, diabetes mellitus, and previous stroke or TIA) score of >/=2 (58.1% versus 67.0%, P<0.001).

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

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

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

193 outcomes in patients with previous stroke or TIA, the absolute benefits of apixaban might be greater

194 group of patients without previous stroke or TIA, the rate of stroke or systemic embolism was 1.01 pe

195 subgroup of patients with previous stroke or TIA, the rate of stroke or systemic embolism was 2.46 pe

196 Among patients with a history of stroke or TIA, the reduction of the primary composite outcome and

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

198 ven primarily by increased risk of stroke or TIA.

199 viduals were followed for incident stroke or TIA.

200 airment in patients with ischaemic stroke or TIA.

201 or acute noncardioembolic ischemic stroke or TIA.

202 tcomes than patients without prior stroke or TIA.

203 to 0.47) in those without previous stroke or TIA.

204 0.2%) than patients without prior stroke or TIA.

205 patients with and without previous stroke or TIA.

206 ents, 1152 (6.2%) had a history of stroke or TIA.

207 78 (8%) had a history of ischemic stroke or TIA.

208 with AF with and without previous stroke or TIA.

209 ulation, 3436 (19%) had a previous stroke or TIA.

210 54-1.32) in those without previous stroke or TIA.

211 ne for the prevention of recurrent stroke or TIA.

212 patients with and without previous stroke or TIA.

213 was the recurrence of an ischemic stroke or TIA.

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

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

216 0 person-years; p=0.0005) and all strokes or TIAs (7.85 vs 2.36 per 100 person-years; p=0.001).

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

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

219 with increased rates of TIAs and strokes or TIAs.

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

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

222 ion about self-administration after possible TIA.

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

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

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

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

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

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

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

230 structurally related stress granule proteins TIA-1 and TIAR.

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

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

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

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

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

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

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

238 ECS of the alpha(1B)-AR that influenced rho-TIA binding.

239 lations using a refined NMR structure of rho-TIA, we identified 14 residues on the ECS of the alpha(1

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

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

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

243 <0.001) and the composite outcome of stroke, TIA, acute coronary syndrome, and all death (risk ratio,

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

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

246 found to be 79% less likely to have a stroke/TIA history (odd ratio: 0.21, 95% confidence interval: 0

247 (p = 0.056) more likely to have had a stroke/TIA.

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

249 Crude stroke/TIA incidence rate was lower in patients treated with rh

250 bstantially increased risk of embolic stroke/TIA.

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

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

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

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

255 ents with a low-intermediate risk for stroke/TIA.

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

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

258 The lower stroke/TIA rate was confirmed in a propensity score-matched coh

259 py was associated with lower rates of stroke/TIA among patients with atrial fibrillation, in particul

260 was associated with a reduced risk of stroke/TIA and no significant difference in heart failure hospi

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

262 y was associated with a lower risk of stroke/TIA in comparison with rate control therapy (adjusted ha

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

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

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

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

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

268 e adjustment for age, sex, history of stroke/TIA, atrial fibrillation, and baseline aspirin/warfarin

269 60 patients (16.9%) with a history of stroke/TIA, were analyzed.

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

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

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

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

274 The prevalence of pre-procedure stroke/TIA in Cactus, Chicken Wing, Windsock, and Cauliflower m

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

276 The association of PFO with stroke/TIA remained significant after multivariable adjustment

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

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

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

280 The TIA-1 polypeptide contains three RNA recognition motifs

281 pite linear separation of the domains in the TIA-1 sequence.

282 X-ray scattering to dissect the roles of the TIA-1 RRMs in RNA recognition.

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

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

285 ed risk score to identify subjects with true TIA or stroke.

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

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

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

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

290 re of the RRM family, it was unknown whether TIA-1 RRM1 contributes to RNA binding as well as documen

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

292 6691 participants in the aspirin group with TIA or minor stroke had a disabling or fatal ischaemic s

293 Individuals with TIA/stroke symptoms often do not seek urgent medical att

294 CONCLUSIONS/SIGNIFICANCE: Individuals with TIA/stroke that are seeking real-time information on sym

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

296 e evaluation and treatment for patients with TIA, with particular attention to urgency and close obse

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 Of 845 patients with TIA/stroke, 587 (69%) were referred directly to outpatie

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