ライフサイエンスコーパス: aura

1 horylation of its substrate Aurora kinase A (AurA).

2 reported migraine was 16% (13% migraine with aura).

3 ine (FHM) is a rare subtype of migraine with aura.

4 graine and in one patient with migraine with aura.

5 support a novel mechanism of activation for AurA.

6 is a key pathogenetic step in migraine with aura.

7 n 4 of 7 patients with otherwise intractable aura.

8 osphorylation is necessary for activation of AurA.

9 re as a therapy for migraine with or without aura.

10 e phenotype in this variant of migraine with aura.

11 that underlie the headache of migraine with aura.

12 d in migraine attacks that begin with visual aura.

13 vascular unit in the development of migraine aura.

14 s cerebral emboli, stroke, and migraine with aura.

15 ree attacks over 3 months while experiencing aura.

16 (CSD) is likely the underlying phenomenon of aura.

17 and efficacy in patients with versus without aura.

18 eatment for some patients with migraine with aura.

19 lmodulin (CaM) binding to multiple motifs on AurA.

20 xtracardiac right-to-left shunts to migraine aura.

21 device for acute treatment of migraine with aura.

22 slow depolarization that underlies migraine aura.

23 rment of noise exclusion in migraine without aura.

24 tween headaches in migraine with and without aura.

25 oglial depolarization implicated in migraine aura.

26 onsidered to be an experimental correlate of aura.

27 tivity, is the most likely cause of migraine aura.

28 e phenotypic diversity of human migraine and aura.

29 is prevalent in patients with migraine with aura.

30 o-left shunts in patients with migraine with aura.

31 accompanied by visual disturbances known as aura.

32 anges may help our understanding of migraine aura.

33 erebral disturbances which subserve migraine aura.

34 TPX2 is a binding partner and activator of AurA.

35 gic migraine than in patients with non-motor aura.

36 derstanding mechanisms subserving the visual aura.

37 clinical characteristics and duration of the aura.

38 hallenging task of capturing patients during aura.

39 redominant sensory phenomenology of migraine aura.

40 n the treatment of migraine with and without aura.

41 l field testing in migraine patients without aura.

42 ed as the cellular correlate of the migraine aura.

43 acute treatment of migraine with and without aura.

44 CSD), the putative mechanism of the migraine aura.

45 electrophysiologic event underlying migraine aura.

46 ura may decrease both headache frequency and aura.

47 re monogenic subtype of common migraine with aura.

48 Migraine (59%), migraine with aura (27%), anxiety and depression were common comorbidi

49 tesla in 131 patients with migraine (38 with aura; 30.8 +/- 9 years old; 109 women; monthly attack fr

50 (56 migraine with aura, 61 migraine without aura, 53 controls).

51 Of 71 patients enrolled in AURA, 53 were eligible for this analysis.

52 170 subjects were enrolled (56 migraine with aura, 61 migraine without aura, 53 controls).

53 ifference was mainly due to migraine without aura (80 [24.0%] vs 335 [15.6%], P < .001).

54 fold and activating its associated Aurora-A (AurA), a kinase crucially required for primary cilia dis

55 A mutant complemented with AurA(KS degrees )-AurA(ACP degrees ).

56 target Thr-295 of AurA to prevent premature AurA activation during interphase and that phosphorylate

57 This unexpected mechanism for AurA activation provides a new context for evaluating th

58 tein for Xklp2 (TPX2), a known MT-localizing AurA activator, is an AurA cofactor in centrosome-driven

59 In contrast with previously characterized AurA activators, NPM does not trigger autophosphorylatio

60 no history of migraine, active migraine with aura, active migraine without aura, and past history of

61 The Cep192-mediated mechanism maximizes AurA activity at centrosomes and appears essential for t

62 t the centrosome, indicating a local loss of AurA activity.

63 Thr-288; Xenopus, Thr-295) by PP6 represses AurA activity.

64 Increasing evidence indicates that AurA also regulates critical processes in normal interph

65 Migraineurs without aura also showed a significant (P < 0.05) though weak re

66 al noise-exclusion deficits in migraine with aura and a minor impairment of noise exclusion in migrai

67 ich is the electrophysiological correlate of aura and a putative trigger for migraine.

68 Conversely, cells lacking AurA and AurB activity exit mitosis without anaphase, fo

69 ts suggest an essential combined function of AurA and AurB in chromosome segregation and anaphase MT

70 Strikingly, inhibition of both AurA and AurB results in a failure to depolymerize spind

71 emonstrate that small molecule inhibitors of AurA and HDAC6 selectively stabilize cilia from regulate

72 common migraine phenotypes because of shared aura and headache features, trigger factors, and underly

73 en-labeled pilot study of patients, reducing aura and headache symptoms in 4 of 7 patients with other

74 We studied patients with migraine with aura and healthy controls with 31P-MRS and with 1H-MRS.

75 of TPX2 on the binding interactions between AurA and inhibitors.

76 a new context for evaluating the function of AurA and its inhibitors in normal and cancerous cells.

77 stic types of migraine, termed migraine with aura and migraine without aura, from the International H

78 Migraine without aura and nonmigraine headache were not associated with a

79 results suggest a novel relationship between AurA and protein phosphatases during progression through

80 l RNFL thinning in migraine patients without aura and pulsative choroidal blood flow may not be affec

81 SD is associated with migraine aura and recently recognized as a novel mechanism of inj

82 o explain the sensory nature of the migraine aura and reveal that sensory cortices are vulnerable in

83 ared with both the migraine patients without aura and the control subjects.

84 n PFO prevalence in those with migraine with aura and those without (26.8% versus 26.1%; odds ratio 1

85 of intracranial origin such as migraine with aura and why this therapeutic approach may not be effect

86 In migraine, both with aura and without aura, patients' choroid thinning should

87 d surface area abnormalities were related to aura and WMHs (P < .01) but not to disease duration and

88 quire the serine/threonine kinase, Aurora A (AurA), and the centrosomal protein of 192 kDa (Cep192)/s

89 Migraine with aura, migraine without aura, and control subjects were prospectively enrolled i

90 electrophysiological surrogate for migraine aura, and develop severe and prolonged motor deficits af

91 sion, the experimental correlate of migraine aura, and further evaluated the response of spontaneous

92 ng depression, the experimental correlate of aura, and inhibited trigeminal activation in in vivo mig

93 migraine with aura, active migraine without aura, and past history of migraine.

94 teral events, prominent automatisms, sensory aura, and post-ictal fear and speech arrest.

95 fects lead to cortical spreading depression, aura, and potentially migraine.

96 Ten migraine with aura, ten migraine without aura, and ten age-matched headache-free subjects partici

97 e initiation and propagation of the migraine aura, and the visual percept that is produces, remain un

98 atrial fibrillation; migraine headache with aura; and the epidemiology of types of stroke, such as a

99 ts activation by either sperm nuclei or anti-AurA antibody (alphaAurA)-induced dimerization.

100 cohort suggest that women with migraine with aura are at increased risk of experiencing TIA or ischem

101 and non-hemiplegic migraine with or without aura are part of a wider clinical spectrum.

102 Migraine attacks with auras are sometimes associated with underlying hereditar

103 cantly thinner in the migraine patients with aura as compared with both the migraine patients without

104 sensory axon remodeling defects in a sensory aura-associated human epilepsy disorder.

105 thermore, an AurA(KS degrees , ACP degrees )-AurA(AT(0)) heterodimer proved to be nonfunctional, wher

106 Most aura attacks originated centrally (within 10 degrees ecc

107 colocalize to centrosomes in G2 phase, where AurA becomes active.

108 rst through lower nasal field (69-77% of all auras) before travelling to upper and temporal fields, o

109 Auras beginning centrally preferentially propagated firs

110 AurA binds, phosphorylates, and reduces the activity of

111 Hence, Cep192 activates AurA by a mechanism different from that previously descr

112 Dephosphorylation of AurA by PP2A (human, Ser-51; Xenopus, Ser-53) destabiliz

113 Early treatment of migraine with aura by sTMS resulted in increased freedom from pain at

114 location, providing direct evidence that the aura can be clinically 'silent'.

115 (CSD)--an event believed to underlie visual aura--can give rise to activation of nociceptors that in

116 type 1 (FHM1) is a subtype of migraine with aura caused by a gain-of-function mutation in the pore-f

117 In the absence of AurA, cells form bipolar spindles but fail to properly a

118 tion of Cep192 or specific interference with AurA-Cep192 binding did not prevent AurA oligomerization

119 The visual percept of the aura changed corresponding with the presumed propagation

120 The visual percept of migraine aura changes depending on the region of the occipital co

121 Familial history of stroke, migraine with aura, circulating antiphospholipid antibodies, discontin

122 depression, the neural correlate of migraine aura, closes the paravascular space and impairs glymphat

123 a known MT-localizing AurA activator, is an AurA cofactor in centrosome-driven spindle assembly.

124 NPM and AurA coimmunoprecipitate and colocalize to centrosomes i

125 gnificantly more common in the migraine with aura compared to control group (73% vs. 51%, p = 0.02),

126 king Wnt5a-induced biochemical steps to HEF1/AurA-dependent cilia disassembly.

127 Most studies of Aurora A (AurA) describe it as a mitotic centrosomal kinase.

128 and its subtypes (presence or absence of an aura) differs between patients whose IS was due to CEAD

129 atio decreased significantly with increasing aura duration and was significantly lower in patients wi

130 ifferent aura phenotypes and with increasing aura duration.

131 la chrysaetos, and turkey vulture, Cathartes aura, during autumn migration across eastern North Ameri

132 risons (migraineurs vs control subjects, the aura effect, the effect of white matter hyperintensities

133 esign of the first human Aurora A kinase (as-AurA) engineered by chemical genetics techniques.

134 cessive maternal-effect mutation in the gene aura exhibit defects including reduced cortical integrit

135 Patients who suffered from migraine with aura, experienced frequent migraine attacks, had previou

136 misdiagnosis for PS and migraine with visual aura for ICOE-G.

137 c centrosomes where the locally accumulating AurA forms homodimers or oligomers.

138 ndently as a function of square root of time aura free, leveling by 2 years of stable seizure (aura)

139 nges parallel length of time seizure free or aura free, stabilize after 2 years, and are unrelated to

140 over time were sensitive to seizure-free and aura-free status.

141 strually related migraine (MRM) and migraine aura frequency.

142 rmed migraine with aura and migraine without aura, from the International Headache Genetics Consortiu

143 arcs, and drug inhibition is consistent with aura function promoting F-actin polymerization and/or st

144 ever, we and others have recently identified AurA functions as diverse as control of ciliary resorpti

145 ith a similar trend for the migraine without aura group (67% vs. 51%, p = 0.08).

146 orty-five patients who had migraines without aura (Group 1), 45 patients who had migraines with aura

147 Group 1), 45 patients who had migraines with aura (Group 2), and 30 healthy participants (control gro

148 gic migraine and in patients with persistent aura >7 days was significantly lower.

149 or stroke, women who reported migraine with aura had adjusted relative risk (95% confidence interval

150 Some auras had limited propagation and spontaneously 'aborted

151 Although migraine with aura has many causes (eg, neuronal network excitability)

152 Migraine-specifically migraine with aura-has been identified as a risk factor for vascular d

153 Migraine patients without aura have normal OPA values, no significant asymmetry of

154 ion of aPKC, AurA, or a downstream target of AurA, HDAC6, restores ciliogenesis in ceramide-depleted

155 20 patients had comorbid migraine, five with aura; (ii) to identify systematically additional visual

156 hanism linking microembolization to migraine aura in an experimental animal model.

157 ue anoxia might be a mechanism for prolonged aura in FHM1.

158 the pathophysiological mechanism of migraine aura in human beings, whereas novel animal studies are u

159 stent with the hypothesis that migraine with aura in midlife is associated with late-life vascular di

160 Migraine with aura in midlife was associated with late-life prevalence

161 h both hemiplegic migraine and migraine with aura in patients.

162 d drawings of his visual percept of migraine aura in real time during more than 1000 attacks of migra

163 ral lobe involvement contributes to migraine aura in some instances.

164 a are consistent with what is known of human aura in that sodium ion channels are those predominantly

165 eractivation of the mitotic kinase Aurora-A (AurA) in cancer is associated with genomic instability.

166 d a conditional deletion of Aurora A kinase (AurA) in Cdk1 analogue-sensitive DT40 cells to analyze A

167 The dimerization of endogenous AurA, in the presence of bound Cep192, triggers potent k

168 In a young man with migraine with aura including hemiplegia, we identified a novel SLC1A3

169 epression (CSD), an animal model of migraine aura, induces a rapid and nearly complete closure of the

170 that there can be multiple distinct sites of aura initiation in a given individual and suggest that t

171 Consistent patterns of aura initiation, propagation and termination were observ

172 modelling, we map two primary regions of CaM-AurA interaction to unfolded sequences in the AurA N- an

173 Migraine aura involves sensory percepts, suggesting that sensory

174 Migraine with aura is a severe debilitating neurological disorder with

175 In this paper, we show that AurA is abundant in normal kidney tissue but is also abn

176 ning approach indicates that the mutation in aura is associated with a truncation of Mid1 interacting

177 Migrainous aura is caused by cortical spreading depression (CSD) -

178 We suggest that migraine with aura is initiated by waves of CSD that lead up to delaye

179 nal analyses revealed that the N-terminus of AurA is not involved in the iteration process, ruling ou

180 Migraine with aura is often the first manifestation of cerebral autoso

181 Migraine aura is sparsely studied due to the highly challenging t

182 In these activities, AurA is transiently activated by noncanonical signals, i

183 The expression of AurA is ubiquitous and cell cycle regulated.

184 Aurora A (AurA) is a major mitotic protein kinase involved in cent

185 The turkey vulture (Cathartes aura) is a widespread, scavenging species in the Western

186 The mitotic kinase Aurora A (AurA) is regulated by a complex network of factors that

187 years, migraine, especially migraine without aura, is consistently associated with CEAD.

188 e electrophysiological substrate of migraine aura, is enhanced in mice expressing a vascular Notch 3

189 ne type 1, a monogenic migraine variant with aura, is linked to gain-of-function mutations in the CAC

190 ation indeed influenced this timing, because AurA isoforms retaining an intact Thr-295 residue furthe

191 emonstrate that NPM is a strong activator of AurA kinase activity at the centrosome and support a nov

192 we report that NPM is a strong activator of AurA kinase activity.

193 HEF1/Cas-L/NEDD9 and the oncogenic Aurora A (AurA) kinase at the basal body of cilia causes phosphory

194 dk1 analogue-sensitive DT40 cells to analyze AurA knockout phenotypes after Cdk1 activation.

195 ored in a DeltaaurA mutant complemented with AurA(KS degrees )-AurA(ACP degrees ).

196 Furthermore, an AurA(KS degrees , ACP degrees )-AurA(AT(0)) heterodimer

197 severe headaches that can be preceded by an aura likely caused by cortical spreading depression (SD)

198 fails to complement the originally isolated aura maternal-effect mutation, confirming gene assignmen

199 These and other findings suggest AurA may be a relevant new biomarker or target in the th

200 e contraceptive use in MRM and migraine with aura may decrease both headache frequency and aura.

201 translatable to humans, a subset of migraine auras may belong to a spectrum of hypoperfusion disorder

202 early two decades to gain insight into basic aura mechanisms.

203 nitoring Instrument (OMI) aerosol index, and Aura Microwave Limb Sounder (MLS) CO.

204 ational Aeronautics and Space Administration Aura Microwave Limb Sounder (MLS) to infer an expression

205 ur studies indicate that maternally provided aura (mid1ip1l) acts during the reorganization of the cy

206 These and other observations suggested that AurA might be involved in pathological conditions, such

207 e were classified as having migraine without aura, migraine with aura, or nonmigraine headache.

208 Compared with migraine with aura, migraine without aura was independently associated

209 Migraine with aura, migraine without aura, and control subjects were p

210 s (MEM) to explore turkey vulture (Cathartes aura) migration decisions at both hourly and daily scale

211 ntemporaneous measurements of ozone from the Aura-MLS satellite, although the short time period makes

212 atory system (DPMS) between migraine without aura (MwoA) patients and healthy controls (HC), and 2) i

213 urA interaction to unfolded sequences in the AurA N- and C-termini.

214 8-10.00]; P < .001), either migraine without aura (n = 142; 73.9% vs 26.5%; OR, 7.01 [95% CI, 4.43-11

215 (n = 3243), those with midlife migraine with aura (n = 361) had an increased risk of late-life infarc

216 CI, 4.43-11.09]; P < .001), or migraine with aura (n = 66; 69.7% vs 26.5%; OR, 5.73 [95% CI, 3.07-10.

217 eferential for migraine with aura or without aura, nor were any associations specific for migraine fe

218 Migraine with aura occurs in up to 20-30% of all migraineurs.

219 xceptions, have not been associated with the aura of fundamental physics breakthroughs.

220 The visual aura of migraine is a subjective phenomenon, and what th

221 hrough the cortex and is associated with the aura of migraine.

222 nts, colleagues, and fellow chemists with an aura of nobility and romanticism.

223 ep, the early and acute psychotic state, the aura of temporal lobe epilepsy and hallucinogenic drug s

224 Deja vu can occur as an aura of temporal lobe epilepsy and in some psychiatric c

225 nce with AurA-Cep192 binding did not prevent AurA oligomerization on MTs but abrogated AurA recruitme

226 NPM induces phosphorylation of AurA on serine 89, and this phosphorylation is necessary

227 NPM does not trigger autophosphorylation of AurA on threonine 288.

228 he clinical manifestations of the migrainous aura once an attack has started.

229 Individuals with auras only after epilepsy surgery had a higher COSY than

230 le risk, it may be suggested that those with auras only in a given year be allowed to drive.

231 ith impaired awareness in those experiencing auras only, those with no seizures and those with contin

232 ly similar whether it occurs as an epileptic aura or normal phenomenon.

233 d for women who experienced migraine without aura or who had a past history of migraine.

234 ociations was preferential for migraine with aura or without aura, nor were any associations specific

235 Inhibition of aPKC, AurA, or a downstream target of AurA, HDAC6, restores ci

236 having migraine without aura, migraine with aura, or nonmigraine headache.

237 hed new light on potential defects caused by AurA overexpression.

238 Aqua Atmospheric Infrared Sounder (AIRS) CO, Aura Ozone Monitoring Instrument (OMI) aerosol index, an

239 channel has been identified in migraine with aura patients in a large pedigree.

240 In migraine, both with aura and without aura, patients' choroid thinning should be considered wh

241 ignificantly between patients with different aura phenotypes and with increasing aura duration.

242 hosphatase would be insufficient to restrict AurA phosphorylation and regulate CDK1 activation, where

243 ous diagnoses, including persistent migraine aura, post-hallucinogen flashback, or psychogenic disord

244 criteria for migraine with aura, with visual aura preceding at least 30% of migraines followed by mod

245 Some auras propagated from peripheral to central regions of t

246 terize and quantify a large number of visual auras recorded by a single individual over nearly two de

247 nt AurA oligomerization on MTs but abrogated AurA recruitment to centrosomes and its activation by ei

248 e disease is brought about and the prolonged aura remain incompletely understood.

249 Attacks of migraine with aura represent a phenomenon in which abnormal neuronal a

250 us may represent therapeutic targets for the aura response in migraine.

251 Ozone Monitoring Instrument (OMI) on NASA's Aura satellite in 2005-2015.

252 ional Aeronautics and Space Administration's Aura satellite suggest an approximately 7-10% decrease i

253 e visual disturbance (36%), whereas migraine aura (seven patients) and consumption of illicit drugs (

254 levels, with performance of migraineurs with aura significantly poorer (P < 0.05) than that of contro

255 al seizures with no impairment of awareness (auras, simple partial seizures) continue, if there is a

256 in the cortex produces sensory disturbances (aura) some 20-40 min before the onset of headache.

257 heric Emission Spectrometer (TES) aboard the Aura spacecraft, to investigate aspects of the atmospher

258 free, leveling by 2 years of stable seizure (aura) status.

259 ients had been enrolled at one centre in the AURA study, had shown resistance to a previous EGFR TKI,

260 of circle of Willis variants, migraine with aura subjects had a higher burden of variants than contr

261 le of Willis is more common in migraine with aura subjects than controls, and is associated with alte

262 on between the multifaceted phenomenology of aura symptoms and the effects of CSD on the brain has no

263 atients were studied during various forms of aura symptoms induced by hypoxia, sham hypoxia, or physi

264 ATION: These findings suggest that different aura symptoms reflect different types of cerebral dysfun

265 In migraine, the nature of aura symptoms suggests that sensory cortex may be prefer

266 ateral CSD recorded by fMRI during bilateral aura symptoms.

267 an event that is widely thought to underlie aura symptoms.

268 lationship with the duration and severity of aura symptoms.

269 Ten migraine with aura, ten migraine without aura, and ten age-matched hea

270 isturbance clinically distinct from migraine aura that can be disabling for patients.

271 autosomal dominant subtype of migraine with aura that is associated with hemiparesis.

272 on during interphase and that phosphorylated AurA(Thr-295) acts as a competitor substrate with a CDK1

273 ivity other than PP1 continuously suppresses AurA(Thr-295) phosphorylation during the early embryonic

274 AurA(Thr-295) phosphorylation indeed influenced this tim

275 However, AurA(Thr-295) phosphorylation is restricted throughout t

276 nsitive to OA caused an abnormal increase in AurA(Thr-295) phosphorylation late during interphase tha

277 Studies have linked migraine with aura to an increased risk of ischemic stroke, particular

278 ep192, through a direct interaction, targets AurA to mitotic centrosomes where the locally accumulati

279 pose that two phosphatases target Thr-295 of AurA to prevent premature AurA activation during interph

280 CSD), the proposed mechanism of the migraine aura, to shape the cortical activity that underlies sens

281 ten begin with warning signs (prodromes) and aura (transient focal neurological symptoms) whose origi

282 our major phenotypes (migraine with multiple auras, transient focal neurological deficits without hea

283 atients who have migraines, with and without aura, using spectral optical coherence tomography (OCT).

284 graine type 1 (FHM1), a severe migraine with aura variant, is caused by mutations in the CACNA1A gene

285 nt of a trans-proteolytic activity assay for Aura virus capsid protease (AVCP) based on fluorescence

286 infarcts 23.0% for women with migraine with aura vs 14.5% for women not reporting headaches; adjuste

287 lence of infarcts for men with migraine with aura vs 21.3% for men not reporting headaches; adjusted

288 ed with migraine with aura, migraine without aura was independently associated with CEAD IS (OR, 1.74

289 on between PFO and migraine (with or without aura) was not modified by diabetes mellitus, hypertensio

290 on documenting the shape and location of the aura wavefront or scotoma in the visual field at one min

291 zed and the spatial and temporal features of auras were quantified and analysed.

292 d from trees, and turkey vultures (Cathartes aura) were the primary scavengers of arboreal carrion, s

293 ypertension and migraine, especially without aura, were confirmed as risk factors for CeAD, in additi

294 ts activation of HDAC6 by cytosolic aPKC and AurA, which promotes acetylation of tubulin in primary c

295 e in patients with episodic migraine without aura who habitually experienced premonitory symptoms dur

296 treating cells exclusively expressing the as-AurA with 1-Na-PP1, we discovered that Aurora A is requi

297 eet international criteria for migraine with aura, with visual aura preceding at least 30% of migrain

298 Patients with only auras within the last 1, 2 or 3 years had a COSY of 11.3

299 me during more than 1000 attacks of migraine aura without headache over 18 years.

300 ulum stores rapidly and transiently activate AurA, without requirement for second messengers.