ライフサイエンスコーパス: aura

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

2 early tonic motor features, and sensorimotor aura.

3 acute treatment of migraine with and without aura.

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

5 electrophysiologic event underlying migraine aura.

6 ura may decrease both headache frequency and aura.

7 re monogenic subtype of common migraine with aura.

8 ion (SD), the phenomenon underlying migraine aura.

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

10 graine and in one patient with migraine with aura.

11 support a novel mechanism of activation for AurA.

12 is a key pathogenetic step in migraine with aura.

13 n 4 of 7 patients with otherwise intractable aura.

14 osphorylation is necessary for activation of AurA.

15 d risk of RAO compared with migraine without aura.

16 e phenotype in this variant of migraine with aura.

17 that underlie the headache of migraine with aura.

18 d in migraine attacks that begin with visual aura.

19 vascular unit in the development of migraine aura.

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

21 ree attacks over 3 months while experiencing aura.

22 eatment for some patients with migraine with aura.

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

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

25 icantly higher than those with migraine with aura.

26 device for acute treatment of migraine with aura.

27 slow depolarization that underlies migraine aura.

28 ophobia from migraine with or without visual aura.

29 rment of noise exclusion in migraine without aura.

30 tween headaches in migraine with and without aura.

31 depolarization thought to underlie migraine aura.

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

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

34 and efficacy in patients with versus without aura.

35 hallenging task of capturing patients during aura.

36 redominant sensory phenomenology of migraine aura.

37 n the treatment of migraine with and without aura.

38 extra-axial tissues in migraine with visual aura.

39 l field testing in migraine patients without aura.

40 ed as the cellular correlate of the migraine aura.

41 g the occipital lobe in migraine with visual auras.

42 gned patients with migraine with and without aura (1:1:1:1 ratio) to oral lasmiditan 200 mg, 100 mg,

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

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

45 re consumed, with Turkey Vultures (Cathartes aura, 47%) and American Alligators (Alligator mississipp

46 (56 migraine with aura, 61 migraine without aura, 53 controls).

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

48 170 subjects were enrolled (56 migraine with aura, 61 migraine without aura, 53 controls).

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

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

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

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

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

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

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

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

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

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

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

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

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

62 %) did not (2177 [7.8%] had migraine without aura and 24 246 [87.0%] had no migraine in the year prio

63 s), among whom 1435 (5.2%) had migraine with aura and 26 423 (94.8%) did not (2177 [7.8%] had migrain

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

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

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

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

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

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

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

71 SD is the basis of migraine aura and is increasingly associated with many other brai

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

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

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

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

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

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

78 nsula functional subdivision correlated with aura and reflex component.

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

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

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

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

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

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

85 providing a novel mechanism in migraine with aura and, by extension, the other neurological disorders

86 was also found between the number of visual auras and tracer uptake in occipital PMT.

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

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

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

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

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

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

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

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

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

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

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

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

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

100 Migraine attacks with auras are sometimes associated with underlying hereditar

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

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

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

104 Most aura attacks originated centrally (within 10 degrees ecc

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

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

107 Auras beginning centrally preferentially propagated firs

108 AurA binds, phosphorylates, and reduces the activity of

109 nhibition of kinetochore-associated pools of AurA blocks phosphorylation of microtubule-kinetochore c

110 X-ray crystal structures comparing AurA bound to activating vs inhibiting monobodies reveal

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 Self-reported migraine with aura compared with migraine without aura or no migraine

127 e distribution of other concomitant types of aura, demographic, clinical or neurosurgical variables.

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

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

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

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 ts were adults with migraine with or without aura experiencing 2 to 8 migraine attacks per month.

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

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

138 rly hypermotor signs, early recovery, and no aura from posterior insula features of early dystonia, e

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

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

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

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

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

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

145 at least 45 years, women with migraine with aura had a higher adjusted incidence rate of CVD compare

146 Patients with migraine with aura had a higher risk for incident RAO compared with th

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

148 Some auras had limited propagation and spontaneously 'aborted

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

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

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

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

153 AO compared with those with migraine without aura (HR 1.58 [95% CI 1.40-1.79]; P < .001).

154 20 patients had comorbid migraine, five with aura; (ii) to identify systematically additional visual

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

156 tical spreading depression model of migraine aura in conditional knockout mice.

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

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

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

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

161 n = 11) who experienced headaches and visual aura in the preceding month.

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

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

164 signed adults with migraine, with or without aura, in a 1:1:1 ratio to receive an initial dose of pla

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

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

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

168 y of Polo-like kinase 1 (Plk1) and Aurora A (AurA) inhibitors attenuates kinase activity, produces sp

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

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

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

172 Migraine aura involves sensory percepts, suggesting that sensory

173 Migraine with aura is a common but poorly understood sensory circuit d

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 d risk of all types of RAO and migraine with aura is associated with increased risk of RAO compared w

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

179 Migraine with aura is known to increase the risk of cardiovascular dis

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

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

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

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

184 Aura is vital to identifying seizure onset and relates t

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

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

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

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

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

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

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

192 risk of stroke in people with migraine with aura, it is important to identify and modify any vascula

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

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

195 losteric pocket of the oncoprotein Aurora A (AurA) kinase, thereby offering the potential for more sp

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

213 and migraine with (MA) and migraine without aura (MO) were identified by a screener, which we valida

214 underlies the neurobiology of migraine with aura (MWA).

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

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

217 8-10.00]; P < .001), either migraine without aura (n = 142; 73.9% vs 26.5%; OR, 7.01 [95% CI, 4.43-11

218 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.

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

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

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 The aura of their younger siRNA relatives had also faded dur

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

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

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

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 , 1.98-2.24) for women with migraine without aura or no migraine (P < .001).

233 ine with aura compared with migraine without aura or no migraine at baseline.

234 VD compared with women with migraine without aura or no migraine.

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

236 was intrainsular, clinical signs related to aura or vegetative signs.

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

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

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

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

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

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

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

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

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

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

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

248 Some auras propagated from peripheral to central regions of t

249 ease in the incidence rate for migraine with aura ranged from 1.01 additional cases per 1000 person-y

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

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

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

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

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

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

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

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

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

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

260 iated with haemorrhagic stroke, the migraine aura status has a small influence on this relationship.

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

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

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

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

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

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

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

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

269 ateral CSD recorded by fMRI during bilateral aura symptoms.

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

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

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 The absolute contribution of migraine with aura to CVD incidence in relation to other CVD risk fact

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

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

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

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

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

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

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

286 CI, 2.72-3.99) for women with migraine with aura vs 2.11 (95% CI, 1.98-2.24) for women with migraine

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

288 incidence rate for women with migraine with aura was significantly higher than the adjusted incidenc

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

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

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

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

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

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

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

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

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

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

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

300 ne is strongly associated with migraine with aura, young age, female sex, use of oral contraceptives