ライフサイエンスコーパス: AIS

1 AIS carries a significant risk of mortality and long-ter

2 AIS expression of Nav beta1 was reduced by approximately

3 AIS was calculated on whole-brain beamformer-reconstruct

4 There were 43 hospitals with 1976 AIS and 59 823 STEMI patients.

5 ic profiles were firstly explored between 30 AIS patients and 31 healthy controls by ultra high-perfo

6 idated in an independent cohort including 31 AIS patients and 44 controls.

7 replicated this association in combined 919 AIS cases (P = 3 x 10(-12), OR = 2.2, CI = 1.8-2.7) and

8 lected, as well as head, thorax, and abdomen AIS, and timing of prophylaxis (within 48 hours, 49-72 h

9 Additionally, AIS finds better model parameters and we find evidence o

10 ent of functional independence 90 days after AIS.

11 tive cohort study examined 38 patients after AIS admitted to a tertiary academic medical center betwe

12 which are not possible in all patients after AIS.

13 st, and neurologic outcome in patients after AIS.

14 xonic synapses did not change position after AIS relocation.

15 d the importance of this feedback on ice age AIS evolution.

16 In agreement, AIS distance inversely correlates with the apical dendri

17 Half of all AIS patients had no angiographic evidence of coronary ar

18 ds today, such teleconnections could amplify AIS mass loss and accelerate global sea-level rise.

19 rip-and-ship and mothership hospitals for an AIS eligible to reperfusion therapy; 11 patients had a b

20 One child had an AIS recurrence.

21 associated with limb movement; most lack an AIS, and some are unmyelinated and have no nodes.

22 et of bulbar dopaminergic neurons possess an AIS and that these AIS-positive cells are morphologicall

23 in both CAD (2.7% versus 5.2%; P<0.0001) and AIS (3.5% versus 5.8%; P<0.0001).

24 Among patients hospitalized with CAD and AIS, smoking is a risk factor for early age of onset, ev

25 more expeditious neuroimaging in both HS and AIS.

26 ocalization of Ank-G at nodes of Ranvier and AIS.

27 ng, here we show that all CA1 PC somatic and AIS synapses contain the alpha1, alpha2, beta1, beta2, b

28 twork was reduced in the somatodendritic and AIS compartments, and both the heavy and light chains of

29 formance is correlated on emergent STEMI and AIS care is unknown.

30 s of the estimation of Bayes factors, VL and AIS agree about which model is best but report different

31 [70.1%] and 32 girls [29.9%]; median age at AIS, 7.7 years [interquartile range, 3.1-13.6 years]).

32 ining axon integrity from their functions at AIS and nodes.

33 mediating concentration of those channels at AISs and nodes of Ranvier.

34 The disruption of Nav beta1 AIS expression by a human epilepsy-causing C121W genetic

35 discharge results from a compromise between AIS and somatodendritic oscillators.

36 etic deletion of ankyrinG from RGCs to block AIS reassembly did not affect axon regeneration, indicat

37 mechanism may be specific to ankyrin G-bound AIS proteins because Nav1.2 channels, but not AIS GABAA

38 ty of spike rate coding at the Purkinje cell AIS in mice.

39 esviruses may act as a trigger for childhood AIS, even if the infection is subclinical.

40 imed to investigate the outcome of childhood AIS 12 months after the event in a population-based coho

41 ective population-based studies of childhood AIS have been completed.

42 irus infection doubled the odds of childhood AIS, even after adjusting for age, race, and socioeconom

43 ly treatable, increase the risk of childhood AIS.

44 of choice in any suspected case of childhood AIS.

45 herpesviruses have been linked to childhood AIS in case reports.

46 onset in 172 patients with imaging-confirmed AIS and 133 stroke-free individuals.

47 than 16 years with radiologically confirmed AIS occurring over a 1-year period residing in southern

48 activity but were contingent on the crucial AIS protein, protein kinase CK2.

49 For detecting AIS at an early stage of invasion when the species is ra

50 die before 1 month of age and have disrupted AIS and many other neurological impairments including se

51 KCNQ channel conductance ratio at the distal AIS and nodes arises from the relative strength of bindi

52 cal GABAergic synaptic boutons to the distal AIS, lacks both sodium channels and local exocytotic mac

53 Under baseline conditions, OB dopaminergic AISs were short and located distally along the axon but,

54 During AIS establishment, a membrane diffusion barrier is forme

55 se experiments on hippocampal neurons during AIS development.

56 cate that treatment of patients experiencing AIS due to a large vessel occlusion with IVT before MT d

57 Counterintuitively, we find AIS mass-loss across the full duration of the Antarctic

58 Following AIS, the presence of ASL collaterals is strongly associa

59 ain and that this interaction is crucial for AIS formation and neuronal polarity in cultured rodent h

60 s, EBs, at the proximal axon is decisive for AIS assembly and neuronal polarity.

61 cores predicting sICH risk following IVT for AIS.

62 ective clinical trials that evaluated MT for AIS (Solitaire With the Intention for Thrombectomy perfo

63 formance of time-critical care processes for AIS and STEMI in a coordinated approach.

64 e show that alphaII spectrin is required for AIS assembly, neuronal excitability, cortical lamination

65 , but the underlying mechanisms required for AIS formation remains unclear.

66 n 18 years treated with bridging therapy for AIS with LVO of the anterior circulation.

67 for STEMI and door-to-needle (DTN) time for AIS, with and without controlling for patient and hospit

68 Hospitals' DTN times for AIS did not correlate with D2B times for STEMI (rho=-0.0

69 ients treated within target time windows for AIS and STEMI (median DTN time <60 minutes: 21% [interqu

70 00-positive patients are often excluded from AIS clinical trials but should probably not be denied th

71 the Strait of Gibraltar, which resulted from AIS expansion and local evaporation of sea water in conc

72 Further, AIS allowed decoding of the cued category on a trial-by-

73 e impact of the feedback mechanism on future AIS retreat over centennial and millennial timescales fo

74 nd dendrites have hampered understanding how AIS properties influence neural coding.

75 We implement AIS using proposals derived from Langevin Monte Carlo (L

76 Importantly, AIS cases harbor mainly non-glycine missense mutations a

77 0.57 versus 0.86 in CAD; 0.56 versus 0.86 in AIS) indicates the presence of substantial confounding b

78 question of how bone quality is affected in AIS remains controversy because there is lack of site-ma

79 f initial neuroimaging was non-diagnostic in AIS, then median time to diagnosis was 44 h.

80 that differential metabolites discovered in AIS could be used as potential diagnostic biomarkers and

81 erve a strong reduction in mobility early in AIS development.

82 matrix genes were significantly enriched in AIS cases compared with controls (P = 6 x 10(-9), OR = 1

83 t lesions are significantly less frequent in AIS patients compared with age- and sex-matched patients

84 set to diagnostic neuroimaging was 24.3 h in AIS and 2.9 h in HS.

85 the prognostic value of thyroid hormones in AIS.

86 nding of endotoxin tolerance implications in AIS.

87 ges at different bone hierarchical levels in AIS.

88 ites indicated disrupted lipid metabolism in AIS, including glycerophospholipid, glycerolipid and fat

89 ur findings of increased lipid metabolism in AIS.

90 ng hours resulted in delayed neuroimaging in AIS (13 vs 3 h, p=0.032).

91 s), have emerged as potential key players in AIS formation.

92 Endovascular approaches to recanalization in AIS developed in the 1980s, and recently, 5 major random

93 From the results, in AIS, patients with a poor outcome had lower levels of tr

94 udy was to analyze coronary vessel status in AIS patients with elevated cTn compared with patients pr

95 To explore the role of rare variants in AIS susceptibility, exome sequence data of 391 severe AI

96 Antarctic sedimentary successions indicate AIS expansion at 6 Ma coincident with major MSC desiccat

97 Nav beta1 in both excitatory and inhibitory AIS, it displayed a marked and fine-grained heterogeneit

98 Patients with severe extracranial injuries (AIS >/= 3), death within 72 hours, or hospital stay <48

99 Inverted AIS plasticity in OB dopaminergic cells was bidirectiona

100 e higher intrinsic frequency of the isolated AIS.

101 kG-knockout neurons completely lacking known AIS components still retain distal axonal polarity and g

102 ed that the coat contains a network of known AIS proteins, including ankyrin G, spectrin betaIV, neur

103 y the neuron-specific deletion of the master AIS scaffold AnkyrinG disrupted microglia-AIS interactio

104 Microglia-AIS interactions appear early in development, persist th

105 er AIS scaffold AnkyrinG disrupted microglia-AIS interactions.

106 and EBs induces the assembly of microtubule-AIS structures in the proximal axon.

107 owever, recent evidence showed that, in most AIS patients, myocardial injury is not caused by coronar

108 ted in the expected loss of pyramidal neuron AIS voltage-gated sodium and potassium channels.

109 axons can be remyelinated and reassemble new AIS and nodes of Ranvier.

110 IS proteins because Nav1.2 channels, but not AIS GABAA receptors, were also endocytosed.

111 our findings demonstrate that Southern Ocean-AIS feedbacks were controlled by global atmospheric tele

112 lagen genes were present in 32% (126/391) of AIS cases compared with 17% (146/843) of in-house contro

113 h The Guidelines from 2002 to 2012; 20.4% of AIS and 30.4% of patients with CAD were past-year smoker

114 injury, we performed a detailed analysis of AIS and node disruption after nerve crush.

115 dy reveals a complex genetic architecture of AIS in which a polygenic burden of rare variants across

116 study to explore the potential biomarkers of AIS for early diagnosis.

117 We enrolled 326 centrally confirmed cases of AIS and 115 stroke-free controls with trauma (29 days to

118 l imaging modality was CT in 68% of cases of AIS.

119 The diagnosis of AIS in children is delayed at every stage of the pathway

120 as to define CT skills in early diagnosis of AIS, to define its contribution to patient's diagnosis a

121 CT was diagnostic of AIS in 66% of cases.

122 ring pattern, while the tapering diameter of AIS may define a trigger zone for action potentials.

123 We found significant disruption of AIS and loss of nodes within days of the crush, and comp

124 es and slices, we triggered a unique form of AIS plasticity by selectively targeting M-type K(+) chan

125 xtension of axon as well as the formation of AIS during the early step of neurodevelopment.

126 Such distinct forms of AIS plasticity in inhibitory interneurons and excitatory

127 x-ray studies revealed several hallmarks of AIS, including postnatal onset of scoliosis without malf

128 bility, surface numbers, and localization of AIS Kv7.2/7.3 heteromers using live imaging.

129 However, loss of AIS proteins by the neuron-specific deletion of the mast

130 Seizures at onset of AIS were associated with a poor outcome (Odds Ratio 3.5

131 6 as a genetic cause for the pathogenesis of AIS and PE in a mouse model.

132 tabolism plays a role in the pathogenesis of AIS.

133 ed to be early key players in the process of AIS formation.

134 he results showed that metabolic profiles of AIS patients generally deviated from healthy controls in

135 elination and promote the reestablishment of AIS and nodes of Ranvier is unknown.

136 tion of Ank-G is consistent with the role of AIS in action potential generation.

137 proved nearly 2 decades ago for treatment of AIS, only a minority of patients receive it due to a nar

138 Mean percentage solid volume of AIS/MIA was 8.2% (95% CI: 2.7%, 13.7%) and had a trend t

139 axodendritic distribution of Tau depends on AIS integrity.

140 alized with a first index CAD (n=158 054) or AIS (n=899 295) event in Get With The Guidelines from 20

141 neurofascin-186 (NF186) expressed in the PC AIS during pinceau synapse formation.

142 betaIV spectrin interact and form a periodic AIS cytoskeleton.

143 with ice-sheet retreat significantly reduces AIS mass loss relative to a simulation without these eff

144 as alpha-band-related and beta-band-related AIS increases in content-specific areas; these AIS incre

145 we found significant reestablishment of RGC AIS, remyelination, and even reassembly of nodes in regi

146 Reconstructions of sampled AIS of dopaminergic neurons revealed variable lengths (1

147 res the use of Annealed Importance Sampling (AIS) to address these restrictions.

148 ea Embayment, which records millennial-scale AIS dynamics across this extensive region.

149 Adolescent idiopathic scoliosis (AIS) and pectus excavatum (PE) are common pediatric musc

150 Adolescent idiopathic scoliosis (AIS) is a complex inherited spinal deformity whose etiol

151 Adolescent idiopathic scoliosis (AIS) is a complex spine deformity, affecting approximate

152 We found that the autoinhibitory segment (AIS), located within the CBD, is progressively removed b

153 he 3D structure of the axon initial segment (AIS) along with the entire somatodendritic domain of adu

154 al organization of the axon initial segment (AIS) and action potential initiation is poorly understoo

155 7.3 are located at the axon initial segment (AIS) and exert strong control over action potential gene

156 ubule fascicles in the axon initial segment (AIS) and hexagonal bundles in neurite-like processes in

157 ductance at the distal axon initial segment (AIS) and nodes of Ranvier in a ratio of approximately 40

158 le domains such as the axon initial segment (AIS) and nodes of Ranvier.

159 through changes at the axon initial segment (AIS) and presynaptic terminals.

160 mammalian neurons, the axon initial segment (AIS) electrically connects the somatodendritic compartme

161 The axon initial segment (AIS) is a specialized structure near the start of the ax

162 The axon initial segment (AIS) is a structure at the start of the axon with a high

163 s) within the neuronal axon initial segment (AIS) is critical for efficient action potential initiati

164 The axon initial segment (AIS) is enriched in specific adaptor, cytoskeletal, and

165 The axon initial segment (AIS) is required for generating action potentials and ma

166 The axon initial segment (AIS) is the site of initiation of action potentials and

167 fts and disruptions in axon initial segment (AIS) morphology.

168 innervate the soma and axon initial segment (AIS) of Purkinje cells (PCs) to form the pinceau synapse

169 The axon initial segment (AIS) serves as the site of action potential initiation i

170 s) are enriched in the axon initial segment (AIS) where they bind to ankyrin-G and coregulate membran

171 B), located within the axon initial segment (AIS), controls retrograde (axon-to-soma) and anterograde

172 ates the Purkinje cell axon initial segment (AIS), exerting final inhibitory control over the integra

173 and overlaps with the axon initial segment (AIS), the site where action potentials are generated.

174 plastic changes in the axon initial segment (AIS), which is pivotal for spike generation.

175 The assembly of the axon initial segment (AIS), which is the hallmark of early neuronal polarizati

176 ainly expressed at the axon initial segment (AIS).

177 organizes the neuronal axon initial segment (AIS).

178 iled maturation of the axon initial segment (AIS).

179 channel clustering at axon initial segments (AIS) and nodes of Ranvier.

180 beta1 was enriched at axon initial segments (AIS) and nodes of Ranvier.

181 channel clustering at axon initial segments (AIS) and nodes of Ranvier.

182 Axon initial segments (AISs) and nodes of Ranvier are sites of clustering of vo

183 cipate in assembly of axon initial segments (AISs) and nodes of Ranvier, it is difficult to uncouple

184 e collected intra-operatively from 28 severe AIS patients and 10 matched controls with similar skelet

185 ptibility, exome sequence data of 391 severe AIS cases and 843 controls of European ancestry were ana

186 f marine sectors of the Antarctic Ice Sheet (AIS) in a warming climate has been identified as the lar

187 tica, indicate that the Antarctic ice sheet (AIS) was highly variable through this key time interval.

188 f >/=600 ppm, a smaller Antarctic Ice Sheet (AIS), restricted to the terrestrial continent, was highl

189 s relationships between Antarctic ice-sheet (AIS) dynamics, climate change and sea level.

190 geological evidence of Antarctic ice-sheet (AIS) expansion at the MSC onset and use a delta(18)O rec

191 71 cases of cervical adenocarcinoma in situ (AIS) and adenocarcinoma in the cohort were positive for

192 n the progression to adenocarcinoma in situ (AIS), minimally invasive adenocarcinoma (MIA) and fully

193 carcinoma (LPA), and adenocarcinoma in situ (AIS)/minimally invasive adenocarcinoma (MIA).

194 early detection of aquatic invasive species (AIS).

195 signals via the active information storage (AIS) measure.

196 children with an arterial ischaemic stroke (AIS) and 43 with a haemorrhagic stroke (HS) were identif

197 Arterial ischaemic stroke (AIS) is an important cause of acquired brain injury in c

198 sed in patients with acute ischaemic stroke (AIS).

199 fusion is critical in acute ischemic stroke (AIS) and ST-segment-elevation myocardial infarction (STE

200 Acute Ischemic Stroke (AIS) can be cured by trombolytic treapy within 3-6 hours

201 omes in patients with acute ischemic stroke (AIS) caused by a large vessel occlusion.

202 tion of patients with acute ischemic stroke (AIS) have elevated levels of cardiac troponins (cTn).

203 Acute ischemic stroke (AIS) is the leading cause of disability worldwide and am

204 ones and prognosis of acute ischemic stroke (AIS) reported conflicting results.

205 Patients with acute ischemic stroke (AIS) suffer from infections associated with mortality.

206 ICH) in patients with acute ischemic stroke (AIS) treated with intravenous thrombolysis (IVT).

207 recommended to treat acute ischemic stroke (AIS) with a large vessel occlusion (LVO).

208 ery disease (CAD) and acute ischemic stroke (AIS), but there are numerous reports of lower in-hospita

209 uently observed after acute ischemic stroke (AIS), indicating poor functional outcome and increased m

210 enous thrombolysis in acute ischemic stroke (AIS).

211 increased risk of arterial ischemic stroke (AIS).

212 for the treatment of acute ischemic stroke (AIS).

213 gic outcome following acute ischemic stroke (AIS).

214 in vitro and in vivo can produce structural AIS changes in excitatory cells that have been linked to

215 is the acquired, or adaptive, immune system (AIS), which is composed of both humoral and cell-mediate

216 dy including patients with blunt severe TBI (AIS >/= 3), those that received LMWH or UH VTE prophylax

217 position relative to the soma and found that AIS distal relocation of both Nav and Kv7 channels elici

218 Myelination starts after the AIS as well as the distribution of Nav channels on the a

219 proximately 190-nm-spaced segments along the AIS axis as early as day in vitro 4, and this pattern al

220 together with Nav and Kv7 segments along the AIS suggests that these channels relocate as a structura

221 eriments indicate that polar climate and the AIS were highly sensitive to relatively small changes in

222 nce of the spectrin cytoskeleton both at the AIS and throughout the nervous system.SIGNIFICANCE STATE

223 Nav beta1 expression at the AIS was detected throughout the brain, predominantly in

224 80AnkG localization and stabilization at the AIS, whereas 480AnkG is required for the specific accumu

225 d that Ank-G colocalized with TH only at the AIS.

226 ctrin to form a periodic cytoskeleton at the AIS.

227 d computational modeling, constrained by the AIS location and realistic dendritic and axonal morpholo

228 ring the basic building blocks composing the AIS, but the underlying mechanisms required for AIS form

229 these amyloid-beta-induced disruptions, the AIS/TDB sorting function failed, causing AD-like Tau mis

230 nisms used by 480 kDa ankyrin-G to drive the AIS formation and thereby to establish neuronal polarity

231 ockdown leads to a reduction of KCNQ2 in the AIS and a reduction in whole-cell KCNQ currents.

232 de-gated (HCN) channels are expressed in the AIS and decrease spike probability, in a manner distinct

233 an organizer of channel localization in the AIS and provide insight into the coordination of KCNQ an

234 ol of spike threshold by HCN channels in the AIS can be altered through serotonergic modulation of 5-

235 effects of voltage-gated ion channels in the AIS from those of the soma and dendrites have hampered u

236 Membrane protein motion in the AIS plasma membrane is confined to a repetitive pattern

237 d, the latter mimicking bundles found in the AIS.

238 ng and decreased microtubule dynamics in the AIS.

239 Therefore, in pyramidal neurons, the AIS location is finely tuned with the somatodendritic ca

240 Normally the AIS performs two tasks in concert, stabilizing neural po

241 eurons results in an outward movement of the AIS and a decrease in the cell's excitability.

242 uditory nucleus lead to a lengthening of the AIS and an increase in neuronal excitability.

243 exon of AnkG is required for assembly of the AIS and nodes of Ranvier and was a transformative innova

244 l axonal polarity as well as assembly of the AIS and normal morphogenesis of nodes of Ranvier all req

245 ules with the nanoscopic organization of the AIS cytoskeleton.

246 ts provide insight into the potential of the AIS for threshold behavior and have implications for its

247 Differences in the size of the AIS likely underlie differences in firing pattern, while

248 hat 480-kDa AnkG is a major component of the AIS membrane "undercoat' imaged by platinum replica elec

249 Few cases of synaptic innervation of the AIS of dopaminergic neurons were observed.

250 confirmed that a more proximal onset of the AIS slightly reduced the efficacy of action potential ge

251 tep construction of a prototype mimic of the AIS that we call an adaptive immune response simulator (

252 rtificial analogues of the components of the AIS to create a system that responds to specific molecul

253 length between the soma and the start of the AIS, and to produce invariant somatic APs, it must scale

254 ational modeling showed that the size of the AIS, but not its position within the somatodendritic dom

255 ein ankyrin-G is the master-organizer of the AIS.

256 -2 for 48 h leads to an outward shift of the AIS.

257 hin axons facilitate the excitability of the AIS.

258 ing rate with both proximity and size of the AIS.

259 ialized extracellular matrix surrounding the AIS, did not disrupt the interaction.

260 These interneurons exclusively target the AIS of pyramidal neurons and form rows of presynaptic bo

261 hannels, which predominantly localize to the AIS and are essential for tuning neuronal excitability.

262 mechanisms governing KCNQ trafficking to the AIS are incompletely understood.

263 ial current is inversely proportional to the AIS distance, denoting the path length between the soma

264 cluding recruitment of beta4 spectrin to the AIS that likely is regulated by phosphorylation, and dem

265 eta; an AD-associated kinase tethered to the AIS) was overexpressed.

266 ions, we examined the effects of varying the AIS position relative to the soma and found that AIS dis

267 ankyrin-G (Ank-G) was used to visualize the AIS of dopaminergic neurons.

268 Here, we investigated whether the AIS is capable of undergoing structural plasticity in ra

269 In contrast, while the AIS in demyelinated axons started more closely to the so

270 icroglia that specifically interact with the AIS in the adult cortex.

271 ng, we observed that microtubules within the AIS appeared highly dynamic, a feature essential for the

272 The TDB (located within the AIS) was impaired when AIS components (ankyrin G, EB1) w

273 h exerting little effect on VGSCs within the AIS.

274 urons, we identified and characterized their AIS in the mouse.

275 gically and functionally distinct from their AIS-negative counterparts.

276 S increases in content-specific areas; these AIS increases were behaviorally relevant in the brain's

277 nergic neurons possess an AIS and that these AIS-positive cells are morphologically and functionally

278 in M-channel activity rapidly trigger unique AIS plasticity to stabilize network excitability.

279 o the most basic responses of the vertebrate AIS, including reaction sequences that mimic both humora

280 B (located within the AIS) was impaired when AIS components (ankyrin G, EB1) were knocked down or whe

281 c basis, few genes have been associated with AIS and the pathogenesis remains poorly understood.

282 6) were recently shown to be associated with AIS in humans.

283 common genetic variants are associated with AIS, they explain only a small portion of disease risk.

284 ning long-term acoustic monitoring data with AIS vessel-tracking data and acoustic propagation modell

285 ied sample size estimation, 29 patients with AIS (median age, 76 years [first-third quartiles, 70-82

286 cally identify the minority of patients with AIS and angiographic evidence of a culprit lesion.

287 g mitochondrial DNA (mtDNA) in patients with AIS correlated with impaired inflammatory response of is

288 y, we show that monocytes from patients with AIS exhibit a refractory state or endotoxin tolerance.

289 ntation did not differ between patients with AIS or NSTE-ACS (95 versus 94 ng/L; P=0.70).

290 Among 2123 consecutive patients with AIS prospectively screened at 2 tertiary hospitals, 13.7

291 pectively gathered registry of patients with AIS to select patients admitted through the Saint-Antoin

292 dently associated with sICH in patients with AIS treated with IVT.

293 d with patients with NSTE-ACS, patients with AIS were less likely to have coronary culprit lesions (7

294 es of sICH complicating IVT in patients with AIS with pretreatment MRI were extracted independently f

295 The study enrolled 14 patients with AIS, without previous treatment, and 10 healthy controls

296 uded 9 studies comprising 2479 patients with AIS.

297 tool for imaging selection in patients with AIS.

298 modal imaging in the triage of patients with AIS.

299 in an independent cohort of 23 patients with AIS.

300 erent zones of histologic progression within AISs and MIAs.