ライフサイエンスコーパス: AIS

1 AIS patients eligible for intravenous r-tPA therapy were

2 igh amounts of uronic acid (179-300 mg g(-1) AIS) and relatively high amounts of cellulosic glucose (

3 unts of cellulosic glucose (118-214 mg g(-1) AIS).

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

5 esected lung nodules including AAH (n = 22), AIS (n = 27), MIA (n = 54) and synchronous ADC (n = 13).

6 In addition, in the parallel study of 99 AIS (27 with severe Cobb angle of 65.8 +/- 14.1 degrees

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

8 ally, Ecm29 KO neurons exhibited accelerated AIS developmental positioning, reflecting a perturbed AI

9 ng outcomes with presence of FLAIR-HAs after AIS.

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

11 which are not possible in all patients after AIS.

12 w data, and reveal that the LIG contained an AIS-derived highstand from ~129.5 to ~125 ka, a lowstand

13 outcomes in patients with and without DM and AIS treated with IVT.

14 esults indicate the transient expression and AIS localization of NuMA1 stabilizes the developing AIS

15 However, the nature and drivers of GrIS and AIS reductions remain enigmatic, even though they may be

16 Mortality was associated with higher ISS and AIS scores.

17 ind that ZDHHC14 controls palmitoylation and AIS clustering of PSD93 and also of Kv1 potassium channe

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

19 we quantify the impact of RCP scenarios and AIS contributions on 21st-century ESL changes at tide-ga

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

21 By tracking vessels with theodolite and AIS, while recording ambient noise levels, we find that

22 [70.1%] and 32 girls [29.9%]; median age at AIS, 7.7 years [interquartile range, 3.1-13.6 years]).

23 odal beta4 spectrin, it cannot compensate at AIS.

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

25 who had early decompression also had better AIS grades at 1 year after surgery, indicating less seve

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

27 Both AIS and ABD geometries were found to be highly variable

28 and more powerful recreational vessels carry AIS-transmitters.

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

30 However, the mechanisms controlling AIS assembly remain poorly defined.

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

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

33 alization of NuMA1 stabilizes the developing AIS by inhibiting endocytosis and removal of AIS protein

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

35 pectrin causes motor impairment and disrupts AIS, loss of beta1 spectrin has no discernable effect on

36 known AIS proteins, and their loss disrupts AIS structure and function.

37 cing NuMA1 or protein 4.1B by shRNA disrupts AIS assembly, but not maintenance.

38 dy reveals feedback-based mechanisms driving AIS assembly.

39 ilencing Lis1 or overexpressing NuMA1 during AIS assembly increased the density of AIS proteins, incl

40 ive serine phosphorylation patterns for each AIS endophenotype resulting in a differential reduction

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

42 motor scores and common odds ratio (cOR) for AIS grade, with corresponding 95% CIs.

43 to direct mechanical thrombectomy (dMT) for AIS patients with large vessel occlusion (LVO).

44 ce for safety concerns, compared to dMT, for AIS patients with LVO.

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

46 We show AnkR lacks the domain necessary for AIS localization.

47 ovide conceptual insights and a resource for AIS molecular organization, the mechanisms of AIS stabil

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

49 with outcome after endovascular therapy for AIS.

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

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

52 associated flux values (1.4 Gmol y(-1)) from AIS to the Fe-deplete Southern Ocean exceed most previou

53 NF1 were found to increase in frequency from AIS and MIA to ADC.

54 r findings reveal a novel role for YKL-40 in AIS pathogenesis and a new molecular mechanism interferi

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

56 as an increase in lacunar volume and area in AIS.

57 tumor heterogeneity establishes early, as in AIS.

58 e in vivo Our data reveal notable changes in AIS length and thickness throughout cell maturation unde

59 How these components cooperate in AIS formation is currently poorly understood.

60 s the 3D patterns of the spinal deformity in AIS patients with the same S shaped sagittal spinal curv

61 arative safety and efficacy of BT and dMT in AIS patients.

62 aratus protein 1 (NuMA1) is downregulated in AIS-deficient neonatal mouse brains and neurons.

63 the prognostic value of thyroid hormones in AIS.

64 nd neuroinflammatory responses implicated in AIS pathogenesis [9].

65 nding of endotoxin tolerance implications in AIS.

66 ges at different bone hierarchical levels in AIS.

67 ently, the cause underlying low bone mass in AIS remains elusive.

68 the observed abnormal bone mineralization in AIS, which may shed light on etiopathogenesis of AIS.

69 s of Vickers hardness and elastic modulus in AIS when compared with controls.

70 l a higher proportion of clonal mutations in AIS/MIA/ADC than AAH suggesting neoplastic transformatio

71 hereas more copy number loss was observed in AIS and MIA.

72 receptor signaling dysfunction occurring in AIS and provides the first evidence for its hereditary n

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

74 ism and mineral homeostasis, but its role in AIS has not been studied.

75 mpairment of melatonin receptor signaling in AIS osteoblasts allowing the classification of patients

76 rons to determine cell-to-cell variations in AIS and ABD geometry, and their influence on neuronal ou

77 and AP shape, such that large variations in AIS geometry negligibly affect neuronal output and are t

78 we describe large cell-to-cell variations in AIS length or distance from the soma in rat substantia n

79 ry of D2R-induced AP threshold plasticity in AISs of stellate cells.

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

81 or baseline score, age, mechanism of injury, AIS grade, level of injury, and administration of methyl

82 th the Ecm29 N-terminal domain and an intact AIS structure are required for transport and tethering o

83 function) with risk of developing ischaemic (AIS), cardioembolic (CES), large artery (LAS), and small

84 a lowstand centred on 125-124 ka, and joint AIS + GrIS contributions from ~123.5 to ~118 ka.

85 are located at the AIS, interact with known AIS proteins, and their loss disrupts AIS structure and

86 , freeze-dried (FD) and cell wall materials (AIS) of raw and processed apples.

87 or gAnkG and its partners than in the mature AIS.

88 Moreover, AIS development can be modulated extrinsically by both n

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

90 b angle of 55.6 +/- 10.61 degrees and 13 non-AIS controls (mean age of 16.5 +/- 4.79 yr old) intraope

91 tions from vessels with and without AIS (non-AIS) in a shallow coastal area within the Inner Danish w

92 rding ambient noise levels, we find that non-AIS vessels have a higher occurrence (83%) than AIS vess

93 anterior circulation large vessel occlusion AIS treated with endovascular-reperfusion therapy with o

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

95 during AIS assembly increased the density of AIS proteins, including ankyrinG and neurofascin-186 (NF

96 a(v)1.6 to the AIS; nor was the diffusion of AIS inserted channels altered relative to WT.

97 trin alone, including profound disruption of AIS Na(+) channel clustering, progressive loss of nodal

98 Here we examined the dynamics of AIS formation in newborn DGCs of young female adult C57B

99 NuMA1 inhibits the endocytosis of AIS NF186 by impeding Lis1's interaction with doublecort

100 which may shed light on etiopathogenesis of AIS.

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

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

103 ms that may facilitate the identification of AIS patients at risk of spinal deformity progression.

104 scanning electron microscopy (SEM) images of AIS demonstrated abnormal osteocytes that were more roun

105 What is the impact of AIS geometry on excitability?

106 and pacemaking frequency were independent of AIS geometry.

107 endocytosis was responsible for the lack of AIS accumulation.

108 Interestingly, the lack of AIS targeting resulted in an elevated percentage of pers

109 While the mechanisms of AIS Na(+) and K(+) channel clustering are understood, th

110 IS molecular organization, the mechanisms of AIS stability, and polarized trafficking in neurons.

111 work thus defines a new preclinical model of AIS and provides tools to realize novel therapeutic stra

112 xon initial segment (AIS), and modulation of AIS size by recruitment or loss of proteins can influenc

113 e chimeras map the molecular organization of AIS intracellular membrane, cytosolic, and microtubule c

114 trials that provided data on the outcomes of AIS patients with LVO stratified by IVT treatment status

115 A long-held assumption in pathogenesis of AIS is that the upright spine in human plays an importan

116 AIS by inhibiting endocytosis and removal of AIS proteins.

117 effects(8), suggesting that the response of AIS grounding lines to Northern Hemisphere sea-level for

118 r levels of factor XI are at reduced risk of AIS compared to those with normal levels of factor XI.

119 results further define the important role of AIS and nodal spectrins for nervous system function.

120 s [4] have confounded basic understanding of AIS biology; thus, treatment options remain limited [5,

121 xcitability and adds to our understanding of AIS maintenance and plasticity, in addition to identifyi

122 information on the role of river barriers on AIS distribution and eDNA detection is important for man

123 opmental positioning, reflecting a perturbed AIS morphological plastic response to hyperexcitability

124 behavioural responses in harbour porpoises (AIS vessels caused 5-24%).

125 signalling dysfunction occurring in primary AIS osteoblasts.

126 o identify molecular determinants of ChC/PyN AIS innervation, we performed an in vivo RNAi screen of

127 to be the only molecule required for ChC/PyN AIS innervation.

128 required for innervation of neocortical PyN AISs by ChCs.

129 erlying their subcellular innervation of PyN AISs are unknown.

130 ation, and that selective innervation of PyN AISs by ChCs requires AIS anchoring of L1CAM by the cyto

131 Under RCP8.5 and rapid AIS mass loss, many tropical sites, including low-lying

132 However, the reduced AIS surface expression of the MAP1B mutant was restored

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

134 We provide a simple formula relating AIS geometry and sodium conductance density to the somat

135 ent (AIS) in vivo Our data reveal remarkable AIS structural remodeling throughout the maturation of t

136 ive innervation of PyN AISs by ChCs requires AIS anchoring of L1CAM by the cytoskeletal ankyrin-G/bet

137 rms microtubule arrays that closely resemble AIS fascicles in neurons.

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

139 ondary endpoints were ASIA Impairment Scale (AIS) grade and change in upper-extremity motor, lower-ex

140 pinal injuries association Impairment Scale (AIS) grades A-C, we induced cord hypothermia (33 degrees

141 erity based on the abbreviated injury scale (AIS) and injury severity score (ISS).

142 classified via the abbreviated injury scale (AIS): 39.3% with AIS = 3, 51.3% with AIS = 4 and 60% wit

143 Adolescent idiopathic scoliosis (AIS) affects 3% to 4% of children between the ages of 11

144 Adolescent idiopathic scoliosis (AIS) is a prevalent spinal deformity occurring during pe

145 Adolescent idiopathic scoliosis (AIS) is a three-dimensional (3D) deformity of the spinal

146 gression in adolescent idiopathic scoliosis (AIS) remain poorly understood.

147 luding an N-terminal autoinhibitory segment (AIS), four predicted cyclic nucleotide-binding domains (

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

149 D(2) R-MSN soma and axonal initial segment (AIS) by GABAergic and cholinergic interneurons.

150 Axon initial segment (AIS) functionality relies on a specific organization of

151 n many neuronal types, axon initial segment (AIS) geometry critically influences neuronal excitabilit

152 n many neuronal types, axon initial segment (AIS) geometry critically influences neuronal excitabilit

153 born DGCs, namely, the axon initial segment (AIS) in vivo Our data reveal remarkable AIS structural r

154 IFICANCE STATEMENT The axon initial segment (AIS) is a specialized region at the proximal axon where

155 The axon initial segment (AIS) is a unique neuronal compartment that plays a cruci

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

157 ectively innervate the axon initial segment (AIS) of excitatory pyramidal neurons; the subcellular do

158 utant Tau-V337M blocks axon initial segment (AIS) plasticity, causing neuronal hyperexcitability.

159 adaptor Ecm29 and the axon initial segment (AIS) scaffold protein ankyrin G.

160 The axon initial segment (AIS) separates the axon from the somatodendritic compart

161 ic transmission at the axon initial segment (AIS) showed that axo-axonic synapses were depolarizing d

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

163 ation at the mammalian axon initial segment (AIS), and modulation of AIS size by recruitment or loss

164 ese cells, namely, the axon initial segment (AIS), has remained unexplored to date.

165 eurons (PyNs) at their axon initial segment (AIS), the site of action potential initiation, allowing

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

167 GUKs, localizes to the axon initial segment (AIS).

168 ts localization at the axon initial segment (AIS).

169 ly concentrated at the axon initial segment (AIS).

170 he cytoskeleton in the axon initial segment (AIS).

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

172 organizes the neuronal axon initial segment (AIS).

173 the distal end of the axon initial segment (AIS).

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

175 ning in the length of axon initial segments (AIS) in the mPFC of PNI mice.

176 does not function at axon initial segments (AIS).

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

178 Axon initial segments (AISs) generate action potentials and regulate the polari

179 Axon initial segments (AISs) initiate action potentials and regulate the traffi

180 tory puncta, longer axonal initial segments (AISs), and higher PV expression when compared with PV+ c

181 ordinates assembly of axon initial segments (AISs), which are sites of action potential generation lo

182 nnels and D2Rs in the axon initial segments (AISs).

183 way (RCP) scenarios and Antarctic Ice Sheet (AIS) melt propagate into uncertainties in projected mean

184 nd, so that substantial Antarctic Ice Sheet (AIS) reduction is implied.

185 ne-based sectors of the Antarctic Ice Sheet (AIS)(1-3).

186 ce Sheet (GrIS) and the Antarctic Ice Sheet (AIS).

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

188 s hyperplasia (AAH), adenocarcinoma in situ (AIS), minimally invasive adenocarcinoma (MIA) or invasiv

189 ods: DNA was extracted from 21 ADCs in situ (AISs), 27 minimally invasive ADCs (MIAs), and 54 fully i

190 in milk (EIM), and aqueous iodine solution (AIS) - subjects collected 24-h urine over 3 d and consum

191 sed for monitoring aquatic invasive species (AIS) such as the American signal crayfish (Pacifastacus

192 and prognosis after acute ischaemic stroke (AIS).

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

194 atus of patients with acute ischemic stroke (AIS) during intravenous r-tPA therapy and associated CA

195 e vessel occlusion in acute ischemic stroke (AIS) is time dependent, but the extent to which it influ

196 inical improvement in acute ischemic stroke (AIS) patients treated with mechanical thrombectomy (MT),

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

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

199 omes of patients with acute ischemic stroke (AIS) treated with intravenous thrombolysis (IVT) are con

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

201 enous thrombolysis in acute ischemic stroke (AIS).

202 ool to assess the significance of structural AIS plasticity for electrical function.

203 ht and electron microscopy approach to study AIS microtubule organization.

204 h surveys (DHSs) and AIDS indicator surveys (AISs) (collected between 2008-2009 and 2015-2016), which

205 905 androgen insensitivity syndrome (AIS)-associated loss-of-function mutants and 168 prostat

206 odels using Automatic Identification System (AIS) data.

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

208 vessels have a higher occurrence (83%) than AIS vessels, and that motorised recreational vessels can

209 We therefore conclude that AIS data would poorly predict vessel noise pollution and

210 Moreover, we demonstrate that AIS development can be modulated extrinsically by both n

211 ed to a global sea-level model, we show that AIS dynamics are amplified by Northern Hemisphere sea-le

212 human neurons with this mutation showed that AIS plasticity is impaired by the abnormal accumulation

213 The AIS (alcohol-insoluble solids) were characterised by hig

214 The AIS is not only the site of action potential initiation,

215 In addition the AIS separates the axon from the somatodendritic compartm

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

217 he AIS complex to the proximal axon, and the AIS channel protein Kv7.3 regulates neuron excitability.

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

219 NuMA1 is transiently located at the AIS during development where it interacts with the scaff

220 exes, TRIM46 levels steadily increase at the AIS during early neuronal differentiation and at the sam

221 urface but reduced surface expression at the AIS of cultured rat embryonic hippocampal neurons from b

222 ses bidirectionally until immobilised at the AIS through its interaction with AnkyrinG.

223 a hyperpolarizing current is present at the AIS, due to resistive coupling with the soma.

224 We show many are located at the AIS, interact with known AIS proteins, and their loss di

225 table accumulation of Neurofascin-186 at the AIS.

226 he steady-state abundance of Na(v)1.6 at the AIS.

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

228 ctrin to form a periodic cytoskeleton at the AIS.

229 ated proteins not previously reported at the AIS.

230 pecific ships whose data are provided by the AIS system.

231 pecialized microtubule tracks that enter the AIS.

232 Interestingly the microtubules entering the AIS form crosslinked bundles, called microtubule fascicu

233 Concentrations are higher from the AIS than the GrIS, highlighting the geochemical conseque

234 lation and mass spectrometry to identify the AIS proteome.

235 ghstand suggests temporal variability in the AIS contributions.

236 he 3D spinal deformity as is observed in the AIS population.

237 ncreases the density of NKCC1 protein in the AIS region, a change that positively correlates with a d

238 ransport and tethering of proteasomes in the AIS region.

239 lation of end-binding protein 3 (EB3) in the AIS submembrane region.

240 ng and decreased microtubule dynamics in the AIS.

241 e in organizing microtubule fascicles in the AIS.SIGNIFICANCE STATEMENT The axon initial segment (AIS

242 Interestingly, the AIS has a characteristic microtubule organization; it co

243 line advance and associated mass gain of the AIS during glaciation, and grounding-line retreat and ma

244 ing in our model increases the volume of the AIS during the Last Glacial Maximum (about 26,000 to 20,

245 eologic reconstructions of the extent of the AIS during the Last Glacial Maximum and subsequent ice-s

246 the physiological form), the binding of the AIS is necessary to keep Plasmodium PKG inactive.

247 A distal shift of the AIS normally produces a (modest) increase in excitabilit

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

249 The assembly of the AIS requires membrane, scaffolding, and cytoskeletal pro

250 crete intermediate stage in formation of the AIS that is regulated through phosphorylation of the neu

251 Both position and length of the AIS vary across and within neuron types, with activity,

252 ity relies on a specific organization of the AIS with high enrichment of structural and functional pr

253 normally occurs early in development of the AIS.

254 if, thus allowing long-term stability on the AIS surface.

255 alizes to the AIS, where it may organize the AIS microtubules.

256 we have studied how these proteins reach the AIS.

257 86) has an essential role in stabilising the AIS complex to the proximal axon, and the AIS channel pr

258 the molecular mechanisms that stabilize the AIS and control neuronal polarity remain obscure.

259 nd electron microscopy approach to study the AIS microtubules during neuron development and identifie

260 Recent studies that indicate that the AIS experienced substantial millennial-scale variability

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

262 eveals how key proteins are delivered to the AIS and thereby how they may contribute to its functiona

263 bule binding protein TRIM46 localizes to the AIS and when overexpressed in non-neuronal cells forms m

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

265 We target the biotin-ligase BirA* to the AIS by generating fusion proteins of BirA* with NF186, N

266 bule-binding protein TRIM46 localizes to the AIS, where it may organize the AIS microtubules.

267 than a failure of forward trafficking to the AIS.

268 Kv7.3 is similarly recruited to the AIS.

269 cruitment of gAnkG and beta4-spectrin to the AIS.

270 and preferential delivery of Na(v)1.6 to the AIS; nor was the diffusion of AIS inserted channels alte

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

272 are in a pentagonal configuration, with the AIS docked in the substrate site of the KD in a swapped-

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

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

275 Comparing AAH to AIS, MIA and ADC, we observe progressive genomic evoluti

276 early lung carcinogenesis model from AAH to AIS, MIA and ADC.

277 Although endocytosis contributes to AIS turnover, how membrane proteins traffic to this prox

278 probability of large ESL changes but due to AIS uncertainties, cannot fully eliminate the probabilit

279 nt modeling suggests that this robustness to AIS variation is mainly explained by the complexity and

280 ute to the prognosis of thrombolysis-treated AIS patients for sICH and mortality.

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

282 e abbreviated injury scale (AIS): 39.3% with AIS = 3, 51.3% with AIS = 4 and 60% with AIS = 5 patient

283 scale (AIS): 39.3% with AIS = 3, 51.3% with AIS = 4 and 60% with AIS = 5 patients underwent surgical

284 ith AIS = 3, 51.3% with AIS = 4 and 60% with AIS = 5 patients underwent surgical interventions.

285 S/CES; and increased factor XI activity with AIS/CES).

286 SVS (e.g. reduced factor VIII activity with AIS/CES/LAS; raised factor VIII antigen with AIS/CES; an

287 is inhibitor activation peptide antigen with AIS.

288 AIS/CES/LAS; raised factor VIII antigen with AIS/CES; and increased factor XI activity with AIS/CES).

289 ateletcrit was significantly associated with AIS/CES, eosinophil percentage of white cells with LAS,

290 fibrinogen was significantly associated with AIS/CES.

291 lotype showed the strongest association with AIS patients in endophenotype FG2 (P = 9.9 x 10(-6) and

292 nor pacemaking frequency is correlated with AIS morphology.

293 posteroanterior radiographs of patients with AIS (age range, 10-18 years, 70% female) were collected

294 tissues were harvested from 21 patients with AIS (mean age of 14.3 +/- 2.20 yr old) with a mean Cobb

295 Among patients with AIS due to large vessel occlusion treated in routine cli

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

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

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

299 in an independent cohort of 23 patients with AIS.

300 contributions from vessels with and without AIS (non-AIS) in a shallow coastal area within the Inner