ライフサイエンスコーパス: CSD

1 CSD analysis revealed no appreciable local generator con

2 CSD and ISD were associated with an increased risk of un

3 CSD decreased sustained VT and ICD shock recurrence in p

4 CSD increased 20-HETE synthesis in brain slices for 120

5 CSD initiated in Ins and S1 induced facilitation and inh

6 CSD is clinically and genetically heterogeneous.

7 CSD reduced ABP in 2K1C+CSD rats and prevented the furth

8 CSD reduced the burden of ICD shocks from a mean of 18 +

9 CSD significantly altered cortical sensory processing on

10 CSD triggered in V1 affects differently Ins and S1 corti

11 CSD was also decreased by the antiepileptic drug topiram

12 CSD was analyzed in rat neocortical slices by imaging of

13 CSD was elicited chemically in adult rats and occurrence

14 CSD was induced in anesthetized male rats by stimulation

15 CSD was induced in the frontal cortex of rats and the co

16 CSD was measured as the percentage of the maximal surfac

17 CSD, elicited by pressure microinjection of KCl, was rec

18 CSD-defined alpha generators were strongest in the supra

19 CSD-dependent open-state trapping is observed during a v

20 CSD reduced ABP in 2K1C+CSD rats and prevented the further progressive increase

21 localization was disrupted by MbetaCD and a CSD peptide.

22 experimental model for the regeneration of a CSD in the axolotl (the Excisional Regeneration Model) t

23 Making use of the intrinsic properties of a CSD microscope, we illuminate stroboscopically, generati

24 Overall, our investigation based on a CSD approach has opened a new strategy towards a general

25 fectly, yet like mammals do not regenerate a CSD.

26 l and expand the search scope for additional CSD binding partners.

27 ngest ages, systemic nicotine did not affect CSD profiles.

28 re we tested the hypothesis that TNF affects CSD, and we explored the direction in which CSD is modif

29 .0 +/- 0.7 at baseline and 1.8 +/- 0.7 after CSD.

30 2 before CSD (baseline) to 6.1 +/- 1.8 after CSD (p < 0.0001) for a period >13 minutes.

31 mice than WT mice and almost abolished after CSD.

32 d sensory responses in rat, before and after CSD, using multielectrode array recordings and two-dimen

33 onitored in vivo in the rat before and after CSD.

34 in 20-HETE cause the reduction in CBF after CSD and that the attenuation of stimulation-induced CBF

35 0-HETE paralleled the reduction in CBF after CSD in vivo.

36 ot the impaired neurovascular coupling after CSD.

37 oconstriction and vascular dysfunction after CSD.

38 gan within 0.9 +/- 0.4 (0-2.5) minutes after CSD in 7 neurons located in laminae I-II, or after a lat

39 ith ICD shock recurrence and mortality after CSD.

40 n of stimulation-induced CBF responses after CSD has a different mechanism.

41 reduced surface area (were sharpened) after CSD.

42 gy residents and patient registrations among CSD member organizations.

43 and show that the oligomerization domain and CSD are protected by tight association with the membrane

44 The discrepancy between LFP and CSD findings appears to be attributable to contamination

45 identified a functional link between TNF and CSD.

46 spreading depolarisations were classified as CSD; 20 patients had at least one ISD.

47 (spikes/s) increased from 3.6 +/- 1.2 before CSD (baseline) to 6.1 +/- 1.8 after CSD (p < 0.0001) for

48 In comparison, before CSD, Ca(2+) and hemodynamic responses to somatosensory s

49 nts taking antiarrhythmic medications before CSD, 39 (32%) no longer required them at follow-up.

50 urthermore, we provide evidence of bilateral CSD recorded by fMRI during bilateral aura symptoms.

51 n of 30 +/- 13%) underwent left or bilateral CSD.

52 zation usually associated with cAMP binding, CSD deletion removes rather than mimics the kinetic effe

53 ccurred simultaneously, with mainly biphasic CSD-associated p(ti)O(2) responses comprising a primary

54 Conclusion Whole-brain CSD-based fiber tractography and super-resolution TDI ma

55 In 25 trigeminovascular neurons activated by CSD, mean firing rate (spikes/s) increased from 3.6 +/-

56 7 trigeminovascular neurons not activated by CSD, mean firing rate was 2.0 +/- 0.7 at baseline and 1.

57 olling the growth of oxide nanostructures by CSD, and some attractive kinetic features will also be p

58 ctric oxide thin films and nanostructures by CSD, with special emphasis on nucleation and growth phen

59 ctivation and sensitization of HT neurons by CSD.

60 elta but not C-type meningeal nociceptors by CSD.

61 ctivation-deactivation cycle is preserved by CSD substitution, but the change in deactivation kinetic

62 similar to yeast (Saccharomyces cerevisiae) CSD.

63 The simple adaptation of conventional CSD equipment allows superresolution investigations of a

64 Lastly, current CSD-based methods for processing of ferroelectric oxide

65 The Cambridge Structural Database (CSD) now stores data for nearly 700,000 structures and i

66 ules from the Cambridge Structural Database (CSD) using the same pharmacophore query further emphasiz

67 data from the Cambridge Structural Database (CSD, a database built over 50 years of community effort)

68 e-brain constrained spherical deconvolution (CSD)-based tractography data and super-resolution track-

69 D and rats exposed to chronic social defeat (CSD) stress, which is used to model depression.

70 ated, resulting in a "critical-size defect" (CSD).

71 d into rat critical-sized calvarial defects (CSD).

72 Carotid sinus nerve denervation (CSD) has recently been shown to relieve hypertension and

73 shown that carotid sinus nerve denervation (CSD) reduces arterial blood pressure (ABP) in SHR.

74 Successful carotid sinus nerve denervation (CSD) was confirmed by testing respiratory responses to h

75 Cardiac sympathetic denervation (CSD) has been shown to reduce the burden of implantable

76 euromodulation using current source density (CSD) analysis in AI of Mongolian gerbils.

77 Current source density (CSD) analysis of laminar LFP profiles revealed alpha cur

78 female), and applied current source density (CSD) analysis to the laminar FP profile.

79 Current source density (CSD) analysis was combined with CSD-MUA coherence to ide

80 g a novel variant of current source density (CSD) analysis.

81 ation of tone-evoked current source density (CSD) profiles in mouse primary auditory cortex from just

82 on by comparing LFP, current source density (CSD), and multiunit activity (MUA) signals in macaque au

83 ly developed inverse current-source density (CSD)-estimation methods are needed for precise assessmen

84 didate is cortical spreading depolarization (CSD)-induced hypoxia.

85 Particularly, chemical solution deposition (CSD) is an ex situ growth approach very promising for hi

86 Chemical solution deposition (CSD) provides a low-cost, versatile approach for process

87 nship between cortical spreading depression (CSD) and headache has not been fully elucidated.

88 Cortical spreading depression (CSD) has long been implicated in migraine attacks that b

89 classified as cortical spreading depression (CSD) if they took place in spontaneously active cortex o

90 Cortical spreading depression (CSD) is a key pathogenetic step in migraine with aura.

91 Cortical spreading depression (CSD) is a propagating event of neuronal depolarization,

92 Cortical spreading depression (CSD) is a transient propagating excitation of synaptic a

93 Cortical spreading depression (CSD) is a wave of neuronal depolarization spreading thro

94 Cortical spreading depression (CSD) is associated with release of arachidonic acid, imp

95 Cortical spreading depression (CSD) is likely the underlying phenomenon of aura.

96 ts, triggered cortical spreading depression (CSD), a propagating slow depolarization that underlies m

97 Cortical spreading depression (CSD), a wave of neuronal depolarization in the cerebral

98 ingle wave of cortical spreading depression (CSD), an animal model of migraine aura, induces a rapid

99 usceptible to cortical spreading depression (CSD), the electrophysiologic event underlying migraine a

100 e report that cortical spreading depression (CSD), the electrophysiological substrate of migraine aur

101 he ability of cortical spreading depression (CSD), the proposed mechanism of the migraine aura, to sh

102 mulations and cortical spreading depression (CSD), the putative mechanism of the migraine aura.

103 often trigger cortical spreading depression (CSD), which aggravates brain damage.

104 rmine whether cortical spreading depression (CSD)--an event believed to underlie visual aura--can giv

105 in naive and cortical spreading depression (CSD)-sensitized trigeminovascular neurons in the spinal

106 ar neurons by cortical spreading depression (CSD).

107 rge variability in cross-sectional diameter (CSD), vertical trajectory, and height of the ST.

108 Congenital sodium diarrhea (CSD) refers to an intractable diarrhea of intrauterine o

109 Substitution of different CSD sequences leads to variation of the degree of open-s

110 ng model of beta4c in complex with dimerized CSD is presented.

111 tachyarrhythmia, conduction system disease (CSD), and DCM vulnerability.

112 cal disease, the Coalition of Skin Diseases (CSD) has for more than two decades provided a base from

113 e how a conventional confocal spinning-disk (CSD) microscope can be converted into a doubly resolving

114 n that levels of Cu/Zn superoxide dismutase (CSD) are down-regulated by miR398.

115 ultilocus conditional sampling distribution (CSD) describes the probability that an additionally samp

116 e use the conditional sampling distribution (CSD), which approximates the probability of sampling an

117 ed to the conditional sampling distribution (CSD), which is at the core of many statistical tools for

118 and the resulting charge state distribution (CSD) and ion mobility spectrum is interpreted as evidenc

119 th its effects on charge state distribution (CSD) as well as at the level of individual charge states

120 ing (FoF), and chronic subjective dizziness (CSD).

121 The chromoshadow domain (CSD) of heterochromatin protein 1 (HP1) was recently sho

122 ologs of HP1 includes a chromoshadow domain (CSD).

123 rresponding to the cav-1 scaffolding domain (CSD) sequence (amino acids 82-101) also attenuated IP(3)

124 nsertion of the caveolin scaffolding domain (CSD), a conserved amphipathic region implicated in inter

125 mbrane-proximal caveolin scaffolding domain (CSD; amino acids 82-101).

126 f cAMP to a cytoplasmic cAMP-sensing domain (CSD).

127 Its chromo shadow domain (CSD) homodimerizes, a requirement for binding protein pa

128 ein interacts with the chromo shadow domain (CSD) of heterochromatin protein 1gamma.

129 l proteins through the chromo-shadow domain (CSD), as well as to recognize key histone modification s

130 ne association of the oligomerization domain/CSD for defined caveola biogenesis and furthermore, high

131 will be signalled by critical slowing down (CSD).

132 quences of this microglial activation during CSD needs to be explored.

133 tissue in a calcium-dependent manner during CSD, and three different CGRP receptor antagonists had a

134 Neuronal [Ca(2+)]i surge during CSD was faster and larger, and post-CSD oligemia and hem

135 uronal excitability in healthy tissue during CSD potentially adds to neuroprotection outside a damage

136 similar to nematode (Caenorhabditis elegans) CSD in retaining activity in the absence of CCS.

137 ur findings provide a mechanism for enhanced CSD susceptibility in hemiplegic migraine.

138 aptic morphology as a mechanism for enhanced CSD susceptibility that we were able to normalize with a

139 Consistently, pY14Cav1 enhanced CSD-dependent vinculin tension in focal adhesions, dampe

140 out the discussion, as specific examples for CSD processing of perovskite ferroelectrics.

141 st-intervention numbers of registrations for CSD member organizations.

142 als, and increased patient registrations for CSD organizations.

143 sociated frequency histograms generated from CSD and PDB data and, derived from the histograms, traff

144 etics of the liganded channel resulting from CSD substitution is not correlated with the change in au

145 est that inbreeding depression stemming from CSD has shaped mating behavior in N. lecontei.

146 Furthermore, CSD improved protein and albuminuria, decreased [Ca(2+)

147 ometry, we demonstrate that this species has CSD.

148 We consequently generalize the historical CSD-PXVXL interaction model and expand the search scope

149 ndicate that the binding surface of the HP1a CSD plus its short CTE provide the needed discrimination

150 anel of amino acid substitutions in the HP1a CSD, we find that Leu-165 in HP1a interacts with HP2 but

151 stinct from that of Pro in the known HP1beta CSD-PXVXL complexes.

152 The crystal structure of the human HP1gamma CSD (CSDgamma) in complex with an H3 peptide suggests th

153 pathway, which was similar to that for human CSD.

154 cific intracortical microstimulation (ICMS), CSD analysis, and pharmacological cortical silencing rev

155 P), the possibility that CGRP is involved in CSD has not been examined in detail.

156 al imaging, we addressed the role of NR2A in CSD.

157 lling self-assembly and self-organization in CSD grown oxides.

158 al role of NR2A-containing NMDA receptors in CSD propagation in vitro; however, whether these recepto

159 This reduction in CSD propagation was also observed with TCN-201, a negati

160 tage-dependent sodium channels play roles in CSD.

161 however, the mechanism underlying increased CSD/migraine susceptibility remains unclear.

162 h pinprick or KCl granule was used to induce CSD in anesthetized rats.

163 rain slices during an experimentally induced CSD.

164 l deficits after ischemic stroke, influences CSD.

165 whereas NMDA receptor antagonism did inhibit CSD.

166 lutamate receptor antagonism did not inhibit CSD, whereas NMDA receptor antagonism did inhibit CSD.

167 tical approximation to a recently introduced CSD derived from the diffusion process associated with t

168 hesion tension, and cancer cell migration is CSD dependent.

169 to measure the LFP and compute band-limited CSD power to identify the laminar sites of persistent cu

170 differ systematically with an order of MUA < CSD < LFP.

171 xpressed phenotype, three of whom manifested CSD and clinically significant arrhythmia in childhood.

172 (HMM) formulation of the sequentially Markov CSD is developed here, yielding an algorithm with time c

173 ro; however, whether these receptors mediate CSD genesis in vivo requires clarification and the role

174 that the improvement in accuracy of the new CSD over previously proposed HMM-based CSDs increases su

175 and spreading depolarisation category (none, CSD only, or at least one ISD) were assessed as outcome

176 The observed CSD(s) are protein dependent, and the short mixing time-

177 istration of PEA stabilized the amplitude of CSD for at least four hours and prevented the run-down o

178 ex reduced dose-dependently the amplitude of CSD.

179 , a downstream target of GC-C, as a cause of CSD and implies primary basal NHE3 malfunction as a pred

180 Clusters of CSD occurred simultaneously, with mainly biphasic CSD-as

181 e release thereby preventing the run-down of CSD amplitudes.

182 o such cortical areas to test the effects of CSD on meningeal nociception.

183 menology of aura symptoms and the effects of CSD on the brain has not been ascertained.

184 query further emphasizes the flexibility of CSD-CrossMiner.

185 ibed four cases of the non-syndromic form of CSD that were caused by dominant activating mutations in

186 The frequency of CSD correlated positively with the duration of the hypox

187 ls have been implicated in the generation of CSD and in the pathophysiology of migraine.

188 strates for the first time that induction of CSD by focal stimulation of the rat visual cortex can le

189 method of cortical stimulation, induction of CSD was recorded in 64 trials.

190 bility to CSD, but also reduced magnitude of CSD genesis in rats.

191 le, considerably suppressed the magnitude of CSD propagation wave and propagation rate in rats.

192 GC-C), the genetic cause for the majority of CSD is still unknown.

193 The occurrence of CSD appeared to be related to the magnitude and duration

194 A indicates that inhibition or prevention of CSD does not underlie PEA's profound neuroprotective eff

195 rs by bicuculline prevented the reduction of CSD amplitudes by TNF.

196 hly specific and sophisticated regulation of CSD activation pathways in planta relative to other know

197 his strategy involves the down-regulation of CSD genes and their copper chaperone CCS through heat-in

198 l conditions, show statistical signatures of CSD after the onset of environmental deterioration and b

199 The stabilization of CSD amplitudes by PEA indicates that inhibition or preve

200 rlying persistent VUD and visual symptoms of CSD.

201 This study assessed the value of CSD and the characteristics associated with outcomes in

202 litude, duration and propagation velocity of CSD was determined prior to and for 6 hours after intrap

203 Having shown that a wave of CSD can trigger long-lasting activation of meningeal noc

204 began approximately 14 min after the wave of CSD.

205 migraine with aura is initiated by waves of CSD that lead up to delayed activation of the trigeminov

206 gating modifier tert-butyl dihydroquinone on CSD in vivo.

207 ts had a dose-dependent inhibitory effect on CSD, suggesting a critical role of CGRP in this phenomen

208 quires clarification and the role of NR2A on CSD propagation is still under debate.

209 Melanomas that arise on mucosal, acral, or CSD skin should be assessed for KIT mutations.

210 TNF receptor (TNFR) 1 or 2 were applied, or CSD was monitored in TNFR1 and TNFR2 knockout mice.

211 ognition of a PxVxL-like motif, as for other CSD partners.

212 D mutants (F92A/V94A) and membrane-permeable CSD-competing peptides, that Src kinase-dependent pY14Ca

213 e during CSD was faster and larger, and post-CSD oligemia and hemoglobin desaturation were more sever

214 The results of the present CSD analysis are supported by calculations.

215 We present CSD-CrossMiner, a novel tool for pharmacophore-based sea

216 irected mutagenesis reveals that the primary CSD interaction occurs through a beta4c C-terminal PXVXL

217 The extent of protein CSD shifting/denaturing can be tailored by acid identity

218 arose within temporal clusters of recurrent CSD.

219 ependent sodium channels by TTX also reduced CSD.

220 lso demonstrate that CGRP antagonism reduces CSD, supporting the possible use of drugs targeting cent

221 The resulting release of GABA reduces CSD amplitudes.

222 Reproducible CSD episodes were induced through repetitive elevations

223 n of H3 by CSDgamma to some extent resembles CSD-PXVXL interaction.

224 n visual FP components accompanied by robust CSD responses and large-amplitude multiunit activity.

225 SD/CSnow), snowmelt (CSD/CSM), and seawater (CSD/CSW) were close to 1 (from 0.44 to 1.4) for all perf

226 nalyzed whether microglial cells might sense CSD by recording membrane currents from microglia in acu

227 rogressive increase in ABP seen in 2K1C+sham CSD rats, with a between-group difference of 14 +/- 2 mm

228 etry, and then underwent CSD (n = 9) or sham CSD (n = 9) 5 weeks after renal artery clipping, in comp

229 In the SHR, CSD reduced both the development of hypertension and its

230 le-locus complementary sex determination (sl-CSD), in which individuals that are diploid and heterozy

231 les, which are often sterile or inviable, sl-CSD can generate substantial inbreeding depression.

232 so show that our data are consistent with sl-CSD.

233 hly deposited snow relative to surface snow (CSD/CSnow), snowmelt (CSD/CSM), and seawater (CSD/CSW) w

234 ative to surface snow (CSD/CSnow), snowmelt (CSD/CSM), and seawater (CSD/CSW) were close to 1 (from 0

235 r pathway for activation of copper/zinc SOD (CSD) involves a copper chaperone for SOD (CCS) and an ad

236 assessment of the underlying spatiotemporal CSD profiles.SIGNIFICANCE STATEMENT Despite its long his

237 To study CSD-induced cerebral oligemia, we used in vivo laser spe

238 In summary, CSD in 2K1C rats reduces the hypertensive burden and imp

239 Syndromic CSD is caused by SPINT2 mutations.

240 the genetic cause for non-GC-C non-syndromic CSD in 18 patients from 16 unrelated families applying w

241 We believe that CSD-CrossMiner closes an important gap in mining structu

242 From these observations we conclude that CSD activates neuronal NMDA receptors, which lead to an

243 Although it is now evident that CSD leads to a signal in microglia, the consequences of

244 We propose that CSD constitutes a nociceptive stimulus capable of activa

245 derlie migraine headache--we now report that CSD can activate central trigeminovascular neurons in th

246 In the present study, we show that CSD ameliorates 2K1C hypertension and reveal the potenti

247 We also show that CSD impairs glymphatic flow, as indicated by the reduced

248 We show that CSD in renovascular hypertension halts further increases

249 In summary, we show that CSD induces changes in the evoked cortical response that

250 These findings suggest that CSD-induced increments in 20-HETE cause the reduction in

251 The CSD has a wide range of applications in both computation

252 The CSD has a wide range of applications, including imputing

253 The CSD interacts with various proteins bearing the PXVXL mo

254 The CSD phenotype is stronger in female R192Q mutants and di

255 The CSD-induced Ca(2+) changes were mitigated by the CaV 2.1

256 ificance of the intramembrane domain and the CSD for defined caveolin-induced membrane deformation.

257 ion between Cav1 Y14 phosphorylation and the CSD promotes focal adhesion traction and, thereby, cance

258 HET0016 blocked the CSD-induced increase in 20-HETE synthesis and ameliorate

259 K(+) channel blocker Ba(2+) blocks both the CSD- and the NMDA-triggered increase in Kir channel acti

260 Briefly, the CSD describes the probability that an additionally sampl

261 structural basis of this interaction for the CSD of HP1alpha.

262 als to patient advocacy organizations in the CSD among Texas dermatologists and dermatology residents

263 we found that one in three compounds in the CSD are polymorphic whilst at least one in two compounds

264 Since there is no observed change in the CSD of buffered proteins exposed to acidic vapors, this

265 showed that the H3 residues that mediate the CSD interaction occur in and adjacent to the alphaN heli

266 an increase in extracellular K(+) mimics the CSD-induced Kir activation.

267 conducted among member organizations of the CSD and among dermatologists and dermatology residents i

268 ally, however, we describe the growth of the CSD and its extensive associated software system, and su

269 binding is dependent on dimerization of the CSD and recognition of a PxVxL-like motif, as for other

270 y exploiting the particular structure of the CSD and typical characteristics of genomic data.

271 Whereas deletion of the CSD mimics the thermodynamic open-state stabilization us

272 the liganded and the unliganded forms of the CSD respectively provide the structural determinants for

273 prominent non-phase-locked component of the CSD that persisted as long as the stimulus was physicall

274 The propagation velocity of the CSD waves was unaltered indicating stable neuronal excit

275 Relative standard deviations of the CSD were between 9 and 15%.

276 When unliganded, the CSD inhibits hyperpolarization-dependent opening of the

277 ng evidence that NR2A subunit contributes to CSD genesis and propagation, suggesting drugs selectivel

278 f11(+/+)) vs Klf11(-/-) when both exposed to CSD stress.

279 eriments in cortical brain slices exposed to CSD.

280 sician awareness and subsequent referrals to CSD member organizations.

281 Monophasic hypoxic p(ti)O(2) responses to CSD were found predominantly in DIND patients.

282 s, markedly reduced cortex susceptibility to CSD, but also reduced magnitude of CSD genesis in rats.

283 nstitute a highly specific strategy treating CSD associated migraine with a likely better safety prof

284 In 31 of those trials, CSD induced a twofold increase in meningeal nociceptor f

285 In a mouse model, microemboli triggered CSD, often without causing microinfarction.

286 cholesterol crystals (<70 microm) triggered CSD in 16 of 28 mice, with 60% of the mice (40% of those

287 Air microemboli reliably triggered CSD without causing infarction.

288 Unfortunately, the true CSD under the coalescent with recombination is not known

289 ed the pharmacological mechanisms underlying CSD and investigated the possibility that endogenous CGR

290 record ABP via telemetry, and then underwent CSD (n = 9) or sham CSD (n = 9) 5 weeks after renal arte

291 Patients with SHD who underwent CSD for refractory VT or VT storm at 5 international cen

292 Here we show, using CSD mutants (F92A/V94A) and membrane-permeable CSD-compe

293 ntributors like proximal cerebral vasospasm, CSD clusters may reduce O(2) supply and increase O(2) co

294 in rats with electrophysiology and in vitro CSD in chick retina with intrinsic optical imaging, we a

295 Using in vivo CSD in rats with electrophysiology and in vitro CSD in c

296 CSD, and we explored the direction in which CSD is modified by TNF.

297 rce density (CSD) analysis was combined with CSD-MUA coherence to identify intracortical alpha curren

298 ed in nine patients from eight families with CSD.

299 ice, with 60% of the mice (40% of those with CSD) showing no infarcts or inflammation on detailed his

300 ases significantly increased stepwise within CSD clusters; particularly in DIND patients, biphasic p(