ライフサイエンスコーパス: CSD

1 CSD activates the trigeminovascular system, evoking a me

2 CSD analysis revealed no appreciable local generator con

3 CSD decreased sustained VT and ICD shock recurrence in p

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

5 CSD indicators may then provide invaluable insights into

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 was also decreased by the antiepileptic drug topiram

11 CSD was analyzed in rat neocortical slices by imaging of

12 CSD was elicited chemically in adult rats and occurrence

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

14 CSD was measured as the percentage of the maximal surfac

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

16 CSD-defined alpha generators were strongest in the supra

17 CSD-FUO patients were identified in the 2004-17 CSD nati

18 CSD-FUO patients were identified in the 2004-2017 CSD na

19 -FUO patients were identified in the 2004-17 CSD national registry.

20 UO patients were identified in the 2004-2017 CSD national registry.

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

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

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

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

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

26 mice than WT mice and almost abolished after CSD.

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

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

29 0-HETE paralleled the reduction in CBF after CSD in vivo.

30 ot the impaired neurovascular coupling after CSD.

31 oconstriction and vascular dysfunction after CSD.

32 ith ICD shock recurrence and mortality after CSD.

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

34 reduced surface area (were sharpened) after CSD.

35 gy residents and patient registrations among CSD member organizations.

36 n = 152, male for 61, and female for 91) and CSD (n = 47, male for 5, female for 42), respectively.

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

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

39 identified a functional link between TNF and CSD.

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

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

42 Evidence for functional connectivity between CSD and CGRP has triggered scientific interest in the po

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

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

45 Deletion of Cav-1 scaffold domain binding (CSD) motif in EphB1 prevented EphB1 binding to Cav-1 as

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

47 ydroethidium administration, was elevated by CSD, and the production was reduced to basal levels in m

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

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

50 ctivation and sensitization of HT neurons by CSD.

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

52 e induction of arterial dilatation or PPE by CSD in female rats, and how these events are affected by

53 e induction of arterial dilatation or PPE by CSD, the inability of fremanezumab to prevent them sugge

54 similar to yeast (Saccharomyces cerevisiae) CSD.

55 This is the first attempt to characterize CSD-FUO as a unique syndrome that may be severe and debi

56 This is the first attempt to characterize CSD-FUO as a unique syndrome which may be severe and deb

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

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

59 ntagonist PLX5622 before and during the 14 d CSD procedure.

60 ow called the Cambridge Structural Database (CSD) has reaped dividends in numerous and diverse areas

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

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

63 ctures in the Cambridge Structural Database (CSD).

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

65 Group DBG: CSD filled with a DBG; group DBG/LV: CSD filled by the c

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

67 CSD protein deletion, resulting in decreased CSD and total SOD enzyme activity.

68 Dedicated CSD methods managed to discover graphs that nearly coinc

69 Chronic social defeat (CSD) in male mice can produce anxiety and aberrant socia

70 The chronic social defeat (CSD) paradigm in mice produces mood alterations and micr

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

72 formation in critical-size calvaria defect (CSD) when combined with a deproteinized bovine graft (DB

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

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

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

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

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

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

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

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

81 vel event type whose current source density (CSD) signature resembled that seen during CA1 SWR, but w

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

83 expressions for the cross-spectral density (CSD) and mutual coherence functions (MCFs) for twisted s

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

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

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

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

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

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

90 Cortical spreading depression (CSD) is a wave of neuronal depolarization thought to und

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

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

93 Cortical spreading depression (CSD) is the propagation of a relatively slow wave in cor

94 Cortical spreading depression (CSD) underlies the neurobiology of migraine with aura (M

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

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

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

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

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

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

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

102 ar neurons by cortical spreading depression (CSD).

103 A 5-mm-diameter CSD was created and three experimental groups (n = 10) w

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

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

106 Causal Structure Discovery (CSD) is the problem of identifying causal relationships

107 a rare manifestation of cat scratch disease (CSD).

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

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

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

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

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

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

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

115 ous dizziness, chronic subjective dizziness (CSD) arises unsteadily by psychological and physiologica

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

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

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

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

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

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

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

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

124 by the phenomenon of critical slowing down (CSD).

125 This paper utilizes Critical Slowing Down (CSD; instability) indicators developed by statistical ph

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

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

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

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

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

131 e useful at detecting future (re-)emergence, CSD needs to be a generic (model-independent) feature of

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

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

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

135 l equation models (which is not designed for CSD) as control.

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

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

138 als, and increased patient registrations for CSD organizations.

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

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

141 and subsequent carboxyl functionalizations (CSD-PLNPs) were rationally fabricated.

142 Data regarding CSD-associated FUO (CSD-FUO), particularly in adults, are limited.

143 Data regarding CSD associated FUO (CSD-FUO), particularly in adults, are limited.

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

145 ometry, we demonstrate that this species has CSD.

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

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

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

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

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

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

152 -viscosity crosslinking agent; group DBG/HV: CSD filled by the combination of DBG and HA in a high-vi

153 dy was to systematically examine whether (i) CSD methods can discover the known causal relationships

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

155 in CSD from the 1900s to 1940s, a decline in CSD between the 1930s and the 1970s, then a further incr

156 g pattern is characterised by an increase in CSD from the 1900s to 1940s, a decline in CSD between th

157 0s and the 1970s, then a further increase in CSD from the 1960s to 2010.

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

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

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

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

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

163 tage-dependent sodium channels play roles in CSD.

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

165 rain slices during an experimentally induced CSD.

166 l deficits after ischemic stroke, influences CSD.

167 whereas NMDA receptor antagonism did inhibit CSD.

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

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

170 up DBG: CSD filled with a DBG; group DBG/LV: CSD filled by the combination of DBG and HA in a low-vis

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

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

173 etween two commonly used models of migraine, CSD induction and systemic CGRP infusion.

174 A national CSD surveillance study has been conducted in Israel sinc

175 A national CSD surveillance study is conducted in Israel since 1991

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 iciencies for the two main emission bands of CSD-PLNPs, resulting from MI-triggered R-PersL signal tr

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

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

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

183 concept sensor array through the ensemble of CSD-PLNPs-COOH and certain MIs was developed and demonst

184 We found evidence of CSD prior to disease re-emergence in all models.

185 query further emphasizes the flexibility of CSD-CrossMiner.

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

187 To assess the generality of CSD, we carried out a simulation study of a hierarchy of

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

189 hosphorylation, indicating the importance of CSD in the interaction.

190 is without shortcomings, the limitations of CSD research are assessed.

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

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

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

194 ly, it is unclear whether the predictions of CSD-derived from simple, low-dimensional systems-pertain

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

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

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

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

199 Our findings are reminiscent of CSD-induced meningeal inflammation and provide the first

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

201 rlying persistent VUD and visual symptoms of CSD.

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

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

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

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

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

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

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

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

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

211 Microglial repopulation of the brain post-CSD reintroduced adverse stress effects, and ROS inhibit

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

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

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

215 ependent sodium channels by TTX also reduced CSD.

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

217 The resulting release of GABA reduces CSD amplitudes.

218 Data regarding CSD associated FUO (CSD-FUO), particularly in adults, ar

219 Data regarding CSD-associated FUO (CSD-FUO), particularly in adults, ar

220 al methods to discover causal relationships, CSD methodologies are gaining popularity.

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

222 For best results, CSD algorithms should be used with longitudinal data pro

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

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

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

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

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

228 By contrast, the ccsd mutant showed CSD protein deletion, resulting in decreased CSD and tot

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

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

246 We show that CSD in renovascular hypertension halts further increases

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

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

249 The CSD also aids the solution of new crystal structures.

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

251 The CSD interacts with various proteins bearing the PXVXL mo

252 The CSD is hypersensitivity reaction due to exposure to comp

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

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

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

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

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

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

259 identify potential ligand molecules from the CSD based on 3D shape and intermolecular interaction mat

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

261 und 138 000 small-molecule structures in the CSD and a series of drug-protein crystal structures.

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

263 utase were significantly deteriorated in the CSD group (p < 0.01 or p < 0.001) as comparing to the he

264 on-gamma were significantly increased in the CSD participants (p < 0.001).

265 to establish features of redox system in the CSD subjects compared to a healthy population.

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

270 normally observed in the serum levels of the CSD group (p < 0.01 or p < 0.001).

271 In a second experiment, at the end of the CSD period, PLX5622 was discontinued to allow microglial

272 ophysiological features and mechanism of the CSD still remains unclearly.

273 years, we chronicle the contribution of the CSD to research into molecular geometries, molecular int

274 lish possible endogenous contributors of the CSD using serum samples from patients with the CSD.

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

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

277 itical contributor of pathophysiology of the CSD, and that is first explored to establish features of

278 s function, we then paraxially propagate the CSD and MCF to any plane [Formula: see text].

279 We found that the CSD-induced brief dilatation and prolonged constriction

280 n species (ROS) production contribute to the CSD stress-induced changes in affective behavior.

281 Finally, we explain why the CSD must evolve with the world around it to ensure it re

282 D using serum samples from patients with the CSD.

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

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

285 eriments in cortical brain slices exposed to CSD.

286 sician awareness and subsequent referrals to CSD member organizations.

287 antagonism may disrupt vascular responses to CSD and the ensuing plasma protein extravasation (PPE).

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

289 Animals susceptible to CSD show activation of microglia, which have elevated le

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

291 We evaluated two CSD methods, Fast Causal Inference (FCI) and Fast Greedy

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

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

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

295 of anticipating disease (re-)emergence using CSD-based early-warning signals (EWS), which are statist

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

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

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

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

300 ed in nine patients from eight families with CSD.