ライフサイエンスコーパス: EDS

1 EDS mapping of a biochar produced from corn stover pyrol

2 EDS mapping showed that magnetosomes are enmeshed in a m

3 EDS results of the irradiated groups showed an increase

4 EDS was also associated with presynaptic dopaminergic dy

5 EDS was measured with the Epworth Sleepiness Scale (ESS)

6 e products generated from 15, 27, 35, and 40 EDS-CF-PCR amplification cycles were collected and analy

7 -62 (FAVQSSSDSS(P)EENGNGDS(P)S(P)EE), 80-91 (EDS(P)DENEDEES(P)E), and 135-145 (EDES(P)DEEEEEE).

8 miting pathogen growth, that many additional EDS genes remain to be discovered, and that direct scree

9 acility using monochromatic radiation and an EDS setup.

10 , energy dispersive X-ray spectral analysis (EDS), scanning electron microscopy (SEM) and reflective

11 zed by FT-IR, TGA/DTA, SEM, BET analysis and EDS.

12 sample (conductive materials) as in DRS and EDS, or through the thin graphite foil (non-conductive m

13 FTIR and EDS analysis suggest these 2D platelets to be Boron Nitr

14 Both HRTEM and EDS results confirmed the formation of bimagnetic core-s

15 10-20 nm range and characterized by STEM and EDS for structural and elemental composition.

16 XRD and EDS confirmed the presence of two NP compositions in thi

17 TEM to study morphology, as well as XRD and EDS to study composition.

18 (EDS), and this type of EDS is classified as EDS type VI, which can also be caused by a deficiency in

19 uracy of results produced with the available EDS quantification routines in the low energy range, sim

20 an independent positive association between EDS and the consumption of some anti-pathogen drugs.

21 en type V gene COL5A1 in a patient with both EDS type I and hypomelanosis of Ito.

22 ion, to the same allele in two large British EDS type II families (LOD scores 4.1 and 4.3).

23 nm) that contained most of the P detected by EDS.

24 oved symptoms of eye dryness, as measured by EDS, versus placebo in participants with DED.

25 Antiepileptic drugs may also cause EDS or influence sleep.

26 g pN-collagen are thinner and weaker causing EDS-like laxity of large and small joints and paraspinal

27 e locus for at least some cases of classical EDS in which the alpha1(V) and alpha2(V) genes have been

28 tely one-third of individuals with classical EDS have mutations of COL5A1 that result in haploinsuffi

29 Eight of 28 probands with classical EDS who were heterozygous for expressed polymorphisms in

30 stable dopaminergic therapy with coexistent EDS, as assessed by an Epworth Sleepiness Scale score of

31 scular form of Ehlers-Danlos syndrome (EDS), EDS type IV, if they alter the sequence in the triple-he

32 y a combination of TEM, single-particle EDS, EDS line scans, XRD analysis, Debye Function simulations

33 has not previously been implicated in either EDS or periodontal disease and contains no known collage

34 e prefrontal cortical neurons and facilitate EDS is consistent with findings implicating LC-norepinep

35 rious analytical techniques including FESEM, EDS, TEM, AFM, FTIR, Raman, Fluorescence and Absorption

36 p correlated with an objective criterion for EDS: a mean sleep latency (MSL) < 10 min.

37 A predictive index for EDS was generated, which included seven baseline charact

38 agility of OI and indirectly responsible for EDS symptoms, by interference with N-propeptide removal.

39 collagen cross-linking, are responsible for EDS types VI and IX.

40 he previously identified EDS5 gene, and four EDS genes that have not been previously described.

41 13.3% and 4.3% reported regular and frequent EDS, respectively.

42 The current study suggests that frequent EDS is independently associated with future vascular eve

43 Moreover, the association with frequent EDS was statistically significant for stroke (HR, 2.10;

44 roke was confined to the group with frequent EDS, and was 1.73x as much as in the group that reported

45 so observed in the cultured fibroblasts from EDS probands.

46 h as in the group that reported never having EDS (HR, 1.73; 95% confidence interval [CI], 1.15-2.60),

47 iodontal management of a case of hypermobile EDS (type III) associated with atypical gingivitis.

48 learning and the lowest dose (2 ng) improved EDS.

49 re change from baseline to days 42 and 14 in EDS.

50 point was change from baseline to day 84 in EDS.

51 Mean changes from baseline in EDS also significantly favored lifitegrast on days 42 (T

52 icantly greater improvement from baseline in EDS versus those receiving placebo (treatment effect [TE

53 en types I and III have been demonstrated in EDS types VII and IV, respectively, while mutations in t

54 Furthermore, in EDS cells at the 7+4d stage, the reduced beta-adrenergic

55 Improvement in EDS was observed as early as day 14.

56 t LT resulted in significant improvements in EDS, as assessed by the Epworth Sleepiness Scale score (

57 ith controls consistent with joint laxity in EDS patients.

58 l three genes as candidates for mutations in EDS.

59 very similar to that previously observed in EDS VIA human and Plod1(-/-) mouse tissues, suggesting t

60 mal connective tissue biogenesis observed in EDS, we analyzed mice heterozygous for a targeted inacti

61 terozygous mutations in COL5A1 can result in EDS type I.

62 n a type V collagen gene, COL5A1, results in EDS type I, and shows the involvement of L1 sequences in

63 V collagen appears to have a causal role in EDS types I and II, which show phenotypic overlap and ma

64 nective tissues is consistent with a role in EDS, and our patient's skin fibroblasts do not synthesiz

65 the M4 module were consistent with roles in EDS and a newly identified hub gene of the M4 module (Na

66 investigate baseline predictors of incident EDS.

67 ications shaped the evolution of HAE-induced EDS in Nicotiana.

68 JHS/EDS-HT patients reported dry eye symptoms more commonly

69 ent in 77 small fibre neuropathy and 167 JHS/EDS-HT patients without itch.

70 ia with abnormal vitreous was found in 7 JHS/EDS-HT eyes (15.9%) and 0 controls (P = .01).

71 s included comparing ocular anomalies in JHS/EDS-HT and control eyes.

72 irmer I test were significantly lower in JHS/EDS-HT eyes (P < .0001).

73 sphere index was significantly higher in JHS/EDS-HT group (P < .01).

74 atients with an established diagnosis of JHS/EDS-HT and 44 eyes of 22 age- and gender-matched control

75 es were significantly more common in the JHS/EDS-HT group (13.6%; P < .05).

76 tent association of eye anomalies in the JHS/EDS-HT group included xerophthalmia, steeper corneas, pa

77 By confocal microscopy, the JHS/EDS-HT group showed lower density of cells in the superf

78 lers-Danlos syndrome hypermobility type (JHS/EDS-HT), characterized by idiopathic chronic itch with p

79 sessment and management of patients with JHS/EDS-HT.

80 We used this system for the two known EDS mutations (Gly-to-Val) in the middle at Gly-910 and

81 Longitudinally, EDS in PD was associated with non-tremor dominant phenot

82 There were no differences in mean EDS scores between the 2 groups at the first and second

83 The mean EDS scores of the 126 case women in the first month afte

84 r discriminating between 13 subjects with no EDS/snoring and 21 patients with EDS and snoring were id

85 he remaining 103 subjects (14 nonsnoring non-EDS, 21 snoring non-EDS, 68 snoring with EDS).

86 jects (14 nonsnoring non-EDS, 21 snoring non-EDS, 68 snoring with EDS).

87 tance of type V collagen in the causation of EDS type II, and the novel collagen mutation indicates t

88 nclear, and data on biological correlates of EDS in PD are limited.

89 ical presentation confirmed the diagnosis of EDS type VIII.

90 ls with a rare recessively inherited form of EDS (characterized by joint hypermobility, skin hyperext

91 1 overlap with those of the vascular form of EDS.

92 ome (EDS) type IV is the most severe form of EDS.

93 molecular bases for the most common forms of EDS (types I, II and III) are unknown.

94 -year-old Caucasian female with a history of EDS type III presented with erythematous mucogingival le

95 ilies with autosomal dominant inheritance of EDS, there appears to be linkage to loci that contain th

96 e precise role of TNX in the pathogenesis of EDS is uncertain, this patient's findings suggest a uniq

97 erials in use for testing the performance of EDS in the low energy range is included.

98 Predictors of EDS are unclear, and data on biological correlates of ED

99 omatic range, from the usual presentation of EDS type IV and thus have been excluded from analysis.

100 lers-Danlos syndrome (EDS), and this type of EDS is classified as EDS type VI, which can also be caus

101 east some cases of the hypermobility type of EDS, a condition marked by gross joint laxity and chroni

102 ndings have been reported with some types of EDS.

103 tinct alpha1(I)-osteogenesis imperfecta (OI)/EDS phenotype.

104 Thus, these OI/EDS collagen mutations are directly responsible for the

105 Patients with OI/EDS form a distinct subset of osteogenesis imperfecta (O

106 In each child with OI/EDS, we identified a mutation in the first 90 residues o

107 The dose-response relationship for CRF on EDS performance resembled an inverted U-shaped curve wit

108 The influence of dopaminergic therapy on EDS is dose dependent.

109 However, linkage studies in other EDS I families indicate the disorder is heterogeneous; l

110 zed by a combination of TEM, single-particle EDS, EDS line scans, XRD analysis, Debye Function simula

111 Erysiphe orontii, suggesting that particular EDS genes have pathogen-specific roles in conferring res

112 lly driven synchronized continuous flow PCR (EDS-CF-PCR) configuration carried out in a microfabricat

113 In early PD, EDS increases significantly over time and is associated

114 of CHD, stroke, or dementia, and self-rated EDS as never, rare, regular, or frequent in response to

115 ng high sensitivity energy dispersive X-ray (EDS) mapping and electron energy loss spectroscopy (EELS

116 high-resolution TEM and SEM, nanometer-scale EDS mapping, and DTA.

117 We compared mean Edinburgh Depression Scale (EDS) scores from a group of women (n = 126 cases) at 32

118 the endoplasmic reticulum (ER) occurs in SCD-EDS patients.

119 splastic form of Ehlers-Danlos syndrome (SCD-EDS), a heritable connective tissue disorder.Those previ

120 We propose that SCD-EDS is the result of vesicular zinc trapping and ER zinc

121 score >/=2.0 (0-4 scale), eye dryness score (EDS) >/=40 (0-100 visual analogue scale [VAS]), and hist

122 were characterized systematically by FE-SEM, EDS, UV/Vis., FTIR spectroscopy, powder XRD, and XPS tec

123 tion of graphene oxide according to the SEM, EDS, XRD, XPS, Raman and TGA results.

124 SEM-EDS analysis shows that the fossils are composed of alum

125 SEM-EDS measurements of SO2-exposed goethite revealed small

126 SEM-EDS was used to obtain the elemental distribution along

127 th energy-dispersive X-ray spectrometer (SEM-EDS) analysis, which it is a analysis that shows the che

128 to energy dispersive X-ray spectrometry (SEM-EDS) and benchtop ED-XRF analyses confirmed these result

129 py-X-ray energy dispersive spectroscopy (SEM-EDS) and X-ray photoelectron spectroscopy (XPS), whereas

130 croscopy-energy dispersive spectroscopy (SEM-EDS) technique, with the significant advantage of drasti

131 croscopy-energy-dispersive spectroscopy (SEM-EDS).

132 SEM/EDS showed diminished content of calcium (Ca) after 15 s

133 copy (OM), scanning electron microscopy (SEM/EDS), micro-infrared spectroscopy (muFTIR/muSR-FTIR), an

134 croscopy/energy dispersive spectrometry (SEM/EDS) after demineralization (n = 3).

135 microscopy and energy dispersive system (SEM/EDS) analysis.

136 xcluded conditions for 6 months prior to SEM/EDS and muXANES analysis to determine V host phases and

137 rsal task and (b) an extradimensional shift (EDS) task.

138 learning, and extradimensional set shifting (EDS) at different doses.

139 e often mediated by early defense signaling (EDS) rapidly activated by the perception of herbivore as

140 ues, such as electrical discharge sintering (EDS) or resistive sintering (RS), have been intensively

141 complaints of excessive daytime sleepiness (EDS) and clinically suspected obstructive sleep apnea (O

142 links between excessive daytime sleepiness (EDS) and vulnerability to infectious diseases in a large

143 orders such as excessive daytime sleepiness (EDS) as well as other sleep or cognitive disorders.

144 icacy of LT on excessive daytime sleepiness (EDS) associated with PD.

145 sessed whether excessive daytime sleepiness (EDS) at baseline was associated with subsequent coronary

146 Excessive daytime sleepiness (EDS) is common and disabling in Parkinson's disease (PD)

147 en obesity and excessive daytime sleepiness (EDS), although for the most part the genetic variance in

148 to symptoms of excessive daytime somnolence (EDS).

149 ure and cause excessive day-time somnolence (EDS).

150 ce of energy dispersive X-ray spectrometers (EDS) in the low energy range below 1 keV.

151 Energy Dispersive X-Ray Spectrometry (EDS) and Raman spectroscopy analysis indicate the presen

152 (XRD), energy dispersive X-ray spectrometry (EDS), UV-vis absorption, and extended X-ray absorption f

153 cope(SEM) and energy dispersive spectrometry(EDS).

154 Energy dispersed spectroscopy (EDS) was employed to reveal that the LAH treatment depos

155 py (SEM) and energy dispersive spectroscopy (EDS) analysis of production debris indicate a complex, m

156 confirmed by energy-dispersive spectroscopy (EDS) and by the fluorescence properties of the granules.

157 on (BSE) and energy-dispersive spectroscopy (EDS) mapping of the same particle, the Pb measured in th

158 Using the electron dispersive spectroscopy (EDS) technique, the particles are confirmed to come from

159 imaging and energy dispersive spectroscopy (EDS) were proved the right synthesis of the GNRs and cor

160 rticle X-ray energy dispersive spectroscopy (EDS) were used to characterize the bimetallic DENs befor

161 scopy (TEM), energy dispersive spectroscopy (EDS), and infrared spectroscopy of adsorbed CO showed th

162 scopy (TEM), energy dispersive spectroscopy (EDS), UV-visible spectroscopy and X-ray diffraction (XRD

163 coupled with energy dispersive spectroscopy (EDS), were used to characterize crystallite morphology a

164 ate by energy-dispersive x-ray spectroscopy (EDS) and a quantitative measurement by Auger electron sp

165 d with energy-dispersive X-ray spectroscopy (EDS) and UV-visible spectrometry.

166 using energy-dispersive X-ray spectroscopy (EDS) and X-ray diffraction (XRD), and microindentation w

167 plying energy-dispersive X-ray spectroscopy (EDS) mapping to the study of two intermetallic phases of

168 es and energy-dispersive X-ray spectroscopy (EDS) showed that Pt-black was growing along GrO(x).

169 ked by energy-dispersive X-ray spectroscopy (EDS) study.

170 M) and energy dispersive X-ray spectroscopy (EDS) to determine their corresponding major element comp

171 Energy dispersive X-ray spectroscopy (EDS) was used to confirm the elemental composition of th

172 ), and energy dispersive X-ray spectroscopy (EDS) were used to characterize galvanostatically deposit

173 scopy, energy-dispersive X-ray spectroscopy (EDS), and surface-sensitive cycling voltammetry.

174 (TEM), energy dispersive X-ray spectroscopy (EDS), fluorescence spectroscopy, and mass spectrometry,

175 RTEM), energy-dispersive X-ray spectroscopy (EDS), selected area electron diffraction (SAED), Raman s

176 RTEM), energy-dispersive X-ray spectroscopy (EDS), X-ray photoelectron spectroscopy (XPS), Raman spec

177 using energy dispersive X-ray spectroscopy (EDS).

178 D) and energy dispersive X-ray spectroscopy (EDS).

179 In early developmental stage (EDS) cells (from 7+3d to 7+5d), the stimulatory response

180 on electron microscopy (STEM), AES, and STEM/EDS analysis.

181 is study also demonstrated that AES and STEM/EDS could be used in a correlative fashion to determine

182 y/energy-dispersive X-ray spectroscopy (STEM/EDS) and inductively coupled plasma atomic emission spec

183 roscopy/energy dispersive spectroscopy (STEM/EDS), inductively coupled plasma-atomic emission spectro

184 h the gravis form of Ehlers-Danlos syndrome (EDS) (type I) in a three generation family.

185 e of the subtypes of Ehlers-Danlos syndrome (EDS) and cutis laxa.

186 ive rise to forms of Ehlers-Danlos syndrome (EDS) because of partial or complete skipping of exon 6,

187 ed mutations causing Ehlers-Danlos syndrome (EDS) classic type result in haploinsufficiency of proalp

188 Ehlers-Danlos syndrome (EDS) designates a heterogeneous group of connective tiss

189 use model of classic Ehlers Danlos syndrome (EDS) had decreased biomechanical stiffness compared with

190 Ehlers-Danlos syndrome (EDS) is a genetically and pathogenetically heterogeneous

191 Ehlers-Danlos syndrome (EDS) is a group of collagen disorders primarily affectin

192 Ehlers-Danlos syndrome (EDS) is a heterogeneous group of connective-tissue disor

193 Vascular Ehlers-Danlos syndrome (EDS) is a rare connective tissue disorder with serious h

194 Vascular Ehlers-Danlos syndrome (EDS) results from mutations in the formation of type III

195 Ehlers-Danlos syndrome (EDS) type I (the classical variety) is a dominantly inhe

196 Vascular Ehlers-Danlos syndrome (EDS) type IV is the most severe form of EDS.

197 Ehlers-Danlos syndrome (EDS) type IV results from mutations in the COL3A1 gene,

198 Ehlers-Danlos syndrome (EDS) types I and II, which comprise the classical variet

199 As in Ehlers-Danlos syndrome (EDS) VIIA/B, fibrils containing pN-collagen are thinner

200 lassical form of the Ehlers-Danlos syndrome (EDS), a heritable connective-tissue disorder that severe

201 phoscoliotic type of Ehlers-Danlos syndrome (EDS), and this type of EDS is classified as EDS type VI,

202 the vascular form of Ehlers-Danlos syndrome (EDS), EDS type IV, if they alter the sequence in the tri

203 e cases of classical Ehlers-Danlos syndrome (EDS), in which aberrant collagen fibrils are associated

204 e characteristics of Ehlers-Danlos syndrome (EDS).

205 with the features of Ehlers-Danlos syndrome (EDS).

206 s are typical of the Ehlers-Danlos syndrome (EDS).

207 Products were characterized by SEM, (S)TEM, EDS, XPS, and SQUID.

208 ution process and characterized by XRD, TEM, EDS, and XPS.

209 have been characterized by powder XRD, TEM, EDS, selected area electron diffraction, and nanobeam el

210 TEM-EDS analysis at 336 h showed secondary precipitates enri

211 croscopy-energy dispersive spectroscopy (TEM-EDS) and field flow fractionation (FFF-ICP-MS).

212 at % Ti, consistently determined by XRD, TEM-EDS, and ICP-OES, was distributed uniformly across the a

213 y process, as confirmed by DLS, SLS, and TEM/EDS analysis.

214 relations, are consistent with the idea that EDS as a proxy of altered sleep quality/quantity may aff

215 h linkage could be excluded, indicating that EDS-VIII is a genetically heterogeneous disorder.

216 d impair learning of the 5 reversals and the EDS task.

217 th similar characteristics who completed the EDS at 32 weeks' gestation during the same summer period

218 ntrations (KCl) to reduce the current in the EDS-CF-PCR device during cycling.

219 The results showed that the EDS-CF-PCR format produced results similar to that of a

220 best quantitative physiological correlate to EDS.

221 one-half of the mutations that give rise to EDS types I and II are likely to lie in the COL5A1 gene,

222 or SC65 mutations may cause as yet undefined EDS variants.

223 the first system capable of being used under EDS or RS conditions independently combining current con

224 s in a patient with a previously undiagnosed EDS type VIII.

225 Vascular EDS is a serious disorder with high mortality, which doe

226 Vascular EDS is associated with a shortened overall survival due

227 old decrease in arterial rupture in vascular EDS patients.

228 nt of complications associated with vascular EDS.

229 Ehlers-Danlos VIII (EDS-VIII) is an autosomal dominant disorder characterize

230 Dopaminergic therapy was associated with EDS at years 2 and 3, as dose increased.

231 Poor healing associated with EDS excluded surgical excision and necessitated the use

232 onnective tissue dysfunction associated with EDS.

233 ariables were assessed for associations with EDS for up to 3 years.

234 ar 1 showed no significant associations with EDS.

235 first report on the folding of collagen with EDS mutations, which demonstrates local delays in the tr

236 Comparable with EDS patients, they had decreased aortic stiffness and te

237 -fos profiles was positively correlated with EDS performance.

238 L5A2 was excluded in two other families with EDS I while a fourth family was concordant for linkage t

239 in 33 unrelated individuals or families with EDS type IV, mutations that affect splicing, of which 30

240 t should be useful in analyzing linkage with EDS and other disease phenotypes.

241 coding region of COL5A1, in one patient with EDS type I.

242 cts with no EDS/snoring and 21 patients with EDS and snoring were identified by receiver operator cur

243 urgical management options for patients with EDS.

244 olding of type III collagen in patients with EDS.

245 kage search in a large Swedish pedigree with EDS-VIII and established linkage to a 7-cM interval on c

246 Analysis of four further pedigrees with EDS-VIII revealed two consistent with linkage to 12p13 a

247 non-EDS, 21 snoring non-EDS, 68 snoring with EDS).

248 0% specificity for identifying subjects with EDS.