ライフサイエンスコーパス: ECD

1 ECD and CCT did not correlate with corneal densitometry,

2 ECD and transplant suitability.

3 ECD binding and cell-based signaling assays with antagon

4 ECD colocalizes and coimmunoprecipitates with PERK and G

5 ECD depletion increased the levels of both phospho-PERK

6 ECD dropped by 33.9% in the first 6 months, and then dec

7 ECD spectra were measured in the stopped-flow mode and c

8 ECD was stable after the initial postsurgical decrease (

9 .01); GAT-IOP: +1.0 +/- 2.3 mm Hg (P = .01); ECD: +31 +/- 400 cells/mm(2) (P = .6); no cases of macul

10 lustrates the functional importance of SID-1 ECD as a dsRNA binding domain that contributes to RNA tr

11 cantly increased the interaction of IL-1Rrp2 ECD with the co-receptor IL-1RAcP.

12 experimentally verified contact of Ser-281 (ECD) and Ile-486 (TMD) was subsequently utilized in dock

13 Up to 2 years of age, ECD was more inversely correlated with CD than with age

14 contact formation, in contrast to the alpha2 ECD, which had no effect.

15 show stable visual acuity and CCT, although ECD decreases.

16 d ECD thresholds is indicated to maintain an ECD that warrants safe future combined pIOL explantation

17 /=25% in ECD, and percentage of eyes with an ECD <1500 cells/mm(2).

18 erly recipients in the United States with an ECD versus non-ECD transplant was only 7 months.

19 as no significant difference in mean CCT and ECD after surgery.

20 The CCT and ECD measures did not change significantly in any group a

21 tutional cohort of 189 patients with ECD and ECD overlapping with Langerhans cell histiocytosis (so-c

22 th a post-mortem time of 20.7 +/- 14.7 h and ECD of 2641.0 +/- 362.8 cells/mm(2).

23 dicate that at least a proportion of LCH and ECD patients have detectable activating kinase mutations

24 cells was indistinguishable between LCH and ECD, although the histiocytic disorders were distinct to

25 immediate cellular precursor in both LCH and ECD.

26 were investigated by (1)H and (19)F NMR and ECD spectroscopy.

27 s were graft survival, BCVA, refraction, and ECD.

28 atient survival exceeded graft survival, and ECD recipients returned to dialysis for an average of 5.

29 n association between graft storage time and ECD decline after DMEK and possibly between donor age an

30 ows that the combination of the film VCD and ECD techniques is a relatively straightforward method to

31 to the end of follow-up and showed an annual ECD decline of 48 cells/mm(2) (standard error, 3.14) and

32 and extracellular domains (AREG-CTD and AREG-ECD), as well as full-length AREG precursor (proAREG).

33 ored by proAREG and AREG-CTD but not by AREG-ECD.

34 BCVA, ECD, and refractive error were compared using linear mix

35 h a tryptic digest of cytochrome c with both ECD and IRMPD as fragmentation modes.

36 Postoperative BSCVA, ECD, and CCT results were comparable in both groups at 6

37 ther methods, the stereochemical analysis by ECD required knowledge of the relative configuration der

38 uration of these enantiomers was assigned by ECD analysis.

39 absolute configuration was again assigned by ECD investigations.

40 bsolute configurations have been assigned by ECD spectroscopy.

41 ural information that cannot be delivered by ECD can be generated by EID.

42 to estimate treatment effect modification by ECD.

43 s suggest that PknB activity is modulated by ECD binding to peptidoglycan substructures, however, the

44 ,3-dihydro-1H,5H-pyrazolo[1,2-a]pyrazoles by ECD and NMR.

45 he extracellular domain of E-cadherin (E-cad-ECD) in a supported membrane.

46 Central ECD was correlated to the duration of active uveitis (r

47 Central ECD was lower among eyes that had undergone cataract or

48 Central ECD was lower in eyes with uveitis than in control eyes

49 gone surgery in either eye (n = 12), central ECD was lower in eyes with uveitis (2324 cells/mm(2) [ra

50 eye bank tissue screening, mean (SD) central ECD was 2746 (297) cells/mm2 in the 0-7d PT group (n = 4

51 compared with results from quantum-chemical ECD calculations to assign the absolute configuration.

52 tional and dispersion dependence of computed ECD spectra.

53 A total of 63 adult patients with confirmed ECD were identified.

54 lly significant correlations between corneal ECD and dry eye severity parameters including the OSDI s

55 The median donor corneal ECD (25th-75th percentiles) was 3005 cells/mm(2) (2852-3

56 ngly, mutant RAMP1 W84A- and RAMP2 E101A-CTR ECD retained AC413/rAmy binding.

57 he human calcitonin receptor ectodomain (CTR ECD) in complex with a truncated analogue of salmon calc

58 integrity and relevance of the isolated CTR ECD.

59 main (ECD) and tethered RAMP1- and RAMP2-CTR ECD fusion proteins and antagonist peptides.

60 ed that the rank order of binding of the CTR ECD is identical to the rank order of binding of the ful

61 The structure of the CTR ECD is similar to other Class B GPCRs and the ligand bin

62 Time of Flight mass spectrometry (UHPLC-DAD-ECD-QTOFMS).

63 Compared with DBD-ECD recipients also at 24 months, DCD-ECD recipients sho

64 ular filtration rate (eGFR) was lower in DCD-ECD recipients at 12 months (41 vs. 53 mL/min, P=0.003)

65 th DBD-ECD recipients also at 24 months, DCD-ECD recipients showed a lower graft function (median, eG

66 Notably, phosphorylation-deficient ECD mutants that failed to bind to PIH1D1 in vitro fully

67 ong-term change in endothelial cell density (ECD) after the implantation of 2 types of rigid iris-fix

68 l thickness (CCT), endothelial cell density (ECD) and complication rates.

69 fect corneal donor endothelial cell density (ECD) and transplant suitability.

70 Endothelial cell density (ECD) at 3 years determined by a central image analysis r

71 ated parameters on endothelial cell density (ECD) decline and detachment rate in this group.

72 vealed a decreased endothelial cell density (ECD) in patient 2, but no signs of corneal decompensatio

73 nation revealed an endothelial cell density (ECD) of 1532/mm(2) in patient 1 and 1620/mm(2) in patien

74 cuity (BSCVA), and endothelial cell density (ECD) prior to DMEK and at 1, 3, 6, 12, and 24 months pos

75 culectomy, corneal endothelial cell density (ECD) significantly decreased by 3.5% (P = .012, paired t

76 mative database of endothelial cell density (ECD) using in vivo specular microscopy in children under

77 ual acuity (BCVA), endothelial cell density (ECD), and complications.

78 l thickness (CCT), endothelial cell density (ECD), and need for regraft.

79 al acuity (BSCVA), endothelial cell density (ECD), central corneal thickness (CCT) at 6 and 12 months

80 ual acuity (CDVA), endothelial cell density (ECD), central corneal thickness (CCT), and graft surviva

81 ual acuity (BCVA), endothelial cell density (ECD), central corneal thickness (CCT), graft survival ra

82 ual acuity (BCVA), endothelial cell density (ECD), pachymetry, and intraoperative and postoperative c

83 , micrometers) and endothelial cell density (ECD).

84 st refraction, and endothelial cell density (ECD).

85 Genetic analyses of a newly developing ECD lesion revealed a somatic KRAS(Q61H) mutation withou

86 spite progress, early childhood development (ECD) remains a neglected issue, particularly in resource

87 re, using a WO3 -film electrochromic device (ECD) array (10 x 10 pixels) and a ZnO-nanowire-matrix pr

88 ectronic and vibrational circular dichroism (ECD and VCD), as well as NMR spectroscopy have been util

89 experimental electronic circular dichroism (ECD) data with TDDFT-ECD calculations for the truncated

90 experimental electronic circular dichroism (ECD) investigations and quantum-chemical circular dichro

91 mirror-image electronic circular dichroism (ECD) spectra for the corresponding absolute configuratio

92 nd calculated electronic circular dichroism (ECD) spectra.

93 solution NMR, electronic circular dichroism (ECD), and single-crystal X-ray diffraction analyses.

94 s by means of electronic circular dichroism (ECD).

95 he presence of extracranial carotid disease (ECD) is associated with less favorable clinical outcomes

96 he non-LCH neoplasm Erdheim-Chester disease (ECD) are heterogeneous neoplastic disorders marked by in

97 iocytosis (LCH) and Erdheim-Chester disease (ECD) are rare histiocytic disorders induced by somatic m

98 Erdheim-Chester disease (ECD) is a rare non-Langerhans cell histiocytosis that mo

99 the pathogenesis of Erdheim-Chester disease (ECD) leading to novel treatment strategies.

100 r manifestations of Erdheim-Chester Disease (ECD) with multimodal imaging.

101 t, and treatment of Erdheim-Chester disease (ECD).

102 neoplasms, such as Erdheim-Chester disease (ECD).

103 y (IRMPD) and electron capture dissociation (ECD) as fragmentation techniques, and D-alpha-tocopheryl

104 que nature of electron capture dissociation (ECD) for cleaving protein backbone bonds while preservin

105 on (ETD), and electron capture dissociation (ECD).

106 ors are composed of an extracellular domain (ECD) and a seven-transmembrane (7TM) domain, and their s

107 ors using purified CTR extracellular domain (ECD) and tethered RAMP1- and RAMP2-CTR ECD fusion protei

108 The soluble LGR4 extracellular domain (ECD) binds RANKL and inhibits osteoclast differentiation

109 The PknB extracellular domain (ECD) consists of four repeats homologous to penicillin-b

110 sized that the soluble extracellular domain (ECD) of long isoform of death receptor 5 (DR5) could blo

111 tion, we expressed the extracellular domain (ECD) of SID-1 and purified it to near homogeneity.

112 ystal structure of the extracellular domain (ECD) of the human neuronal alpha2 nicotinic acetylcholin

113 otherapy augments HER2 extracellular domain (ECD)-specific antibodies.

114 featured with a large extracellular domain (ECD).

115 a characteristic large extracellular domain (ECD).

116 bound GPR56 or GPR110 extracellular domains (ECDs) from the respective seven-transmembrane (7TM) doma

117 the large N-terminal extracellular domains (ECDs) of alpha1, alpha2, beta2, and gamma2 subunits were

118 P < 0.001), but not with the baseline donor ECD (r = -0.04; P = 0.78).

119 71% (53%-80%) relative to the baseline donor ECD, comparable with the 76% (70%-82%) median cell loss

120 Use of expanded criteria donor (ECD) kidneys, which are associated with a reduced graft

121 viability of human extended criteria donor (ECD) livers is not well known.

122 donor status: SCD, expanded criteria donor (ECD), or LD (by donor age: <60, 60-64, 65-69, >/=70 year

123 nts and the use of extended criteria donors (ECD).

124 ar outcomes in recipients of single and dual ECD kidneys.

125 Ecdysoneless (ECD) is an evolutionarily conserved protein whose germ l

126 Mammalian Ecdysoneless (ECD) is a highly conserved ortholog of the DrosophilaEcd

127 observed that, overexpression of ectodomain (ECD) of Il-1Rrp2 or IL-1RAcP exhibited dominant-negative

128 Eighteen ECD livers that were declined for transplantation underw

129 ith photodiode array (DAD), electrochemical (ECD), charged aerosol (CAD), and mass spectrometry (MS)

130 cycle arrest, which is rescued by exogenous ECD, demonstrating a requirement of ECD for normal mamma

131 y comparison of theoretical and experimental ECD spectra.

132 Comparison of the experimental ECD and VCD spectra with the density functional theory s

133 n assigned by comparison of the experimental ECD spectra with DFT and semiempirical calculations.

134 r PknB signal transduction, a fully extended ECD and a conserved, membrane-distal putative ligand-bin

135 Significant changes were observed for ECD values (1741+/-274.5 cells/mm(2) at last visit befor

136 ortunities to advance political priority for ECD, including an increasingly favourable political envi

137 To advance global priority for ECD, proponents will need to surmount the framing and go

138 atomic resolution, built a model of the full ECD, and discovered a region on the C-terminal PASTA dom

139 g HEK293 cells, the alpha1, beta2, or gamma2 ECD each caused a significant reduction in contact forma

140 y coupled with electron capture detector (GC-ECD), and validated for screening and quantification of

141 coupled to electron capture detection (HS-GC-ECD) were evaluated.

142 tography with electron capture detection (GC/ECD) for the determination of nine pesticides (chlorotha

143 terviews with individuals involved in global ECD leadership, practice, and advocacy, as well as peer-

144 -PRESS implantation and in the control group ECD did not change either at 1 month or at 3 months afte

145 ethods for AC determination as AXRD >> VCD > ECD, while the synergy of all three methods provides ver

146 therapy induced immune responses beyond HER2-ECD and, importantly, whether those immune responses wer

147 IgG to HER2 intracellular domain (ICD), HER2-ECD, p53, IGFBP2, CEA, and tetanus toxoid were examined.

148 ed antibodies to IGFBP2, p53, HER2-ICD, HER2-ECD, and CEA, but not to tetanus toxin, relative to cont

149 is HPLC with electrochemical detection (HPLC-ECD).

150 A levels were increased, suggesting impaired ECD translation as the mechanism for reduced protein lev

151 Ten years after implantation, ECD had decreased by >/=25% in 7.9% and 6.3%, whereas EC

152 centage of eyes with a decrease of >/=25% in ECD, and percentage of eyes with an ECD <1500 cells/mm(2

153 avourable political environment, advances in ECD metrics, and the existence of compelling arguments f

154 The linear decline in ECD after DSEK was consistent with shorter-term endothel

155 2 years of life there is a rapid decline in ECD, which is likely related to growth in CD and hence s

156 A mild decrease in ECD may occur, but there is a low probability of severe

157 gh" mode, we observed a large enhancement in ECD efficiency by introducing a short ion trapping perio

158 ctivating mutation during BRAF inhibition in ECD.

159 reduce (preexisting) hepatobiliary injury in ECD livers.

160 ce of compelling arguments for investment in ECD.

161 iopsies, and gauge the treatment response in ECD patients.

162 AF/MEK inhibition as a promising strategy in ECD.

163 ection, postoperative complication, and late ECD decay is reduced when compared to standard penetrati

164 upled to liquid chromatography (LC), this LC-ECD workflow provides good sequence coverage for both tr

165 the neoplastic clone in 20 adults with LCH, ECD, and HCL.

166 CD34(+) cells from patients with ECD and LCH/ECD, including detection of shared origin of LCH and acu

167 e trimeric langerin extracellular domain (Lg-ECD).

168 tion state and the global architecture of Lg-ECD.

169 e interface between protomers of trimeric Lg-ECD, thereby explaining the defective oligomerization of

170 f RSPOs1-4 using purified RSPO Fu1-Fu2, LGR4 ECD, and ZNRF3 ECD proteins in Wnt signaling and recepto

171 Moreover, LGR4-ECD therapeutically abrogated RANKL-induced bone loss in

172 (days), longer PT was associated with lower ECD (mean difference by days, 15 cells/mm2; 95% CI, 4-26

173 Mean ECD was 2733 cells/mm(2).

174 The mean ECD loss at 6 months, 1 year, 2 years, 3 years, and 5 ye

175 - 1.4 years (range 0.1-5 years) and the mean ECD was 3746 +/- 370 cells/mm(2) (range 3145-5013 cells/

176 ouse embryonic fibroblasts (MEFs); moreover, ECD mRNA levels were increased, suggesting impaired ECD

177 cularly evident for kidneys coming from most ECDs.

178 directly compared with a conventional GC-MS/ECD detection system.

179 rometry or electron capture detection (GC-MS/ECD) as of yet, which often limits the ability to conduc

180 ion gas chromatograph (TDS-PTV-GC) with a mu-ECD detector.

181 s given to eight patients with multisystemic ECD with CNS and/or cardiac involvement.

182 afenib) in three patients with multisystemic ECD.

183 nd sustained efficacy in BRAF(V600E)-mutated ECD as second-line therapy.

184 t interactions in a wild type neuronal nAChR ECD and the full ligand binding pocket conferred by two

185 on to the waiting list than with delayed non-ECD transplantation >/=3 years after activation to the w

186 in the United States with an ECD versus non-ECD transplant was only 7 months.

187 ) deficits, white matter lesions, and Notch3(ECD) deposition, were evaluated between 6 and 20 months

188 ular deposition of NOTCH3 ectodomain (Notch3(ECD) ) on the vessels.

189 roteins that abnormally accumulate in Notch3(ECD) -containing deposits on brain vessels of mice and p

190 and vitronectin, acting downstream of Notch3(ECD) deposition, play a role in CADASIL, producing diver

191 mice was not associated with reduced Notch3(ECD) deposition in brain vessels.

192 rioretinal biopsy confirmed the diagnosis of ECD in 1 case, with the presence of histiocytic infiltra

193 patients with confirmed tissue diagnosis of ECD that showed intraocular manifestations and were imag

194 Their median age at diagnosis of ECD was 54 years (age range, 18-80 years), and 67% (42 o

195 In all eligible cases, the diagnosis of ECD was made using clinical criteria in conjunction with

196 of GRP78 reversed the attenuating effect of ECD overexpression on PERK signaling.

197 ion of the linker region at the interface of ECD and TMD are of particular importance.

198 Rare intraocular manifestations of ECD confirmed on histopathology can be imaged with multi

199 Intraocular manifestations of ECD seen on multimodal imaging include histiocytic choro

200 Measurements of ECD and CT during the course of postkeratoplasty follow-

201 Reciprocally, overexpression of ECD led to marked decreases in p-PERK, p-eIF2alpha, and

202 Significantly, overexpression of ECD provided a survival advantage to cells upon ER stres

203 T) is an underused way to expand the pool of ECD kidneys and to rapidly transplant elderly patients w

204 the knowledge on the relative positioning of ECD and TMD and the conformation of the linker region at

205 To examine whether the presence of ECD modified the effect of IAT for intracranial proximal

206 Because of the relative rarity of ECD, key clinical features of the disease may not be wel

207 e first and second year of life, the rate of ECD decrease was significantly higher than between 2 and

208 xogenous ECD, demonstrating a requirement of ECD for normal mammalian cell cycle progression.

209 nal example of the pronounced sensitivity of ECD toward molecular conformation, and a clear warning a

210 has been assigned using TD-DFT simulation of ECD spectra.

211 derate clinical efficacy in the treatment of ECD and can be considered a treatment option in cases wi

212 hloro-2'-deoxyadenosine) in the treatment of ECD.

213 tion, and a clear warning against the use of ECD spectral correlations to assign absolute configurati

214 It is not known if adult LCH or ECD arises from hematopoietic stem cells (HSCs), nor whi

215 rmined the crystal structures of overlapping ECD fragments at near atomic resolution, built a model o

216 nalysis of labile N-phosphorylated peptides, ECD and ETD are emerging as a complementary method.

217 ell loss of 32% in the perioperative period, ECD declined at a linear rate of approximately 110 cells

218 Efficient UVPD and photo-ECD of a model peptide and proteins within the ICR cell

219 ral and genetic characterization of the PknB ECD.

220 CD correlated with the 6-month postoperative ECD (r = 0.56; P < 0.001), but not with the baseline don

221 matrix method, a popular approach to predict ECD spectra of compounds which can be treated with an in

222 The mean preoperative ECD was 2761 +/- 285 cells/mm(2).

223 ewed for patients with pathologically proven ECD.

224 C digests of bovine serum albumin, providing ECD spectra for doubly charged precursor ions with very

225 ER stress induction led to a reduced ECD protein level, but this effect was not seen in PKR-l

226 Refraction, ECD loss (40% at 3 months; P < 0.001), donor loss (DSAEK

227 Modification of preoperative age-related ECD thresholds is indicated to maintain an ECD that warr

228 At 3 years, the mean (SD) ECD decreased from baseline by 37% (21%) in the 0-7d PT

229 nd 209 eyes in the 8-14d PT group (mean [SD] ECD, 1537 [683] cells/mm2 and mean [SD] ECL, 44% [23%])

230 the 203 eyes in the 0-7d PT group (mean [SD] ECD, 1620 [673] cells/mm2 and mean [SD] ECL, 41% [23%])

231 comparison of the experimental and simulated ECD data generated at different theory levels.

232 ical or histological scores, dual and single ECD transplantations yield similar results in terms of p

233 are seen between the full-length and soluble ECD structures, rationalizing previous experimental data

234 ansfer studies, we demonstrated that soluble ECD disrupts endogenous DR5-DR5 interactions.

235 Available extension study ECD results at 4 years mirrored those at 3 years in the

236 theory-electronic circular dichroism (TDDFT-ECD) calculations of the solution conformers.

237 nic circular dichroism (ECD) data with TDDFT-ECD calculations for the truncated model compound 8.

238 VA, lower astigmatism, and similar long-term ECD compared with PK for FED and PBK.

239 t as short as possible to improve short-term ECDs.

240 eir subunit composition, with the N-terminal ECDs of each of the subunits directly participating in i

241 s had better graft and overall survival than ECD recipients.

242 Taken together, our data demonstrate that ECD promotes survival upon ER stress by increasing GRP78

243 Subsequent analyses demonstrated that ECD transplants do not provide a lifetime of allograft f

244 Here we present evidence that ECD regulates the endoplasmic reticulum (ER) stress resp

245 nalyse the challenges and opportunities that ECD proponents face in advancing global priority for the

246 r tetra-O-substituted resorcin[4]arenes, the ECD exciton couplet at longer wavelength depends on the

247 inhibition of TRAIL-induced apoptosis by the ECD predominantly comes from the disruption of DR5 oligo

248 cing ligand (TRAIL)-induced apoptosis by the ECD, although TRAIL is still able to bind to the recepto

249 The coloration and bleaching process in the ECD component show good cyclic stability, and over 85% o

250 d directly expressed by color changes in the ECD.

251 y utilized in docking homology models of the ECD and the TMD to create a full-length model of a glyco

252 The critical role of the ECD is manifested by disease-causing mutations on ZIP4,

253 were used to guide homology modeling of the ECD.

254 tion and indicates that rearrangement of the ECD/extracellular loop 1 (ECL1) interface is a critical

255 dependence of solvent and temperature on the ECD spectra were examined.

256 without (standard criteria donor [SCD]) the ECD criteria.

257 After the cornea reaches adult size, the ECD decreases at a rate similar to that reported in adul

258 The analysis indicates that the ECD community faces two primary challenges in advancing

259 firm the expected binding mode of TSH to the ECD as well as the general fold of the domains and were

260 by binding of the hormone ligand TSH to the ECD.

261 ded 17 unique distance restraints within the ECD of the TSHR, its ligand TSH, and the hormone-recepto

262 In contrast, after the age of 2 years, the ECD was inversely correlated with age but not with CD (r

263 resolved by enantioselective HPLC, and their ECD spectra have been recorded online by stopped-flow me

264 satisfactory, and a high proportion of these ECD kidneys are discarded.

265 Demographics, death-to-preservation time, ECD, lens status, medical history, time on mechanical ve

266 disease (no change in symptoms attributed to ECD), and progressive disease (worsening of symptoms att

267 omplete resolution of symptoms attributed to ECD), partial response (partial resolution of symptoms a

268 partial resolution of symptoms attributed to ECD), stable disease (no change in symptoms attributed t

269 disease (worsening of symptoms attributed to ECD).

270 change in proven or suspected lesion due to ECD for >/=3 months), and progressive disease (progressi

271 olution of proven or suspected lesion due to ECD), partial response (partial resolution of proven or

272 olution of proven or suspected lesion due to ECD), stable disease (no significant change in proven or

273 rsening of proven or suspected lesion due to ECD).

274 heir structures were determined by NMR, VCD, ECD, and X-ray diffraction.

275 ecreased by >/=25% in 7.9% and 6.3%, whereas ECD was <1500 cells/mm(2) in 3.9% and 4.0% in the myopic

276 urvival defects, but the mechanisms by which ECD functions are largely unknown.

277 However, the exact mechanism by which ECD regulates cell cycle is unknown.

278 We quantified the extent to which ECD kidneys provide recipients with a lifetime of allogr

279 t storage time in medium was associated with ECD decrease (ie, the longer the storage time, the large

280 on of novel somatic mutation associated with ECD enabled treatment with a new-targeted systemic agent

281 ions are rarely observed in association with ECD.

282 tioning allograft at 5 years was higher with ECD transplantation within 1 year after activation to th

283 We report a patient with ECD who carried the BRAF(V600E) mutation and developed t

284 ti-institutional cohort of 189 patients with ECD and ECD overlapping with Langerhans cell histiocytos

285 mediates in CD34(+) cells from patients with ECD and LCH/ECD, including detection of shared origin of

286 nce of myeloid neoplasms among patients with ECD and MH.

287 ay be at least as effective in patients with ECD as in those without ECD, and it should not be withhe

288 Some 10.1% (19/189) of patients with ECD have an overlapping myeloid neoplasm, most commonly

289 n the prespecified subgroup of patients with ECD versus 1.3 (CI, 0.9 to 1.9) in patients presenting w

290 fied 752 grafts (75%) in 590 recipients with ECD measurements at 1 or more postoperative examinations

291 , 0.9 to 1.9) in patients presenting without ECD.

292 ive in patients with ECD as in those without ECD, and it should not be withheld in these complex pati

293 The 10-year ECD correlated with the 6-month postoperative ECD (r = 0

294 One-year ECD was lower after EK vs PK (1472 vs 1859 cells/mm(2),

295 At 3 years, ECD did not differ between EK and PK.

296 may remain stable up to at least 4-7 years; ECD shows a constant, slow decrease; and complications a

297 dings lead to working hypotheses on how ZIP4-ECD exerts critical functions in zinc transport.

298 The conserved dimeric architecture in ZIP4-ECD is also demonstrated to be a common structural featu

299 first crystal structure of a mammalian ZIP4-ECD, which reveals two structurally independent subdomai

300 g purified RSPO Fu1-Fu2, LGR4 ECD, and ZNRF3 ECD proteins in Wnt signaling and receptor binding assay