ライフサイエンスコーパス: EC

1 c acid components of the elongation complex (EC).

2 disease (worsening of symptoms attributed to ECD).

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

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

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

6 in retinal and choroidal endothelial cells (ECs).

7 as a result, to lower genetic diversity than EC.

8 ing pathway were found to be dysregulated in EC.

9 y regulation of E-selectin on the cocultured EC.

10 ignificant gap in the metabolomic studies of EC.

11 proliferation and migration in VSMCs but not EC.

12 on the European Commission Decision 2002/657/EC.

13 ctivating mutation during BRAF inhibition in ECD.

14 ewed for patients with pathologically proven ECD.

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

16 immediate cellular precursor in both LCH and ECD.

17 to estimate treatment effect modification by ECD.

18 d directly expressed by color changes in the ECD.

19 , 0.9 to 1.9) in patients presenting without ECD.

20 ell sources capable of generating functional ECs.

21 T mutants and in HHT patient blood outgrowth ECs.

22 ot M2-polarized macrophages induced EndMT in ECs.

23 (E2) treatment activates Notch signaling in ECs.

24 ondrial respiratory capacity in human aortic ECs.

25 t mediate the key actions of Hh signaling in ECs.

26 tory MKL1/2 target genes in VSMCs but not in ECs.

27 at Y361 via proline-rich kinase 2 (Pyk2) in ECs.

28 family member and is localized in nuclei of ECs.

29 (SMCs) and promoted the tube formation from ECs.

30 alian cells via choline dehydrogenase (CHDH; EC 1.1.99.1), we assessed whether this enzyme was expres

31 LPMOs are copper-dependent enzymes (EC 1.14.99.53-56) that, with glycoside hydrolases, parti

32 adenosine 5'-phosphosulfate reductase (APR, EC 1.8.99.2), was significantly higher in Salicornia tha

33 zed by diacylglycerol acyltransferase (DGAT, EC 2.3.1.20).

34 c patches were created from spheroids (CM:FB:EC = 70:15:15, 70:0:30, 45:40:15) using a 3D bioprinter.

35 determined that aging of endothelial cells (ECs), a critical component of the BM microenvironment, w

36 d whether resulting metabolic changes induce EC activation, is unknown.

37 associated with classical endothelial cell (EC) activation signs, such as Vegfa/VEGFR1+2 upregulatio

38 ssary to promote angiogenesis and to protect ECs against hydrogen peroxide-induced oxidative stress.

39 coronary syndrome (ACS) to promote premature EC aging and thrombogenicity.

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

41 Our data highlight the significance of CCN1-EC and CCN1-pericyte communication signals in driving ph

42 BQ were 41, 47 and 53microW/cm(2), while CA, EC and EPC electrodes with BQ showed 260, 330 and 500mic

43 m power densities of biofuel cells using CA, EC and EPC electrodes without BQ were 41, 47 and 53micro

44 et of cortical synaptic terminals within the EC and in this way, constrain non-action potential-depen

45 s a difference in their capacity to activate EC and support the secondary recruitment of flowing neut

46 We found that ADAR2 is overexpressed in EC and that the increase in expression positively correl

47 revealed a twofold increase in proliferative ECs and a 1.35-fold increase in proliferative alpha-smoo

48 carbons in the tricyclic acid (TCA) cycle of ECs and contributes to lipid biosynthesis via reductive

49 tify a set of cytokines that are elevated in ECs and define their effects on cellular activation, HIV

50 the inherent cross-diffusion issue of redox ECs and has the added benefit of greatly stabilizing the

51 in IL-37 induced pro-angiogenic response in ECs and in the mouse model of Matrigel plug and oxygen-i

52 Mutants of gamma-ECS and PCS1 were hypersensitive to As and had higher ro

53 entify significantly mutated genes (SMGs) in ECs and use them as biomarkers for the classification of

54 n of 5-LOX from nucleus to cytoplasm in both ECs and VSMCs, potentially facilitating SPM biosynthesis

55 ch paired activation of entorhinal cortical (EC) and Schaffer collateral (SC) inputs to hippocampal C

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

57 RPE), fenestrated choroid endothelial cells (ECs) and Bruch's membrane, a highly organized basement m

58 ing (equalisation of parental contributions (EC)) and the other forcing it (circular sib mating (CM))

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

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

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

62 (PGI2, also called prostacyclin) in Cav-1 KO EC, and this PGI2 increase appeared to stimulate cAMP/PK

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

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

65 The ECs are antigenically stable at temperatures above the c

66 Electro-chromic materials (EC) are a new class of electronically reconfigurable thi

67 battery (LIB) and electrochemical capacitor (EC) are considered as the most widely used energy storag

68 Endothelial cells (ECs) are critical determinants of vascular homeostasis a

69 ression level and role in endothelial cells (ECs) are still unclear.

70 Human endothelial cells (ECs) are widely used to study mechanisms of angiogenesis

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

72 of protein kinase B was increased in hIRECO EC as was Nox2 NADPH oxidase-dependent generation of sup

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

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

75 nce of Cav-1 increased cAMP/PKA signaling in EC, as indicated by elevated phosphorylation of hormone-

76 irin), and a delayed-release enteric-coated (EC) aspirin.

77 PGA2 enhanced the EC barrier and protected against barrier dysfunction cau

78 s by which molecules cross endothelial cell (EC) barriers in normal tissues and in solid tumors, incl

79 To examine its role in endothelial cell (EC) biology, we generated mice with catalytic inactivati

80 gene induced by electroconvulsive seizures (ECS), blocks its antidepressant efficacy.

81 on of growth persistence specifically within EC branched protrusions.

82 of MCAK expression on MT growth dynamics and EC branching morphology.

83 characterize lipid droplet (LD) formation in EC by manipulating pathways leading to the formation and

84 We therefore hypothesize that ECs can directly activate basophils via cell-to-cell int

85 While ECs can take up asparagine, silencing asparagine synthet

86 entation of contact precautions for all ESBL-EC carriers remains weak.

87 of and against contact precautions for ESBL-EC carriers.

88 d contactless conductivity detection (hybrid EC-CE-C(4)D) is herein described.

89 ectric and the optical characteristics of an EC cell can be engineered to suit a variety of applicati

90 However, the molecular mechanism of EC cell mechanotransduction is unknown.

91 The EC cell model released 5-HT in response to stretch, and

92 We show that EC cells express specific chemosensory receptors, are el

93 Here, we found that EC cells in mouse primary cultures fired spontaneous bur

94 We conclude that the EC cells in the human and mouse small bowel GI epitheliu

95 munoreactivity localized specifically within EC cells of human and mouse small bowel epithelium.

96 We tested the susceptibility of human EC cells to transduction by retroviral vectors derived f

97 In human EC cells, MLV integration occurs normally, but no viral

98 Embryonic carcinoma (EC) cells are malignant counterparts of embryonic stem (

99 Human embryonic carcinoma (EC) cells are shown to restrict the expression of murine

100 packaged in the extracellular vesicles from EC-CM.

101 atopoietic stem and progenitor cell/EC (HSPC/EC) coculture system as well as in vivo EC infusions fol

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

103 ic carbon (TOC) and/or the elemental carbon (EC) contents in the atmospheric aerosol may have a stron

104 gs highlight an important mechanism by which EC contribute to atherogenesis under hyperlipidemic cond

105 om the perspective of how endothelial cells (ECs) coordinate migration and proliferation in response

106 findings define critical roles for Stac3 in EC coupling and human disease.

107 h domain 3) is an essential component of the EC coupling apparatus and a mutation in human STAC3 caus

108 that MCAK promotes fast MT growth speeds in ECs cultured on compliant 2D ECMs but promotes slow MT g

109 D ECMs but promotes slow MT growth speeds in ECs cultured on compliant 3D ECMs, and these effects are

110 col (PEG) hydrogel NPs by endothelial cells (ECs) cultured in a microchannel compared to uptake of ei

111 e non-canonical Wnt5a in pericyte but not in EC cultures.

112 osis factor (TNF) compared with normal donor EC cultures.

113 FS was 87.9% (95% CI, 85.6% to 89.8%) in the EC-D arm and 88.3% (95% CI, 86.1% to 90.1%) in the DC ar

114 Patients receiving EC-D reported significantly more stomatitis, myalgia or

115 d by three cycles of docetaxel (100 mg/m(2); EC-D).

116 etation gas exchange parameters derived from EC data are subject to scale-dependent and method-specif

117 ross primary productivity (GPP) derived from EC data to calculate a measure of iWUE (G1 , "stomatal s

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

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

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

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

122 However, patient-derived ECs demonstrate a greater increase in permeability and i

123 Inhibition of glutamine metabolism in ECs did not cause energy distress, but impaired tricarbo

124 EC differentiation, capillary engraftment, reduced capil

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

126 rom in vivo angiogenesis models and cultured EC document that TSP-4 mediates upregulation of angiogen

127 The SMOC-EC domain bound HSPGs with a similar affinity to BMP2 an

128 , inhibited BMP2 signaling, whereas SMOC-EC (EC domain only) enhanced BMP2 signaling.

129 , lacking the extracellular calcium binding (EC) domain, inhibited BMP2 signaling, whereas SMOC-EC (E

130 ll (SMC) proliferation and endothelial cell (EC) dysfunction are critical in the pathogenesis of athe

131 Rab7 inhibition reversed lal(-/-) EC dysfunctions, including decreasing their enhanced mig

132 somal proteins that are involved in lal(-/-) EC dysfunctions.

133 Endoplasmic reticulum (ER) stress elicits EC dysregulation in metabolic syndrome.

134 main, inhibited BMP2 signaling, whereas SMOC-EC (EC domain only) enhanced BMP2 signaling.

135 of angiopoietins with Tie2 in cis and across EC-EC junctions in trans Except for the binding of the C

136 ctivation of one SHIP2 allele selectively in ECs (ECSHIP2(Delta/+)).

137 ns than PFIs due to higher elemental carbon (EC) emissions.

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

139 Taken together, our results suggest that ECs enhance EMT-induced TNBC cell metastasis via PAI-1 a

140 Under increased electric fields, both EC entropy and adiabatic temperature changes increase qu

141 aorta, oleic acid treatment generates LD in EC ex vivo.

142 Endothelial cells (ECs) express O-glycoproteins that are believed to play i

143 Stabilized ECs, expressed recombinantly as VLPs, could be ideal can

144 s induced the entry of Ca(2+) in ECs via the EC-expressed TRPM2.

145 Here we report that lal(-/-) ECs facilitated in vivo tumor angiogenesis, growth, and

146 ECs from LAL-deficient (lal(-/-)) mice possess enhanced

147 ystemic cytokine responses may differentiate ECs from subjects with uncontrolled viral replication or

148 ever, it is not known how endothelial cells (EC) from large vessels process a postprandial surge of F

149 strate that microvascular endothelial cells (ECs) from Anxa2(-/-) mice display reduced barrier functi

150 nt stem cell-derived endothelial cells (iPSC-ECs) from three families with unaffected mutation carrie

151 ereas Sox17 expression is required to confer EC function.

152 By applying an electrochemical (EC) gate voltage to the molecule, we switch the redox gr

153 The findings reveal novel features of human EC gene regulation not present in their murine counterpa

154 In addition, in the EC-H2O2 system, Mn(II) removal efficiency increased as p

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

156 Glutamine metabolism in endothelial cells (ECs) has been poorly studied.

157 x-enhanced electrochemical capacitors (redox ECs) have, however, performed poorly due to cross-diffus

158 Human dermal microvascular ECs (HDMECs) treated with TLR3 [Poly(I:C)], TLR4 (LPS),

159 vivo hematopoietic stem and progenitor cell/EC (HSPC/EC) coculture system as well as in vivo EC infu

160 (MAECs) from these mice, and human umbilical ECs (HUVEC) treated with Kindlin-2 siRNA showed enhanced

161 sive injury in mice to demonstrate that aged ECs impair the repopulating activity of young HSCs and i

162 th concerns associated with long-term use of EC in relatively young users who did not also smoke toba

163 at reported for uptake of similar PEG NPs by ECs in a static culture, where the smaller disks were fo

164 all ECs in wild-type cells, and 5-7% of all ECs in cells lacking proofreading factors are, in fact,

165 lic and cytoskeleton changes in target organ ECs in gene array and proteomic analyses.

166 for blood flow; however, the involvement of ECs in the process of triple-negative breast cancer (TNB

167 omyces cerevisiae and found that 1-3% of all ECs in wild-type cells, and 5-7% of all ECs in cells lac

168 actively transcribing elongation complexes (ECs) in Escherichia coli and Saccharomyces cerevisiae an

169 an important role for BM endothelial cells (ECs) in regulating hematopoietic aging and support furth

170 Endothelial cells (ECs) in the tumor microenvironment have been reported to

171 PMN interaction with ECs induced the entry of Ca(2+) in ECs via the EC-expres

172 HSPC/EC) coculture system as well as in vivo EC infusions following myelosuppressive injury in mice t

173 Microvascular ECs instruct neighboring cells in their organ-specific v

174 athway of cytokine-mediated signaling at the EC interface, and we propose that this is a mechanism fo

175 rol epoxide hydrolase (ChEH) metabolizes 5,6-EC into cholestane-3beta,5alpha,6beta-triol, which is tr

176 ochrome B (phyB) at multiple sites where the EC is bound provides a mechanism for integrating environ

177 ok distribution patterns when the passage of ECEs is most likely to occur from 2012 to 2016 using pas

178 results suggest blocking TRPM2 activation in ECs is a potentially important means of therapeutically

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

180 calized on the surface of endothelial cells (ECs) is a key determinant of the magnitude and duration

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

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

183 Here we report that EC lacking Cav-1 exhibit impaired LD formation.

184 SMOC deletion constructs we found that SMOC-EC, lacking the extracellular calcium binding (EC) domai

185 itatory post-synaptic currents (mEPSCs) onto EC layer III pyramidal neurons, suggesting that these ch

186 nhancing insulin sensitivity specifically in EC leads to a paradoxical decline in endothelial functio

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

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

189 or ZEA and T-2 toxin) or at one third of the EC level (for DON: 400microg/kg).

190 tors specify non-vascular, amniotic cells to EC-like cells, whereas Sox17 expression is required to c

191 METHODS AND LD were present in EC lining the aorta after the peak in plasma triglycerid

192 ) groups, respectively, resulting in a total EC loss of 16.6% and 21.5% from 6 months to 10 years pos

193 Chronic EC loss was calculated from 6 months postoperatively to

194 A significant linear chronic EC loss was reported after implantation with myopic or t

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

196 using electrochemical liquid phase epitaxy (ec-LPE) at low temperatures (T </= 90 degrees C).

197 (RC) (>/=2 PIMT/year); 2) erratic compliers (EC) (<2 PIMT/year); and 3) non-compliers (NC) (no PIMT).

198 fected individuals termed elite controllers (ECs) maintain CD4(+) T cell counts and control viral rep

199 or-stimulatory myeloid cells, and suppressed EC-mediated stimulation of in vitro tumor cell transmigr

200 However, how DF alters EC metabolism, and whether resulting metabolic changes i

201 In ECs, MKL1 was constitutively nuclear and MKL2 cytoplasmi

202 utive Akt signalling increases expression of EC morphogenesis genes, including Sox17, shifts the geno

203 tinal symptoms with mycophenolate mofetil or EC-MPS in combination with Tac and cyclosporin, but this

204 (Tac), enteric-coated mycophenolate sodium (EC-MPS) and sirolimus (SRL) in oral dosage forms was wel

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

206 EC N1ICD expression in melanoma correlated with shorter

207 LP) vaccines that mimic the "empty" capsids (ECs) normally produced in viral infection.

208 receptors (N1ICD) are frequently observed in ECs of human carcinomas and melanoma, and in ECs of the

209 r silencing of poly ADP-ribose polymerase in ECs of mice prevented PMN transmigration.

210 ecombinant AAV serotype 1 (rAAV1) transduces ECs of pathologic vessels, and that editing of genomic V

211 ECs of human carcinomas and melanoma, and in ECs of the pre-metastatic niche in mice.

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

213 This study examined the impact of ECEs on the resident UK butterfly species (n = 41) over

214 We cultured endothelial cells (ECs) on collagen-coupled stiff or compliant polyacrylami

215 tect against apoptosis of endothelial cells (ECs), one of the hallmarks of endothelial dysfunction le

216 Combining gamma-ECS or PCS1 with HAC1 mutation did not alter As toleranc

217 ial of MPs from senescent endothelial cells (ECs) or from patients with acute coronary syndrome (ACS)

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

219 Snail was also expressed in EC overlying atherosclerotic plaques in coronary arterie

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

221 lso play important roles in the prognosis of EC patients, has not been extensively studied.

222 fects of PGA2 on pulmonary endothelial cell (EC) permeability and inflammatory activation and identif

223 work, we show that Fe(0) electrocoagulation (EC) permits the oxidative removal of Mn(II) from solutio

224 shear stress, which alters endothelial cell (EC) physiology.

225 ), gamma-glutamyl-cysteine synthetase (gamma-ECS), phytochelatin synthase (PCS1) and phosphate efflux

226 gets to ameliorate and, perhaps, reverse the EC plexiform phenotype in severe human PAH.

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

228 on of phosphodefective STIM1-Y361F mutant in ECs prevented the increase in vascular permeability indu

229 al monolayers to macromolecules by promoting EC proliferation and migration.

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

231 Loss of Bmp6 in ECs recapitulated the hemochromatosis phenotype of globa

232 fact that the spontaneous endothelial cell (EC) regeneration is a slow and insufficient process, it

233 g blank wheat and wheat spiked either at the EC regulated levels (100microg/kg for ZEA and T-2 toxin)

234 itionally, jagged-2 expressed in bone marrow ECs regulated HSPC cell cycle and quiescence during rege

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

236 The Commission Regulation (EC) Regulation N.

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

238 esults demonstrate that neurons in the human EC represent space with an enhanced flexibility relative

239 vity per weight of CNTs than those of CA and EC, respectively.

240 Our work demonstrates that nontransformed ECs respond differently to excess centrosomes than do mo

241 nstability in tumor cells, how untransformed ECs respond to excess centrosomes is poorly understood.

242 Furthermore, platelet removal by ECs resulted in a corresponding decrease in platelet-leu

243 resulting in increased interepithelial cell (EC) scanning, expression of antimicrobial genes, and gly

244 longitudinal analyses, higher HEI and lower EC scores were observed in Hispanic compared with white

245 n, a commonly IV-administered antibiotic and EC-SERS to detect dobutamine, a drug commonly administer

246 s where we use NRS and electrochemical SERS (EC-SERS) to detect IV therapy analytes within their clin

247 fects are fully rescued by endothelial cell (EC)-specific overexpression of Kir2.1.

248 we generated a mouse with endothelial cell (EC)-specific overexpression of the human insulin recepto

249 EC-specific deletion in mice of glutaminase, the initial

250 rms a complex with VEC and its phosphatases, EC-specific protein tyrosine phosphatase (VE-PTP) and Sr

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

252 bsolute configurations have been assigned by ECD spectroscopy.

253 array scan patterns, only found on high-end EC-SPM setups such as hopping mode scan, were easily imp

254 t electrochemical-scanning probe microscope (EC-SPM) is presented.

255 trogen and aspartate to asparagine) impaired EC sprouting even in the presence of glutamine and aspar

256 ion, miR-424 and miR-503 reduced LPS induced EC sprouting, migration and tube formation.

257 n internal networks that are responsible for EC stability.

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

259 and functionally distinct endothelial cell (EC) subtypes from cardiogenic versus hemogenic mesoderm

260 ensitive TRPM2 mutant channel (C1008-->A) in ECs suppressed the Ca(2+) entry response.

261 A layer of KCl deposited by e-beam to the eC surface without breaking vacuum protects the surface

262 is incorporated into synaptic vesicles, from EC synaptic terminals using two photon microscopy in sli

263 er and describe one solution: an inexpensive EC system that could help by making spatial replication

264 fects of TL alterations on the rate at which ECs terminate from effects of the TL on the nucleotide a

265 d factor-1 (SDF-1) levels were 43% higher in ECs than in NCs.

266 fy the rejuvenating factors elaborated by BM ECs that restore HSC function and the immune repertoire

267 n blood-brain barrier endothelial cells (BBB-ECs) that was previously shown to be involved in leukocy

268 ta lay the groundwork for the exploration of EC therapies that can serve as adjuvant modalities to en

269 ow shear stress induces dedifferentiation of EC through a process termed endothelial-to-mesenchymal t

270 to upregulation of angiopoietin-2 (Ang2) in ECs through FOXO1 activation and triggering a positive f

271 es, increasing the concentration of FAEs and ECs through the inhibition of degrading enzymes has been

272 elet disposal mediated by endothelial cells (ECs) through phosphatidylserine (PS) and examined the ef

273 essential for the discovery of biomarkers in ECs to further investigate the non-SMGs that were highly

274 t action of ECT and implicate the ability of ECS to induce dendritic arborization of differentiating

275 Exposure of P1 ECs to MPs shed from senescent P3 cells or circulating M

276 and Wnt7b-specific signals in mammalian CNS ECs to promote angiogenesis and regulate the BBB.

277 further proved crucial in glutamine-deprived ECs to restore protein synthesis, suppress ER stress, an

278 from LAL deficiency enhances the ability of ECs to stimulate tumor cell proliferation and metastasis

279 of these enzymes converts 5-ethynylcytosine (EC) to 5-ethynyluridine monophosphate that is subsequent

280 ximity ligation assays in endothelial cells (ECs) to demonstrate compound-induced inhibition of Pfn1-

281 dium channel (ENaC) subunits in enterocytes (ECs) to maintain osmotic and ISC homeostasis.

282 Transplanting vascular endothelial cells (ECs) to support metabolism and express regenerative para

283 nsitizes retinal vascular endothelial cells (ECs) to VEGF-A, leading to upregulation of angiopoietin-

284 Thus, tumor-induced EC-to-OSB conversion is one mechanism that leads to oste

285 entified in PDX-conditioned medium, promoted EC-to-OSB conversion of 2H11 endothelial cells.

286 While individual EC towers are well suited to providing fluxes from the f

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

288 t precautions for preventing nosocomial ESBL-EC transmission in nonepidemic settings, without harming

289 Cytokine activation of endothelial cells (EC) upregulates VCAM-1 receptors that target monocyte re

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

291 tion with ECs induced the entry of Ca(2+) in ECs via the EC-expressed TRPM2.

292 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

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

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

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

296 ly recognized as a focal adhesion protein in EC, was not anticipated to have a role in vascular barri

297 Aortic EC were stimulated with low-dose TNFalpha (0.3 ng/ml) in

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

299 Here, we demonstrate that ECs-when mixed with TNBC cells-could increase TNBC cell

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