ライフサイエンスコーパス: CME

1 CME is initiated by the formation of clathrin-coated pit

2 CME suppression was also phenocopied by HSC70 RNAi deple

3 CME was defined as central retinal thickness greater tha

4 oidal organization (P<0.001), VMT (P<0.001), CME (P<0.001), exudation (P<0.001), and disruption of th

5 CME and intraretinal fluid (IRF) status: (1) CME, (2) IRF without CME, (3) neither CME nor IRF.

6 mprints in a linear range of 1-64 ng mL(-1) (CME) and 0.25-64 ng mL(-1) (HME), respectively.

7 y block (n = 1), choroidal effusion (n = 2), CME (n = 4), and redislocation (n = 1) in the exchange g

8 ex (TPC), which is proposed to function as a CME adaptor complex, is only conserved in plants and a f

9 cells by inhibition of GSK3beta accelerates CME, alters CCP dynamics and, unexpectedly, increases th

10 This indicates that the presence of active CME is essential for the pluripotency of embryonic stem

11 CLCb/Dyn1-dependent adaptive CME selectively altered EGF receptor trafficking, enhanc

12 We define molecular mechanisms for adaptive CME in cancer cells and a role for the reciprocal crosst

13 This "adaptive CME" resulted from upregulation of dynamin-1 (Dyn1) and

14 cells contributes to a program of "adaptive" CME that alters signaling to enhance cancer cell surviva

15 vitreal aflibercept injection for addressing CME in RP seems to be an effective treatment.

16 .04; P = .038); CILP was 0.14 +/- 0.01 after CME and 0.27 +/- 0.03 after IME (P < .002).

17 ression (CILP) was significantly lower after CME (0.17 +/- 0.01) compared with IME (0.30 +/- 0.02; P

18 vious treatment (33% vs. 67%; P = 0.04), and CME progression after treatment (0% vs. 100%; P = 0.006)

19 r confounding factors) for vitreous cell and CME for those treated with cryotherapy compared to contr

20 of anterior chamber cell, vitreous cell, and CME in the cryotherapy-treated eyes.

21 ng the more potent inhibitors of dynamin and CME yet reported.

22 All FTMHs had some element of ERM and CME.

23 Hard exudates and CME regressed completely in 15 of 15 and 5 of 6 eyes, re

24 ion especially in those with small holes and CME.

25 RD or RD surgery, infectious keratitis, and CME were 1.0%, 0.8%, and 4.1%, respectively.

26 (IC50 = 10.6 +/- 1.3 to 1.6 +/- 0.3 muM) and CME (IC50(CME) = 65.9 +/- 7.7 to 3.7 +/- 1.1 mM), which

27 use of aflibercept in a patient with RP and CME.

28 e reciprocal crosstalk between signaling and CME in cancer progression.

29 , and the absence of posterior synechiae and CME characterize RV-associated uveitis.

30 Arabidopsis CME appears to follow the constant curvature model and t

31 ind that the positively curved membranes are CME hotspots, and that key CME proteins, clathrin and dy

32 ches, which cluster near exocytic sites, are CME sites.

33 hort CCS intensity trace fragments to assess CME dynamics.

34 required for efficient Ede1 localization at CME sites are the third EH domain, the proline-rich regi

35 groups were created on the basis of baseline CME and intraretinal fluid (IRF) status: (1) CME, (2) IR

36 Because CME entails substantial local remodeling of the plasma m

37 phostinA23, which is routinely used to block CME, displays similar properties, thus questioning its u

38 s simian virus 40 (SV40) was not affected by CME-specific treatments.

39 s near Earth and Mars confirm the channelled CME motion, and are consistent with an ellipse shape of

40 Chronic CME was the most common cause of MVL (3.55%), and macula

41 Classical CME proceeds via the formation of clathrin-coated pits (

42 These studies identified conserved CME mechanisms and species-specific adaptations with bro

43 Analysis of constitutive CME is difficult because the initiation of endocytic eve

44 Genetics and live-cell imaging revealed core CME spatiodynamic similarities between the two yeasts, a

45 The imprints created with cysteine (CME) and histidine modified epitopes (HME) could detect

46 critical specifically for activity-dependent CME of synaptic glutamate receptors.

47 images of sufficient quality for determining CME and IRF at baseline, 92 (8.1%) had CME, 766 (67.7%)

48 in the follow-up cohort, 105 (40%) developed CME during a median follow-up of 31 months (mean, 34; ra

49 eroid therapy none of the patients developed CME subsequently (P = .003).

50 significantly reduced the odds of developing CME as compared to topical corticosteroids in nondiabeti

51 significantly reduced the odds of developing CME as compared to topical corticosteroids in nondiabeti

52 rticosteroids reduced the odds of developing CME in nondiabetic and diabetic patients, as compared to

53 significantly reduced the odds of developing CME, as compared to topical corticosteroids, in nondiabe

54 During CME in yeast, actin polymerization is triggered and coor

55 During CME, endocytic adaptor proteins bind cargoes at the cell

56 dynamics and premature actin assembly during CME through a PtdIns(4,5)P2-dependent mechanism.

57 temporal regulation of actin assembly during CME.

58 itment and actin polymerization onset during CME.

59 ent and function of specific proteins during CME is achieved remains unclear.

60 nonredundant, early regulatory roles during CME in nonneuronal cells.

61 mportance of this "checkpoint." Dysregulated CME also alters EGF receptor signaling and leads to cons

62 mutant cells displaying rapid, dysregulated CME are defective in early endosomal trafficking, matura

63 euronal cells to trigger rapid, dysregulated CME.

64 Cystoid macular edema (CME) before intraocular surgery was not encountered.

65 urrent treatments for cystoid macular edema (CME) in retinitis pigmentosa (RP) are not always effecti

66 Cystoid macular edema (CME) in retinitis pigmentosa (RP) has been managed in se

67 s. 3.2 mm; P = 0.01), cystoid macular edema (CME) involving the foveola (30% vs. 70%; P = 0.001), ret

68 Cystoid macular edema (CME) is a leading cause of blindness.

69 Cystoid macular edema (CME) occurred in 5 eyes (0.87%): 3 in group A and 2 in g

70 e score of >/=1.5+ or cystoid macular edema (CME) of >300 mum were enrolled.

71 ations, resolution of cystoid macular edema (CME), and anterior chamber and vitreous inflammation wer

72 visual acuity (BCVA), cystoid macular edema (CME), and the highest fluorescein angiography (FA) score

73 foveal architecture, cystoid macular edema (CME), intraretinal exudates and subretinal lipid aggrega

74 , retinal detachment, cystoid macular edema (CME), macular scarring, macular hole, optic neuropathy,

75 l membrane (ERM), and cystoid macular edema (CME), were analyzed.

76 in eyes with uveitic cystoid macular edema (CME).

77 P) increase (n = 12), cystoid macular edema (CME; n = 3), and nonarteritic anterior ischemic optic ne

78 infectious keratitis, cystoid macular edema [CME], retinal detachment [RD], or RD surgery) following

79 E) and the component-wise mediation effects (CME), respectively.

80 Loss of efficient CME in twd40-2-3 resulted in the unregulated overaccumul

81 its own internalization by regulating either CME initiation rates or frequency of abortive events, ou

82 rocesses like clathrin-mediated endocytosis (CME) across a diverse range of organisms and mechanical

83 e presence of clathrin-mediated endocytosis (CME) and bulk endocytosis.

84 urred through clathrin-mediated endocytosis (CME) and independently of choline binding protein A (Cbp

85 Clathrin-mediated endocytosis (CME) and its core endocytic machinery are evolutionarily

86 or uptake via clathrin-mediated endocytosis (CME) and subsequent intracellular sorting for degradatio

87 s involved in clathrin-mediated endocytosis (CME) and synaptic vesicle recycling.

88 Clathrin-mediated endocytosis (CME) begins with the nucleation of clathrin assembly on

89 ntral role in clathrin-mediated endocytosis (CME) by recruiting cargo and clathrin to endocytic sites

90 Clathrin-mediated endocytosis (CME) constitutes the major pathway for uptake of signali

91 tion phase of clathrin-mediated endocytosis (CME) determines where and when endocytosis occurs.

92 erstanding of clathrin-mediated endocytosis (CME) dynamics is based on detection and tracking of fluo

93 inhibitor of clathrin-mediated endocytosis (CME) in different systems and that ES9 induces inhibitio

94 e-1) inhibits clathrin-mediated endocytosis (CME) in mammalian cells by aggregate-driven sequestratio

95 Clathrin-mediated endocytosis (CME) in mammalian cells is driven by resilient machinery

96 essure during clathrin-mediated endocytosis (CME) in yeast, but precise molecular details are still u

97 Clathrin-mediated endocytosis (CME) involves nanoscale bending and inward budding of th

98 Clathrin-mediated endocytosis (CME) involves the recruitment of numerous proteins to si

99 Clathrin-mediated endocytosis (CME) is a fundamental process in cell biology and has be

100 membrane via clathrin-mediated endocytosis (CME) is a key mechanism for regulating synaptic strength

101 Clathrin-mediated endocytosis (CME) is a key pathway for transporting cargo into cells

102 Clathrin-mediated endocytosis (CME) is a major internalization route for PM proteins.

103 Clathrin-mediated endocytosis (CME) is facilitated by a precisely regulated burst of ac

104 Clathrin-mediated endocytosis (CME) is key to maintaining the transmembrane protein com

105 Clathrin-mediated endocytosis (CME) is the major internalisation route for many differe

106 Clathrin-mediated endocytosis (CME) is the major route of receptor internalization at t

107 Clathrin-mediated endocytosis (CME) is the primary mechanism eukaryotic cells use to in

108 Clathrin-mediated endocytosis (CME) is used to internalize a diverse range of cargo pro

109 s of the core clathrin-mediated endocytosis (CME) machinery.

110 Clathrin-mediated endocytosis (CME) manages the sorting and uptake of the bulk of membr

111 Clathrin-mediated endocytosis (CME) occurs via the formation of clathrin-coated vesicle

112 ed either via clathrin-mediated endocytosis (CME) or independently of clathrin (CIE) remains segregat

113 omplex of the clathrin-mediated endocytosis (CME) pathway.

114 ast for early clathrin-mediated endocytosis (CME) proteins facilitated by the phase separation of the

115 Clathrin-mediated endocytosis (CME) regulates signaling from the plasma membrane.

116 In plants, clathrin mediated endocytosis (CME) represents the major route for cargo internalisatio

117 ot abolished; clathrin-mediated endocytosis (CME) was severely impaired at the step of membrane fissi

118 component for clathrin-mediated endocytosis (CME), display a loss of pluripotency and an enhanced exp

119 During clathrin-mediated endocytosis (CME), endocytic-site maturation can be divided into two

120 ainly through clathrin-mediated endocytosis (CME), endosomal recycling, or degradation.

121 hich inhibits clathrin-mediated endocytosis (CME), impaired the AtPep1-PEPR1 internalization and comp

122 During clathrin-mediated endocytosis (CME), over 50 different proteins assemble on the plasma

123 indicator for clathrin-mediated endocytosis (CME), we find that alpha-Syn involvement in endocytosis

124 roteins drive clathrin-mediated endocytosis (CME), which from yeast to humans involves a burst of act

125 ission during clathrin-mediated endocytosis (CME).

126 regulated by clathrin-mediated endocytosis (CME).

127 es, including clathrin-mediated endocytosis (CME).

128 hich to study clathrin-mediated endocytosis (CME).

129 ing classical clathrin-mediated endocytosis (CME).

130 t to occur by clathrin-mediated endocytosis (CME).

131 A53T mutations in alpha-Syn further enhance CME in neuronal and nonneuronal cells.

132 olipid binding, are ineffective in enhancing CME.

133 tion included complete macroscopic excision (CME) in 1,172 patients (77%) and incomplete macroscopic

134 h excision (PME) and complete mesh excision (CME).

135 as investigated using a crude melon extract (CME) as well as a commercial serine protease (Alcalase).

136 rom seven different space missions of a fast CME, which originated in an active region near the disk

137 Deletion of EDE1 results in fewer CME initiations and defects in the timing of vesicle mat

138 e constant curvature model and the bona fide CME population generates vesicles of a predominantly hex

139 existing paradigm, actin is dispensable for CME events at the plasma membrane but plays a unique rol

140 ific for fission yeast and not essential for CME.

141 es of all CATT study eyes were evaluated for CME.

142 s known about how PM proteins are sorted for CME and whether similar motifs are required.

143 Hydrolysates from CME exhibited better emulsifying properties compared to

144 of NSAID therapy to prevent vision loss from CME at 3 months or more after cataract surgery.

145 are at significantly higher risk for future CME.

146 y) had a significantly higher rate of future CME (n = 66; 50%) compared with eyes without subclinical

147 ining CME and IRF at baseline, 92 (8.1%) had CME, 766 (67.7%) had IRF without CME, and 273 (24.1%) ha

148 Most patients had CME in both eyes (n = 24).

149 (n=22), the mean score for children who had CME (n=31) was 7.3 points (95% confidence interval [CI],

150 Compared with children who did not have CME as infants (n=22), the mean score for children who h

151 Group A was more likely to have CME (63.6% vs. 27.3%; P < 0.001) at final follow-up with

152 .8 mum; P < 0.001), were more likely to have CME (93.9% vs. 48.2%; P < 0.001), and received more anti

153 .6 +/- 1.3 to 1.6 +/- 0.3 muM) and CME (IC50(CME) = 65.9 +/- 7.7 to 3.7 +/- 1.1 mM), which makes this

154 In CME and growth inhibition cell-based assays, the data ob

155 omplex revealed that the roles of TWD40-2 in CME are both distinct from and cooperative with the AP2

156 inery and the membrane, leading to arrest in CME.

157 time monitoring of spatiotemporal changes in CME dynamics and is less prone to errors associated with

158 A role for the F-actin cytoskeleton in CME is well established, and recently, PKA-dependent ass

159 ifferential functions of dynamin isoforms in CME using domain swap chimeras.

160 ver rates of membrane-associated proteins in CME.

161 tant signaling lipid with conserved roles in CME and actin assembly regulation.

162 X9 and AP2 and potently and acutely inhibits CME.

163 TDD) or without (TD) the distal leg inhibits CME and CCP dynamics by perturbing clathrin interactions

164 al Initiative on Thrombosis and Cancer (ITAC-CME), established to reduce the global burden of VTE in

165 his Review, we provide an update of the ITAC-CME consensus recommendations based on a systematic revi

166 ved membranes are CME hotspots, and that key CME proteins, clathrin and dynamin, show a strong prefer

167 At a given DH level, CME hydrolysates showed higher oil and water holding cap

168 long been assumed that cargo triggers local CME site assembly in Saccharomyces cerevisiae based on t

169 During mammalian CME, a reversible phosphorylation event occurs on Thr156

170 s and general ME framework, the coherent ME (CME), that overcomes both limitations.

171 llular processes; however, rhomboid-mediated CME regulation has not been described.

172 s: (1) CME, (2) IRF without CME, (3) neither CME nor IRF.

173 RF without CME (43.8%) and eyes with neither CME nor IRF (32.5%; P < 0.001).

174 s with IRF without CME and eyes with neither CME nor IRF (52 vs. 60 vs. 66 letters, P < 0.001); highe

175 , other membrane-associated proteins and non-CME endocytic protein caveolin1 show no such curvature p

176 to report a case of cystoid macular oedema (CME) associated with Rosai-Dorfman Disease (RDD).

177 ed a side-by-side quantitative comparison of CME in two distantly related yeast species.

178 Development of CME detected by macular SD OCT during 6 months postopera

179 actors associated with future development of CME included female gender (P = 0.004), increasing tumor

180 om the Sun results in geometric expansion of CME plasma parcels at a speed faster than the local wave

181 edema in uveitic patients with a history of CME who underwent phacoemulsification.

182 ut mice revealed a significant impairment of CME of transferrin.

183 rophylactic treatment to reduce incidence of CME after triple-DMEK surgery.

184 t systems and that ES9 induces inhibition of CME not because of its effect on cellular ATP, but rathe

185 mplicate this mechanism in the inhibition of CME.

186 Inhibitors of CME that interfere with clathrin function have been desc

187 coded reporters that allow the initiation of CME on demand.

188 Interpretation of CME observations and their interaction with the solar wi

189 coherence of CMEs suggests interpretation of CME observations requires accurate reconstruction of the

190 he foveola (0% vs. 100%; P = 0.002), lack of CME regardless of foveola involvement at presentation (7

191 e visual acuity, smaller tumor size, lack of CME, and lack of treatment before PDT.

192 minor effects on biochemical measurements of CME, thus providing inconclusive/misleading information

193 the variation in biochemical measurements of CME.

194 en made toward elucidating the mechanisms of CME, and the field is becoming increasingly complex, wit

195 rns progression from the initiation phase of CME to the internalization phase.

196 namin2 recruitment during the late phases of CME, and promoted dynamin recruitment.

197 ce tomography (OCT) revealed the presence of CME in the left eye.

198 amber and vitreous inflammation, presence of CME, and prior use of regional corticosteroid injections

199 screened for ROP and graded for presence of CME, central foveal thickness (CFT), inner nuclear layer

200 tly express CLCb, exhibit increased rates of CME and altered clathrin-coated pit dynamics.

201 /or stalled, hence impairing global rates of CME.

202 vo systems by demonstrating the reduction of CME dynamics during dorsal closure of Drosophila melanog

203 talk between signaling and the regulation of CME, leading to autoregulation of endocytosis and signal

204 sure high spatial and temporal regulation of CME.

205 cell surface receptors to the regulation of CME.

206 Standardized reporting of CME based on OCT may allow for more uniform quantitation

207 ed successful hole closure and resolution of CME with concurrent improvement in visual acuity after a

208 sights into the plasticity and robustness of CME.

209 ntified in our genome-wide genetic screen of CME.

210 Severity of CME, as assessed by foveal-to-parafoveal thickness ratio

211 analyses to measure discrete early stages of CME and show how sequential, allosterically regulated co

212 their role in fission at the late stages of CME, many studies have suggested that dynamin also plays

213 TPase dynamin also regulates early stages of CME.

214 d by dynamin isoforms during early stages of CME.

215 a regulatory role during the early stages of CME; however, detailed studies regarding isoform-specifi

216 which is required to drive multiple steps of CME.

217 al study was pivotal to our understanding of CME and its progression into ever-increasing complexity

218 The results enhance our understanding of CME propagation and shape, which can help to improve spa

219 ics in vivo through a mechanism depending on CME and F-actin remodeling.

220 In seedlings of twd40-2-3 and other CME-deficient mutants, a direct correlation was revealed

221 ons, actin dynamics is required to carry out CME successfully.

222 nd tracking of single fluorescent particles, CME dynamics is not characterized in vivo, so the effect

223 asma membrane, where it recruited late-phase CME proteins and supported productive endocytosis, ident

224 astructure, dynamics and mechanisms of plant CME as allowed by our advancement in electron microscopy

225 light the independent evolution of the plant CME mechanism during the autonomous rise of multicellula

226 RCTs comparing medical strategies to prevent CME after uncomplicated cataract surgery in nondiabetic

227 Prior retinal surgery, history of prior CME.

228 dosome movement that itself actively promote CME events.

229 e use DASC-resolved ACs and CCPs to quantify CME progression in 11 EAP knockdown conditions.

230 Finally, we show that Sbf/Rab35/CME directs the plasma membrane to Rab11 endosomes throu

231 ortant role in development of post-radiation CME.

232 ng whether an iodine supplement could reduce CME in RP.

233 atory drug therapy was effective in reducing CME detected by angiography or optical coherence tomogra

234 nd safety of tocilizumab (TCZ) in refractory CME.

235 o better understand mechanisms that regulate CME.

236 form-specific role for dynamin in regulating CME and reveal a feed-forward pathway that could link si

237 cancer-cell specific function in regulating CME in non-small-cell lung cancer (NSCLC) cells.

238 ing diseases associated with uveitis-related CME are juvenile idiopathic arthritis (n = 9), Behcet di

239 tration of TCZ in refractory uveitis-related CME.

240 There is no uniform method of reporting CME in the literature, which prevents accurate assessmen

241 is maintained in mitotic cells with restored CME, indicating that direct phosphorylation of the CME m

242 According to the results of this study, CME can be suggested as a new source of proteolytic enzy

243 tive week, we observed 9 cases of subsequent CME (12%).

244 As such, CME regulates signaling from cell-surface receptors, but

245 ability of dephosphorylated Dyn1 to support CME, even at substoichiometric levels compared with Dyn2

246 e this entire complex while still supporting CME.

247 Of ten CME-related proteins we examined, all show preferences f

248 We demonstrate that CME can be 'restarted' in mitotic cells despite high mem

249 Extensive studies have shown that CME proteins actively modulate the plasma membrane curva

250 The CME predicts strong deviations from Haus ME, which we su

251 Thus information cannot propagate across the CME.

252 ent for the actin cytoskeleton to assist the CME machinery to overcome the increased load.

253 in imprinting factors of 8.8 and 11 for the CME and HME imprints, respectively.

254 ickness, although higher at baseline for the CME group, was similar at 1 and 2 years follow-up for al

255 st antioxidant activity was obtained for the CME hydrolysates with 5.0% DH level.

256 Furthermore, the CME paves the way for exploiting the rich phenomenology

257 We show how the CME can be represented in QTT format, then use the expon

258 improvement in VA at follow-up; however, the CME group started and ended with the worst VA among the

259 However, the CME is demonstrated to be channelled during eruption int

260 stability, we envisage the usefulness of the CME for describing self-modelocking and spontaneous freq

261 ndicating that direct phosphorylation of the CME machinery does not account for shutdown.

262 The AP2 complex of the CME pathway is conserved in yeast, animals, and plants,

263 s facilitated by the phase separation of the CME protein, Ede1, which acts as an intrinsic autophagy

264 rcome the infinite dimensional nature of the CME through projections or other means, a common feature

265 are consistent with an ellipse shape of the CME-driven shock provided by the new Ellipse Evolution m

266 alerkin discretization in time to reduce the CME evolution problem to a set of QTT-structured linear

267 ignaling receptors reciprocally regulate the CME machinery remains an open question.

268 The TME test was more powerful than the CME test when the two mediation effects are in the same

269 d spatially describe progression through the CME pathway and pinpoint a cargo-sensitive regulatory tr

270 Whereas the CME of constitutively internalized transferrin receptors

271 effects are in the same direction, while the CME test was more powerful than the TME test when the tw

272 al-to-parafoveal thickness ratio, within the CME group correlated with poorer cognitive (R2=0.16, P=0

273 oma who have responded to induction therapy, CME of the primary tumor is associated with improved sur

274 n addition to regulating cargo entry through CME, Syp1 can promote internalization of Ptr2 through a

275 duce plant defense responses, likely through CME of cell surface-located signaling components.

276 The mechanisms that link NMDAR activation to CME of AMPARs remain elusive.

277 ent domains contribute to its recruitment to CME sites, site selection, and site maturation.

278 t this cytotoxicity could be abrogated using CME inhibitors or antioxidants, attesting to intracellul

279 articipants with current or resolved uveitic CME.

280 Fifty-six eyes of 42 patients with uveitic CME were prospectively imaged as part of the VISUAL-1 tr

281 t IHCs use dynamin-dependent endocytosis via CME to support vesicle cycling during mild stimulation b

282 lead to a radically different view of which CME steps are regulated and which steps are deterministi

283 mum in the first and third patient, in whom CME was the indication for DEX implantation.

284 .3 for EFS associated with IME compared with CME was observed before and after the introduction of im

285 More eyes with CME (65.3%) developed scarring during 2 years of follow-

286 In CATT, eyes with CME had worse baseline and follow-up VA, although all gr

287 At baseline, eyes with CME had worse mean VA (letters) than eyes with IRF witho

288 th less central foveal swelling in eyes with CME.

289 .45 +/- 0.02) were significantly higher with CME compared with IME (5-year EFS, 0.33 +/- 0.03; 5-year

290 Patients with CME secondary to noninfectious uveitis who had inadequat

291 s lead to the diagnosis of bilateral RP with CME in the right eye.

292 notherapy, outcomes were still superior with CME versus IME (5-year EFS, 0.47 +/- 0.02 v 0.39 +/- 0.0

293 tion age 33.6 +/- 18.9 years; 17 women) with CME were assessed.

294 o directly measure molecular turnover within CME sites for the first time.

295 on UIC separately for eyes with and without CME showed a strong inverse significant relationship for

296 ollow-up compared with eyes with IRF without CME (43.8%) and eyes with neither CME nor IRF (32.5%; P

297 mean VA (letters) than eyes with IRF without CME and eyes with neither CME nor IRF (52 vs. 60 vs. 66

298 fluid (IRF) status: (1) CME, (2) IRF without CME, (3) neither CME nor IRF.

299 (8.1%) had CME, 766 (67.7%) had IRF without CME, and 273 (24.1%) had neither.

300 Retinitis pigmentosa with or without CME.