ライフサイエンスコーパス: effacement

1 d substantial vacuolization and foot process effacement.

2 n proteinuria with only minimal foot process effacement.

3 plete or significant improvement of podocyte effacement.

4 asement membrane thickening and foot process effacement.

5 nt sFlt-1 mice exhibited severe foot process effacement.

6 cellular junctions during a process known as effacement.

7 e presence of circulating factors causing FP effacement.

8 membrane reaction and podocyte foot process effacement.

9 deposits and extensive podocyte foot process effacement.

10 AK, followed by proteinuria and foot process effacement.

11 with attenuated albuminuria and foot process effacement.

12 nd splitting including podocyte foot process effacement.

13 ar basement membrane, and focal foot process effacement.

14 can lead to proteinuria without foot process effacement.

15 an be observed without podocyte foot process effacement.

16 /- mice, even before widespread foot process effacement.

17 en are associated with podocyte foot process effacement.

18 iffuse visceral epithelial cell foot process effacement.

19 y from a nonnephrotic patient exhibited >20% effacement.

20 re (ripening) that facilitate dilatation and effacement.

21 the filtration slits resembling foot process effacement.

22 ion, loss of stress fibers, and foot process effacement.

23 to the loss of cell adhesion and microvillus effacement.

24 nalyses showed a focal podocyte foot process effacement.

25 evelopment, leading to podocyte foot process effacement.

26 ding new light on mechanisms in foot process effacement.

27 nge in cell morphology known as foot process effacement.

28 phrin-Nck1/2 association during foot process effacement.

29 roteinuria and partial podocyte foot process effacement.

30 ing in proteinuria and podocyte foot process effacement.

31 lin1 cleavage, albuminuria, and foot process effacement.

32 reased demand during the disease state of FP effacement.

33 led to albuminuria and podocyte foot process effacement.

34 ent wall thickening, enhanced wall, and fold effacement.

35 responsible for proteinuria and foot process effacement.

36 ped spontaneous proteinuria and foot process effacement.

37 differentiated enterocytes in relation to MV effacement.

38 ose with mild (</=25%) podocyte foot process effacement (13,030 vs. 4806 pg/mL; P=0.02).

39 oteinuria with morphologic changes (podocyte effacement), a condition that presents a major obstacle

40 s(nls) mouse exhibited podocyte foot process effacement, absence of slit diaphragms, and massive prot

41 Effacement activity caused by the EPEC protein Map in th

42 MV effacement activity of the EPEC protein EspF in the TC-7

43 Microvillous effacement and actin rearrangement, characteristic of A/

44 solated glomeruli, resulting in foot process effacement and albumin leakage.

45 d hypertension-induced podocyte foot process effacement and albuminuria.

46 podocyte injury and attenuated foot process effacement and associated proteinuria in a delayed fashi

47 hat Robo2 cKO mice display less foot process effacement and better-preserved slit-diaphragm density c

48 orresponding restructuring, characterized by effacement and blebbing of its apical surface.

49 d actinomyosin contractility in foot process effacement and compromised filtration capacity.

50 tural studies revealed podocyte foot process effacement and deposition of extracellular matrix.

51 alteration of glomerular features including effacement and disorganization of the slit diaphragm, fo

52 Podocyte foot process effacement and disruption of the slit diaphragm are typi

53 les and causes diffuse podocyte foot process effacement and F-actin collapse via nephrin, alphavbeta3

54 dneys revealed diffuse podocyte foot process effacement and focal podocyte hypertrophy by 3 wk of age

55 smission electron microscopy showed podocyte effacement and fusion and morphologically normal endothe

56 rocess effacement in young mice, and diffuse effacement and globally disrupted podocyte morphology in

57 es were edematous with areas of foot process effacement and glomerular basement membrane thickening a

58 a by 6 weeks and focal podocyte foot process effacement and glomerulosclerosis at 3 months.

59 uria and azotemia), structural (foot-process effacement and glomerulosclerosis) and molecular (gene-e

60 binding domain of SHROOM3 may cause podocyte effacement and impairment of the glomerular filtration b

61 in the podocytes, with complete foot process effacement and irregular and thickened glomerular baseme

62 cture, and eventual progression to cartilage effacement and joint instability.

63 from protamine sulfate-induced foot process effacement and lipopolysaccharide-induced nephrotic synd

64 oli by two distinctive phenotypes, attaching effacement and localized adherence.

65 Podocyte foot process effacement and loss of slit diaphragm followed with prog

66 ter birth and preceded podocyte foot process effacement and loss of slit diaphragms by at least 7 day

67 ostnatal day 28, accompanied by foot process effacement and loss of slit diaphragms.

68 he epithelium, as they preceded foot process effacement and loss of slit diaphragms.

69 e sulfate-induced podocyte foot process (FP) effacement and LPS-induced nephrotic syndrome.

70 n a cluster with more prominent foot process effacement and microvillous transformation had the highe

71 Individual podocyte descriptors such as effacement and microvillous transformation were associat

72 e knockout mice had distinctive foot process effacement and microvillus formation.

73 d segmental glomerulosclerosis and extensive effacement and microvillus transformation of podocyte fo

74 f adult zebrafish, resulting in foot-process effacement and podocyte loss.

75 into the mechanisms of podocyte foot process effacement and points out a promising strategy to treat

76 There was an association between FP effacement and proteinuria (P = 0.04).

77 yte dysfunction, represented by foot process effacement and proteinuria, is often the starting point

78 The mice developed podocyte foot process effacement and proteinuria, which were prevented by FK50

79 similar phenotypes of podocyte foot process effacement and proteinuria.

80 ch is a key factor for podocyte foot process effacement and proteinuria.

81 mice from LPS-induced podocyte foot process effacement and proteinuria.

82 vating SFKs and FAK, leading to foot process effacement and proteinuria.

83 reased, accompanied by podocyte foot process effacement and proteinuria.

84 nal pathway leading to podocyte foot process effacement and proteinuria.

85 l intestine enterocytes, causing microvillus effacement and rearrangement of the host cell cytoskelet

86 amatically more albuminuria and foot process effacement and reduced glomerular nephrin mRNA and immun

87 II activation, reduced podocyte foot process effacement and reduced levels of proteinuria during neph

88 P3) from severe glomerulopathy with podocyte effacement and segmental glomerular basement membrane sp

89 signaling in podocytes leads to foot process effacement and urinary protein loss via a mechanism that

90 rular basement membrane thickening, podocyte effacement, and albuminuria.

91 ion barrier integrity, podocyte foot process effacement, and an edematous phenotype.

92 3 integrin on podocytes, causes foot process effacement, and contributes to proteinuric kidney diseas

93 ollapsed capillaries, extensive foot process effacement, and dysmorphic mitochondria in podocytes.

94 rly onset albuminuria, podocyte foot process effacement, and elevated systolic BP.

95 lt mice results in proteinuria, foot process effacement, and glomerulosclerosis.

96 ted in progressive albuminuria, foot process effacement, and histology consistent with ESRD.

97 el barium study showed fold thickening, fold effacement, and increased luminal fluid in 80% of patien

98 egulates BB assembly as well as pathological effacement, and indicate that it is an important regulat

99 structure, loss of readherence, microvillus effacement, and interruption of signal transduction.

100 tes display severe proteinuria, foot process effacement, and kidney failure.

101 ceptor and reduced albuminuria, foot-process effacement, and mesangial matrix expansion.

102 glomerular basement thickening, foot process effacement, and podocyte loss, resulting in marked reduc

103 proteinuria, increased podocyte foot process effacement, and to decreased podocyte number in the sett

104 e mesangial matrix and podocyte foot process effacement are attenuated.

105 on microscopy revealed an early foot process effacement, as well as morphologic abnormality, in ILK-d

106 thelial damage similar to the attachment and effacement associated with enteropathogenic Escherichia

107 of the bone marrow revealed almost complete effacement by neutrophils, eosinophils, and their precur

108 e suggested that the bacteria respond to the effacement by up-regulating genes associated with anaero

109 FP effacement can be observed within minutes after reperfus

110 sociated with profound podocyte foot process effacement, cell death, and sustained p38 and JNK activa

111 The degree of podocyte effacement correlates with suPAR levels at time of diagn

112 to 2.1+/-2.8 mg/dL (P=0.003), mean podocyte effacement decreased from 57%+/-33% to 22%+/-22% (P=0.00

113 rovillus assembly during differentiation and effacement during bacterial pathogenesis.

114 Accordingly, the effacement effector protein Tir from enterohemorrhagic E

115 x vivo derived enterocytes with regard to MV effacement, enabling a better dissection of the process.

116 ighly conserved non-LEE (locus of enterocyte effacement)-encoded effector F (NleF) shows both diffuse

117 The locus of enterocyte effacement-encoded regulator (Ler) of enteropathogenic a

118 e lpf1 operon while Ler (locus of enterocyte effacement-encoded regulator) acts as an antisilencer.

119 Cells with the most advanced cytoplasmic effacement expressed the C/EBP-homologous protein (CHOP)

120 e protected from acute podocyte foot process effacement following protamine sulfate perfusion.

121 rs developed heavy proteinuria, foot process effacement, GBM thickening, and renal failure by 3 month

122 ient and necessary for podocyte foot process effacement, however, Rac1 inhibition is not an option fo

123 focal glomerular sclerosis and foot process effacement; however, its etiology and pathogenesis are u

124 ar to those used in vivo during foot process effacement in a subset of glomerular diseases.

125 inuria, nephrinuria, FSGS, and podocyte foot effacement in Ang II-induced hypertension; and early mor

126 also reduced Adriamycin-induced foot process effacement in both the COX-2 transgenic mice and Balb/C

127 opy revealed prominent podocyte foot process effacement in Daf1(-/-) mice with more widespread and se

128 ar basement membrane thickening and podocyte effacement in eNOS(-/-) mice with podocyte-specific VEGF

129 n improved creatinine clearance and podocyte effacement in eNOS-deficient sFlt-1 mice.

130 ic deletion of Crk1/2 prevented foot process effacement in one model of podocyte injury and attenuate

131 The mean score of FP effacement in postreperfusion allograft biopsies was 0.7

132 We evaluated the degree of FP effacement in postreperfusion KT biopsies by counting th

133 hat the degree of podocyte foot process (FP) effacement in postreperfusion transplant biopsies can be

134 final common pathway leading to foot process effacement in proteinuric diseases.

135 ed with diffuse epithelial cell foot process effacement in the absence of peripheral glomerular immun

136 podocytes confirmed more robust foot process effacement in the knockout animals.

137 ockdown model and mild podocyte foot process effacement in the mouse model, whereas all other structu

138 ucleoside, an agent that causes foot process effacement in vivo, disrupted actin and nephrin simultan

139 n shows focal areas of podocyte foot-process effacement in young mice, and diffuse effacement and glo

140 inuria, improvement of podocyte foot process effacement, increased glomerular AMPK activation, and re

141 K abrogated the proteinuria and foot process effacement induced by glomerular injury.

142 eruli of mutant mice, including foot process effacement, irregular and split areas of the glomerular

143 ion barrier, including podocyte foot process effacement, irregular thickening of the glomerular basem

144 se data establish that podocyte foot process effacement is a migratory event involving a novel interp

145 Although in most cases, podocyte effacement is associated with proteinuria and glomerular

146 In C57BL/6J mice podocyte effacement is delayed, prolonging normal renal function.

147 Microvillus effacement is inhibited after exposure of calpastatin-ov

148 s leak into urine, and podocyte foot process effacement is the common pathway of all proteinruic dise

149 Podocyte effacement is the first pathologic manifestation of FSGS

150 pathogenic E. coli gene locus for enterocyte effacement; it did not display mannose-resistant adheren

151 he mechanisms by which podocyte foot process effacement leads to proteinuria and kidney failure, we s

152 ) that is encoded by the locus of enterocyte effacement (LEE) and is necessary for causing attaching

153 notypes are found on the locus of enterocyte effacement (LEE) and the EPEC adherence factor (EAF) pla

154 the presence of both the locus of enterocyte effacement (LEE) and the plasmid-encoded bundle-forming

155 ires the products of the locus of enterocyte effacement (LEE) and, in particular, the type III secret

156 3,359-bp sequence of the locus of enterocyte effacement (LEE) from EDL933, an enterohemorrhagic Esche

157 attle and to repress the locus of enterocyte effacement (LEE) genes important for colonization of the

158 gulate expression of the locus of enterocyte effacement (LEE) genes in a metabolite-dependent manner.

159 Transcription of the locus of enterocyte effacement (LEE) genes in enterohemorrhagic Escherichia

160 gulate expression of the locus of enterocyte effacement (LEE) genes positively and negatively, respec

161 resses expression of the locus of enterocyte effacement (LEE) genes, whose expression is not required

162 d by the presence of the locus of enterocyte effacement (LEE) genomic island, which encodes a type II

163 tes to expression of the locus of enterocyte effacement (LEE) in an EA-dependent manner.

164 sion of the genes in the locus of enterocyte effacement (LEE) in enterohaemorrhagic Escherichia coli

165 The locus of enterocyte effacement (LEE) is a chromosomal pathogenicity island t

166 nicity island termed the locus of enterocyte effacement (LEE) is found in diverse attaching and effac

167 The locus of enterocyte effacement (LEE) is necessary for enteropathogenic Esche

168 The locus of enterocyte effacement (LEE) of Escherichia coli O157:H7 (O157) enco

169 anscription from several locus of enterocyte effacement (LEE) operons (LEE1 to LEE5) and from bfp dur

170 f STEC strains carry the Locus of Enterocyte Effacement (LEE) pathogenicity island (PAI), which encod

171 encoded together on the locus of enterocyte effacement (LEE) pathogenicity island and display high l

172 eins encoded in the EHEC locus of enterocyte effacement (LEE) pathogenicity island are known to contr

173 The locus of enterocyte effacement (LEE) pathogenicity island encodes many genes

174 The locus of enterocyte effacement (LEE) pathogenicity island of enterohemorrhag

175 orf2 gene located on the locus of enterocyte effacement (LEE) pathogenicity island of enteropathogeni

176 , is an activator of the locus of enterocyte effacement (LEE) pathogenicity island via the LEE1 promo

177 ctors encoded within the locus of enterocyte effacement (LEE) pathogenicity island, including the adh

178 oded outside of the EPEC locus of enterocyte effacement (LEE) pathogenicity island, non-LEE-encoded e

179 m (TTSS), encoded by the locus of enterocyte effacement (LEE) pathogenicity island, to deliver effect

180 ation of the chromosomal locus of enterocyte effacement (LEE) pathogenicity island, which confers the

181 lesion is encoded by the Locus of Enterocyte Effacement (LEE) pathogenicity island, which encodes a t

182 he essential role of the locus of enterocyte effacement (LEE) pathogenicity island, which encodes eff

183 TTSS are located on the locus of enterocyte effacement (LEE) pathogenicity island.

184 islands, including the locus for enterocyte effacement (LEE) region, which encodes a T3SS and effect

185 in, and genes within the locus of enterocyte effacement (LEE) responsible for attaching and effacing

186 perplasia and contains a locus of enterocyte effacement (LEE) similar to that found in enteropathogen

187 (SPI-1), SPI-2, and the locus of enterocyte effacement (LEE) T3SSs.

188 des the genes within the locus of enterocyte effacement (LEE) that are largely organized in five oper

189 nicity island called the locus of enterocyte effacement (LEE) that is organized in five major operons

190 not mediated through the locus of enterocyte effacement (LEE) transcriptional regulator GrlA or Ler.

191 in the regulation of the locus of enterocyte effacement (LEE), a PAI of enteropathogenic and enterohe

192 ctors are encoded on the locus of enterocyte effacement (LEE), a pathogenicity island required for th

193 taining mutations in the locus of enterocyte effacement (LEE), a pathogenicity island required for vi

194 proteins encoded on the locus of enterocyte effacement (LEE), and a LEE-encoded regulator (Ler) is p

195 e factors encoded by the locus of enterocyte effacement (LEE), as well as Shiga toxin.

196 on system encoded in the locus of enterocyte effacement (LEE), but lack the virulence factors (stx, b

197 icity island, termed the locus of enterocyte effacement (LEE), contains all the genes necessary for t

198 een genes encoded on the locus of enterocyte effacement (LEE), including ler, showed a significant in

199 icity island, termed the locus of enterocyte effacement (LEE), which contains eae encoding intimin as

200 egative regulator of the locus of enterocyte effacement (LEE), which encodes most of the proteins inv

201 The locus of enterocyte effacement (LEE), which includes five major operons (LEE

202 ese, eight mapped to the locus of enterocyte effacement (LEE), which is required for the formation of

203 C. rodentium possess the locus of enterocyte effacement (LEE), which is the canonical virulence trait

204 proteins encoded by the locus of enterocyte effacement (LEE), which plays a key role in the host-cel

205 Escherichia coli (EPEC) locus of enterocyte effacement (LEE)-encoded effectors EspF and Map are mult

206 amined the expression of locus of enterocyte effacement (LEE)-encoded factors in individual bacteria.

207 arries two copies of non-locus of enterocyte effacement (LEE)-encoded protein H, designated NleH1 and

208 (per) gene, by the locus for the enterocyte effacement (LEE)-encoded regulator (ler) gene, and by se

209 The locus of enterocyte effacement (LEE)-encoded type 3 secretion system (T3SS)

210 intestinal environment, locus of enterocyte effacement (LEE)-encoded virulence genes are activated a

211 wed global increases in Locus for Enterocyte Effacement (LEE)-negative STEC infection.

212 notably those within the locus of enterocyte effacement (LEE).

213 S) system encoded by the locus of enterocyte effacement (LEE).

214 nicity island termed the locus of enterocyte effacement (LEE).

215 nicity island called the locus of enterocyte effacement (LEE).

216 es the expression of the locus of enterocyte effacement (LEE).

217 E are encoded within the locus of enterocyte effacement (LEE).

218 ity islands known as the locus of enterocyte effacement (LEE).

219 nicity island called the locus of enterocyte effacement (LEE).

220 system specified by the locus of enterocyte effacement (LEE).

221 nicity island called the locus of enterocyte effacement (LEE).

222 enicity island named the locus of enterocyte effacement (LEE).

223 nicity island termed the locus of enterocyte effacement (LEE).

224 nicity island called the locus of enterocyte effacement (LEE).

225 on system encoded by the locus of enterocyte effacement (LEE).

226 a global regulator, Ler (locus of enterocyte effacement [LEE]-encoded regulator), which activates exp

227 ower numbers and caused fewer attachment and effacement lesions than the parent strain.

228 rular basement membranes and severe podocyte effacement, matching human diabetic nephropathy.

229 The significant degree of foot process effacement (mean 34%, five of 14 cases with >50%) sugges

230 of human renal disease, such as foot process effacement, mesangial expansion, and glomerulosclerosis.

231 ice also manifested significant foot-process effacement, moderate mesangial expansion, and segmental

232 e report that, in this model of foot process effacement, nephrin dislocates to the apical pole of the

233 gnificant proteinuria, podocyte foot process effacement, nephrin down-regulation, and nephrinuria.

234 endent complex is necessary for foot process effacement observed in distinct subsets of human glomeru

235 ial form of sinusoidal capillarization, with effacement of endothelial zonation functionally parallel

236 The locus of enterocyte effacement of enteropathogenic Escherichia coli encodes

237 ness of more than 3 mm, and partial or total effacement of fatty hilum were included in the study.

238 clerosis, with reduced podocytes, widespread effacement of foot processes, and modest proteinuria.

239 s on the effect of suPAR on podocyte injury, effacement of foot processes, and proteinuria.

240 and activity, hyaluronan fragmentation, and effacement of HA from the vessel wall of small pulmonary

241 ypic abnormalities such as pleuritis and the effacement of lymphoid follicles in the regional lymph n

242 d into the host cell membrane with resultant effacement of microvilli and loss of the glycocalyx.

243 erent to intestinal epithelial cells without effacement of microvilli or cup-and-pedestal formation.

244 demonstrated intimate bacterial attachment, effacement of microvilli, submucosal edema, mucosal hete

245 collapse of nephrocyte lacunar channels and effacement of nephrocyte slit diaphragms.

246 ression in glomerular podocytes and revealed effacement of podocyte foot processes in Neph1(-/-) mice

247 lapsing glomerulopathy, as well as extensive effacement of podocyte foot processes with abnormal junc

248 litting of the glomerular basement membrane, effacement of podocyte foot processes, and reduced sialy

249 of collagen alpha1alpha2alpha1(IV) in GBMs, effacement of podocyte foot processes, gradual loss of g

250 of the glomerular filtration barrier lead to effacement of podocyte foot processes, leakage of albumi

251 gnificant increase in albuminuria and showed effacement of podocyte foot processes.

252 merular injury is often characterized by the effacement of podocytes, loss of slit diaphragms, and pr

253 dose (100 mug), did not induce proteinuria, effacement of podocytes, or disruption of the cytoskelet

254 ly, we observed severe podocyte foot process effacement of remaining podocytes, activation of proxima

255 ilient, less elastic, and was accompanied by effacement of rete ridges with reduced deposition of bot

256 e that gastric distension causes progressive effacement of the abdominal portion of the LES, exposing

257 The lymph node revealed effacement of the architecture by an interfollicular inf

258 at the corticomedullary junction and diffuse effacement of the epithelial foot processes and microvil

259 cortical mass/thickening, and replacement or effacement of the fatty hilum.

260 Effacement of the lateral ventricle was used as a radiog

261 Effacement of the nuclear cleft was only applicable in 1

262 -null mice were significantly protected from effacement of the podocyte foot processes, albuminuria,

263 ular basement membrane, but does not prevent effacement of the podocyte foot processes.

264 reater than 50% within 15 minutes after full effacement of the stenosis by the angioplasty balloon.

265 pansion of the human leukocytes and complete effacement of the tumor compared with tumor progression

266 efining feature of EPEC disease is the loss (effacement) of absorptive microvilli (MV) from the surfa

267 We observed pronounced podocyte foot process effacement on long stretches of the filtration barrier i

268 le score, absence of specific abnormalities (effacement or hypodensity of >33% of the middle cerebral

269 min D3 or 1,25-vitamin D2 prevented podocyte effacement or reversed glomerular and tubulointerstitial

270 einuria is a result of podocyte foot process effacement or the cause of it.

271 s of synaptopodin, nephrin, and foot process effacement, partly regulated by angiopoietins.

272 C) which do not have the locus of enterocyte effacement pathogenicity island carry the STEC autoagglu

273 s, other products of the locus of enterocyte effacement pathogenicity island, and an immunogenic remn

274 cated within the 35.6-kb locus of enterocyte effacement pathogenicity island.

275 tion system borne on the locus of enterocyte effacement pathogenicity island.

276 hly prevalent among LEE (locus of enterocyte effacement)-positive E. coli strains associated with sev

277 acterial motility, modulating attachment and effacement processes, and upregulating the expression of

278 ve and grafted kidneys, causing foot process effacement, proteinuria and FSGS-like glomerulopathy.

279 reased expression of the locus of enterocyte effacement regulon, which is known to play a pivotal rol

280 of their foot process (FP) architecture (FP effacement) results in urinary protein loss.

281 The FP effacement score in the postreperfusion KT biopsy may be

282 The FP effacement score predicts early recurrence with a sensit

283 K activation regulates podocyte foot process effacement, suggesting that pharmacologic inhibition of

284 itical gene outside the locus for enterocyte effacement that regulates bacterial colonization, crypt

285 on all strains carry the locus of enterocyte effacement, the effector repertoires of different clonal

286 ce revealed widespread podocyte foot process effacement, thickening of the glomerular basement membra

287 g mesangial sclerosis, podocyte foot process effacement, tubular atrophy, interstitial fibrosis, and

288 Podocytes showed foot process effacement, vacuolar degeneration, detachment and downre

289 Podocyte pathology included effacement, vacuolization, and hypertrophy with crescent

290 iated with glomerulomegaly, uniform podocyte effacement, very few and wide foot processes joined by o

291 py was performed on 74 biopsies and podocyte effacement was detected in 88%.

292 While microvillus effacement was detected in both 388- and 388DeltaS-treat

293 ed in both 388- and 388DeltaS-treated cells, effacement was more prevalent and rapid in cells exposed

294 ients demonstrated at least 80% foot process effacement, whereas no biopsy from a nonnephrotic patien

295 ement membrane (GBM) charge and foot process effacement, whereas transgenic expression specifically i

296 ation of the cell shape, called foot process effacement, which is a classic feature of proteinuric ki

297 Podocytes showed focal foot process effacement, which was the most likely cause for transien

298 ase in proteinuria and podocyte foot process effacement with a reduction in the expression of podocyt

299 nstrate that renal ischemia induces podocyte effacement with loss of slit diaphragm and proteinuria.

300 GTPases was identified as a key mechanism in effacement, with increased membrane activity and motilit