ライフサイエンスコーパス: effacement

1 e presence of circulating factors causing FP effacement.

2 membrane reaction and podocyte foot process effacement.

3 evelopment, leading to podocyte foot process effacement.

4 deposits and extensive podocyte foot process effacement.

5 AK, followed by proteinuria and foot process effacement.

6 with attenuated albuminuria and foot process effacement.

7 ding new light on mechanisms in foot process effacement.

8 nd splitting including podocyte foot process effacement.

9 ar basement membrane, and focal foot process effacement.

10 can lead to proteinuria without foot process effacement.

11 an be observed without podocyte foot process effacement.

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

13 en are associated with podocyte foot process effacement.

14 nge in cell morphology known as foot process effacement.

15 iffuse visceral epithelial cell foot process effacement.

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

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

18 roteinuria and partial podocyte foot process effacement.

19 re (ripening) that facilitate dilatation and effacement.

20 the filtration slits resembling foot process effacement.

21 to the loss of cell adhesion and microvillus effacement.

22 ing in proteinuria and podocyte foot process effacement.

23 lin1 cleavage, albuminuria, and foot process effacement.

24 reased demand during the disease state of FP effacement.

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

26 responsible for proteinuria and foot process effacement.

27 ped spontaneous proteinuria and foot process effacement.

28 differentiated enterocytes in relation to MV effacement.

29 d substantial vacuolization and foot process effacement.

30 n proteinuria with only minimal foot process effacement.

31 plete or significant improvement of podocyte effacement.

32 asement membrane thickening and foot process effacement.

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

34 cellular junctions during a process known as effacement.

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

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

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

38 Effacement activity caused by the EPEC protein Map in th

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

40 Microvillous effacement and actin rearrangement, characteristic of A/

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

68 similar phenotypes of podocyte foot process effacement and proteinuria.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

97 FP effacement can be observed within minutes after reperfus

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

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

100 rovillus assembly during differentiation and effacement during bacterial pathogenesis.

101 Accordingly, the effacement effector protein Tir from enterohemorrhagic E

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

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

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

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

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

107 se mice revealed membrane-bound melanin with effacement f the organelle structure of severely affecte

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

133 Microvillus effacement is inhibited after exposure of calpastatin-ov

134 Podocyte effacement is the first pathologic manifestation of FSGS

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

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

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

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

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

140 3,359-bp sequence of the locus of enterocyte effacement (LEE) from EDL933, an enterohemorrhagic Esche

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

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

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

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

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

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

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

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

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

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

151 nd of 35 kb known as the locus of enterocyte effacement (LEE) is necessary and sufficient for this ef

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

214 The locus of enterocyte effacement of enteropathogenic Escherichia coli encodes

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

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

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

218 H. pylori attachment resulted in (i) effacement of microvilli at the site of attachment, (ii)

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

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

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

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

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

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

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

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

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

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

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

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

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

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

233 Effacement of the lateral ventricle was used as a radiog

234 Effacement of the nuclear cleft was only applicable in 1

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

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

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

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

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

240 racteristic histologic change is retraction (effacement) of the distal "foot" processes of glomerular

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

256 The FP effacement score predicts early recurrence with a sensit

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

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

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

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

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

262 n of nephrotic syndrome and GEC foot process effacement using the puromycin aminonucleoside rat model

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

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

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

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

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

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

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

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

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

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

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

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

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