ライフサイエンスコーパス: villous

1 ssion; specimens of inflammatory bowel and a villous adenoma also had no detectable CRD-BP.

2 enoma with a diameter of at least 10 mm or a villous adenoma in 7.9 percent, an adenoma with high-gra

3 es, having a distal tubulovillous adenoma or villous adenoma was the strongest predictor of advanced

4 adenomas, seven tubulovillous adenomas, one villous adenoma with marked dysplasia, and two cancers.

5 ination had neoplasms (one carcinoma and one villous adenoma) at colonoscopy.

6 Of patients with a distal tubulovillous or villous adenoma, 12.1% had advanced proximal neoplasia.

7 denoma that was 10 mm or more in diameter, a villous adenoma, an adenoma with high-grade dysplasia, o

8 d as an adenoma 10 mm or more in diameter, a villous adenoma, an adenoma with high-grade dysplasia, o

9 denoma that was 10 mm or more in diameter, a villous adenoma, an adenoma with high-grade dysplasia, o

10 a > or =10 mm, 6.05 (95% CI: 2.48-14.71) for villous adenoma, and 6.87 (95% CI: 2.61-18.07) for adeno

11 us adenoma with high grade dysplasia, n = 3; villous adenoma, n = 3), and 20 cases with newly diagnos

12 n malignant renal cell carcinoma and colonic villous adenoma, regulates TET2 protein expression.

13 4-21.45; P < .001), as was the prevalence of villous adenomas (5.5% vs 1.3% in unexposed; mOR = 6.28;

14 Villous adenomas (n = 545; 3.6 %), dysplasia (n = 49; 0.

15 and expression of T-antigen in precancerous villous adenomas and regions of invasive adenocarcinoma.

16 s (i.e., adenomas at least 1 cm in diameter, villous adenomas, adenomas with high-grade dysplasia, or

17 VR1814 replicated in villous and cell column cytotrophoblasts and reduced for

18 Intestinal IR injury causes villous and crypt damage, which has so far been attribut

19 of IL-8, activity was noted predominantly in villous and crypt epithelium but also in a few immunores

20 HB-EGF mRNA and protein were expressed in villous and extravillous cytotrophoblast cells up to wee

21 ominantly in the syncytiotrophoblast and the villous and extravillous cytotrophoblasts.

22 idua revealed the expression of CD1d on both villous and extravillous trophoblasts, the fetal cells t

23 membrane, where it induces the formation of villous and ruffled structures from the surface of trans

24 ing asymptomatic after the diet, with normal villous architecture on repeat biopsy, if performed.

25 f difference 17.7-95.9 mum; P = 0.006), mean villous area was 27.6% greater (27623 v.

26 h WD534tc/C or NCDV/A alone caused only mild villous atrophy (jejunum and/or ileum), whereas dual inf

27 n 2010-2013), presence of total and subtotal villous atrophy (OR 4.2 (2.5-7.0) and OR 2.0 (1.3-3.2) v

28 d was greater among patients with persistent villous atrophy (SIR, 3.78 [CI, 2.71 to 5.12]) than amon

29 h documented moderate or severe symptoms and villous atrophy (villous height:crypt depth ratio of </=

30 caused mild to severe (duodenum and jejunum) villous atrophy and fusion.

31 Capsule endoscopy could detect villous atrophy and severe complications in patients wit

32 ents with conventional celiac disease (CCD) (villous atrophy beyond D1) and individuals without celia

33 Persistent villous atrophy compared with mucosal healing was associ

34 h celiac disease; 9.7% of these patients had villous atrophy confined to D1 (USCD; P < .0001).

35 ents with celiac disease who have persistent villous atrophy despite a GFD.

36 Patients with persistent symptoms and/or villous atrophy despite strict adherence to a gluten-fre

37 All subjects showed villous atrophy in duodenal biopsies, were HLA-DQ2/DQ8-p

38 T cells to kill epithelial cells and induce villous atrophy in patients with active celiac disease.

39 n trace gluten may be the cause of continued villous atrophy in some patients.

40 WT PEC, and all pigs developed diarrhea and villous atrophy in the small intestines resembling that

41 to detect ultra-short celiac disease (USCD, villous atrophy limited to D1), and the clinical phenoty

42 effects of gluten-sensitive enteropathy with villous atrophy limited to the duodenal bulb (D1) have n

43 ion of the characteristic mucosal changes of villous atrophy may replace biopsy as the mode of diagno

44 Tropical enteropathy is an asymptomatic villous atrophy of the small bowel that is prevalent in

45 The rate of LPM in patients with persistent villous atrophy was compared with that of those with muc

46 Villous atrophy was defined as a Marsh 3 lesion or villo

47 Villous atrophy was found in 87%, while 13% had minor le

48 Mild (duodenum and jejunum) or no (ileum) villous atrophy was observed in histologic sections of t

49 Moderate villous atrophy was observed in the small intestines, an

50 values for diagnosis of celiac disease were villous atrophy with 40 intraepithelial lymphocytes (IEL

51 m assays identified patients with persistent villous atrophy with high levels of specificity: 0.83 fo

52 However, they detected villous atrophy with low levels of sensitivity: 0.50 for

53 on 2,933 individuals with CD (Marsh stage 3; villous atrophy) to the Swedish Prescribed Drug Register

54 tinal mucositis in the proximal jejunum with villous atrophy, accumulation of damaged DNA, CD11b(+)-m

55 f rye and barley that leads to inflammation, villous atrophy, and crypt hyperplasia in the intestine.

56 Diagnosis requires the presence of duodenal villous atrophy, and most patients have circulating anti

57 ration, intestinal bacterial overgrowth with villous atrophy, and rectal prolapse.

58 characterized by chronic secretory diarrhea, villous atrophy, associated autoantibodies, and a partia

59 ntified individuals with biopsy-verified CD (villous atrophy, histopathology stage Marsh III) through

60 d by inflammation of the small bowel mucosa, villous atrophy, malabsorption, and increased intestinal

61 sk of neuropathy in 28,232 patients with CD (villous atrophy, Marsh 3) with that of 139,473 age- and

62 a about 26,995 individuals with CD (equal to villous atrophy, Marsh stage 3), 12,304 individuals with

63 Although IND/A alone caused villous atrophy, more-widespread small intestinal lesion

64 Villous atrophy, the hallmark of celiac disease, is patc

65 Coeliac disease is characterised by villous atrophy, which usually normalises after gluten w

66 a higher risk among patients with persistent villous atrophy.

67 and various techniques may identify areas of villous atrophy.

68 bodies detected in serum or small intestinal villous atrophy.

69 inflammatory cells, with varying degrees of villous atrophy.

70 ivity (below 50%) in detection of persistent villous atrophy.

71 tissue transglutaminase 2 in the absence of villous atrophy.

72 ial cytotoxic T cells and the development of villous atrophy.

73 follow-up biopsy, 3308 (43%) had persistent villous atrophy.

74 n and not in epithelia located higher on the villous axis.

75 However, villous B cells are reduced in the absence of invariant

76 Small intestinal (villous) B cells are diminished in genotypes that alter

77 re it then causes epithelial cell damage and villous blunting that leads to diarrhea and cramping.

78 t predictive, terminal ileum eosinophils and villous blunting were significant predictors of active i

79 histological changes in ill animals included villous blunting with sloughing of epithelial cells, sub

80 ntraepithelial lymphocytes, eosinophils, and villous blunting.

81 pression in subepithelial fibroblasts and in villous, but not crypt, epithelial cells.

82 a with vascular dilatation and congestion of villous capillaries.

83 ly related to overall measures of peripheral villous capillarization.

84 TSA), or sessile serrated adenoma (SSA) with villous characteristics (>/=25% villous component), and/

85 rvention may therefore selectively influence villous compartment remodelling.

86 per 100 mum muscularis mucosa (a measure of villous compartment volume) were measured in orientated

87 ed advanced histologic features, including a villous component (n = 11), high-grade dysplasia (n = 4)

88 mas as multiple adenomas and adenomas with a villous component or high-grade dysplasia.

89 as > or = 10 mm in diameter, adenomas with a villous component or moderate-to-severe dysplasia, carci

90 a (SSA) with villous characteristics (>/=25% villous component), and/or high-grade dysplasia and/or d

91 al adenoma that was pathologically advanced (villous component, high-grade dysplasia, or >/=1 cm); 21

92 nomas (adenomas with high-grade dysplasia, a villous component, or a size >/=10 mm) and after 5 years

93 years) and polyp characteristics (>/= 1 cm, villous components or high-grade dysplasia, >/= 3 polyps

94 one polyp >/= 1 cm, at least one polyp with villous components), and those with and without polypect

95 al analysis revealed severe mucosal erosion, villous congestion, and inflammatory infiltrates.

96 on in tubulovillous adenomas with increasing villous content.

97 s had no effect on epithelial restitution or villous contraction, indicating that elevations in trans

98 reas cytotrophoblasts and other cells of the villous core expressed viral proteins.

99 (a measure of epithelial surface area), and villous cross sectional area per 100 mum muscularis muco

100 member, is highly expressed in proliferative villous CTB and required for induction of the trophoblas

101 Although proximally continuous with villous cytotrophoblast (CTB) distally, these cells diff

102 discrete subpopulations of placental cells, villous cytotrophoblast (vCTB) cells and mesenchymal cel

103 cy (two female and three male concepti), and villous cytotrophoblast cells (vCTBs) were isolated at 1

104 Although both isolated placental villous cytotrophoblast cells and chorion membrane extra

105 t ELF5 is expressed in the human placenta in villous cytotrophoblast cells but not in post-mitotic sy

106 nd have localized the signal to the layer of villous cytotrophoblast cells.

107 e BeWo choriocarcinoma cell line, a model of villous cytotrophoblast fusion.

108 ion of DLX5, TLX1 and HOXA10 in primary term villous cytotrophoblast resulted in decreased proliferat

109 In situ, pVHL immunolocalized to villous cytotrophoblast stem cells, and expression was e

110 dentified immunoreactive EPO associated with villous cytotrophoblast, endovascular and intravascular

111 Terminal differentiation of villous cytotrophoblasts (CT) ends in formation of the m

112 ration of primary trophoblasts as well as of villous cytotrophoblasts and cell column trophoblasts in

113 Villous cytotrophoblasts are epithelial stem cells of th

114 14 isolated villous cytotrophoblasts from control (n = 3), IUGR (n =

115 ion from epidermal growth factor receptor(+) villous cytotrophoblasts into human leukocyte antigen-G(

116 asts that breach the uterine vasculature and villous cytotrophoblasts underlying syncytiotrophoblasts

117 Fusion of placental villous cytotrophoblasts with the overlying syncytiotrop

118 orionic villi of the rhesus placenta, within villous cytotrophoblasts, and occasionally within cells

119 ophoblast cells differentiate from precursor villous cytotrophoblasts, but the essential regulating f

120 , two regulators controlling self-renewal of villous cytotrophoblasts.

121 after SMAO, although the incidence of ileal villous damage was significantly higher in both the iNOS

122 anslocation to mesenteric lymph nodes, ileal villous damage, and cecal bacterial population were eval

123 ompanied by hepatocyte injury and intestinal villous damage.

124 bacterial population levels, or cause ileal villous damage.

125 of leukocytes and lymphocytes, resulting in villous degeneration and lipid malabsorption.

126 A-induced neutrophil recruitment by 92% and villous destruction by 90%.

127 imensional reconstruction to assess directly villous development in human pregnancy in vivo in 20 unc

128 GATA-4 protein is expressed exclusively in villous differentiated epithelial cells of the proximal

129 05) by decreasing the histologic indices for villous distortion and active inflammation.

130 eter of at least 1 cm or at least 25 percent villous elements or evidence of high-grade dysplasia, in

131 ntestines, and viral antigen was detected in villous enterocytes of the small and large intestines by

132 Higher numbers of PEC antigen-positive villous enterocytes were detected by immunofluorescent (

133 hibition of bacterial binding to porcine gut villous enterocytes.

134 becomes progressively more expressed in the villous epithelial cells during the suckling-weaning tra

135 apoptosis was seen in the crypts and denuded villous epithelial cells of both saline- and modified Un

136 An occasional normal and some denuded villous epithelial cells of stored bowels exhibited apop

137 sue, with substantially reduced levels after villous epithelial differentiation.

138 Both MDE and IPN comprised papillary villous epithelial neoplasms involving the main and larg

139 derlies the expansive single-cell absorptive villous epithelium and contains a large population of DC

140 duced in the differentiated small intestinal villous epithelium during the suckling-weaning transitio

141 here high-level expression is limited to the villous epithelium of the duodenum.

142 Intracellular pH (pH(i)) of intact jejunal villous epithelium was measured by ratiometric microfluo

143 -) exchange activity in the DraKO and Nhe3KO villous epithelium, respectively.

144 inant Cl(-)/HCO(3)(-) exchanger in the lower villous epithelium.

145 crofluorometry of intracellular pH in intact villous epithelium.

146 Concentrations were measured in placental villous explant conditioned media of 14 amino acids that

147 We employed villous explant cultures to study viral effects on diffe

148 as bile acids-treated trophoblast cells and villous explant in vitro.

149 Interferon-gamma, which increases villous explant indoleamine 2,3-dioxygenase expression,

150 2 inflammatory signaling in vitro by using a villous explant system.

151 d 2.3-fold following in vitro culture of the villous explant.

152 a dose- and time-dependent manner from human villous explants and cultured trophoblasts but not from

153 by IgG from women with PE in human placental villous explants and that endothelial cells are a key so

154 Villous explants from normal placentas delivered by elec

155 R-1 than normal pregnancies, suggesting that villous explants in vitro retain a hypoxia memory reflec

156 ing pathways during hypoxia-reoxygenation of villous explants in vitro.

157 Conditioned medium (CM) from normal villous explants induced endothelial cell migration and

158 L-Tryptophan influx into villous explants is supported exclusively by transport s

159 Preeclamptic villous explants secreted high levels of sFlt-1 and sEng

160 pernatants taken from preeclamptic placental villous explants showed a four-fold increase in sVEGFR-1

161 Exposure of normal villous explants to hypoxia increased sVEGFR-1 release c

162 ecreased angiogenesis seen in human placenta villous explants was attenuated by tumor necrosis factor

163 medium previously conditioned by culture of villous explants was markedly reduced when placental ind

164 Villous explants were exposed to hydrogen peroxide to te

165 , we demonstrated that challenging placental villous explants with a specific TLR2 agonist (Pam3Cys)

166 sis in the placentas of pregnant mice, human villous explants, and human trophoblast cells.

167 ins stimulated sFlt-1 release from placental villous explants, in a dose- and time-dependent manner.

168 ing organotypic human midgestation chorionic villous explants, we show that syncytiotrophoblasts isol

169 induce trophoblast outgrowth from placental villous explants.

170 -like tyrosine kinase-1 secretion from human villous explants.

171 duction from endothelial cells and placental villous explants.

172 been studied using human placental chorionic villous explants.

173 nomas (P < .0001 for trend), the presence of villous features (OR, 1.28; 95% CI, 1.07-1.52), and prox

174 noma 10 mm or more in size, any adenoma with villous features or high-grade dysplasia, any dysplastic

175 adenocarcinoma or TAs 1 cm or larger or with villous features or severe dysplasia located beyond sigm

176 proximal neoplasia, defined as a polyp with villous features, a polyp with high-grade dysplasia, or

177 he occurrence of advanced lesions (> or =25% villous features, high-grade dysplasia, size > or =1 cm,

178 er 3 or more adenomas, high-grade dysplasia, villous features, or an adenoma 1 cm or larger in size.

179 st 1 cm in diameter or with tubulovillous or villous features, severe dysplasia, or invasive cancer),

180 Features of vascularity, villous formation, pannus, granularity, and capillary hy

181 siological conditions using intact placental villous fragments suggest a contribution of SNAT4 to sys

182 oblast of first trimester and term placental villous fragments was measured by microfluorimetry using

183 o dissected from each animal to evaluate the villous height (VH) and crypt depth (CD).

184 MM improved small bowel villous height and absorptive area, but not crypt depth,

185 In adults, villous height and crypt depth measurements showed that

186 Groups with stress and PD showed decreased villous height and crypt depth.

187 Median villous height to crypt depth ratio in distal duodenal b

188 patients given MM compared to placebo, mean villous height was 24.0% greater (293.3 v.

189 Villous height, crypt depth, villous width, villous peri

190 median villous height-to-crypt depth ratios (2.60-2.63; P = .98

191 At t0, the median villous height/crypt depth (Vh/Cd) in the small-intestin

192 s atrophy was defined as a Marsh 3 lesion or villous height:crypt depth ratio below 3.0.

193 rate or severe symptoms and villous atrophy (villous height:crypt depth ratio of </=2.0) were assigne

194 nd placebo groups in change from baseline in villous height:crypt depth ratio, numbers of intraepithe

195 The primary end point was a change in the villous height:crypt depth ratio.

196 After 1 year on the GFD, the mean mucosal villous height:crypt depth values increased (P < .001),

197 We evaluated ratios of small-bowel mucosal villous height:crypt depth, serology and laboratory test

198 ma at least 1 cm in diameter, a polyp with a villous histologic appearance, a polyp with high-grade d

199 noma > or = 1 cm in diameter or a polyp with villous histologic features or high-grade dysplasia), or

200 noma at least 1 cm in diameter, a polyp with villous histologic features or severe dysplasia, or a ca

201 enomas (estimated diameter, >/=1 cm; or with villous histologic findings, high-grade dysplasia, or ca

202 , 1.82; 95% CI, 1.66-2.00) and adenomas with villous histology (HRR, 2.43; 95% CI, 1.96-3.01) also we

203 mas (P < 0.0001 for trend), in adenomas with villous histology (odds ratio [OR], 3.2; 95% confidence

204 a size >/=10 mm (OR = 1.7; 95% CI: 1.2-2.3), villous histology (OR = 2.0; 95% CI: 1.2-3.2), proximal

205 ject age (P = 0.01 for trend), tubulovillous/villous histology (OR, 2.3; 95% CI, 1.5-3.7), and high-g

206 histologic features of adenoma progression (villous histology and high-grade dysplasia) rather than

207 Similarly, two studies identified that villous histology in an index polyp was associated with

208 anced adenomas that measured <1.0 cm but had villous histology or high-grade dysplasia, and 9.9% (357

209 lar adenomas 10 mm or greater, adenomas with villous histology or high-grade dysplasia, or invasive c

210 Adenomas with tubulovillous or villous histology were frequently methylated: 73% (17 of

211 of advanced adenomas (>1 cm or tubulovillous/villous histology) was higher among individuals with ade

212 de dysplasia, and conventional adenomas with villous histology) were seen in 4.3% of patients aged <5

213 s more common in adenomas with tubulovillous/villous histology, a characteristic associated with more

214 enoma greater than > or =10 mm, adenoma with villous histology, adenoma with high-grade dysplasia, or

215 ng adenoma number, size, grade of dysplasia, villous histology, and location with recurrence of advan

216 Large size and number, villous histology, proximal location of adenomas, insuff

217 ned as an adenoma 1 cm or larger or one with villous histology, severe dysplasia, or cancer) was meas

218 , including all those with simple tubular or villous histology.

219 Vascularity and villous hypertrophy are the most reliable features of sy

220 kappa> or =0.8) for features of vascularity, villous hypertrophy, and pannus.

221 N induction in single infected and bystander villous IECs in vivo.

222 The magnitude of villous injury was less in the iNOS-/- mice than the iNO

223 We show that the repeated evolution of villous interdigitation is associated with reduced offsp

224 occurrence of hypoxemia considerably alters villous intestinal perfusion as it decreases the fractio

225 it journeys from the crypt to the tip of the villous is proposed.

226 istic manner, thereby increasing the risk of villous ischemia.

227 nd in 6 of 6 cases of splenic lymphomas with villous lymphocytes (SLVLs) and hairy cell leukemia.

228 oma markers and villous lymphocytes, and the villous lymphocytes were found to be WA B cells.

229 th a WA BCE had splenic lymphoma markers and villous lymphocytes, and the villous lymphocytes were fo

230 , though PP, isolated lymphoid follicle, and villous M cells are all derived from intestinal crypt st

231 to form M cell-DC functional units, whereas villous M cells did not consistently engage underlying D

232 th RANKL also induced the differentiation of villous M cells on all small intestinal villi with the c

233 SF-1R by macrophage lineage cells, including villous macrophages and the syncytiotrophoblast layer of

234 By considering villous membrane to capillary membrane transport, statio

235 identified on syncytiotrophoblast but not in villous mesenchymal cells; amnion epithelial cells were

236 llular injury, its capacity to influence the villous microcirculation after intestinal I/R is unclear

237 The changes in villous microvasculature correlated with histologic inju

238 BD-stereoenterotypes ('cobblestones' versus 'villous mini-aggregation') cluster separately within two

239 , and prolonged fasting when peristalsis and villous motility are decreased and the mucosal barrier f

240 uring normal digestion due to peristalsis or villous motility may be trophic for the intestinal mucos

241 epetitive deformation during peristalsis and villous motility, whereas the mucosa atrophies during se

242 titively deformed by shear, peristalsis, and villous motility.

243 9 g; control 641 + or - 22 g; P = 0.08), but villous, nonparenchymal, trophoblast, and capillary volu

244 in the placenta and placental bed but not by villous or extravillous trophoblasts in normal or pathol

245 ced histology was defined as an adenoma with villous or serrated histology, high-grade dysplasia, or

246 High risk adenomas (villous or tubulovillous or high grade dysplasia or size

247 ere larger than 10 mm or were tubulovillous, villous, or malignant.

248 rs; adenomas >/=10 mm, high-grade dysplasia, villous, or tubulovillous) and 400 age- and sex-matched

249 Constant maternal villous oxygen concentration and perfect fetal capillary

250 A strong link between various measures of villous oxygen transport efficiency and the number of ca

251 Villous height, crypt depth, villous width, villous perimeter per 100 mum muscularis mucosa (a measu

252 18-11130 mum2/100 mum; P = 0.03), and median villous perimeter was 29.7% greater (355.0 v.

253 (VUE), a destructive inflammatory lesion of villous placenta, is characterized by participation of H

254 cells and a decrease in their differentiated villous progeny.

255 g at formative stages in mouse embryos, when villous projections appear and crypt precursors occupy i

256 They possess villous projections on their apical surfaces and contain

257 d stimulation in mice to determine that both villous protrusions and floating cysts contribute to PEC

258 rated less, lost polarity and failed to form villous protrusions and floating cysts.

259 mic cavity caused a severe disruption of the villous protrusions of the PE and Wilms tumor 1 and tran

260 ssociated to hemorrhagic shock, it decreased villous RBCs velocity in an additive manner and the frac

261 uclear, extravillous trophoblasts anchor the villous region to the uterus.

262 ells and fetal cells (trophoblasts): (i) the villous region where maternal blood bathes syncytialized

263 recurrence of high-risk polyps (> or = 1 cm, villous, severe atypia).

264 ated pigs, in contrast to moderate to severe villous shortening and blunting in the duodenum and jeju

265 equency of enucleated RBCs was higher in the villous stroma than in circulation.

266 Cytotrophoblast, villous stroma, and Hofbauer cells showed focal staining

267 blasts, and occasionally within cells of the villous stroma.

268 ew placental development with a focus on how villous structure relates to function.

269 y into the eye's venous system, and that the villous structures are sites of communication between la

270 The walls of the large veins contain villous structures that protrude into their lumina and a

271 Villous surface area, capillary surface area, membrane t

272 , Mamu-AG glycoprotein also was expressed in villous syncytiotrophoblasts, and accumulation of Mamu-A

273 The gastrointestinal villous tip lesions were accompanied by varying degrees

274 Dra expression increased from villous tip to crypt.

275 ha messenger RNA expression localized to the villous tips of the small intestine and the surface epit

276 irred fluid extended from 20 microm over the villous tips throughout the intervillous space.

277 er extent in cytotrophoblasts, isolated from villous tissue of full-term placentae.

278 gic entities representing abnormal placental villous tissue with unique genetic profiles and a wide s

279 Maldevelopment of placental villous trees and their blood vessels results in impaire

280 The chronology of villous trees was much the same in 3-dimensional CPA, sc

281 Feto-placental macrophages regulate villous trophoblast differentiation during placental dev

282 trimester before a protective zone of mature villous trophoblast has been established.

283 005 vs. control group) but no differences in villous trophoblast staining.

284 ellular level and loss of functional mass of villous trophoblast via cell death pathways are key cont

285 describe the differentiation and turnover of villous trophoblast while highlighting selected features

286 and key pathways that regulate apoptosis in villous trophoblast, including increased p53 activity, a

287 late of most components (intervillous space, villous, trophoblast, and capillary volumes, all P < 0.0

288 Here highly purified HLA-G+ EVT and HLA-G- villous trophoblasts (VT) were isolated.

289 ta1, -beta2, and -beta3 are not expressed in villous trophoblasts but are present within the placenta

290 dy considers the apoptotic susceptibility of villous trophoblasts from normal, PE, and IUGR pregnanci

291 escription of enhanced apoptosis in isolated villous trophoblasts in PE and IUGR.

292 ch1 is additionally expressed in clusters of villous trophoblasts underlying the syncytium, suggestin

293 xpression is conserved only in the placental villous trophoblasts, an essential part of the placenta

294 tal JEG3 and BeWo cells and in primary human villous trophoblasts, and this induction was abrogated b

295 Villous tumors may be flat, lobulated lesions, also know

296 the maternal spiral arterioles, dysregulated villous vasculogenesis, and abundant fibrin deposition a

297 in vivo, was increased in these cells and in villous vessels.

298 ffects may account for the reduced placental villous volume, and contribute to the low birth weight t

299 Villous height, crypt depth, villous width, villous perimeter per 100 mum muscularis

300 was no significant effect on crypt depth or villous width.