ライフサイエンスコーパス: villous

1 (Odds ratio (OR) 1.07, 95% CI 0.69-1.66) or villous adenoma (OR 1.26, 95% CI 0.17-9.42).

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

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

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

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

6 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

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

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

9 4-21.45; P < .001), as was the prevalence of villous adenomas (5.5% vs 1.3% in unexposed; mOR = 6.28;

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

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

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

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

14 assages [SAPs]) that are localized to the SI villous and crypt region.

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

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

17 cental sample, showing SUPYN localization in villous and extravillous trophoblast subtypes, the decid

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

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

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

21 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

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

23 uals with CD, defined as duodenal or jejunal villous atrophy (stage 3 Marsh score), were matched with

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

25 predisposing HLA-DQ8 molecule, and develops villous atrophy after ingestion of gluten.

26 celiac disease who are seronegative but have villous atrophy and genetic risk factors for celiac dise

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

28 Patients without severe villous atrophy at baseline received a gluten challenge

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

30 Persistent villous atrophy compared with mucosal healing was associ

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

32 ients with treated but unhealed CeD (n = 81; villous atrophy despite a adhering a gluten-free diet),

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

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

35 k factors associated with the development of villous atrophy in children with potential celiac diseas

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

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

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

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

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

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

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

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

44 The cumulative incidence of progression to villous atrophy was 43% at 12 years.

45 , the cumulative incidence of progression to villous atrophy was 43% over a 12-year period.

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

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

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

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

50 most strongly associated with development of villous atrophy were numbers of gammadelta intraepitheli

51 is still depends on the presence of duodenal villous atrophy while the patient is on a gluten-contain

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

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

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

55 CeD (n = 82) and disease controls (n = 27), villous atrophy without CeD), and healthy controls (n =

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

57 itive results from tests for anti-TG2 but no villous atrophy), 30 patients with untreated celiac dise

58 patients with untreated celiac disease (with villous atrophy), and 5 patients with treated celiac dis

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

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

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

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

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

64 observed in the absence of HAI-2, including villous atrophy, luminal bleeding, loss of mucin-produci

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

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

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

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

69 p period, 42 (15%) of 280 children developed villous atrophy, whereas 89 (32%) children no longer tes

70 a propria is required for the development of villous atrophy, which demonstrates the location-depende

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

72 gluten-free diet to evaluate improvements in villous atrophy.

73 tissue transglutaminase 2 in the absence of villous atrophy.

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

75 istories to identify potential etiologies of villous atrophy.

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

77 a higher risk among patients with persistent villous atrophy.

78 and various techniques may identify areas of villous atrophy.

79 ntify factors associated with progression to villous atrophy.

80 and 11 patients did not because of baseline villous atrophy.

81 sed to identify children at highest risk for villous atrophy.

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

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

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

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

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

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

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

89 rvention may therefore selectively influence villous compartment remodelling.

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

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

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

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

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

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

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

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

98 on in tubulovillous adenomas with increasing villous content.

99 omal fibroblasts and Hofbauer macrophages in villous cores.

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

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

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

103 During human placentation, villous cytotrophoblast (CTB) progenitors differentiate

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

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

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

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

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

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

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

111 The villous cytotrophoblastic cells have the ability to fuse

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

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

114 Villous cytotrophoblasts are epithelial stem cells of th

115 olating first and second trimester placental villous cytotrophoblasts followed by culture in TSC medi

116 14 isolated villous cytotrophoblasts from control (n = 3), IUGR (n =

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

118 Genome-wide comparisons of primary villous cytotrophoblasts overexpressing constitutively a

119 Differentiated primary villous cytotrophoblasts showed that CORIN was expressed

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

121 Villous cytotrophoblasts were isolated from 7 placentas

122 Fusion of placental villous cytotrophoblasts with the overlying syncytiotrop

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

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

125 ompanied by hepatocyte injury and intestinal villous damage.

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

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

131 hibition of bacterial binding to porcine gut villous enterocytes.

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

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

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

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

136 showed crypt hyperplasia and dissociation of villous epithelium from adjacent mesenchyme.

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

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

139 phometry, using the mRNA expression ratio of villous epithelium-specific gene APOA4 to crypt prolifer

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

141 crofluorometry of intracellular pH in intact villous epithelium.

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

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

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

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

146 2 inflammatory signaling in vitro by using a villous explant system.

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

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

149 Human in vitro studies using placental villous explants demonstrated that increased HIF-1alpha

150 n human trophoblast cell lines and anchoring villous explants from first-trimester placentas infected

151 Villous explants from normal placentas delivered by elec

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

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

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

155 ug/ml) exposure of first trimester placental villous explants resulted in secretion of inflammatory c

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

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

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

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

160 Villous explants were exposed to hydrogen peroxide to te

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

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

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

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

165 ZIKV increased the permeability of anchoring villous explants.

166 induce trophoblast outgrowth from placental villous explants.

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

168 duction from endothelial cells and placental villous explants.

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

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

171 eatures (cancer, high-grade dysplasia, >=25% villous features), 3 or more diminutive or small (6-9 mm

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

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

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

175 UDCA inhibited OATP4A1 activity in placental villous fragments and oocytes.

176 ethodological approaches including placental villous fragments and Xenopus laevis oocytes were used t

177 Quantitative proteomic analysis of villous fragments showed direct effects of TC on multipl

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

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

180 n cutoff of >=3 adenomas or any adenoma with villous growth pattern, high-grade dysplasia, or >=10 mm

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

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

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

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

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

186 The study was powered to detect changes in villous height to crypt depth, and stopped at planned in

187 Villous height to crypt depth, video capsule endoscopy e

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

189 at irradiated Cebpd(-/-) mice show decreased villous height, crypt depth, crypt to villi ratio and ex

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

191 ercentage change from baseline to week 12 in villous height-to-crypt depth (VHCD) ratio.

192 elial cells; intestinal histological scores (villous height-to-crypt depth ratio; VHCD); intraepithel

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

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

195 Digital quantitative villous height: crypt depth ratio (VH: CrD) measurements

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

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

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

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

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

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

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

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

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

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

206 , 1.82; 95% CI, 1.66-2.00) and adenomas with villous histology (HRR, 2.43; 95% CI, 1.96-3.01) also we

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

208 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

209 ine 1 to 2 small adenomas (<1cm, and without villous histology or high-grade dysplasia) and no neopla

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

211 a (defined as adenomas >=10mm, adenomas with villous histology or high-grade dysplasia, or colorectal

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

231 By considering villous membrane to capillary membrane transport, statio

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

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

234 The changes in villous microvasculature correlated with histologic inju

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

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

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

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

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

240 9 g; control 641 + or - 22 g; P = 0.08), but villous, nonparenchymal, trophoblast, and capillary volu

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

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

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

244 Constant maternal villous oxygen concentration and perfect fetal capillary

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

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

247 18-11130 mum2/100 mum; P = 0.03), and median villous perimeter was 29.7% greater (355.0 v.

248 ) to D12 peri-implantation period before the villous placenta forms.

249 trophoblast organoids closely resembles the villous placenta with a layer of cytotrophoblast (VCT) t

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

251 with a safe and adequate blood supply and a villous placenta-blood interface from which nutrients an

252 cells and a decrease in their differentiated villous progeny.

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

254 They possess villous projections on their apical surfaces and contain

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

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

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

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

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

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

261 Microarray data of chorionic villous samples (CVSs) obtained from women of ~11.5 gest

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

263 STB, which is distinct from the STB of later villous STB, had a phenotype consistent with intense pro

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

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

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

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

268 Villous surface area, capillary surface area, membrane t

269 Dra expression increased from villous tip to crypt.

270 Placental villous tissue (n = 823) and edge biopsies (n = 488) fro

271 NOx levels in placental villous tissue are increased in fetal growth restriction

272 Furthermore, NOx levels in placental villous tissue are increased in FGR vs. placentas from w

273 nse to low oxygen, first trimester chorionic villous tissue from pregnancies at increased risk of dev

274 tration of CD8(+) T-cells into the placental villous tissue occurred in both fetal growth restriction

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

276 Pathological abnormalities in villous tissue were reported in 21.4% (88/411) of compli

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

278 , we used scRNA-seq to profile the placental villous tree, basal plate, and chorioamniotic membranes

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 eral effects of LPS on both extravillous and villous trophoblast physiology, and the involvement of t

284 proteins, C4BPA, binds to CD40 of placental villous trophoblast to activate p100 processing to p52,

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

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

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

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

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

290 man placentas displayed strong expression in villous trophoblasts and a gradual decrease from proxima

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

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

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

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

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

296 ) cytotrophoblasts and syncytial sprouts vs. villous trophoblasts.

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

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.