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1 lls of the crypts and only marginally in the villi.
2 ly repopulate multiple contiguous crypts and villi.
3 s clusters and results in exceptionally wide villi.
4 t the crypt base, and by apoptotic events in villi.
5 ped its genome occupancy in adult intestinal villi.
6  the proliferative compartment of intestinal villi.
7 ffusional screening may operate in placental villi.
8  after which macrophages had migrated to the villi.
9 ive RBCs occurs in first trimester placental villi.
10 reduction in Ki67 positive cells and blunted villi.
11 on from the capillary network at the tips of villi.
12 tor to the brush border membrane of duodenal villi.
13 ect underlying cytotrophoblasts in chorionic villi.
14 idence for Wnt signaling after appearance of villi.
15  epithelium and lamina propria of the apical villi.
16  to crypts and the lower third of intestinal villi.
17 17H BChE were in the epithelial cells of the villi.
18 , and markedly lower in the upper portion of villi.
19  layer of the crypts, and Akt2 was mostly in villi.
20 roliferating crypts of Lieberkuhn but not in villi.
21 clusters and changes the pattern of emerging villi.
22 to round cystic structures without crypts or villi.
23 ltured lymphocytes, amniocytes, or chorionic villi.
24 last hyperplasia and overgrowth of placental villi.
25 villous trophoblasts (EVTs) at the anchoring villi.
26 kedly involuted however, most notably in the villi.
27 roduces a dramatic, very unusual widening of villi.
28 (CCR5)-positive macrophage-like cells in the villi.
29 al cells in lymph node sinuses and placental villi.
30 y prominent within the lamina propria of the villi.
31 ure of explants of human placental chorionic villi.
32 pts as well as a reduction in the density of villi.
33 ia, embryonic hair follicles, and intestinal villi.
34 les and in enterocytes lining the intestinal villi.
35 L-10 was also substantially increased in the villi.
36 served in the interfollicular region and the villi.
37 zation of CD4+ T cells within the intestinal villi.
38  with the epithelial cells of the intestinal villi.
39 on of mucin filled cysts, and lengthening of villi.
40 d was localized to absorptive enterocytes on villi.
41 l cells, especially in the upper half of the villi.
42 an anatomically correct model of rat jejunal villi.
43 rentiated absorptive epithelial cells in the villi.
44 ive higher tissue oxygenation at the base of villi.
45 oes not determine the pattern of clusters or villi.
46 tiated poorly and exhibited severely stunted villi.
47 rincipal driving force for cell migration on villi.
48 m cells become restricted to the base of the villi.
49 nchronized response of cell migration on the villi.
50 separation, pulmonary alveoli and intestinal villi.
51 apoptosis and, consequently, loss of nascent villi.
52 ypts and subsequent shrinkages of crypts and villi.
53 oth muscle cells encircling arteries in stem villi.
54 then a zigzag pattern, and lastly individual villi.
55 i but did not alter the fraction of perfused villi.
56 l cell shape as well as in the morphology of villi.
57 rding to cell production demands of adjacent villi.
58 erved a more than 8-fold decrease in injured villi (4% vs 34% in saline-pretreated animals).
59 so slightly altered the fraction of perfused villi (94% +/- 2% in hemorrhagic shock group vs 100% +/-
60 nd neutrophil infiltration in the intestinal villi, accompanied by elevated cholesterol but reduced c
61  neutrophil infiltration into the intestinal villi, administration of D-4F mitigated macrophage infil
62                          DraKO and wild-type villi also demonstrated regulation of apical Na(+)/H(+)
63                           We detected longer villi, an expanded zone of PCNA expression, and increase
64 maged cells followed by rapid destruction of villi and accelerated lethality.
65 y overlapping, functions in early intestinal villi and adult crypts.
66 from basal and parietal decidua to chorionic villi and amniochorionic membranes and that targeting TI
67 fibroblasts, and Hofbauer cells in chorionic villi and amniotic epithelial cells and trophoblast prog
68         When the cells reach the apex of the villi and are fully differentiated, they undergo cell de
69 roscopy revealed that albumin accumulated in villi and at the base of the brush border.
70 um, active total Akt was present most in the villi and basal layer of the crypts, and Akt2 was mostly
71       An increase in the number of chorionic villi and blood vessels over that in controls suggested
72 full aPKC down-regulation in small intestine villi and colon surface epithelium using a conditional e
73 11 alone produced serious damage to duodenal villi and colonic crypts.
74 (-/-)Eat2b(-/-) mice, indicated by flattened villi and crypt hyperplasia.
75 ly modulated epithelial morphologies such as villi and crypts is usually associated with the epitheli
76  prediction and 2D-DIGE/mass spectrometry on villi and crypts samples, we found that ablation of PepT
77 as apoptosis was clearly observed in jejunal villi and crypts, (42 times more M30 positivity compared
78 onfined to crypts and apoptosis occurring in villi and crypts.
79  axis and changed the miRNA profiles of both villi and crypts.
80 ts syncytiotrophoblasts that cover chorionic villi and cytotrophoblasts that invade uterine vessels,
81 ochemistry localized CYP2J2 in trophoblastic villi and deciduas at 12 weeks and term.
82 iated syncytiotrophoblast (STB) in chorionic villi and extravillous trophoblast (EVT) at the implanta
83 bited a 2-fold increase in length of jejunal villi and have normal growth on a normal diet but were l
84 D34(+)CD45(low)-that were found in chorionic villi and in the chorioamniotic membrane.
85 seen in the lamina propria of the intestinal villi and in the liver.
86 ytiotrophoblasts on the surfaces of floating villi and invasive CTBs that remodel the uterine vascula
87 thesis, we exposed first-trimester chorionic villi and isolated cytotrophoblasts to CMV in vitro.
88 n of the absorptive surface of the tube into villi and microvilli.
89 6 mice began dying), massive necrosis of the villi and mucosal cells in the ilea were observed in B6
90            Blunting and fusion of intestinal villi and multifocal infiltration of mononuclear cells w
91                          MML from individual villi and numbers of adherent leukocytes within villi we
92 ly seen in folded structures from intestinal villi and pollen grains to wrinkled membranes and progra
93 entalized intestinal epithelium comprised of villi and terminally differentiated cells.
94 th muscle cells in blood vessels of floating villi and the chorion.
95 n mRNA localized predominantly in intestinal villi and the corticomedullary junction of the kidney, w
96 nd to enterocytes in rat pups at the tips of villi and to intestinal epithelial cells (IEC-6) in cult
97 phoblasts and endothelial cells of chorionic villi and uterine arteries.
98 ube to form finger-like luminal projections (villi) and flask-shaped invaginations (crypts).
99 ce of the normal columnar epithelial lining, villi, and Brunner's glands, which are replaced by a GLU
100 MC appeared in the crypts at the base of the villi, and by wk 2 the number of MC throughout the villi
101 pithelial cells at the tip of the intestinal villi, and colocalized with tyrosine nitration, an index
102 ical degradation, complete denudation of the villi, and crypt injury (especially in the ileum) after
103 sive fibrinoid deposits, fibrosis, avascular villi, and edema, which could impair placental functions
104 a and Firmicutes penetrated small intestinal villi, and flagellated bacteria breached the colonic muc
105 creas, surface colonocytes, small intestinal villi, and gastric isthmus cells.
106 ctural degeneration with the loss of crypts, villi, and glandular structure by 7 days.
107 ll hypertrophy of blood vessels, blunting of villi, and lacteal dilatation with lymphocytes and polym
108 rypts, somewhat less in the lower portion of villi, and markedly lower in the upper portion of villi.
109 ng caloric uptake and increasing intestinal, villi, and microvilli lengths.
110 elial barrier, severe blunting of intestinal villi, and recruitment and activation of myeloid cells.
111  of conventional B cells in small intestinal villi, and suggest an immunologic link between CD1-restr
112 nt at the tips of the villi, the base of the villi, and the submucosa, respectively.
113 e synovial lining and the stroma of synovial villi, and to a lesser extent in CD68-positive cells of
114 vasculatures in endocrine glands, intestinal villi, and uterus are the most affected in response to V
115 flammatory infiltrate in placental chorionic villi are associated with adverse pregnancy results.
116 ithelial cell migration velocities along the villi are coupled to cell proliferation rates within the
117 al intestinal epithelium is stratified, that villi are formed by an epithelial remodeling process inv
118  the numbers of enteroendocrine cells in the villi are greatly reduced.
119  essentially the same way as in mammals: the villi are lined with non-dividing differentiated cells,
120 d laboratory strain AD169 in human placental villi as explants in vitro and xenografts transplanted i
121 nine deficiency blunts mastocytosis in ileal villi as well as bacterial translocation, measured as nu
122 d syncytiotrophoblast derived from placental villi at term and colonies of trophoblast differentiated
123 As and their target proteins along the crypt-villi axis in the jejunum of PepT1 KO mice.
124 rophoblast stem cells in anchoring chorionic villi become invasive.
125 tive erythroid cells were found in placental villi between 5-7 weeks of development, at which time th
126 tion with dramatic atrophy of the intestinal villi, bone marrow, and spleen, and with hematopoietic f
127 ic shock not only decreased RBCs velocity in villi but also slightly altered the fraction of perfused
128 oxemia decreased RBCs velocity in intestinal villi but did not alter the fraction of perfused villi.
129 that the enzyme is expressed not only in the villi, but also in the crypt regions of the small intest
130 li K1 bacteria are physically separated from villi by the mucus layer and their numbers controlled by
131                       Capillaries in jejunal villi can absorb nutrients at rates several hundred time
132 ation of stem and progenitor cells along the villi, caused a mild defect in the apical junction orien
133 t global X reactivation is also inducible in villi cells from first-trimester spontaneous abortions b
134  mesenchymal cores of their small intestinal villi, compared with conventionally raised animals that
135 at remodeling of resistance arteries in stem villi contributes to IUGR by compromising umbilical bloo
136 with the earliest steps in the growth of new villi, contributing to virus transmission and impairing
137            Cytotrophoblasts of the anchoring villi convert during human placentation from a transport
138           The morphometric parameters of the villi, crypts, muscular layer and total wall generally i
139                          Microfluorimetry of villi demonstrated that Dra is the dominant Cl(-)/HCO(3)
140 tion in a 2D+1D geometry for a wide range of villi densities.
141                        The predicted optimal villi density 0.47+/-0.06 is compatible to previous expe
142                                The effect of villi density on oxygen transfer efficiency is assessed
143 ters, we observe the existence of an optimal villi density providing a maximal oxygen uptake as a tra
144 additive manner and the fraction of perfused villi dropped in a synergistic manner (69% +/- 3% in hyp
145 th shortening and widening of the intestinal villi due to diffuse edema and infiltration by a mixed i
146 nected vessels developed in small intestinal villi during the period of postnatal development that co
147  hair follicles, limb digits, and intestinal villi, during development.
148 e placenta leads to development of avascular villi, edema, and hypoxia associated with symptomatic co
149              Large fibrinoids with avascular villi, edema, and inflammation were significantly increa
150 explant culture of first-trimester chorionic villi enhanced extravillous trophoblast differentiation
151 we confirmed by analyzing purified placental villi, enriched in endothelium, by immunoblotting with a
152       1-2% of 129/Sv (DeltaN89 beta-catenin) villi exhibited an abnormal branched architecture.
153                       During late gestation, villi extend into the intestinal lumen to dramatically i
154 ians, this instability is a precursor of the villi, finger-like projections into the lumen.
155                                              Villi first emerge at embryonic day (E) 14.5 from a prev
156 tion of the crypts and extreme shortening of villi following 1500 cGy total body irradiation.
157 -lymphocyte population within the intestinal villi following Cryptosporidium parvum infection was cha
158                              However, as the villi form, the putative stem cells become restricted to
159 ough enteral losses improve along with graft villi formation, electrolyte abnormalities continue, to
160  cytotrophoblasts in explants, and anchoring villi formed normally in vitro.
161          Isolated small bowel and intestinal villi from alpha-gustducin null mice showed markedly def
162      Isolated small intestine and intestinal villi from gustducin null mice displayed markedly defect
163 gmented digital photomicrographs of terminal villi from the Pregnancy, Infection and Nutrition study
164  activity, are markedly reduced on placental villi from women with this syndrome.
165 resent in the villi, indicating that MUCTag6 villi goblet cells do not progress into M phase.
166 Ag mice expressing large T-antigen solely in villi had ectopic enterocyte proliferation with increase
167 tric foveolar cells, whereas small intestine villi had only a few (<1%) positive cells.
168                     Moreover, the intestinal villi have a steep oxygen gradient from the hypoxic epit
169 ose endings to the apical tips of intestinal villi, immediately subjacent to the epithelial wall.
170 ation process of primitive RBCs in placental villi, implying an unexpectedly broad role for the place
171 al calcification of the maternal surface and villi in a cohort of smokers and nonsmokers at risk for
172 senchymal clusters determines the pattern of villi in a manner that mimics the spread of a self-organ
173 ion as it decreases the fraction of perfused villi in a synergistic manner, thereby increasing the ri
174 ound in the crypts in neonatal and along the villi in adult tissues.
175 ound in epithelial cells of small intestinal villi in all puppies and the colon in 2 of the 10 puppie
176 velopment, but does not prevent emergence of villi in areas where clusters have already formed.
177 nta, FOS was expressed in proximal anchoring villi in conjunction with phospho-ERK.
178 intestine but are present in both crypts and villi in MUCTag6.
179 py confirmed mild shortening and blunting of villi in the duodenum and jejunum of the TC-PEC-inoculat
180                   Injury and swelling of the villi in the duodenum was present in untreated mice afte
181         This is analogous to the function of villi in the intestine or sulci in the brain, where an e
182 d to the mesenchymal cells at the tip of the villi in the small intestine and directly underlying the
183 anylin mRNA was localized in both crypts and villi in the small intestine and to superficial epitheli
184 ces, including reaching the surfaces between villi in the small intestine.
185 s of N2 or glucose were directed at duodenal villi in vitro, labeling by FM1-43 or FM2-10 was observe
186 phoblasts and reduced formation of anchoring villi in vitro.
187 arious exogenous molecules in the intestinal villi in vivo.
188 s most prevalent near the tips of intestinal villi, in the lamina propria, just basal to epithelial c
189 phoblasts and cytotrophoblasts, in chorionic villi-in clinical cases of congenital infection.
190  and by wk 2 the number of MC throughout the villi increased by approximately 25-fold.
191 number of CD8+ T cells within the intestinal villi increased following a challenge infection.
192 yncytial trophoblast of term human placental villi incubated in vitro with D-[1-3H]galactose ([3H]gal
193 cellular trophoblast of term human placental villi incubated in vitro with tritiated leucine ([3H]leu
194 ling present in the syncytial trophoblast of villi incubated the longest times (4 h+) remained in ass
195 trast, mitotic cells were not present in the villi, indicating that MUCTag6 villi goblet cells do not
196  by histologic analysis of terminal ileum (% villi injured).
197 replaced sodium chloride in contact with the villi, intestinal blood flow decreased to 58.6 +/- 2.8%
198      Bacteria were shed back from intestinal villi into the small intestinal lumen and reinfected the
199 r, foci unexpectedly varied in the number of villi involved and were associated with the presence of
200 re L. monocytogenes replicates in intestinal villi, is shed into the lumen, and reinfects intestinal
201 ls of neutrophil influx and extravasation in villi lamina propriae, including elastase-positive cells
202 poietic organs, extensive loss of intestinal villi, obstructive enterocolitis, and lethality within 1
203                                    Arachnoid villi occlude and degenerate.
204                                              Villi of mutant mice became stunted, and enterocytes lac
205         Antigens were also seen in chorionic villi of one of the first trimester placentas.
206 A is expressed at high levels only along the villi of the duodenal epithelium, principally if not exc
207 ) is expressed at high levels only along the villi of the duodenal epithelium.
208 asolateral surface of enterocytes lining the villi of the duodenum and jejunum.
209                                          The villi of the human and chick gut are formed in similar s
210 ished a vital defensive perimeter within the villi of the ileum in the small intestine.
211  T cells (70%) present within the intestinal villi of the infected ileum.
212 al cells on the upper half of the intestinal villi of the jejunum and ileum.
213  squamous epithelium of the stomach, and the villi of the jejunum.
214 ands, uterine decidua, and injured chorionic villi of the placenta, demonstrating both its induction
215 in the syncytiotrophoblasts of the chorionic villi of the rhesus placenta, within villous cytotrophob
216     Basal expression was found in crypts and villi of the small and large intestine, bronchiolar epit
217 d of surface IgM(+) IgD(+) cells residing in villi of the small intestine and superficial lamina prop
218                                          The villi of the small intestine maintain a hypertonic inter
219 and enteroendocrine cells in both crypts and villi of the small intestine, with no changes observed i
220 o syncytiotrophoblasts in floating chorionic villi or extravillous trophoblasts (EVTs) at the anchori
221 were increased more than fourfold in MUCTag6 villi (P < 0.0001), and apoptotic goblet cells were evid
222 cm(3); P = 0.02) with anisomorphic growth of villi (P = 0.025).
223 ytokine IL-8 (p = 0.0271), longer intestinal villi (p<0.0001), deeper crypts (p = 0.0053), and a thin
224 d toxin A-mediated destruction of intestinal villi, p21(WAF1/CIP1) expression, and enterocyte apoptos
225 es of the kidney and those of the intestinal villi, pancreas, and adrenals.
226 ee within the epithelial cells higher up the villi, paralleling the gradient in expression of the pol
227                In the intestine, finger-like villi provide abundant surface area for nutrient absorpt
228 zed array of finger-like projections, called villi, provide an enormous epithelial surface area for a
229 nated in the liver, whereas small intestinal villi provided a niche for bacterial replication, indica
230 phoblastic lacunae or newly formed chorionic villi remained largely Mamu-AG-negative.
231 fusion can be numerically solved in terminal villi represented by digital photomicrographs.
232 0 (SV40) TAg in choroid plexus or intestinal villi requires at least one activator E2F.
233 eculiar intestinal morphology with very long villi resulting from increased enterocyte lifespan and a
234 icroscopic examination of MUCTag6 intestinal villi revealed the presence of degraded cell remnants co
235 dysregulation, and atrophy of the intestinal villi, skin, thymus, and spleen.
236  limited to the epithelium of the developing villi strictly within the duodenal region of the small i
237 enous molecular markers that illustrated the villi structures and confirmed the different absorption
238                                 In chorionic villi, syncytiotrophoblasts did not become infected, alt
239                                 In placental villi, syncytiotrophoblasts express the virion receptor
240 e rise to the mature cell types of chorionic villi-syncytiotrophoblasts on the surfaces of floating v
241                      Covering the surface of villi that float in blood, syncytiotrophoblasts express
242 med self-regenerating cell clusters, forming villi that resemble intestinal epithelium.
243                                 In chorionic villi that were infected with CMV in utero, syncytiotrop
244 ng mMCP-2 as they present at the tips of the villi, the base of the villi, and the submucosa, respect
245 hen the epithelium is folded into crypts and villi, the epithelium is a single-cell layer once again.
246 ished physically in the human, the placental villi, the exocoelomic cavity, and the secondary yolk sa
247 ifferentiation during a 48-72-h migration up villi, there is a marked and rapid fall in the levels of
248 ll intestinal crypts to the base of adjacent villi, they rapidly lose their ability to undergo apopto
249 phoblasts in vivo by transplanting placental villi to the fifth mammary fat pads or beneath the kidne
250      Tubule cell injury, as shown by loss of villi, tubule dilation, and cellular protrusions into th
251 psule endoscopy showed delayed appearance of villi until the proximal to mid jejunum and jejunal muco
252 nding smooth muscle fold the epithelium into villi via mucosal buckling.
253 DNA methylation in first-trimester chorionic villi was assessed in chromosomally normal miscarriages
254                          The failure to form villi was not attributable to the absence of HH or PDGF
255 at [3H]gal incorporation into term placental villi was predominantly localized to cytotrophoblast.
256           Absorption of metals in intestinal villi was simulated by means of ultrafiltration over sem
257 n the jejunum, but the percentage of damaged villi was still reduced considerably (18% vs 42%).
258 rs of adherent leukocytes within, individual villi were determined every 15 min for 2 hr after remova
259 li and numbers of adherent leukocytes within villi were determined for 2 to 4 hours after clamp remov
260 ayed spontaneous duodenal lesions, and ileal villi were truncated and fragile with reduced cellular p
261  in the submucosa and muscle layers, but the villi were unaffected.
262 d apoptosis, specifically at the tips of the villi, where there is highest sheer.
263 out 4 days to migrate out to the tips of the villi, where they die.
264 l epithelial cells throughout the crypts and villi, where we also observed infiltration of activated
265  ACAT-2 is concentrated at the apices of the villi, whereas ACAT-1 is uniformly distributed along the
266 d in the nuclei of superficial layers of the villi, whereas Ki67-positive cells were confined to the
267 , PPARgamma expression occurs throughout the villi, whereas the expression of both SRC-1 and PBP is c
268 mester through term) that contained floating villi (which include cytotrophoblasts differentiating in
269 ing into syncytiotrophoblasts) and anchoring villi (which include cytotrophoblasts differentiating in
270 ne, endothelial, and immune cells; placental villi, which are bathed in maternal blood, and fetal mem
271 xposure caused remodelling of the intestinal villi, which increased the surface area available for ir
272  in the IFR and lamina propria of intestinal villi, while F4/80+ cells were found only in the latter.
273  overexpressed revealed multiple well-formed villi with crypt-like units, whereas those in which epim
274 n of villous M cells on all small intestinal villi with the capacity for avid uptake of Salmonella an
275  and explants from first-trimester chorionic villi with the prototype Ugandan and a recently isolated
276 xpression at the level of the invasive fetal villi within the placental junctional zone, where tropho

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