ライフサイエンスコーパス: crypt

1 wn-6 (18-c-6) and with Cs in the presence of crypt.

2 epithelial stem/progenitor cells within the crypt.

3 e proliferative process in the upper colonic crypt.

4 small pool of stem cells at the base of each crypt.

5 generating 2 daughter crypts from 1 parental crypt.

6 cells (IESCs) positioned at the base of each crypt.

7 h genes in the villus but Bcl-2 alone in the crypt.

8 sion, in which 2 crypts fuse into 1 daughter crypt.

9 mucosa without effects on normal intestinal crypts.

10 cells and lowest in the apoptosis-sensitive crypts.

11 nd blocked G1/S transition in the intestinal crypts.

12 R3C1 bind to the CLDN1 promoter in rat colon crypts.

13 adenoma formation, also found in irradiated crypts.

14 ormal mucin glycocalyx from WT cells over KO crypts.

15 epithelial cell proliferation and lengthens crypts.

16 es; most reside at the +4 position in normal crypts.

17 rains was the ability to colonize intestinal crypts.

18 ons, compared with the adjacent normal colon crypts.

19 division of a single crypt into two daughter crypts.

20 proaches to the in vitro culture of ISCs and crypts.

21 changed the miRNA profiles of both villi and crypts.

22 blet cells, resulting in enlarged intestinal crypts.

23 s express LGR5 at the base of normal colonic crypts.

24 elopment and the establishment of intestinal crypts.

25 o epithelial cells distributed along colonic crypts.

26 high degree of plasticity within intestinal crypts.

27 s units with stem cells at the bottom of the crypts.

28 crypts and apoptosis occurring in villi and crypts.

29 (crypt)}2{[(R2N)3Sc]2[mu-eta(1):eta(1)-N2]} (crypt = 2.2.2-cryptand, R = SiMe3), has been isolated fr

30 h metal with an end-on dinitrogen bridge, {K(crypt)}2{[(R2N)3Sc]2[mu-eta(1):eta(1)-N2]} (crypt = 2.2.

31 f up to 20 K, as observed for the complex [K(crypt-222)][(Cp(Me4H)2Tb)2(mu-[Formula: see text])].

32 M](+) = [(18-C-6)K(thf)(2)](+) (1, 76%) or [(crypt-222)K](+) (2, 54%)).

33 tal X-ray diffraction in the compound (K[222-crypt])4 [Sn14 Ni(CO)]DMF.

34 geometry of cells (such as that of a colonic crypt), a 2D lattice and a mass-action (complete graph)

35 e results showed that the number of aberrant crypts, aberrant crypt foci (ACF) and crypts/focus in ra

36 pertrophic phenotype with features including crypts, abnormal mitral leaflets and trabeculae.

37 ication of the model to data from irradiated crypts after an extended recovery period permitted deduc

38 ed mice, with the number of Paneth cells per crypt also significantly reduced.

39 The intestinal crypt and its stem cells are dependent on the Wnt pathwa

40 ferentiated compartment of the mouse colonic crypt and P2-HNF4alpha in the proliferative compartment.

41 interprets the Wnt levels in the intestinal crypt and translates the continuous Wnt signal into a di

42 decreased crypt proliferation and increased crypt and villus apoptosis.

43 testinal epithelium is a repetitive sheet of crypt and villus units with stem cells at the bottom of

44 tudied expansion of organoids generated from crypts and adenomas, stimulated by HGF or EGF, that were

45 t epithelium, with proliferation confined to crypts and apoptosis occurring in villi and crypts.

46 s results in loss of stem cells from colonic crypts and disrupts gut homeostasis and colon organoid g

47 ressed mainly in the epithelial cells of the crypts and only marginally in the villi.

48 great house of Pueblo Bonito, unusual burial crypts and significant quantities of exotic and symbolic

49 dent mechanisms that radioprotect intestinal crypts and that ATM inhibition promotes GI syndrome afte

50 -1-infected cells localized predominantly to crypts and the lower third of intestinal villi.

51 se in tuft and enteroendocrine cells in both crypts and villi of the small intestine, with no changes

52 )3 with K in the presence of 2.2.2-cryptand (crypt) and 18-crown-6 (18-c-6) and with Cs in the presen

53 lial tissues, most notably in the intestinal crypts, and is highly up-regulated in many colorectal, h

54 e crypt base and the pattern reversed at the crypt apex.

55 prior to radiation blocked proliferation and crypt apoptosis and improved crypt regeneration.

56 e of these changes was revealed by rescue of crypt apoptosis and Wnt pathway gene expression upon tre

57 Septic bi-transgenic animals had decreased crypt apoptosis but had a paradoxical increase in villus

58 In contrast, villus and crypt apoptosis were increased in septic fabpi-TAg mice.

59 Our findings indicate that mammalian crypt architecture protects stem/progenitor cell prolife

60 mucosal damage was characterized by loss of crypt architecture, increased epithelial cell apoptosis,

61 Crypts are a normal part of cardiac development but, alo

62 nal stem cells (ISCs) located at the base of crypts are the primary driver of regeneration.

63 f expansion and the spatial structure of the crypt arises as a balance between this expansion and the

64 gulates both the number of stem cells in the crypts as well as the sloughing of cells from the villus

65 h) had higher baseline numbers of epithelial crypt-associated integrin alphaE(+) cells (P < .01 for b

66 (P < .01 for both), but a smaller number of crypt-associated integrin alphaE(+) cells after etrolizu

67 t not mutant CR, elevated EZH2 levels in the crypt at days 6 and 12 (peak hyperplasia) coincided with

68 how that nine individuals buried in an elite crypt at Pueblo Bonito, the largest structure in the can

69 ATM inhibition also increased cell death in crypts at 4 h in Cdkn1a(p21(CIP/WAF1))-/-, earlier than

70 ar how the continuous Wnt gradient along the crypt axis is translated into discrete expression of Asc

71 function via different mechanisms along the crypt axis.

72 to replicate cell differentiation along the crypt axis.

73 d glucocorticoid receptor (NR3C1) low at the crypt base and the pattern reversed at the crypt apex.

74 inal epithelium results in apoptotic loss of crypt base columnar stem cells and bias towards differen

75 nes in intestinal crypt epithelia, including crypt base columnar stem cells and Paneth cells, and in

76 the small intestine, where it is enriched in crypt base columnar stem cells, one of the most active s

77 g-lived, radiation-resistant cells above the crypt base that generate Lgr5(+) CBCs in the colon and i

78 We observed that Gpr182 is expressed at the crypt base throughout the small intestine, where it is e

79 xpressing cells at the +4 position above the crypt base.

80 The first contains rapid cycling crypt-based columnar (CBC) Lgr5(+) cells, and the second

81 the expanded proliferative zone observed in crypts before adenoma formation, also found in irradiate

82 As that were differentially expressed in the crypt bottom, creating an SC signature for normal coloni

83 or 5-positive (Lgr5(+)) stem cells reside at crypt bottoms of the small and large intestine.

84 are intermingled with Lgr5(+) stem cells at crypt bottoms.

85 and discrete specification of stem cells at crypt bottoms.

86 ed in vitro crypt organoid proliferation and crypt budding was abrogated by the Wnt inhibitor IWP2.

87 e abundance of Lgr5-expressing stem cells in crypts, but rather exerted its effects on intermediate p

88 e virions were present in 10% of intestinal crypts by 10-12 days.

89 from eyes of each participant and graded for crypts (by number and size) and furrows (by number and c

90 ay regulate B0AT1 in villus and SN2/SNAT5 in crypt cell is unknown.

91 Homeostatic adult small intestinal crypt cell proliferation, survival, and canonical wingle

92 ediated by B0AT1), while it is stimulated in crypt cells (mediated by SN2/SNAT5).

93 hile ATR inhibition may potentiate arrest in crypt cells after TBI.

94 esicles (BBMV) were prepared from villus and crypt cells and uptake studies were performed using rapi

95 lycytidylic acid challenge and expression by crypt cells clearly distinguish Clr-a from the likewise

96 nt signaling status, and in mouse intestinal crypt cells in vivo.

97 of Clr-a by intestinal epithelial cells and crypt cells throughout the gut.

98 Apoptotic positive crypt cells were 15-fold higher in WT-TPN versus TLR4KO-

99 r capture microdissection to isolate colonic crypt cells, differentiated surface epithelium, adenomas

100 In contrast, in crypt cells, Na-glutamine co-transport stimulation was r

101 s of aberrant differentiation of uncommitted crypt cells-these differentiated toward the secretory ce

102 ng bone marrow and differentiated intestinal crypt cells.

103 ansporters, B0AT1 in villus cells and SN2 in crypts cells that are uniquely altered in the chronicall

104 the intestine can rapidly occur from Lgr5(+) crypt columnar stem cells.

105 e number of Lgr5EGFP-positive stem cells per crypt compared with IgG-treated mice, with the number of

106 We identified multifocal aberrant crypt-containing endocrine cell clusters (ACECs) that co

107 mAb injection, but it significantly reduced crypt damage and inflammatory cytokine secretion in NOD2

108 T cell activation did not worsen crypt damage in mice carrying either cell-specific delet

109 In the Tet1-deficient crypt, decreased expression of Wnt target genes such as

110 Intestines of EED knockout mice had massive crypt degeneration and lower numbers of proliferating ce

111 WD also increased crypt depth and colon cell proliferation.

112 efined as a Marsh 3 lesion or villous height:crypt depth ratio below 3.0.

113 Median villous height to crypt depth ratio in distal duodenal biopsies was not si

114 symptoms and villous atrophy (villous height:crypt depth ratio of </=2.0) were assigned randomly to g

115 ps in change from baseline in villous height:crypt depth ratio, numbers of intraepithelial lymphocyte

116 end point was a change in the villous height:crypt depth ratio.

117 median villous height-to-crypt depth ratios (2.60-2.63; P = .98) did not decrease

118 eases in ileum and jejunum villus height and crypt depth were observed in comparison to sow-fed anima

119 No changes in villus height/crypt depth were observed.

120 th; ileum p < 0.001 villus height, p < 0.002 crypt depth).

121 sed on BrdU incorporation, villus height and crypt depth, and cell number.

122 s (jejunum, p < 0.01 villus height, p < 0.04 crypt depth; ileum p < 0.001 villus height, p < 0.002 cr

123 Human intestinal crypt-derived enteroids are a model of intestinal ion tr

124 Injection of mice with TNF or incubation of crypt-derived enteroids with TNF reduced their expressio

125 her confirm the crucial role of Dnmt1 during crypt development using the in vitro organoid culture sy

126 Intestinal crypts display robust regeneration upon injury.

127 icantly greater inflammation in the stomach, crypt distortion in the colon, and eosinophilia in the r

128 Gastritis and colonic crypt distortion were present in the IBD group at a grea

129 tants appeared unable to colonize intestinal crypts due to an inability to pass through the intestina

130 e intestinal submucosa and expand around the crypts during the third week of life in mice, independen

131 -Ires-CreERT2) mice, we monitored individual crypt dynamics over multiple days with single-cell resol

132 ed for a periodic acidification of the adult crypts each night.

133 endocrine cell clusters (ACECs) that contain crypt EC cell microtumors in patients with familial SI-N

134 Homozygous loss of Apc alone resulted in crypt elongation, activation of the Wnt signature and ac

135 HNF-6 expression was observed only in crypt epithelia expressing insulin and not in epithelia

136 egulation of Wnt pathway genes in intestinal crypt epithelia, including crypt base columnar stem cell

137 tial gradients of these factors insures that crypt epithelial cell proliferation and development proc

138 n specimens exhibited survivin in most basal crypt epithelial cells of normal mucosa.

139 taltic reflex activity, and proliferation of crypt epithelial cells.

140 Tegaserod increased proliferation of crypt epithelial cells.

141 on (LCM)-harvested ileal and colonic tip and crypt epithelial fractions from germ-free and convention

142 Crypt epithelial survival and regeneration after injury

143 cells both in vitro and in vivo and that the crypt epithelium also expressed IL-6.

144 Using normal colonic crypt epithelium as a comparator, we identify enhancers

145 YAMC and intestinal crypts expressed lower levels of XIAP, cIAP1, cIAP2, and

146 ifying the mechanisms that regulate rates of crypt fission and fusion could provide insights into int

147 As counteracting processes, crypt fission and fusion could regulate crypt numbers du

148 In the adult intestine, crypt fission is observed at a low frequency.

149 usion, an almost exact reverse phenomenon of crypt fission, in which 2 crypts fuse into 1 daughter cr

150 In addition, TgfbetaR2 loss in vivo reduced crypt fission, irradiation-induced crypt regeneration, a

151 Crypt number increases by a process called crypt fission, the division of a single crypt into two d

152 that the number of aberrant crypts, aberrant crypt foci (ACF) and crypts/focus in rats of the KJT + A

153 examined the colonic microbiota and aberrant crypt foci (ACF) in C57BL/6N female mice fed various die

154 ed DNA methylation changes in human aberrant crypt foci (ACF), the earliest putative precursor to CRC

155 xpression levels, and the number of aberrant crypt foci in the colon endothelium.

156 e changes preceded the formation of aberrant crypt foci or adenoma.

157 e number of mutagen-induced aberrant colonic crypt foci.

158 errant crypts, aberrant crypt foci (ACF) and crypts/focus in rats of the KJT + AOM group were signifi

159 Destruction of clonogenic cells in the crypt following irradiation are thought to cause altered

160 tes directed epithelial evaginations to form crypts for implantation in mice.

161 d role for PCP in executing spatial cues for crypt formation and implantation.

162 at Hmga1 drives hyperproliferation, aberrant crypt formation and polyposis in transgenic mice.

163 sdirected epithelial evaginations, defective crypt formation, and blastocyst attachment, leading to s

164 Intestinal crypt fractions were prepared for ex vivo bactericidal a

165 multiply via fission, generating 2 daughter crypts from 1 parental crypt.

166 shifted cells within hyperplastic intestinal crypts from a stem cell to a transit amplifying phenotyp

167 We isolated intestinal crypts from C57BL/6 mice, cultured enteroids, incubated

168 -) mice did not expand to the same extent as crypts from Cd44(+/+) mice on stimulation with HGF, but

169 Intestinal crypts from Cd44(-/-) mice did not expand to the same ex

170 Intestinal crypts from EED knockout mice had signs of aberrant diff

171 Furthermore, crypts from EED-knockout mice had impaired Wnt signaling

172 erse phenomenon of crypt fission, in which 2 crypts fuse into 1 daughter crypt.

173 We discovered the existence of crypt fusion, an almost exact reverse phenomenon of cryp

174 s 4.1 +/- 0.9% of all crypts were undergoing crypt fusion.

175 ta [change in iris volume in millimeters per crypt grade increment] = -1.43, 95% confidence interval

176 ta [change in iris volume in millimeters per crypt grade increment] = 0.23, 95% CI, 0.06-0.40; P = 0.

177 In light condition, higher iris crypt grade was associated independently with smaller ir

178 tinal abnormalities in neonates and disrupts crypt homeostasis in adults, whereas Dnmt3a loss was com

179 -6 signaling in the gut epithelium regulates crypt homeostasis through the Paneth cells and the Wnt s

180 mbined, these provide an alternative view of crypt homeostasis where the niche is in a constant state

181 ized that IL-6 signaling could also modulate crypt homeostasis.

182 benzazepine to diminish Notch-driven colonic crypt hyperplasia curtailed the fitness advantage confer

183 II secretion system (T3SS) to induce colonic crypt hyperplasia in mice, thereby gaining an edge durin

184 artially regulate Wnt/beta-catenin-dependent crypt hyperplasia in response to CR infection.

185 . rodentium infection, manifested by reduced crypt hyperplasia, reduced epithelial expression of IL-6

186 Here, we show that by triggering colonic crypt hyperplasia, the C. rodentium T3SS induced an exce

187 (-/-) mice, indicated by flattened villi and crypt hyperplasia.

188 llele and mosaic deletion of Cosmc in 50% of crypts (IEC-Cosmc(+/-)) were protected from spontaneous

189 Examining 819 crypts in 4 mice, we found that 3.5% +/- 0.6% of all cry

190 irradiation reduced numbers of proliferating crypts in Ah(Cre)/Met(fl/fl)/LacZ mice.

191 upled to cell proliferation rates within the crypts in all conditions.

192 rast, ATR inhibition decreased cell death in crypts in Cdkn1a(p21(CIP/WAF1))-/- mice at 4 h after TBI

193 onocytes within the epithelium of dysplastic crypts in mouse colon.

194 The morphological orientation of crypts in rodent uteri was recognized more than a centur

195 malized cell-cell adhesion, and formation of crypts in tissue cultures.

196 by increasing the number of S phase cells in crypts in wild-type but not Cdkn1a(p21(CIP/WAF1))-/- mic

197 Crypts incubated with EGF or HGF expanded into self-orga

198 ession patterns at the implantation chamber (crypt) inMsx1(f/f)/Msx2(f/f)females; the patterns were l

199 lled crypt fission, the division of a single crypt into two daughter crypts.

200 r segment abnormalities included absent iris crypts, iris transillumination, lens subluxation, and ca

201 conclude that cell proliferation within the crypt is the primary force that drives cell migration al

202 l regeneration, LIG4 mainly expressed in the crypts is conditionally upregulated in ISCs, accompanied

203 Cell proliferation within small intestinal crypts is the principal driving force for cell migration

204 ed epithelial morphologies such as villi and crypts is usually associated with the epithelium-stroma

205 Dark maroon [K(crypt)](+) , [K(18-c-6)](+) , and [Cs(crypt)](+) salts o

206 was a clear association of S. flexneri with crypts, key morphological features of the colonic mucosa

207 mucosal injury or application to a naturally crypt-less host organism led to inhibition of proliferat

208 neration of which is fueled by proliferative crypt Lgr5(+) intestinal stem cells (ISCs).

209 cancer cells Caco-2/TC7 and SW480 and normal crypt-like HIEC-6 cells, PrP(c) interacts, in cytoplasm

210 Undifferentiated or crypt-like, and differentiated or villus-like, human ent

211 th ATM inhibition prior to TBI was increased crypt loss within the intestine epithelium.

212 ial cells differentiate along the intestinal crypt-luminal axis.

213 upon withdrawal of WNT3A, yielding decreased crypt markers and increased villus-like characteristics.

214 Crypt markers, surface cell enzymes, and membrane ion tr

215 a model of the healthy and cancerous colonic crypt microenvironment.

216 l model of the healthy and cancerous colonic crypt microenvironments.

217 ial cells are derived from stem cells in the crypts, migrate up the villus as they differentiate and

218 the colon demonstrated a rapid disruption of crypt morphology, aberrant proliferation, cell-death act

219 During postnatal development, crypts multiply via fission, generating 2 daughter crypt

220 zed the expression of Dnmt3a in murine colon crypts, murine colon adenomas and human colorectal cance

221 The morphometric parameters of the villi, crypts, muscular layer and total wall generally increase

222 erve as Paneth cell equivalents in the colon crypt niche.

223 Crypt number increases by a process called crypt fission

224 ses, crypt fission and fusion could regulate crypt numbers during the lifetime of a mouse.

225 ority of gut colonization determines colonic crypt occupancy.

226 V. fischeri colonizes the crypts of a host organ that is used for behavioral light

227 In the mammalian intestine, crypts of Leiberkuhn house intestinal epithelial stem/pr

228 The crypts of the intestinal epithelium house the stem cells

229 rse and colonize the mucus-filled intestinal crypts of their host, a necessary step required to trigg

230 We found that small intestinal crypts of Villin(Cre);Dclk1(f/f) mice were hypoplastic a

231 Although few Chinese persons have multiple crypts on their irides, irides with more crypts were sig

232 c3-targeted knock-out (KO) mice we show that crypts (one or two) are a normal part of wildtype develo

233 cultures developed from isolated intestinal crypts or stem cells (termed enteroids/colonoids) and fr

234 Using mouse in vitro crypt organoid and in vivo models, this study first demo

235 to IL-6 significantly reduced in vitro basal crypt organoid proliferation and budding, and in vivo si

236 dies demonstrated that IL-6-induced in vitro crypt organoid proliferation and crypt budding was abrog

237 st demonstrated that exogenous IL-6 promoted crypt organoid proliferation and increased stem cell num

238 mouse appearance), and augmented intestinal crypt Paneth cell bactericidal potency via a mechanism t

239 y contrast, HO and HET embryos had increased crypt presence, abnormal mitral valve formation and alte

240 wing to direct differentiation of epithelial crypt progenitor cells.

241 vival curve showed a significant increase in crypt progenitors in irradiated mice treated with AA-ORS

242 s to secrete IL-13, which acts on epithelial crypt progenitors to promote differentiation of tuft and

243 ia cecal ligation and puncture had decreased crypt proliferation and increased crypt and villus apopt

244 4 deletion significantly enhanced intestinal-crypt proliferation and inflammation induced by azoxymet

245 ared with unmanipulated littermates, whereas crypt proliferation was decreased.

246 reted by stromal myofibroblasts of the lower crypt, promotes proliferation through canonical beta-cat

247 al growth in nonirradiated mice and enhanced crypt regeneration after radiation.

248 ys was observed 3.5 days post-TBI, when peak crypt regeneration occurs.

249 +) ISC/progenitor population maintenance and crypt regeneration postinjury require mTOR.

250 o reduced crypt fission, irradiation-induced crypt regeneration, and differentiation toward Paneth ce

251 ally converts to that of Lgr5(+) ISCs during crypt regeneration.

252 intestinal epithelium and induce subsequent crypt regeneration.

253 rge reservoir of potential stem cells during crypt regeneration.

254 oliferation and crypt apoptosis and improved crypt regeneration.

255 with the epithelium, particularly within the crypt regions.

256 capture microdissected Mtgr1(-/-) intestinal crypts revealed Notch activation, and secretory markers

257 rvasive apoptosis was observed in intestinal crypts, revealing an important role for BET bromodomain

258 nd, which was isolated as a stable [K([2.2.2]crypt)](+) salt, featuring a [Au2 Sb16 ](4-) cluster cor

259 Er, Lu), which were isolated as the K([2.2.2]crypt) salts and identified by single-crystal X-ray diff

260 oon [K(crypt)](+) , [K(18-c-6)](+) , and [Cs(crypt)](+) salts of the [Sc(NR2 )3 ](-) anion are formed

261 n and 2D-DIGE/mass spectrometry on villi and crypts samples, we found that ablation of PepT1 further

262 sis to form the monomeric Sc(2+) complex, [K(crypt)][Sc(NR2)3], was observed.

263 Whereas the colon lacks Paneth cells, deep crypt secretory (DCS) cells are intermingled with Lgr5(+

264 prise 2 molecularly distinct layers: a basal crypt segment that expressed TFF2 and overlying papillar

265 chniques such as image restoration, cell and crypt segmentation, and cancer grading.

266 trengthen cell-cell adhesion in normal adult crypt stem cells and colon cancer cells.

267 LGR5 ablation in colon cancer cells and crypt stem cells resulted in loss of cortical F-actin, r

268 es of Wnt and RSPO ligands in the intestinal crypt stem-cell niche.

269 reproduces proliferation patterns in normal crypts stipulates that proliferative fate and cell cycle

270 Wnt/beta-catenin signaling is required for crypt structure maintenance.

271 g dysplastic and malignant clones within the crypt-structured BE tissue.

272 In profiling miRNA expression in SC-enriched crypt subsections isolated from fresh, normal surgical s

273 /Cl uptake, protein mistargeting, and longer crypts, suggesting that keratins contribute to intestina

274 A single-hit, multi-target crypt survival curve showed a significant increase in cr

275 initrogen complex was not observed with this crypt system, but it did occur with the 18-crown-6 (crow

276 is within specialized implantation chambers (crypts) that originate within the evaginations directed

277 ies, we use a hybrid stochastic model of the crypt to investigate how exogenous niche signaling (from

278 thelial cells are highly regulated along the crypt vertical axis, which, when perturbed, can result i

279 s miRNAs and their target proteins along the crypt-villi axis in the jejunum of PepT1 KO mice.

280 ing stem cells generated numerous long-lived crypt-villus "ribbons," indicative of dedifferentiation

281 B maintains a Cu gradient along the duodenal crypt-villus axis and buffers Cu levels in the cytosol o

282 altered the distribution of miRNAs along the crypt-villus axis and changed the miRNA profiles of both

283 phrinB interactions position cells along the crypt-villus axis and compartmentalize incipient colorec

284 d dysregulated miRNAs and proteins along the crypt-villus axis are highly related to this process.

285 f expression and function of PepT1 along the crypt-villus axis demonstrated that this protein is cruc

286 sorption for each of the compounds along the crypt-villus axis, as well as confirming a proximal-dist

287 testinal epithelial cell migration along the crypt-villus axis.

288 nteroids represent distinct points along the crypt-villus axis; they can be used to characterize elec

289 mor tissues of different stages and isolated crypts were analyzed by in situ hybridization and immuno

290 n 4 mice, we found that 3.5% +/- 0.6% of all crypts were in the process of fission, whereas 4.1 +/- 0

291 Small intestinal crypts were isolated and subsequently cultured to grow o

292 Crypts were isolated, enteroids were propagated in cultu

293 Normal appearing single crypts were laser microdissected in placebo- and sulinda

294 Intestinal crypts were obtained from surgical resection specimens o

295 ple crypts on their irides, irides with more crypts were significantly thinner and lost more volume o

296 In scarce normal human embryos, crypts were sometimes present.

297 cess of fission, whereas 4.1 +/- 0.9% of all crypts were undergoing crypt fusion.

298 rate from the vasculature into the symbiotic crypts, where they lyse and release particulate chitin,

299 estinal stem cells reside at the base of the crypt, which contains adjacent epithelial cells, stromal

300 The epithelium of the small intestinal crypt, which has a vital role in protecting the underlyi