ライフサイエンスコーパス: hindgut

1 t region (foregut+salivary gland, midgut and hindgut).

2 12.5 pc in the distal developing intestine (hindgut).

3 across all three germ layers, including the hindgut.

4 ssed around ENCCs as they enter the ceca and hindgut.

5 re length of the gut, including the terminal hindgut.

6 y-G3, was highly expressed in the midgut and hindgut.

7 both rodent and avian sacral crest into the hindgut.

8 tribute to the enteric nervous system in the hindgut.

9 nd both before and after colonization of the hindgut.

10 into the posterior endoderm that becomes the hindgut.

11 ages and a gut consisting of fore-, mid- and hindgut.

12 C motility, both in the allantois and in the hindgut.

13 ndent on Steel factor when they colonize the hindgut.

14 e specification in the developing C. elegans hindgut.

15 ution of sacral NCC is mainly limited to the hindgut.

16 NS formation, in sacral NCC within the chick hindgut.

17 the gonadal ridge, remaining trapped in the hindgut.

18 ding the neurogenic ectoderm, stomadeum, and hindgut.

19 prising lack of expression of factors in the hindgut.

20 salivary glands and pgant5 in the developing hindgut.

21 idventral row running beneath the midgut and hindgut.

22 to the region of the endoderm that forms the hindgut.

23 ed for asymmetric left--right looping of the hindgut.

24 the rest of the foregut, the midgut and the hindgut.

25 e transport within the Malpighian tubule and hindgut.

26 arts with the formation and extension of the hindgut.

27 e morphologically distinct subregions of the hindgut.

28 udal mesoderm and endoderm of the developing hindgut.

29 ccumulation within the Malpighian tubule and hindgut.

30 pression in the neuroepithelium, retina, and hindgut.

31 ll rearrangement in the Drosophila embryonic hindgut.

32 number of ENS cells primarily to the distal hindgut.

33 48 requires egl-38 for its expression in the hindgut.

34 he development of the Caenorhabditis elegans hindgut.

35 ract and pull more cells into the elongating hindgut.

36 nd Melainabacteria in the murine foregut and hindgut.

37 nts resulted in 80%-100% colonization of the hindgut.

38 e digestion of lignocellulose in the termite hindgut.

39 nt cells to control late invagination of the hindgut.

40 (44%) foregut, 100 (51%) midgut, and 10 (5%) hindgut.

41 that efficiently transport virus across the hindgut.

42 ophic lakes, geothermal springs, and termite hindguts.

43 esodermal cell types, including cells in the hindgut; (3) two genes, lin-49 and lin-59, affect develo

44 In the hindgut, 5,6-dihydroxyindole was further oxidized by pro

45 oregut (80%), and the insoluble fibre in the hindgut (95%).

46 ls (OB-ISCs) is regulated by the neighboring hindgut, a developmentally distinct organ.

47 on, other peb-1 mutant phenotypes, including hindgut abnormalities, appeared independent of the molti

48 ng in cultured avian intestine also leads to hindgut aganglionosis.

49 rs, myenteric and submucosal plexuses in the hindgut almost entirely composed of transplanted vagal N

50 Here we show that the development of the hindgut also depends on cellular interactions, in this c

51 ch, 6h in the midgut and less than 2h in the hindgut although in many cases shorter periods were obse

52 ik(-/- )embryos fail to develop somites or a hindgut and are truncated posteriorly.

53 alo rumen metagenome with cow rumen, termite hindgut and chicken caecum metagenome.

54 suggested that in order to migrate into the hindgut and differentiate into enteric neurons and glia,

55 e maintenance of structural integrity in the hindgut and egg-laying system in adults.

56 in a number of sites including the foregut, hindgut and epidermis, but not in the central nervous sy

57 precursors from the mesenchyme colonize the hindgut and form intramural ganglion cells that express

58 egion of the neuraxis, to colonise the chick hindgut and form the ENS in an experimentally generated

59 d identify smooth muscles around the midgut, hindgut and heart that resemble their vertebrate counter

60 as a myosuppressin agonist on the cockroach hindgut and locust oviduct, mimicked the effect of dromy

61 ditis elegans mab-9 mutants are defective in hindgut and male tail development because of cell fate t

62 ralian fate maps (such as the origins of the hindgut and mesoderm from the 4d mesentoblast), but also

63 or example, Bmp4 is expressed throughout the hindgut and midgut, but is not expressed in the early gi

64 gh levels of Bla g 1 were found in cockroach hindgut and proventriculus.

65 rmal cells that evaginate from the primitive hindgut and subsequently undergo a sequence of orderly e

66 ctoderm boundary that will give rise both to hindgut and to border ectoderm.

67 ell mass that divides the cloaca into dorsal hindgut and ventral urogenital sinus.

68 precursors in the colonic epithelium of the hindgut and within the urogenital system.

69 Spirochetes from termite hindguts and freshwater sediments possessed homologs of

70 -edge, foregut atrium cells, nervous system, hindgut, and anal pad cells.

71 ocesses during development of the Drosophila hindgut, and compare these to related processes in other

72 patterning in the epithelia of the foregut, hindgut, and imaginal discs.

73 When such ablations were performed, the hindgut, and in some cases also the cecal region, lacked

74 ginal discs, the central nervous system, the hindgut, and salivary glands.

75 depolymerization continues in the posterior hindgut, and that the beetle excretes an energy- and nut

76 erm, migrate into and through the developing hindgut, and traverse to the genital ridge where they cl

77 s and outside the pharynx in the hypodermis, hindgut, and vulva.

78 affect development of many cells, including hindgut; and (4) three genes, mab-9, egl-38, and lin-48,

79 ar of the JAK/STAT activator Unpaired at the hindgut anterior, may play a role in controlling hindgut

80 Enteric ganglia in the hindgut are derived from separate vagal and sacral neura

81 Microbial communities in the termite hindgut are essential for degrading plant material.

82 lanogaster, ISCs of the posterior intestine (hindgut) are confined to an anterior narrow segment, whi

83 ry-which are expressed in various bilaterian hindguts-are expressed in a small region at the posterio

84 sser contribution, that is restricted to the hindgut, arises from the sacral region of the neuraxis.

85 hlight the use of the Malpighian tubules and hindgut as accessible models of human disease biology.

86 Using the embryonic Drosophila hindgut as an in vivo model for organogenesis, we show t

87 eurons as efficiently in the Ednrb-deficient hindgut as did wild-type NCSCs.

88 loped a mathematical model of the developing hindgut, based on the differential interfacial tension h

89 The elongating hindgut becomes subdivided into domains -- small intesti

90 r of extrinsic fibers that travel within the hindgut between circular and longitudinal muscles and wi

91 -38 in the development of one structure, the hindgut, but not in other tissues such as the egg-laying

92 hat the cells do not internalize through the hindgut, but rather through the closing blastopore; and

93 e conclude that sacral crest cells enter the hindgut by advancing on extrinsic fibers and, in agangli

94 approximately 90% develop a prolapse of the hindgut by the late prism stage ( approximately 8 h afte

95 Hindgut cell proliferation was stimulated specifically b

96 e ligand plays a cell non-autonomous role in hindgut cell rearrangement.

97 gut anterior, may play a role in controlling hindgut cell rearrangement.

98 ing fates within the hindgut, making certain hindgut cells different from others.

99 e in the larva, where it generates all adult hindgut cells including ISCs.

100 Defective proliferation of hindgut cells is a key component of the pathogenic seque

101 hindgut domains, and show that ventrolateral hindgut cells populate the majority of the colonic epith

102 als, these genes are expressed in subsets of hindgut cells rather than in individual cell types.

103 Drosophila gene ovo and is expressed in the hindgut cells that develop abnormally in lin-48 mutants.

104 t PEB-1 was detectable in all hypodermal and hindgut cells underlying the cuticle.

105 idence that lin-48 is a target for EGL-38 in hindgut cells.

106 Most rodents house microbes in hindgut chambers, such as the caecum and colon.

107 pression to the most posterior region of the hindgut (cloaca), in controlling adjacent endodermal dif

108 arker for living PGCs, their behavior before hindgut colonization has not been previously studied.

109 rmal behavior of PGCs in live embryos before hindgut colonization, and the roles of Steel factor, usi

110 ibutes to a subset of enteric ganglia in the hindgut, colonizing the colon in a caudal-to-rostral wav

111 nd the pools of microbial metabolites in the hindgut compartment, underlining that both gut developme

112 Lower termites harbor in their hindgut complex microbial communities that are involved

113 om the renal organs (Malpighian tubules) and hindgut contractions by activating a G protein-coupled k

114 l anatomy (flight musculature, midgut shape, hindgut convolutions, brain shape and size) and external

115 rganogenesis, we show that the tightening of hindgut curvature that normally occurs between embryonic

116 the pancreas, differentiation of foregut and hindgut derivatives is unaffected.

117 Hindgut-derived endoderm can differentiate into rectal,

118 al and brachyenteron) required for embryonic hindgut development also act during pupation to construc

119 should identify additional genes controlling hindgut development and thus shed light on a variety of

120 nesis during both embryonic segmentation and hindgut development, we suggest that they may be require

121 rent factors contribute to normal C. elegans hindgut development.

122 similarity with bowl required for Drosophila hindgut development; (b) it lies in a chromosomal region

123 cral neural crest-derived neurons within the hindgut did not appear to be sufficiently high to compen

124 incubation duration for a published in vitro hindgut digestibility assay using ileal digesta (sampled

125 tance of correcting for this in the in vitro hindgut digestion assay.

126 surrounding the cloaca, the terminal end of hindgut dilation.

127 was little difference in estimated in vitro hindgut DMD between 18 and 24h incubation durations.

128 considered optimal based on observed in vivo hindgut DMD values in humans, but there was little diffe

129 coordinate growth between dorsal and ventral hindgut domains to regulate the extension of the hindgut

130 oaches, we describe novel dorsal and ventral hindgut domains, and show that ventrolateral hindgut cel

131 However, injury to the adult HZ/hindgut drives upregulation of unpaired-3 cytokine, whic

132 For two assays, hindgut dry matter digestibility (DMD) generally increas

133 ved values with previously published in vivo hindgut dry matter digestibility for similar diets.

134 n Hoxa-4 known to express in the stomach and hindgut during development.

135 intermediate 5,6-dihydroxyindole reached the hindgut either by passing directly through the midgut, o

136 We show that the defect in hindgut elongation in drm, bowl, and lin mutants is due,

137 The midgut and hindgut endoderm of the mouse embryo give rise to the in

138 ll type-specific proliferation defect in the hindgut endoderm, and we find that Grhl3 is expressed sp

139 Sp5/8 pathway, which is active in the dorsal hindgut endoderm, is required for hindgut extension and

140 is of surface ectoderm, cloacal mesoderm and hindgut endoderm.

141 he role of ET3 during formation of the avian hindgut ENS.

142 mak and a subpopulation of sacral NCC within hindgut enteric ganglia.

143 s migrate posteriorly and differentiate into hindgut enterocytes, a group of the progenitor cells, un

144 genitors that differentiate as midgut versus hindgut enterocytes.

145 hways, implying nutrient scarcity within the hindgut environment.

146 ions were not acquired by aphids through the hindgut epithelial cells and were not transmitted when i

147 in severe dehydration without damage to the hindgut epithelial cells, implicating a physiological fa

148 ssed in the basolateral membrane of anterior hindgut epithelial cells.

149 g differences between the communities at the hindgut epithelium and the luminal fluid of newly moulte

150 er cell signaling molecules expressed in the hindgut epithelium are required to establish its normal

151 portantly, specific expression of ine in the hindgut epithelium can completely restore disrupted syst

152 ransduce Hedgehog signals in fetal life; the hindgut epithelium expresses Ptch but not Gli1 at E10.5;

153 Elongation of the Drosophila embryonic hindgut epithelium occurs by a process of oriented cell

154 r external hypertonicity, loss of ine in the hindgut epithelium results in severe dehydration without

155 significant cell division or apoptosis, the hindgut epithelium undergoes morphogenesis by changes in

156 e appearance of STAT92E in a gradient in the hindgut epithelium, these results support a model in whi

157 in honey bees, specialized in colonizing the hindgut epithelium.

158 cal effects of these defenses in the form of hindgut expansion and gut melanization.

159 Using hindgut explants cultured in collagen gel, we find that

160 We also found that hindgut expression of ine is required for water conserva

161 the dorsal hindgut endoderm, is required for hindgut extension and colon formation.

162 ity of the neural tube remains open, and the hindgut fails to close.

163 GLT1 is made possible by the contribution of hindgut fermentation to carbohydrate digestion.

164 en turtles are endangered marine herbivorous hindgut fermenters that contribute to a variety of marin

165 s that novel Fibrobacter diversity exists in hindgut fermenters, we performed culturing and 16S rRNA

166 certain phylotypes with either ruminants or hindgut-fermenters.

167 hich are generally grouped into foregut- and hindgut-fermenters.

168 microbial fermentation in both foregut- and hindgut-fermenting folivorous primates.

169 s in the gastrointestinal tracts of numerous hindgut-fermenting herbivores, but their physiology is p

170 cluding several that were only isolated from hindgut-fermenting hosts, and four previously unrepresen

171 olutionarily ancient role for these genes in hindgut formation.

172 e gradient that drives cell movements in the hindgut-forming endoderm, enabling tissue-scale posterio

173 also act during pupation to construct a new hindgut from imaginal cells.

174 cryptorchidism, incomplete separation of the hindgut from the urogenital sinus (UGS), absence of the

175 caudal is not sufficient for hindgut gastrulation and development, however, as it doe

176 However, at earlier stages in the hindgut, germ cells are unaffected in CXCR4(-/-) embryos

177 Similarly, segments of murine hindgut harvested prior to the arrival of vagal crest ce

178 olin receptor immunosignals are found in the hindgut, heart, and in distinct neuronal populations of

179 d that Klf6 is expressed in neuronal tissue, hindgut, heart, lung, kidney, and limb buds during midge

180 , and lin are required for patterning of the hindgut, i.e., for correct expression in the prospective

181 ys in mammals and the Malpighian tubules and hindgut in insects, can increase water conservation and

182 ge at which sacral NCC begin to colonise the hindgut in large numbers, myenteric and submucosal plexu

183 n an experimentally generated hypoganglionic hindgut in ovo model.

184 In order to generate aneural hindgut in vivo, it was necessary to ablate the vagal ne

185 es a deleterious infection of the C. elegans hindgut initiated by adhesion to rectal and anal cuticle

186 CapI-hh is expressed in a ring of the hindgut internal to that of CapI-Wnt1, as well as in a s

187 data show BMP-dependent patterning of human hindgut into HCOs, which will be valuable for studying d

188 utants suggest that proper patterning of the hindgut into small intestine and large intestine is like

189 himeras by transplanting preganglionic quail hindguts into the coelomic cavity of chick embryos.

190 aginating Malpighian tubule buds, elongating hindgut, invaginating salivary glands, intersegmental gr

191 The Drosophila embryonic hindgut is a robust system for the study of patterning a

192 , the absence of Wnt activity in the ventral hindgut is crucial for proper hindgut morphogenesis, as

193 lonic aganglionosis, a disorder in which the hindgut is devoid of neurons.

194 Therefore, ine in the Drosophila hindgut is essential for the maintenance of systemic wat

195 We find that the hindgut is formed by collective cell movements through a

196 The Drosophila hindgut is fruitful territory for investigation of event

197 en descriptively characterized(8,9), but the hindgut is likely to form by a distinct mechanism that h

198 ession is localized to the developing midgut-hindgut junction and is required to establish the small

199 rostral gradient, being most numerous in the hindgut, less so in the intestine, and absent in the pro

200 n, than those arising from either foregut or hindgut locations.

201 suppressin receptor binding in the cockroach hindgut, locust oviduct, and fruit fly crop are similar.

202 fficient to mediate virus transport from the hindgut lumen into the hemocoel.

203 are required for patterning fates within the hindgut, making certain hindgut cells different from oth

204 te that a stable boundary between midgut and hindgut/Malpighian tubules is not established during ear

205 cluding the endodermal midgut and ectodermal hindgut/Malpighian tubules, maintain populations of divi

206 ites, and in some cases, the expression of a hindgut marker in hermaphrodite animals.

207 recombinations were constructed using avian hindgut mesenchyme and non-intestinal epithelium from th

208 xtramural ganglion and secondarily enter the hindgut mesenchyme.

209 Furthermore, when compared with the termite hindgut microbiome, there are fundamental differences in

210 In horses, high-starch diets alter the hindgut microbiota.

211 he sacral neuraxis extensively colonised the hindgut, migrated in a caudorostral direction, different

212 ecursor cells and thus create an aganglionic hindgut model in vivo.

213 in the ventral hindgut is crucial for proper hindgut morphogenesis, as ectopic stabilization of beta-

214 whereas FGF4 alone is sufficient to promote hindgut morphogenesis.

215 r epithelial structures, such as foregut and hindgut morphogenesis.

216 ne, drumstick, that affects only foregut and hindgut morphogenesis.

217 specific blast cells within the hindgut, the hindgut morphology in both males and hermaphrodites, and

218 ines (lin), are required to establish normal hindgut morphology.

219 raenteric ganglion of Remak and colonize the hindgut much later, after vagal crest-derived neural pre

220 strulation and a loss of cardiac tissues and hindgut musculature.

221 sgenic embryos is apposed with nontransgenic hindgut, neural precursors from the mesenchyme colonize

222 enteric precursors in order to colonise the hindgut, nor are capable of dramatically altering their

223 rest, research on the Malpighian tubules and hindgut of Drosophila have uncovered important paradigms

224 sate for the lack of ganglia in the terminal hindgut of Hirschsprung's disease in humans or aganglion

225 we analysed the bacterial microbiota in the hindgut of Odontotermes formosanus and its fungus comb t

226 Twelve proteins were predicted to act in the hindgut of the aphid, while six proteins were predicted

227 g archenteron, and finally to the midgut and hindgut of the pluteus larva.

228 totic index was elevated in neural folds and hindgut of treated embryos, consistent with a proposed m

229 mparative microarray of the embryonic distal hindgut of wild-type and EdnrB(NCC-/-) mice that model H

230 The optimised assay gave realistic hindgut OMD values ranging from 55% to 79% (Wheat Bran D

231 umors originated in the pancreas, midgut, or hindgut or were of unknown origin.

232 DPP signals, resulting in a lethal defect in hindgut organogenesis.

233 ion of CCLM from midgut origin (n = 238) and hindgut origin (n = 487) was analyzed.

234 Compared with CCLM from hindgut origin, CCLM from midgut origin are associated w

235 educe spontaneous muscle contractions of the hindgut, oviduct, and heart.

236 artments (foregut, midgut, mixed segment and hindgut p1, p3, p4, and p5 segments) and salivary glands

237 migrated along normal, previously described hindgut pathways and formed isolated ganglia containing

238 of genes involved in bilaterian foregut and hindgut patterning during the development of the acoel C

239 ed to brachyury have also been implicated in hindgut patterning, and our results support models for a

240 s of the bacterial community resident in the hindgut paunch of a wood-feeding 'higher' Nasutitermes s

241 his study, we compared the microbiota in the hindgut paunch of Amitermes wheeleri collected from cow

242 g in concert: the Malpighian tubules and the hindgut perform essential roles in excretion and ionic a

243 on of a neuropeptide that arrests midgut and hindgut peristalsis; and attaching to the midgut to avoi

244 ghian tubules of Drosophila develop from the hindgut primordium and visceral mesoderm.

245 Elongation of the internalized Drosophila hindgut primordium is similar to elongation of the arche

246 el, ectopic expression of Drm throughout the hindgut produces a lin phenotype.

247 l tract digestibilities in rats and in vitro hindgut production of short-chain fatty acids (SCFAs).

248 As the majority of the hindgut progenitor cells migrate posteriorly and differe

249 signaling acts to balance the proportion of hindgut progenitors that differentiate as midgut versus

250 k-in reporter line to track the emergence of hindgut progenitors, we follow the kinetics of CDX2 expr

251 ed the transcriptomes of Xenopus foregut and hindgut progenitors, which are conserved with mammals.

252 entiation of midgut enterocytes derived from hindgut progenitors.

253 as a genome-wide toggle between foregut and hindgut programs.

254 n anterior narrow segment, which we name the hindgut proliferation zone (HPZ).

255 conditions such as kidney stones, while the hindgut provides an outstanding model for processes such

256 The development of the Drosophila hindgut provides, in microcosm, a genetic model system f

257 Hindgut reconstruction was adopted in 1993 and preservat

258 acterized by an absence of the terminal-most hindgut (rectum) and formation of a fistula that aberran

259 l, for the normal morphology and function of hindgut (rectum) cells in both males and hermaphrodites

260 on, while a thicker gut wall in the anterior hindgut reduces oxygen diffusion and favours hydrogen ac

261 ammalian kidney and insect Malpighian tubule/hindgut requires a region of hypertonicity within the or

262 apical surface of wild-type trachea and the hindgut reveals previously unrecognized spatial patterns

263 One hypothesizes early colonization of the hindgut shortly after neurulation, and the other states

264 GF/Wnt-induced posterior endoderm pattering, hindgut specification and morphogenesis, and a pro-intes

265 d activity of WNT3A and FGF4 is required for hindgut specification whereas FGF4 alone is sufficient t

266 During this patterning step, 3D mid- or hindgut spheroids bud from the monolayer epithelium atta

267 rgence, focusing on measurable parameters of hindgut spheroids, the intermediate step between definit

268 over methanogenesis as an H2 sink in termite hindguts, suggest that the motility of termite gut proto

269 The AJCC Hindgut Taskforce sought population-based validation tha

270 The AJCC Hindgut Taskforce sought population-based validation tha

271 d from three broad domains: fore-, mid-, and hindgut that have distinct functional, morphological, an

272 gut domains to regulate the extension of the hindgut that leads to colon formation.

273 between the endodermal midgut and ectodermal hindgut that shares molecular signatures of both organs,

274 In vessel-rich areas, such as the midgut and hindgut, the distribution of migrating ENCC did not supp

275 of the male-specific blast cells within the hindgut, the hindgut morphology in both males and hermap

276 ly, in miRet(51) mice, which lack ENS in the hindgut, the vascular network in this region appeared to

277 In the midgut and hindgut, these stem cells originate from within larger p

278 ic ganglia in the mesenchyme surrounding the hindgut, they are not found in the gut prior to the arri

279 l crest origin fail to colonize the terminal hindgut, this aganglionic region becomes non-functional

280 em cells are patterned into CDX2(+) mid- and hindgut tissue using FGF4 and WNT3a.

281 In aganglionic hindguts, TNC expression is strong throughout the outer

282 rest cells (NCCs) that enter the foregut and hindgut to become enteric neural-crest-derived cells (EN

283 t it acts cell autonomously in the posterior hindgut to direct cell fate.

284 sue-scale posterior extension of the forming hindgut tube.

285 d better survival than those with foregut or hindgut tumors.

286 enic mice, they manifested an altered midgut-hindgut union and agenesis of the cecum.

287 stabilization of beta-catenin in the ventral hindgut via gain- or loss-of-function mutations in Ctnnb

288 p and Hh), and to establish and maintain the hindgut visceral mesoderm (Wg and Hh).

289 over sequential but interdependent phases of hindgut visceral mesoderm development.

290 to promote the proper differentiation of the hindgut visceral mesoderm itself.

291 of cellulases and hemicellulases in termite hindgut was observed when we compared glycoside hydrolas

292 microbial community residing in the termite hindgut, we found genus-wide infection patterns displayi

293 ning events within one organ, the C. elegans hindgut, we have analyzed the expression pattern of seve

294 vagal-derived neural crest cells within the hindgut, we mapped the contribution of various vagal neu

295 se, a failure to form enteric ganglia in the hindgut, were highly up-regulated in gut neural crest st

296 ll-2, -3, and -4 are highly expressed in the hindgut (where cellulolytic protists are harbored).

297 ignaling during ENS development in the avian hindgut, where it influences NCC proliferation, differen

298 regulation of the cell cycle, except in the hindgut, where Wnt5a is highly expressed.

299 or development of the Caenorhabditis elegans hindgut, whereas several vertebrate Tbx20 genes promote

300 e rumen (forages and legumes) or the termite hindgut (wood).