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 nd Melainabacteria in the murine foregut and hindgut.

4 nd both before and after colonization of the hindgut.

5 into the posterior endoderm that becomes the hindgut.

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

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

8 ndent on Steel factor when they colonize the hindgut.

9 e specification in the developing C. elegans hindgut.

10 e digestion of lignocellulose in the termite hindgut.

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

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

13 the gonadal ridge, remaining trapped in the hindgut.

14 ding the neurogenic ectoderm, stomadeum, and hindgut.

15 prising lack of expression of factors in the hindgut.

16 salivary glands and pgant5 in the developing hindgut.

17 idventral row running beneath the midgut and hindgut.

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

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

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

21 e transport within the Malpighian tubule and hindgut.

22 e morphologically distinct subregions of the hindgut.

23 udal mesoderm and endoderm of the developing hindgut.

24 ccumulation within the Malpighian tubule and hindgut.

25 pression in the neuroepithelium, retina, and hindgut.

26 ll rearrangement in the Drosophila embryonic hindgut.

27 number of ENS cells primarily to the distal hindgut.

28 48 requires egl-38 for its expression in the hindgut.

29 he development of the Caenorhabditis elegans hindgut.

30 further specification and development of the hindgut.

31 n only induce Hoxd-13 in the mesoderm of the hindgut.

32 m to the morphology and mucin content of the hindgut.

33 rate of myogenic contractions of the larval hindgut.

34 cally in the caudal portion of the embryonic hindgut.

35 t cell populations in the dorsal and ventral hindgut.

36 x preferentially affect foregut, and one the hindgut.

37 eron tip followed by the foregut, midgut and hindgut.

38 nt cells to control late invagination of the hindgut.

39 (44%) foregut, 100 (51%) midgut, and 10 (5%) hindgut.

40 that efficiently transport virus across the hindgut.

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

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

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

44 both rodent and avian sacral crest into the hindgut.

45 tribute to the enteric nervous system in the hindgut.

46 ophic lakes, geothermal springs, and termite hindguts.

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

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

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

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

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

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

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

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

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

56 ls constituted nearly all of the prospective hindgut and about half of the prospective midgut, while

57 byn expression in the hindgut and anal pad primordia is required for the regul

58 e engulfment), resulting in severely reduced hindgut and anal pads.

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

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

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

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

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

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

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

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

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

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

69 at body, the developing midgut endoderm, the hindgut and Malpighian tubules, and the epidermis and ce

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

71 g1-derived cells that will contribute to the hindgut and midgut in accordance with lineage tracing ob

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

73 development, is permanently activated in the hindgut and midgut.

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

75 efects in terminal derivatives including the hindgut and proventriculus.

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

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

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

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

80 Spirochetes from termite hindguts and freshwater sediments possessed homologs of

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

100 nduce Bmp4 in the mesoderm of the midgut and hindgut, Bmp4 is not induced in the stomach region of th

101 -38 in the development of one structure, the hindgut, but not in other tissues such as the egg-laying

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

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

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

105 Hindgut cell proliferation was stimulated specifically b

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

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

108 eg1 clones contributed only small numbers of hindgut cells but large patches of ectoderm cells that e

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

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

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

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

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

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

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

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

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

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

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

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

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

122 than 10(-9) M and increase the frequency of hindgut contractions at concentrations above 10(-8) M.

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

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

125 related gene (Trg), DNA of which rescues the hindgut defects of deficiency 68D/E.

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

127 Hindgut-derived endoderm can differentiate into rectal,

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

147 c endoderm and small portions of the foregut/hindgut endoderm.

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

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

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

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

152 genitors that differentiate as midgut versus hindgut enterocytes.

153 hways, implying nutrient scarcity within the hindgut environment.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

171 certain phylotypes with either ruminants or hindgut-fermenters.

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

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

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

175 olutionarily ancient role for these genes in hindgut formation.

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

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

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

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

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

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

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

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

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

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

186 n an experimentally generated hypoganglionic hindgut in ovo model.

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

188 ar epithelia (salivary glands, tracheae, and hindgut) in much same manner as they alter the shape of

189 dominal ganglion were found to innervate the hindgut, indicating that YXFGLamides may be involved in

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

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

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

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

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

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

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

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

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

199 The Drosophila hindgut is fruitful territory for investigation of event

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

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

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

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

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

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

206 several cell types, including the posterior hindgut, Malpighian tubules, anal plate, garland cells,

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

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

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

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

211 xtramural ganglion and secondarily enter the hindgut mesenchyme.

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

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

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

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

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

217 whereas FGF4 alone is sufficient to promote hindgut morphogenesis.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

241 lethal over deficiencies of 68D/E and show a hindgut phenotype.

242 caudal is essential for invagination of the hindgut primordium and for further specification and dev

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

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

245 d to promote development of the internalized hindgut primordium.

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

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

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

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

250 entiation of midgut enterocytes derived from hindgut progenitors.

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

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

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

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

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

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

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

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

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

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

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

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

263 The AJCC Hindgut Taskforce sought population-based validation tha

264 The AJCC Hindgut Taskforce sought population-based validation tha

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

291 cally absent from the ventral portion of the hindgut, whereas they contributed efficiently to the dor

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