ライフサイエンスコーパス: GI tract

1 GI tract biopsy and qPCR results were available for 81 k

2 idney and liver transplant recipients with a GI tract biopsy and plasma CMV qPCR result within 15 day

3 encapsulation to protect probiotics against GI tract insults and improve their adhesion and growth o

4 y frequencies of Th17 cells in the blood and GI tract.

5 events within the peripheral blood (PB) and GI tract during AEI.

6 , quality of life and functional status, and GI tract imaging.

7 Here we analyzed Th17 cells in the blood, GI tract, and broncheoalveolar lavage of HIV-infected an

8 l isolate strain V583 was actively killed by GI tract flora, whereas commensal enterococci flourished

9 firm that systemic inflammation triggered by GI tract bacteria plays a pivotal role in tumorigenesis

10 CMV GI tract disease was defined as histopathologic evidence

11 splant recipients; 20 cases of confirmed CMV GI tract disease were identified.

12 , the sensitivity of qPCR for diagnosing CMV GI tract disease was 85% (95% confidence interval [CI],

13 ensitivity and excellent specificity for CMV GI tract disease in kidney and liver transplant recipien

14 ishment of vegetative bacteria in the distal GI tract.

15 The Drosophila GI tract is an accessible model to address this question

16 istribution of enterococci in the Drosophila GI tract was determined by immunohistochemical staining

17 vivo small intestinal total ischemia during GI-tract surgery.

18 Thus, to enhance GI tract physiology, we treated SIV-infected pigtail mac

19 in neonatal lethality, with mice exhibiting GI tract abnormalities.

20 with a history of adverse reactions to food, GI tract symptoms, and birch pollen pollinosis and five

21 CMV DNA as an adjunct diagnostic method for GI tract disease in kidney and liver transplant recipien

22 Gastrointestinal (GI) tract disease/inflammation is a hallmark of HIV/SIV

23 We show here that a gastrointestinal (GI) tract bacterial infection is sufficient to enhance p

24 annel, was identified as a gastrointestinal (GI) tract cancer susceptibility gene in multiple Sleepin

25 eart, muscles, nerves, and gastrointestinal (GI) tract tissue.

26 uch as the oral cavity and gastrointestinal (GI) tract.

27 pollen allergy experience gastrointestinal (GI) tract symptoms that are possibly caused by pollen-as

28 rbed onto SWCNTs in a fish gastrointestinal (GI) tract.

29 ing K1 to translocate from gastrointestinal (GI) tract to blood.

30 rug stability in the harsh gastrointestinal (GI) tract environment, providing opportunities for targe

31 rder to colonize the human gastrointestinal (GI) tract and cause disease, EHEC must be able to sense

32 The human gastrointestinal (GI) tract is the habitat for hundreds of microbial speci

33 nsal organism of the human gastrointestinal (GI) tract primarily transmissible via the fecal-oral rou

34 HIV infection results in gastrointestinal (GI) tract damage, microbial translocation, and immune ac

35 p1a1 expression deleted in gastrointestinal (GI) tract epithelial cells develop immunotoxicity and di

36 ern induced by morphine in gastrointestinal (GI) tract.

37 s from the tongue or lower gastrointestinal (GI) tract colonization.

38 Lower gastrointestinal (GI) tract graft-versus-host disease (GVHD) is the predom

39 The mammalian gastrointestinal (GI) tract harbors a diverse population of commensal spec

40 The mammalian gastrointestinal (GI) tract is colonized by a complex consortium of bacter

41 The mammalian gastrointestinal (GI) tract is colonized by trillions of beneficial commen

42 h toxin to systemic and/or gastrointestinal (GI) tract disease.

43 the mucosa of the proximal gastrointestinal (GI) tract.

44 cted to tissues within the gastrointestinal (GI) tract (jejunum, ileum and colon).

45 flammatory response in the gastrointestinal (GI) tract and alters GI motility, but little is known ab

46 us system and vital to the gastrointestinal (GI) tract and its communication with the rest of the bod

47 on (BMT) that involves the gastrointestinal (GI) tract and lungs.

48 ubmucosal plexuses) of the gastrointestinal (GI) tract and the areas of the dorsal vagal complex (DVC

49 on-induced toxicity in the gastrointestinal (GI) tract and the main cellular compartments studied in

50 ells of Cajal (ICC) in the gastrointestinal (GI) tract are described based on observations of laborat

51 e dynamic ecosystem of the gastrointestinal (GI) tract by translating chemical cues from the environm

52 In the gastrointestinal (GI) tract CFTR promotes chloride and bicarbonate secreti

53 competitive growth in the gastrointestinal (GI) tract consortium.

54 The gastrointestinal (GI) tract contains much of the body's serotonin (5-hydro

55 microbial community of the gastrointestinal (GI) tract determines susceptibility to Clostridium diffi

56 The gastrointestinal (GI) tract epithelium is continuously replenished by acti

57 onic devices placed in the gastrointestinal (GI) tract for prolonged periods have the potential to tr

58 The gastrointestinal (GI) tract forms from the endoderm (which gives rise to t

59 etic axons innervating the gastrointestinal (GI) tract has not been available.

60 particles delivered to the gastrointestinal (GI) tract improve oral absorption or local targeting of

61 The primacy of the gastrointestinal (GI) tract in dictating the outcome of graft-versus-host

62 urological function in the gastrointestinal (GI) tract in health and disease.

63 ernal organs including the gastrointestinal (GI) tract in mice.

64 gm of T cell homing to the gastrointestinal (GI) tract involves the induction of alpha4beta7 and CCR9

65 iated drug delivery in the gastrointestinal (GI) tract is a bourgeoning area of study.

66 host disease (GVHD) of the gastrointestinal (GI) tract is an often lethal complication of allogeneic

67 The gastrointestinal (GI) tract is composed of a diverse set of organs that to

68 The gastrointestinal (GI) tract is essential for the absorption of nutrients,

69 Drug delivery to the gastrointestinal (GI) tract is highly challenging due to the harsh environ

70 emand drug delivery to the gastrointestinal (GI) tract is highly desirable due to the high instances

71 The lumen of the gastrointestinal (GI) tract is home to an enormous quantity of different b

72 The gastrointestinal (GI) tract is the largest immune organ; in vertebrates, i

73 The complexity of the gastrointestinal (GI) tract lies in its anatomy as well as in its physiolo

74 is a normal member of the gastrointestinal (GI) tract microbiota of healthy humans, but during host

75 The involvement of the gastrointestinal (GI) tract occurs in 25% of all cases of PTLD.

76 al events occur within the gastrointestinal (GI) tract of Asian macaques with progressive simian immu

77 ompartmentalization of the gastrointestinal (GI) tract of metazoans is critical for health.

78 In the gastrointestinal (GI) tract of multiple species, there are resident plasma

79 e disease that affects the gastrointestinal (GI) tract of premature infants.

80 teroendocrine cells of the gastrointestinal (GI) tract play a central role in metabolism, digestion,

81 The gastrointestinal (GI) tract presents a major site of immune modulation by

82 hronic inflammation of the gastrointestinal (GI) tract that includes debilitating diseases, such as u

83 transport and fate in the gastrointestinal (GI) tract through multiple mechanisms including enhancem

84 ting the microbiota in the gastrointestinal (GI) tract through the use of probiotics (PBio) is a safe

85 alts from the lumen of the gastrointestinal (GI) tract to the liver via the portal vein.

86 n VPI 10463 throughout the gastrointestinal (GI) tract using a murine model of infection.

87 evere malabsorption by the gastrointestinal (GI) tract was the primary cause of death in CFTR-knockou

88 Mucosal damage to the gastrointestinal (GI) tract with resulting microbial translocation is hypo

89 cause lethal damage to the gastrointestinal (GI) tract, a condition called the GI syndrome.

90 spores, germination in the gastrointestinal (GI) tract, and then colonization of the large intestine.

91 enic microorganisms in the gastrointestinal (GI) tract, but the influence of IECs on the development

92 In the gastrointestinal (GI) tract, ICC are pacemaker cells that generate spontan

93 ide hormones all along the gastrointestinal (GI) tract, making it one of the largest endocrine organs

94 to epithelial cells of the gastrointestinal (GI) tract, mediating toxicities restricting the therapeu

95 c inflammation outside the gastrointestinal (GI) tract, such as eosinophilic airway inflammation seen

96 s specific for GVHD of the gastrointestinal (GI) tract, the GVHD target organ most associated with no

97 In the gastrointestinal (GI) tract, TMEM16A is absent from smooth muscle cells, b

98 to endocrine cells in the gastrointestinal (GI) tract, where it is important for endocrine different

99 gnal was restricted to the gastrointestinal (GI) tract, which was validated by directly measuring the

100 n of CD4(+) T cells in the gastrointestinal (GI) tract.

101 elial cell toxicity in the gastrointestinal (GI) tract.

102 m the genital tract to the gastrointestinal (GI) tract.

103 , frequently affecting the gastrointestinal (GI) tract.

104 get organs, especially the gastrointestinal (GI) tract.

105 acterized in detail in the gastrointestinal (GI) tract.

106 paracrine mediators in the gastrointestinal (GI) tract.

107 crobial species within the gastrointestinal (GI) tract.

108 y at specific sites in the gastrointestinal (GI) tract.

109 es is important within the gastrointestinal (GI) tract.

110 oxemia) originating in the gastrointestinal (GI) tract.

111 ss of CD4 T cells from the gastrointestinal (GI) tract.

112 resent in abundance in the gastrointestinal (GI) tract.

113 e tunica muscularis of the gastrointestinal (GI) tract.

114 17 months old outside the gastrointestinal (GI) tract.

115 nanoparticles (NPs) in the gastrointestinal (GI) tract.

116 T-cell accumulation in the gastrointestinal (GI) tract.

117 t, with an emphasis on the gastrointestinal (GI) tract.

118 d a major reservoir to the gastrointestinal (GI) tract.

119 twork in the mucosa of the gastrointestinal (GI) tract.

120 e) disease anywhere in the gastrointestinal (GI) tract.

121 In the upper gastrointestinal (GI) tract, there have been many anterograde tracing stud

122 s that innervate the upper gastrointestinal (GI) tract.

123 he human body exist within gastrointestinal (GI) tract communities, where they contribute to many asp

124 lines the respiratory and gastrointestinal (GI) tracts is an important portal of entry for pathogens

125 from the reproductive and gastrointestinal (GI) tracts of six species (bovine, ovine, equine, porcin

126 commensal organisms of the gastrointestinal (GI) tracts of a broad range of mammalian and insect host

127 us species are truly indigenous to the human GI tract or the oral cavity.

128 ed prevalence of C. trachomatis in the human GI tract.

129 uman primate (Macaca fascicularis) and human GI tracts.

130 tion in HIV-infected individuals may improve GI tract immunity and thereby mitigate inflammatory sequ

131 diated by ILC2 production of IL-13, improved GI tract barrier function, and a preserved graft-versus-

132 It is possible that differences in GI tract and immune development are related to shifts in

133 confirm that Kcnq1 has a functional role in GI tract cancer, we created Apc(Min) mice that carried a

134 sion GPCRs points to their important role in GI tract functioning and defines them as a potentially c

135 ecum and colon is an important early step in GI tract colonization.

136 p excretions also developed the long-lasting GI tract infection.

137 occurred in the upper GI tract (48%), lower GI tract (23%), and rectum (29%) without differences bet

138 liver (RR, 2.1; 95% CI, 1.8-2.5), and lower GI tract (RR, 1.9; 95% CI, 1.7-2.2).

139 scuss new insights into the biology of lower GI tract GVHD and focus on intrinsic pathways and regula

140 stasis may improve treatment of severe lower GI tract aGVHD.

141 Recent data indicate that lower GI tract GVHD is a complicated process mediated by donor

142 2 innate lymphoid cells (ILC2s) in the lower GI tract are sensitive to conditioning therapy and show

143 with grade III or greater aGVHD of the lower GI tract, who do not respond to therapy with corticoster

144 present a late onset, and involve the lower GI tract.

145 the lethality of aGVHD and in treating lower GI tract disease.

146 rity of visceral organs (e.g., heart, lungs, GI tract, etc) and their activation is critical for defe

147 s that most commonly originate in the lungs, GI tract, and pancreas.

148 ensal bacteria associated with the mammalian GI tract can be anatomically defined as (i) luminal, (ii

149 show that chemical sensing in the mammalian GI tract determines the niche specificity for colonizati

150 host species for SIV that does not manifest GI tract damage or chronic immune activation during infe

151 lexus along different segments of the monkey GI tract.

152 kappa-AL had more GI tract and liver involvement, where as renal involveme

153 bacterial populations in the infected mouse GI tract using 16S rRNA gene sequence analysis of bacter

154 f irradiated endothelial cells of the murine GI tract.

155 ese cells were relatively rare in the murine GI tract.

156 Notably, GI tract clones display extensive sharing of sequence va

157 in increased frequency and functionality of GI tract APCs, enhanced reconstitution and functionality

158 in 13 of 16 patients (81%) with a history of GI tract symptoms associated with the ingestion of Bet v

159 o the GI tract and systemic translocation of GI tract microbial products.

160 urons that is more prominent in the proximal GI tract.

161 argets, innervate the mucosa of the proximal GI tract.

162 pression of all 30 Adhesion GPCRs in the rat GI tract divided into twelve subsegments.

163 administered UAPs could survive the animal's GI tracts for as long as 18h.

164 While this model may be useful for studying GI tract neurodegeneration, in its present state it does

165 er these results support the hypothesis that GI tract damage leading to local and systemic microbial

166 city and die within 32 days, indicating that GI tract inducible CYP1A1 is absolutely required for det

167 opism of microbes across mucus and along the GI tract, providing unique insights into the mechanisms

168 s from specialized endocrine cells along the GI tract.

169 ic traits of microbial communities along the GI tract.

170 o electronics at various locations along the GI tract.

171 dysbiosis and epithelial dysplasia along the GI tract.

172 d environments in both food products and the GI tract.

173 n striking contrast, water absorption by the GI tract rapidly and uniformly transported non-mucoadhes

174 his mouse model, P. aeruginosa colonizes the GI tract and then disseminates systemically once Cy or R

175 Because a single bacterium can escape the GI tract to colonize deeper tissues, heterogeneous gene

176 We present a drug delivery system for the GI tract based on coating standard gelatin drug capsules

177 quantified in CD4+ T cells derived from the GI tract and PB by using real-time PCR.

178 There is evidence that signals from the GI tract are modulated by long term changes in diet, pos

179 stant stream of interoceptive input from the GI tract, integrates this information with other interoc

180 eption of interoceptive information from the GI tract, or recall of interoceptive memories of such in

181 erstanding of drug-lipid interactions in the GI tract and exploitation of such interactions to achiev

182 iated with severe, irreparable damage in the GI tract and extremely low survival.

183 OR is crucial for T-cell accumulation in the GI tract and for establishing local adaptive immunity ag

184 m particulate gels can persist longer in the GI tract and may be useful in inducing satiety and thus

185 elial cells can provide CFTR activity in the GI tract and nasal epithelium of recipient cystic fibros

186 Infectious organisms produced in the GI tract and reaching the rectum may then chronically co

187 improve delivery to particular sites in the GI tract are discussed.

188 cificity not determined) was detected in the GI tract as early as 18 days postinfection.

189 neurotoxin from proteolytic digestion in the GI tract as well as from adverse environmental condition

190 d proliferating T cells were detected in the GI tract compared to the PB, and a robust cytotoxic resp

191 ut the ecological role of enterococci in the GI tract consortia.

192 evidence that motor neurotransmission in the GI tract does not occur through poorly defined structure

193 n regulating the inflammatory process in the GI tract during aGVHD are needed.

194 rapies that might restore homeostasis in the GI tract during GVHD are highlighted.

195 indolent clonal T-cell proliferations in the GI tract have been described.

196 n peripheral vagal afferent processes in the GI tract modulate responsiveness to GI stimuli.

197 ere is significant loss of Th17 cells in the GI tract of HIV-infected patients; (5) Th17 cells are no

198 its target genes, the FDG-PET signal in the GI tract of these mice is abolished by rapamycin treatme

199 investigators that lactobacilli found in the GI tract originate in the oral cavity by proposing that

200 The use of low-frequency ultrasound in the GI tract represents a novel tool for the delivery of a w

201 about the oral properties of stimuli in the GI tract suggests a new account of delayed taste aversio

202 ucture between different biopsy sites in the GI tract than 8 primary therapy-responsive patients.

203 ) is an important metabolite for EHEC in the GI tract, and EA is also a signal that EHEC uses to acti

204 ificant influence over tumor location in the GI tract, and that both cecal and duodenal tumors initia

205 for pacemaker current and slow waves in the GI tract, but the precise mechanism of electrical rhythm

206 distribution, and thus drug delivery, in the GI tract, including to ulcerated tissues.

207 tunities for targeting specific sites in the GI tract, increasing drug solubility and bioavailability

208 es EA and choline, which are abundant in the GI tract, promoted expression of these fimbriae.

209 In the GI tract, the microbiota express beta-glucuronidase enzy

210 sion on distribution of nanoparticles in the GI tract, we orally and rectally administered nano- and

211 nd establish a long-lasting infection in the GI tract.

212 Amyloid was also detected in the GI tract.

213 on by nucleases, which are ubiquitous in the GI tract.

214 P-A in regulating the immune response in the GI tract.

215 1-associated food allergy manifesting in the GI tract.

216 n-associated food allergy manifesting in the GI tract.

217 on of effector or regulatory response in the GI tract.

218 ta-cells and incretin releasing cells in the GI tract.

219 s of dendritic cells and CD4+ T cells in the GI tract.

220 d limiting type 1 cytokine production in the GI tract.

221 ormal as well as in neoplastic tissue in the GI tract.

222 e important physiological role of ICC in the GI tract.

223 atients, including 3.8% with bleeding in the GI tract.

224 lity, and providing sustained release in the GI tract.

225 aded by the large amount of proteases in the GI tract.

226 and structural abnormalities persist in the GI tract.

227 nisms, focusing on defense mechanisms in the GI tract.

228 s in mammals and the microbes inhabiting the GI tract.

229 cells, leading to their emigration into the GI tract where they mediate fulminant disease.

230 ia in neurological diseases that involve the GI tract.

231 patients develop megasyndromes involving the GI tract, in particular, the esophagus and the colon.

232 in the stomach (37%) versus the rest of the GI tract ( approximately 10%), and catecholamine neurons

233 ssary to recast our conceptualization of the GI tract and its resident microbial communities in ecolo

234 3%) were restricted to a few segments of the GI tract and two were not expressed in any segment.

235 tanding of the anatomy and physiology of the GI tract by focusing on the ENS and the mucosal immune s

236 A breach of the epithelial barrier of the GI tract can result in local and eventually systemic dis

237 Inflammation of the GI tract causes marked changes in the release and extrac

238 em is optimized to assure homeostasis of the GI tract during physiological perturbations and to adapt

239 ments aimed at augmenting restoration of the GI tract hold promise in returning cART recipients to fu

240 his suggests that nutrient activation of the GI tract may potentiate learning about nonnutritive flav

241 n in peripheral blood, reconstitution of the GI tract occurs at a much slower pace, and both immunolo

242 re among the most challenging cancers of the GI tract to treat, associated with poor median survivals

243 on can readily be applied to any area of the GI tract within any species, including humans.

244 We propose the name "indolent T-LPD of the GI tract" for these lesions that can easily be mistaken

245 nhances Candida albicans colonization of the GI tract, a risk factor for haematogenously-disseminated

246 omote crypt hyperplasia and neoplasia of the GI tract, and Hic1(+/-), Apc(+/Delta716) double heterozy

247 l taxa present in different locations of the GI tract, and their specific metabolic features.

248 failed to develop in various regions of the GI tract, but no major changes in the smooth muscle laye

249 olid malignancies, especially cancers of the GI tract, cervix, and head and neck.

250 The bacterial microbiome of the GI tract, including lactic acid bacteria (LAB), plays a

251 In this region of the GI tract, the protective mucus barrier is poorly develop

252 ew, we focus on the tubular structure of the GI tract, tools for innervation, and, finally, evaluatio

253 in found in Lactobacillus inhabitants of the GI tract.

254 d thereby regulate the motor function of the GI tract.

255 ovine rumen but absent in other areas of the GI tract.

256 the visceral mesoderm in the ontogeny of the GI tract.

257 hin various regions and tissue layers of the GI tract.

258 ppress eosinophilic inflammation outside the GI tract.

259 Several different cell types populate the GI tract, adding to the complexity of cell sourcing for

260 accomplish these many and varied tasks, the GI tract relies on endogenous enteric hormones produced

261 Collectively, these data confirm that the GI tract is a key player in the immunopathogenesis of HI

262 suggests that allergen exposure through the GI tract induces tolerance.

263 716)) develop multiple polyps throughout the GI tract as early as 4 weeks after birth.

264 p increased numbers of polyps throughout the GI tract at 60 days.

265 rplasia in all classes of ICC throughout the GI tract of Kit(V558Delta)/+ mice, except for ICC in the

266 unique and diverse physiology throughout the GI tract, including wide variation in pH, mucus that var

267 had exon 19 deleted from Rb1 throughout the GI tract.

268 plasia of most classes of ICC throughout the GI tract.

269 vity, and disease progression throughout the GI tract.

270 These contribute to structural damage to the GI tract and systemic translocation of GI tract microbia

271 did not induce hydrosalpinx or spread to the GI tract even when delivered to the oviduct by intraburs

272 Delivery of luciferase plasmid to the GI tract in TNFDeltaARE mice was achieved by insonating

273 in vivo, and induce T cell migration to the GI tract in vivo.

274 accelerated the chlamydial spreading to the GI tract.

275 ucosal tissues to recruit lymphocytes to the GI tract.

276 (1) the patterns of biodiversity within the GI tract and (2) the scales of time, space, and environm

277 impervious to chemical conditions within the GI tract and is completely melted within two minutes whe

278 Localized molecules within the GI tract were then identified in situ by surface samplin

279 s safely and effectively anywhere within the GI tract.

280 onse back to various target cells within the GI tract.

281 esentation and cytokine secretion within the GI tract.

282 We investigated the fungal burdens in the GI tracts of germfree mice and mice with a disturbed mic

283 t strains because of their occurrence in the GI tracts of insects and simple organisms living and fee

284 we paraffin embedded and then sectioned the GI tracts of infected mice at various days postinfection

285 organisms spreading from the genital to the GI tracts were detected in different mouse strains and a

286 Upon crossing the GI-tract (125)I-PrP(Sc) became associated to blood cells

287 f IL-22-producing RORgammat(+) ILCs in their GI tract.

288 lucose utilization in focal regions of their GI tract corresponding to these gastrointestinal hamarto

289 xt dependent, p53-induced activation of this GI tract-specific miRNA during ischemia could promote an

290 the chlamydial spreading from the genital to GI tracts is discussed.

291 were sutured on the serosal surface of upper GI tract to record the circular muscle contractions in e

292 GI bleeding events occurred in the upper GI tract (48%), lower GI tract (23%), and rectum (29%) w

293 served in most neurons innervating the upper GI tract (fundus, 97%; corpus, 95%; duodenum, 98%).

294 isk of late-onset complications of the upper GI tract (rate ratio [RR], 1.8; 95% confidence interval

295 wise, most neurons that innervated the upper GI tract expressed NR2B-IR (fundus, 98%; corpus, 85%; du

296 y spinal afferent nerve endings in the upper GI tract of mice.

297 ogical, and endoscopic findings of the upper GI tract on 201 patients who underwent allogeneic hemato

298 tion of spinal afferent endings in the upper GI tract.

299 in 897 consecutive patients undergoing upper GI tract endoscopy.

300 mean plasma CMV copy number in patients with GI tract disease was 3.84 log10 (38 334 copies/mL).