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 udy to visualize Pb dynamics in the lung and GI tract using XRF microscopy and link the inhalation an

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

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

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

8 Examining the chicken GI tract with immunofluorescence microscopy demonstrates

9 CMV GI tract disease was defined as histopathologic evidence

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

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

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

13 ins permissive of migration into the damaged GI tract, resulting in the lethal feed-forward cascade o

14 ishment of vegetative bacteria in the distal GI tract.

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

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

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

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

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

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

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

22 Gastrointestinal (GI) tract involvement is the major cause of morbidity an

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

26 ess is severely limited by gastrointestinal (GI) tract toxicity caused by gut bacterial beta-glucuron

27 characteristics of the CF gastrointestinal (GI) tract, including inflammation, maldigestion and mala

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

29 c acid (LCA) to facilitate gastrointestinal (GI) tract colonization.

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

31 ion of NIR-II emitters for gastrointestinal (GI) tract imaging remains challenging due to fluorescenc

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

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

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

35 er-metabolism in the human gastrointestinal (GI) tract and respiratory system are largely unknown and

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

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

38 ome varies along the human gastrointestinal (GI) tract with exposure to luminal and mucosal factors.

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

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

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

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

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

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

45 inked to the disruption of gastrointestinal (GI) tract epithelial barrier integrity and subsequent mi

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

47 The gastrointestinal (GI) tract (GIT) holds significant potential as a target

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

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

50 ion and progression in the gastrointestinal (GI) tract and associated organs.

51 DNA shed from cells of the gastrointestinal (GI) tract and has great potential as a bio-specimen for

52 phil infiltration into the gastrointestinal (GI) tract and is characterized by various digestive symp

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

54 many of which involve the gastrointestinal (GI) tract and liver.

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

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

57 rial composition along the gastrointestinal (GI) tract and to assess SIBO in IBS.

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

59 hways mutation rate in the Gastrointestinal (GI) tract cancers in a systematic review and meta-analys

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

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

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

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

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

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

66 and poor absorption in the gastrointestinal (GI) tract generally limit their administration to parent

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

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

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

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

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

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

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

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

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

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

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

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

79 The gastrointestinal (GI) tract is the primary site of copper entry into the b

80 host disease (GVHD) in the gastrointestinal (GI) tract is the principal determinant of lethality foll

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

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

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

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

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

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

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

88 atory mediator that in the gastrointestinal (GI) tract plays a physiological role in gut-brain signal

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

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

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

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

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

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

95 The gastrointestinal (GI) tract was the most common site of increased major bl

96 The key sites within the gastrointestinal (GI) tract where T cells mediate effector responses and t

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

98 zed by inflammation of the gastrointestinal (GI) tract, and it is associated with different neurologi

99 yos, adult brains, and the gastrointestinal (GI) tract, and many cancers, including epithelial GI tum

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

101 transmitter signals in the gastrointestinal (GI) tract, facilitating normal motility patterns.

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

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

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

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

106 imarily synthesized in the gastrointestinal (GI) tract, where it is secreted into the lumen and subse

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

108 reatment of lesions in the gastrointestinal (GI) tract.

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

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

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

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

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

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

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

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

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

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

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

120 crobial communities in the gastrointestinal (GI) tract.

121 , frequently affecting the gastrointestinal (GI) tract.

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

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

124 paracrine mediators in the gastrointestinal (GI) tract.

125 crobial species within the gastrointestinal (GI) tract.

126 ), particularly within the gastrointestinal (GI) tract.

127 e periphery, including the gastrointestinal (GI) tract.

128 s upon passage through the gastrointestinal (GI) tract.

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

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

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

132 ted in the respiratory and gastrointestinal (GI) tracts.

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

134 edictability of drug absorption in the human GI tract than a Caco-2 Transwell system (Spearman's corr

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

136 he capacity to elaborate Tff2 did not impact GI tract integrity or the thickness of the small-intesti

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

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

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

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

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

142 lity, showing >50-fold higher sensitivity in GI tract, and migrated homogenously during gastrointesti

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

144 wn to partially alleviate irinotecan-induced GI tract damage and resultant diarrhea in mice.

145 particles in the lung and gastro-intestinal (GI) tract were visualized using X-ray fluorescence (XRF)

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

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

148 Upper and lower GI tract endoscopic examinations found no bleeding.

149 /- 12.3 years) who underwent upper and lower GI tract endoscopy in Germany from December 2015 through

150 elayed bleeding after EMR of upper and lower GI tract lesions.

151 8-12/2018 for lesions in the upper and lower GI tract.

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

153 section procedures of the upper and/or lower GI tract in 6 patients in 2 endoscopy centers.

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

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

156 2 innate lymphoid cells (ILC2s) in the lower GI tract are sensitive to conditioning therapy and show

157 tinomyces) were almost absent from the lower GI tract, where the microbial communities mainly compris

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

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

160 y the Shannon index) than those in the lower GI tract.

161 l consortia in saliva, upper GI tract, lower GI tract, and fecal samples.

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

163 Lesions in upper and lower GI tracts that underwent EMR between January 2012 and De

164 at dysplastic mucosal lesions of the luminal GI tract can be challenging.

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

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

167 ping microbial biogeography of the mammalian GI tract and more accurate analyses of changes in microb

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

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

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

171 f irradiated endothelial cells of the murine GI tract.

172 -negative bacteria, is present in the normal GI tract and levels increase during high-fat feeding and

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

174 is a promising target for the development of GI tract therapies, yet it has been under-exploited due,

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

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

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

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

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

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

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

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

183 The GI tract is also host to diverse bacterial populations,

184 al (GI) cancers, such as those affecting the GI tract, liver, and pancreas, on which this review is f

185 cterial communities at 8 locations along the GI tract using high-throughput sequencing techniques.

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

187 o electronics at various locations along the GI tract.

188 dysbiosis and epithelial dysplasia along the GI tract.

189 s from specialized endocrine cells along the GI tract.

190 ads in lumenal and mucosal samples along the GI tract.

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

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

193 pneumoniae can asymptomatically colonize the GI tract in immunocompetent mice and modifies the host G

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

195 iae isolate was able to translocate from the GI tract and cause hepatic infection that mimicked the r

196 ne increased major bleeding, mainly from the GI tract.

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

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

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

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

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

202 Subsequently, donor DCs in the GI tract are activated by DAMP/PAMP signals in the colon

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

204 ions due to impaired water absorption in the GI tract can be used as unique tracers to track the onse

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

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

207 ells and mediates pathological damage in the GI tract during GVHD.

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

209 revealed a host-microbial interaction in the GI tract involved in the regulation of copper transport.

210 the isotopic fractionation of copper in the GI tract of mice with intestinal microbiota significantl

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

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

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

214 complex, large mucosal-based lesions in the GI tract using standard endoscopic equipment and a novel

215 tor (IF), critical for B12 absorption in the GI tract via the cubilin receptor, could be used as a ta

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

217 ntigen-specific mucosal IgA responses in the GI tract, and enhanced antigen-specific IgG responses in

218 cretion and visceral hypersensitivity in the GI tract, and has been implicated in diseases such as ir

219 rod1 expression has not been examined in the GI tract, and it is not known whether Neurod1 can simila

220 a cytokine that mediates inflammation in the GI tract, but the transcriptional program that governs G

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

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

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

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

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

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

227 Amyloid was also detected in the GI tract.

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

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

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

231 and structural abnormalities persist in the GI tract.

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

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

234 1-associated food allergy manifesting in the GI tract.

235 s a nonredundant inflammatory pathway in the GI tract.

236 ing on the inhibition of APC function in the GI tract.

237 evented the initiation of lethal GVHD in the GI tract.

238 on IECs and initiation of lethal GVHD in the GI tract.

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

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

241 ia in neurological diseases that involve the GI tract.

242 emonstrate that during the disruption of the GI tract and increased microbial translocation, we find

243 3%) were restricted to a few segments of the GI tract and two were not expressed in any segment.

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

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

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

247 fection can influence the composition of the GI tract immune responses and its microbiome in the nonh

248 Endoscopic examination of the GI tract is necessary to exclude ulcers and polyps or ca

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

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

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

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

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

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

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

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

257 mon cause of foreign body perforation of the GI tract.

258 c target for preneoplastic conditions of the GI tract.

259 in found in Lactobacillus inhabitants of the GI tract.

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

261 ualization of the detailed structures of the GI tract.

262 nd samples per day) of whole segments of the GI tract.

263 to analyze the bacterial communities of the GI tract.

264 primary pacemaker conductance in ICs of the GI tract.

265 ppress eosinophilic inflammation outside the GI tract.

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

267 enteric adipose tissue (MAT) surrounding the GI tract.

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

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

270 vity, and disease progression throughout the GI tract.

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

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

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

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

275 accelerated the chlamydial spreading to the GI tract.

276 ucosal tissues to recruit lymphocytes to the GI tract.

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

278 Colonization density within the GI tract and levels of shedding in the feces differed am

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

280 sentation and pathological damage within the GI tract, positioning GM-CSF as a key regulator of GVHD

281 to growing microbial communities within the GI tract.

282 esentation and cytokine secretion within the GI tract.

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

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

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

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

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

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

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

290 istinct microbial consortia in saliva, upper GI tract, lower GI tract, and fecal samples.

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

292 The predominant genera in the upper GI tract (Gemella, Veillonella, Neisseria, Fusobacterium

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

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

295 The bacterial communities in the upper GI tract were characterized by greater richness and hete

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

297 tected Helicobacter pylori in only the upper GI tract.

298 in 897 consecutive patients undergoing upper GI tract endoscopy.

299 or or life-threatening, 48 (35.0%) was upper GI tract in origin, 43 (31.4%) was lower GI in origin, a

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