ライフサイエンスコーパス: gluten

1 ing wheat gluten (oral challenge) or without gluten.

2 etention capacity (WRC) of WU-AX compared to gluten.

3 in addition to genetic variants and dietary gluten.

4 s in modulating the epithelium's response to gluten.

5 nt but increased the beta-sheet structure of gluten.

6 used to modulate the epithelial response to gluten.

7 by an inappropriate immune reaction against gluten.

8 3 and 19.5) to investigate how PA polymerize gluten.

9 hat may promote loss of tolerance to dietary gluten.

10 develops villous atrophy after ingestion of gluten.

11 acterized by autoimmune reactions to dietary gluten, affects up to 3 million in the US and approximat

12 total flour weight basis) to modify semolina gluten aggregation reactions in dough production and pas

13 sease (CeD) is triggered by the ingestion of gluten, although the relative roles of genetic and envir

14 The reliability and comparability of gluten analytical results in gluten-free foods is hamper

15 f serologic testing to determine exposure to gluten and accuracy of test results.

16 of T helper 1 (TH1) immunity against dietary gluten and celiac disease (CeD).

17 onobese diabetic/DQ8 mice were sensitized to gluten and fed an ATI diet, a gluten-containing diet or

18 st time the mineral bioavailability from the gluten and gluten-free flakes was evaluated and compared

19 erent chemical compounds on conformations of gluten and its subunits.

20 Celiac disease (CD) is triggered by gluten and related prolamines in genetically susceptible

21 tive interactions between BFLs and starch or gluten and relocated more lipids than did hex.

22 morphological, and rheological properties of gluten and their subunits were studied.

23 rm rye bread, endosperm rye bread with added gluten and wheat bread.

24 complexity, model systems containing starch, gluten and/or water-unextractable arabinoxylan (WU-AX) w

25 tein, dietary fiber, containing less fat and gluten, and enriched with lactic acid, vitamins, and min

26 samples used for the prediction of protein, gluten, and moisture content.

27 zed(3), but no pathophysiologically relevant gluten- and HLA-dependent preclinical model exists.

28 This article provides an overview of gluten- and wheat-related disorders.

29 disease (CD), dermatitis herpetiformis (DH), gluten ataxia (GA), wheat allergy (WA), and non-celiac g

30 e 1, and TG6 in gluten axonal neuropathy and gluten ataxia.

31 me polyglandular syndrome type 1, and TG6 in gluten axonal neuropathy and gluten ataxia.

32 materials were included in this study, both gluten (barley, rye, spelt, wheat) and gluten-free (amar

33 Practice Advice 7: Reduction or avoidance of gluten before diagnostic testing is discouraged, as it m

34 disease or other enteropathies unrelated to gluten, but negative results from serologic tests.

35 rom patients with celiac disease who consume gluten, but not from patients on gluten-free diets.

36 Therefore, chemical modification of gluten can be mainly conducted via acylation, glycosylat

37 s have been reported regarding the effect on gluten celiac-immunotoxicity.

38 evere villous atrophy at baseline received a gluten challenge (2-4 g daily) during weeks 2-12.

39 49 patients underwent the gluten challenge (per-protocol 1 population) and 11 pati

40 distinction between paired baseline and post-gluten challenge biopsies as quantitative histomorphomet

41 preliminary framework for rational design of gluten challenge for CeD research.

42 Gluten challenge is used to diagnose celiac disease (CeD

43 istologic and molecular markers suitable for gluten challenge studies can be obtained from a single p

44 in patients with coeliac disease undergoing gluten challenge, was not significantly different betwee

45 ble-blind crossover, placebo-controlled oral gluten challenge, which had a fixed sequence, and biopsy

46 All assessments showed changes with gluten challenge.

47 MG 714 did not prevent mucosal injury due to gluten challenge.

48 patients with coeliac disease who underwent gluten challenge.

49 one dose of study drug and who underwent the gluten challenge.

50 rioration in all coeliac disease patients on gluten challenge.

51 tative histology within 2 weeks without oral gluten challenge.

52 blood and central nervous system, similar to gluten-challenge studies of patients with coeliac diseas

53 In this randomized, double-blind, 2-dose gluten-challenge trial conducted in 2 US centers (Boston

54 l epitopes were inefficient at taking up TG2-gluten complexes for presentation to gluten-specific T c

55 to be explored in dough systems with reduced gluten concentration.

56 ase autoimmunity for every 1-g/d increase in gluten consumption (hazard ratio [HR], 1.30 [95% CI, 1.2

57 f celiac disease for every 1-g/d increase in gluten consumption (HR, 1.50 [95% CI, 1.35-1.66]; absolu

58 eased nutritional quality as compared to the gluten containing counterparts.

59 tudy was to provide new approach in creating gluten-containing and gluten-free breads without additiv

60 Gluten-containing cereals have by far the highest concen

61 um of conditions induced by the ingestion of gluten-containing cereals, have been increasing in preva

62 sensitized to gluten and fed an ATI diet, a gluten-containing diet or a diet with ATIs and gluten fo

63 al villous atrophy while the patient is on a gluten-containing diet, along with findings from serolog

64 small intestinal mucosal histology during a gluten-containing diet.

65 disease (based on anti-TG2 and anti-EMA) on gluten-containing diets, the cumulative incidence of pro

66 ry status of fermented products derived from gluten-containing grains for patients with celiac diseas

67 The gluten content in semolina flour determined with the che

68 sy-proven CeD were randomized to 3 g or 10 g gluten/d for 14 days.

69 Gluten deamidation by human tissue transglutaminase is c

70 sing gliadin was compared with that of other gluten-degrading enzymes.

71 models 1 and 2), ear swelling (in model 1), gluten-dependent enteropathy (in model 3), and body weig

72 Gluten-derived peptides accounted for approximately 50%

73 uten sensor that integrates food processing, gluten detection, result interpretation and data transmi

74 nd gives new insights into the complexity of gluten digestion from a physiologically relevant food ma

75 ainly made up by protein from non-repetitive gluten domains.

76 ime to maximal change, change magnitude, and gluten dose-response relationship varied.

77 kers to assess disease activity induced by 2 gluten doses, and aimed to identify biomarkers to supple

78 complex of HLA-DQ2.5 and the immunodominant gluten epitope DQ2.5-glia-alpha1a using phage display.

79 ccounts for HLA-DQ2.2 additionally requiring gluten epitopes possessing a serine at the P3 position o

80 t and highly homologous HLA-DQ2.5-restricted gluten epitopes, DQ2.5-glia-alpha1a (PFPQPELPY) and DQ2.

81 esponses against these two highly homologous gluten epitopes.

82 mized trials, but the quantity of early-life gluten exposure has been a major focus of prevention eff

83 ecially convenient approach to assess recent gluten exposure in celiac patients and appears to accura

84 Sustained gluten exposure reliably induces histologic changes but

85 Celiac disease is provoked by gluten exposure, but the complete pathogenic process in

86 n biomarkers are sensitive and responsive to gluten exposure, potentially allowing less invasive, low

87 ally indicates ongoing intestinal damage and gluten exposure.

88 is an immune-mediated disorder triggered by gluten exposure.

89 the earliest, most sensitive marker of acute gluten exposure.

90 pect to both the PQQPFPQQ analyte and a real gluten extract from semolina flour.

91 uten-containing diet or a diet with ATIs and gluten for 2 weeks.

92 This allows for the use of gluten for a variety of purposes in the food and non-foo

93 inefficiency as a treatment to detoxify the gluten for celiac disease patients.

94 torage proteins, collectively referred to as gluten, found in wheat (Triticum aestivum).

95 iation of water with the starch-fraction and gluten-fraction in doughs, and this effect was cultivar-

96 nulin can improve the nutritional quality of gluten free (GF) bread and have a prebiotic activity.

97 both gluten (barley, rye, spelt, wheat) and gluten-free (amaranth, buckwheat, corn, quinoa, millet,

98 ration coupled with adequate water levels on gluten-free (GF) batter rheology, bread quality and sens

99 f the addition of onion waste fractions into gluten-free (GF) bread to promote its health benefits.

100 Gluten-free (GF) breads often lack proteins, minerals an

101 The interest in gluten-free (GF) products increases together with the in

102 value sufficient for discriminating between gluten-free and non-gluten-free food products.

103 aining diet compared with mice that were fed gluten-free and thus ATI-free diet.

104 Gluten-free bread was fortified with modified dietary fi

105 e used as an alternative food ingredient for gluten-free bread.

106 Gluten-free breads were harder, less elastic with more g

107 w approach in creating gluten-containing and gluten-free breads without additives by combining therma

108 perties and in vitro starch digestibility of gluten-free cakes of brown, black, and red rice, as well

109 d beverages, such as functional products and gluten-free cereals, thereby providing extra health bene

110 sed in designing value-added traditional and gluten-free cookies.

111 , CM and CF are interesting alternatives for gluten-free cracker formulation.

112 A gluten-free diet (GFD) is the only effective treatment f

113 eatment of celiac disease (CD) is a lifelong gluten-free diet (GFD).

114 s a confirmatory test before initiation of a gluten-free diet (GFD).

115 esult of disease and/or its treatment with a gluten-free diet (GFD).

116 While typically managed by gluten-free diet and dapsone, treatment of DH refractory

117 nosis of coeliac disease, and adherence to a gluten-free diet for at least 12 months before screening

118 ctive to or replacing a burdensome life-long gluten-free diet for coeliac disease.

119 isorders, and they should remain on a strict gluten-free diet indefinitely.

120 A strict, lifelong gluten-free diet is the only treatment.

121 ed celiac disease should immediately start a gluten-free diet or be monitored on their regular diet.

122 o endoscopic evaluation after 1-3 years on a gluten-free diet to evaluate improvements in villous atr

123 ct is particularly important for people on a gluten-free diet who often represent mineral deficiencie

124 in diagnosis to be made in the context of a gluten-free diet without intestinal biopsy.

125 with celiac disease (35 untreated and 5 on a gluten-free diet) as well as 18 subjects with confirmed

126 5 patients with treated celiac disease (on a gluten-free diet), as well as 43 individuals without cel

127 n = 81; villous atrophy despite a adhering a gluten-free diet), patients with untreated CeD (n = 82)

128 t signs and symptoms who do not respond to a gluten-free diet, and for whom no etiology of enteropath

129 lenge of 59 individuals on a self-instituted gluten-free diet, for whom celiac disease had been exclu

130 c alternative other than the observance of a gluten-free diet.

131 rds the development of an alternative to the gluten-free diet.

132 e aimed to be a potential alternative to the gluten-free diet.

133 and histologic markers of improvement on the gluten-free diet.

134 ent for coeliac disease is a lifelong strict gluten-free diet; however, the diet is restrictive and g

135 ter COVID-19 can impact on CeD treatment and gluten-free dieting, the only available therapy for CeD.

136 who consume gluten, but not from patients on gluten-free diets.

137 king, were analyzed and compared to standard gluten-free doughs.

138 Novel gluten-free extruded foods (composed of rice: 50-80%, be

139 rated into a range of foodstuffs, especially gluten-free flakes and extruded products.

140 mineral bioavailability from the gluten and gluten-free flakes was evaluated and compared.

141 In this work, 18 gluten-free flours (prepared from cereals, pseudocereals

142 These findings highlight that gluten-free flours are able to deliver bioaccessible pol

143 r discriminating between gluten-free and non-gluten-free food products.

144 disease, and more widespread availability of gluten-free food.

145 omparability of gluten analytical results in gluten-free foods is hampered by the lack of reference m

146 he use of sprouted oat powder as a promising gluten-free functional ingredient.

147 ating that cricket powder provides to bakery gluten-free goods high nutritional value proteins and an

148 is aimed to produce and characterize a novel gluten-free ingredient from oat through sprouting at 18

149 Acorn flour was used as a gluten-free ingredient to produce acorn muffins.

150 characteristics of commercial pasta to fresh gluten-free pasta from proso millet varieties differing

151 The utilization of proso millet in gluten-free pasta is promising, however, processing opti

152 The demand for gluten-free products has been growing over the last few

153 and corn as ingredients for whole grain and gluten-free products.

154 t the shelf life of an experimental batch of gluten-free rusks with a lower content of antioxidant.

155 ug/kg), correlated with rancid perception in gluten-free rusks, was also speculated.

156 to develop a shelf life prediction model of gluten-free rusks.

157 great potential in the development of novel gluten-free snacks that are healthier than traditional s

158 ge (CM) and cladode flour (CF) for producing gluten-free snacks.

159 this work, cricket flour was used to produce gluten-free sourdough breads, suitable for celiac people

160 plantain flour exhibited good potential for gluten-free spaghetti having highest content of fiber an

161 rice and maize flours for the production of gluten-free sponge cakes.

162 im of this paper was to assess the impact of Gluten-Friendly (GF) technology (Italian priority patent

163 olating recombinant phage-antibodies against gluten from a non-immunized library of human single-doma

164 y reflecting the complex interaction between gluten, genetics and IL-15-driven tissue inflammation, t

165 microstructure of dough by the inclusion of gluten, glutenin and LMW-GS, which lacks resemblance amo

166 rties of base flour dough by the addition of gluten, glutenin and purified low molecular weight glute

167 crowave heating of wheat kernels, flour, and gluten, has attracted attention lately because it has be

168 en accurate and scalable, assays that detect gluten-HLA tetramer complexes might be used in diagnosis

169 Detoxification of gluten immunogenic epitopes is a promising strategy for

170 In vivo, gluten immunogenic epitopes were decreased by 60% in the

171 o determine the clinical usefulness of urine gluten immunogenic peptides (GIP) as a biomarker monitor

172 of this method to achieve the measurement of gluten in food samples, after the extraction with pure e

173 most appropriate clone for the detection of gluten in foods (dAb8E-phage) was further applied in an

174 that allow a comprehensive determination of gluten in foods, whilst replacing the need for animal im

175 rrently the most popular methods to quantify gluten in foods.

176 d by an immune-mediated reaction to ingested gluten in genetically susceptible persons.

177 Moreover, it was capable of determining gluten in real samples in the concentration range of 4-2

178 ild-type mice and exacerbate inflammation to gluten in susceptible mice.

179 dwich-based sensor for the quantification of gluten in the DES ethaline.

180 eased intestinal inflammation in response to gluten in the diet.

181 pted efforts to identify methods of lowering gluten in wheat, one of the most important cereal crops.

182 inosa producing elastase as a model, we show gluten-independent, PAR-2 mediated upregulation of infla

183 posure to dietary antigen can be controlled, gluten-induced inflammation triggered a profound depleti

184 ake (from 75% to 94%) and with biomarkers of gluten ingestion.

185 less invasive, lower-dose, shorter-duration gluten ingestion.

186 High gluten intake during childhood may confer risk of celiac

187 Higher gluten intake during the first 5 years of life was assoc

188 gluten was consumed, 20.7%; absolute risk if gluten intake was 1-g/d higher than the reference amount

189 gluten was consumed, 28.1%; absolute risk if gluten intake was 1-g/d higher than the reference amount

190 Daily gluten intake was associated with higher risk of celiac

191 Daily gluten intake was associated with higher risk of celiac

192 Gluten intake was estimated from 3-day food records coll

193 Data on gluten intake were available in 6605 children (98%) by S

194 e diet; however, the diet is restrictive and gluten is difficult to avoid.

195 in the duodenum and the loss of tolerance to gluten is not well understood.

196 mance allows the quantification of 20 mug of gluten/kg of food when 1 g of food is extracted with 10

197 with that determined with a commercial ELISA gluten kit.

198 The ingestion of gluten leads to the generation of harmful gluten peptide

199 assay is useful for the analysis of residual gluten levels in foods, thus facilitating the evaluation

200 This is complemented with a Gluten-like repeat pattern detection.

201 the dough strength in the order of LMW-GS < gluten < glutenin.

202 This analysis suggests immunogenic gluten may peak within the intestinal duodenum and gives

203 edients including sunflower meal (SFM), corn gluten meal (CGM), and dried distillers' grains with sol

204 The changes in gluten molecular conformation and network structure indu

205 ic peptide comprising repetitive immunogenic gluten motifs.

206 ysis were used to investigate changes in the gluten network arrangement as affected by the microwave

207 granules of soft wheat flour and reduces its gluten network forming capacity and apparent content of

208 The resultant thermoset gluten network in bread crumb is mainly made up by prote

209 interactions and larger cavities within the gluten network, both caused by starch swelling.

210 erall, Pembina was found to develop stronger gluten networks that were more resilient than those of H

211 or selective determination of an immunogenic gluten octamer epitope, PQQPFPQQ.

212 ed significant changes from baseline at 10 g gluten only; symptoms were significant at 3 g.

213 with an AIN-76A-based diet containing wheat gluten (oral challenge) or without gluten.

214 dant cell type presenting the immunodominant gluten peptide DQ2.5-glia-alpha1a in the tissues from th

215 We used these mAbs to assess gluten peptide presentation and phenotypes of presenting

216 s of gluten proteins and digestion-resistant gluten peptides (synthetic 33-mer peptide and pentapepti

217 e and kinetic release pattern of immunogenic gluten peptides in a physiologically relevant food matri

218 response of CD4(+) T cells toward deamidated gluten peptides in the intestinal mucosa of individuals

219 xpresses B-cell receptors (BCR) specific for gluten peptides or the autoantigen transglutaminase 2 (T

220 isease is an autoimmune illness activated by gluten peptides produced during gastrointestinal digesti

221 enesis of celiac disease (CeD) by presenting gluten peptides to CD4(+) T cells.

222 The release profile of six gluten peptides was defined by quantitative LC-MS/MS; no

223 and the deamidation state of six immunogenic gluten peptides within bread was investigated.

224 of gluten leads to the generation of harmful gluten peptides, which, in predisposed individuals, can

225 on of mTG to bread does not create activated gluten peptides.

226 disease patients were challenged with 4 g of gluten per day for 10 weeks and 24 non-coeliac patients

227 immune-mediated enteropathy against dietary gluten present in wheat, rye and barley and is one of th

228 Gluten protein as one of the plant resources is suscepti

229 composition, protein secondary structure or gluten protein composition.

230 tment on hydrated durum wheat kernels blocks gluten protein conformation through SS bonds formation a

231 lease by Aq1 of peptides from the repetitive gluten protein domains during baking.

232 15) on wheat kernel endosperm morphology and gluten protein structure, using SEM, light and immunoflu

233 ines and chaperones, notably involved in the gluten-protein folding process, were up-regulated in sup

234 protease in kiwifruit, on the hydrolysis of gluten proteins and digestion-resistant gluten peptides

235 d herbicide timing on the chemistry of wheat gluten proteins and shikimic acid accumulation.

236 transmission in a portable device, detecting gluten proteins at or below the accepted 20 ppm threshol

237 ed similar changes in secondary structure of gluten proteins concerning formation of aggregates (1604

238 cterized by a breakdown of oral tolerance to gluten proteins in genetically predisposed individuals,

239 potential to strongly reduce the ability of gluten proteins to stimulate a T-cell-mediated immune re

240 mmune responses, but the contribution of non-gluten proteins to symptoms in patients with celiac dise

241 Actinidin is able to hydrolyse gluten proteins under simulated gastric conditions.

242 transglutaminase-catalysed transamidation of gluten proteins using ethylamine as amine nucleophile, s

243 The gastric degree of hydrolysis of gluten proteins was influenced by an interaction between

244 ry autoimmune disease caused by ingestion of gluten proteins, mainly gliadin.

245 ith the usual solvents for the extraction of gluten proteins.

246 t enhanced the macromolecular aggregation of gluten proteins.

247 stricted responses of CD4+ T cells to cereal gluten proteins.

248 scosity, swelling characteristics as well as gluten proteins; it removes the sulfhydryl group and lea

249 The protein content, gluten quantity and quality found to be reduced in high

250 credence to a model of celiac disease where gluten-reactive T cells provide help to autoreactive TG2

251 The incidence of gluten-related disorders (GRDs) continues to increase an

252 In this review, the current definitions of gluten-related disorders, focusing on their clinical fea

253 Gluten-related disorders, including celiac disease, whea

254 food by people with celiac disease or other gluten-related disorders.

255 r characterized by a variable combination of gluten-related signs and symptoms and disease-specific a

256 y T (Treg) cells in the loss of tolerance to gluten remains poorly understood.

257 Exclusion of dietary gluten restored BTNL8 expression but was insufficient to

258 Gluten's structure was altered when mTG exceeded 100 U.k

259 he ability of mTG (0-2000 U.kg(-1)) to alter gluten's structure, digestibility and the deamidation st

260 Gluten secondary structure was affected by the microwave

261 portable gluten testing device would enable gluten-sensitive individuals to safeguard their food saf

262 ucts increases together with the increase in gluten-sensitive people.

263 (+) IELs was accompanied by the expansion of gluten-sensitive, interferon-gamma-producing Vdelta1(+)

264 xia (GA), wheat allergy (WA), and non-celiac gluten sensitivity (NCGS) are the five major GRDs that p

265 celiac disease, wheat allergy, and nonceliac gluten sensitivity (NCGS), are increasingly reported wor

266 ase and a related condition called nonceliac gluten sensitivity is increasing.

267 Administration of ATIs to gluten-sensitized mice expressing HLA-DQ8 increased inte

268 We developed a novel solution, Nima(TM), a gluten sensor that integrates food processing, gluten de

269 emical analyses, which affects the choice of gluten source to be applied for RM production.

270 ial leukocyte counts, and HLA-DQ2-restricted gluten-specific CD4 T cells showed significant changes f

271 ry and RNA sequencing analysis, we find that gluten-specific CD4(+) T cells in the blood and intestin

272 des that include immunodominant epitopes for gluten-specific CD4-positive T cells.

273 Additional end points included gluten-specific cluster of differentiation (CD)4 T-cell

274 Patients with celiac disease have gluten-specific immune responses, but the contribution o

275 up TG2-gluten complexes for presentation to gluten-specific T cells.

276 ain antigen-presenting cells for pathogenic, gluten-specific T cells.

277 In dough prepared from gluten-starch blends (GSB) differing in PIN levels, PINs

278 Final viscosity, gluten strength, extensibility, and falling number exhib

279 lutenin of gluten were analyzed to elucidate gluten structure changes induced by salt.

280 and the effect of the microwave treatment on gluten structure, conformation, functionality and celiac

281 have increased proteolytic activity against gluten substrates that correlates with increased Proteob

282 onomic, simple, accurate, rapid and portable gluten testing device would enable gluten-sensitive indi

283 entiation (CD)4 T-cell analysis with HLA-DQ2-gluten tetramers and enzyme-linked immune absorbent spot

284 Combining HLA-DQ-gluten tetramers with mass cytometry and RNA sequencing

285 ctive TG2-specific B cells by involvement of gluten-TG2 complexes, and they outline a general mechani

286 ry enteropathy caused by exposure to dietary gluten that occurs in a subset of genetically susceptibl

287 Gluten, the major protein component of wheat, did not in

288 enes, P. aeruginosa elastase synergizes with gluten to induce more severe inflammation that is associ

289 anding of the early steps leading to loss of gluten tolerance.

290 ately because it has been claimed to abolish gluten toxicity for celiac patients.

291 in coeliac disease patients challenged with gluten using PAXgene fixed paraffin-embedded biopsies.

292 rmine the efficacy and safety of vital wheat gluten (VWG) oral immunotherapy (OIT).

293 A simulated in vitro digestion of gluten was conducted to define the profile and kinetic r

294 by age of 3 years if the reference amount of gluten was consumed, 20.7%; absolute risk if gluten inta

295 he age of 3 years if the reference amount of gluten was consumed, 28.1%; absolute risk if gluten inta

296 ological point of view, the functionality of gluten was retained.

297 ure, and extractable gliadin and glutenin of gluten were analyzed to elucidate gluten structure chang

298 ce were placed on diets that lacked wheat or gluten, with or without wheat amylase trypsin inhibitors

299 In a starch-gluten-WU-AX-water model and in wheat flour, water was d

300 X did not affect the water distribution in a gluten-WU-AX-water system, despite the higher water rete