ライフサイエンスコーパス: gluten

1 milar elasticity and viscous flow balance to gluten.

2 atients mount an abnormal immune response to gluten.

3 s subsequently triggered by the ingestion of gluten.

4 ory disorder of the gut triggered by dietary gluten.

5 een for celiac disease in patients consuming gluten.

6 for their capability to detect and quantify gluten.

7 reatment abolishes the antigenic capacity of gluten.

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

9 c disease, a permanent immune intolerance to gluten.

10 ghest overall GSRS-IBS score after consuming gluten, 24 had the highest score after consuming fructan

11 ssigned to groups placed on diets containing gluten (5.7 g), fructans (2.1 g), or placebo, concealed

12 s who are genetically susceptible to dietary gluten, a protein complex found in wheat, rye, and barle

13 and stability of wheat by cross-linking into gluten aggregates through inter-chain disulfide bonds.

14 The gluten aggregation and dehydration processes were also r

15 are like gluten 'pills', shown here to skew gluten analysis results.

16 conditions should be considered for accurate gluten analysis.

17 A step-wise, 'test-all-positive-gluten' analytical methodology has been developed and ve

18 ll deformation rheological properties of the gluten and a strain hardening behaviour of both dough an

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

20 erial is crucial for accurate measurement of gluten and evaluating assay performance.

21 We aimed to investigate the effect of gluten and fructans separately in individuals with self-

22 potential co-protein effects in mixtures of gluten and globular proteins during heating at 100 degre

23 was no difference in GSRS-IBS scores between gluten and placebo groups.

24 line wheat starch, gelatinized wheat starch, gluten, and formed gluten network.

25 had T cells that proliferated in response to gluten antigen in vitro.

26 Milk and wheat/gluten are the most common food triggers.

27 hich enhance polymerization in mixtures with gluten are unknown.

28 y disperse gluten to allow a single accurate gluten assessment.

29 clonotypes can be identified and that common gluten associated immune response features can be charac

30 that the introduction of small quantities of gluten at 4-6 mo of age did not reduce the risk of celia

31 The commonest cause of sporadic ataxia was gluten ataxia (25%).

32 Gluten avoidance without celiac disease was defined as a

33 Gluten avoidance without celiac disease was more common

34 We examined T-cell responses against gluten by generating T-cell lines and T-cell clones from

35 Ingestion of gluten by persons with celiac disease causes immune-medi

36 The source of gluten can influence gluten quantitation due to variabil

37 rticipants were randomly assigned after oral gluten challenge and 20 (71%) of 28 participants were ra

38 duals with suspected celiac disease to avoid gluten challenge and duodenal biopsy, but requires valid

39 ng gluten-specific CD4(+) T cells after oral gluten challenge of patients with celiac disease.

40 ipants who completed the post-treatment oral gluten challenge per protocol, interferon gamma release

41 to Nexvax2 peptides after the screening oral gluten challenge were discontinued before dosing.

42 s with refractory celiac disease, undergoing gluten challenge, or consuming a prescribed oats-contain

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

44 tative histology within 2 weeks without oral gluten challenge.

45 vaccine resembled those associated with oral gluten challenge.

46 ble-blind crossover, placebo-controlled oral gluten challenge.

47 criteria, cultivars that possessed a typical gluten composition were identified.

48 onsumption patterns as well as the amount of gluten consumed at 11-36 mo of age do not influence CD d

49 resent study was the impact of the amount of gluten consumed from age 10 mo onward on CD development.

50 iables country, sex, intervention group, and gluten consumption pattern did not show significant asso

51 This study reports the gluten consumption pattern in children at risk of CD fro

52 , the interaction between HLA risk group and gluten consumption pattern showed no significant risk on

53 e (HR: 5.81; 95% CI: 1.18, 28.74; P = 0.031).Gluten consumption patterns as well as the amount of glu

54 Four gluten-containing (white wheat, wholemeal wheat, spelt a

55 We selected 38 different gluten-containing and gluten-free products, either unpro

56 Gluten-containing cereals have by far the highest concen

57 food-group elimination diet (TFGED; milk and gluten-containing cereals).

58 ng a qLAMP based-method for the detection of gluten-containing cereals, along with its evaluation in

59 ncentrations of ATIs found in a normal daily gluten-containing diet increased low-level intestinal in

60 etected individuals with celiac disease on a gluten-containing diet vs controls with an area under th

61 ediatric patients (18 years or younger) on a gluten-containing diet who tested positive for TGA-IgA f

62 identified subjects with celiac disease on a gluten-containing diet with 100% sensitivity (95% CI 1.0

63 ivity], 10 subjects with celiac disease on a gluten-containing diet, and 52 presumed healthy individu

64 mples from subjects with celiac disease on a gluten-containing diet.

65 stologic evidence requires patients to be on gluten-containing diets.

66 ions in gluten quantitation depending on the gluten-containing grain and their cultivars.

67 riggers in TFGED responders were milk (52%), gluten-containing grains (16%), and both (28%).

68 l symptoms, or both, related to ingestion of gluten-containing grains, with symptomatic improvement o

69 Modern gluten-containing staples had levels of TLR4-activating

70 eveloped and verified to assess kernel-based gluten contamination (i.e., wheat, barley and rye kernel

71 thods are required to detect the presence of gluten contamination.

72 44s), protein content (12.0-12.3g/100gd.m.), gluten content (9.7-10.5g/100gd.m.), yellow index (18.0-

73 ELISA methods do not give rise to equivalent gluten content measurement results.

74 s on robust markers and their conversion to "gluten content" are required.

75 that indicates the presence of cereals with gluten content.

76 bability of mis-assessment to sample average gluten content.

77 antly in the samples with lower moisture and gluten content.

78 fants received 100 mg immunologically active gluten/d or placebo from 4 to 6 mo of age, with a stepwi

79 Bacterial colonizations produced distinct gluten-degradation patterns in the mouse small intestine

80 Gluten describes a complex mixture of proteins found in

81 yme-linked immunosorbent assays (ELISAs) for gluten detection each have specific characteristics, but

82 Biopsies were incubated with gluten digested with chymotrypsin (modified or unmodifie

83 we characterized signatures associated with gluten directed immune activity and identified gluten-in

84 However, the consumption of high amounts of gluten early in life has been suggested to increase CD r

85 ally examines the feasibility of harmonizing gluten ELISA assays by the introduction of: a common ext

86 ot mount a T cell response to immunodominant gluten epitopes of CD.

87 We studied the repertoire of gluten epitopes recognized by T cells from children and

88 in children recognize deamidated and native gluten epitopes, whereas T cells from adults only recogn

89 children and adults each reacted to multiple gluten epitopes.

90 of public clonotypes associated with dietary gluten exposure identified subsets of highly similar clo

91 d, but the global immune response to in vivo gluten exposure in CD has not been systematically invest

92 s, and increased diversity in the gut during gluten exposure.

93 -DQ2.5, do not develop CD despite continuous gluten exposure.

94 ocedure; a common calibrator, such as a pure gluten extract and an incurred matrix material.

95 llergens became strongly insolubilized after gluten formation and heating.

96 protein was extracted from wheat flour, and gluten fractions were also extracted by adding SDS.

97 Gluten free (GF) diets are prone to mineral deficiency,

98 o the attractive nutritional profile such as gluten free and high dietary fiber content.

99 to NF in order to prepare corn tortillas and gluten free cookies characterized in terms of dimensions

100 evices for an efficient, simple and accurate gluten free diet (GFD) monitoring as well as therapy fol

101 market, and has been used to produce various gluten free food items such as pasta and bread.

102 at, wholemeal wheat, spelt and rye) and four gluten-free (chick pea, lupin, buckwheat, amaranth) flou

103 to increase the nutritional value of common gluten-free (GF) cereal-based foods, GF cookies using al

104 describes the successful development of new gluten-free (GF) mini sponge cakes fortified with brocco

105 (i.e., wheat, barley and rye kernels) during gluten-free (GF) oat production.

106 Gluten-free bakery products usually exhibit weak aroma.

107 ing technological and nutritional quality of gluten-free bread during 5day shelf life by means of che

108 tes (GMPH) utilization for the enrichment of gluten-free bread followed by characterization of flavou

109 essary in order to improve the weak aroma of gluten-free breads.

110 th 30 of 52 patients who did not adhere to a gluten-free diet (58%) (P < .0001).

111 45 of 148 patients who adhered strictly to a gluten-free diet (98%) had reduced symptoms, compared wi

112 n gastrointestinal symptoms compared with no gluten-free diet (difference less than 1 point on a scal

113 growing number of individuals adhering to a gluten-free diet (GFD) without exclusion of celiac disea

114 tients with celiac disease should maintain a gluten-free diet (GFD), excluding wheat, rye, and barley

115 coming a fraction of individuals following a gluten-free diet (GFD).

116 tment for celiac disease (CeD) is a lifelong gluten-free diet (GFD).

117 y are commonly used to monitor patients on a gluten-free diet (GFD).

118 : A man in his 80s with DH not controlled by gluten-free diet (with poor adherence), dapsone, and con

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

120 ive serologic findings found initiation of a gluten-free diet associated with small improvement in ga

121 Many patients following a gluten-free diet continue to have symptoms and have smal

122 bers of individuals are empirically trying a gluten-free diet for a variety of signs and symptoms.

123 Participants reported following a gluten-free diet for at least 1 year before the study be

124 Difficulties adhering to a gluten-free diet have led to the development of non-diet

125 ciated with prevalence of celiac disease and gluten-free diet in the United States.

126 Although a gluten-free diet is an effective treatment in most indiv

127 ening for celiac disease must occur before a gluten-free diet is implemented, since once a patient in

128 A gluten-free diet is the only means to manage coeliac dis

129 celiac disease was defined as adherence to a gluten-free diet without a diagnosis of celiac disease.

130 Although both conditions are treated with a gluten-free diet, distinguishing between celiac disease

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

132 ure, omega-3 fatty acid supplementation, and gluten-free diet, may have additional benefits, as do po

133 mplemented, since once a patient initiates a gluten-free diet, testing for celiac disease is no longe

134 isorders is based on a lifelong, and strict, gluten-free diet.

135 years who had coeliac disease and were on a gluten-free diet.

136 treatment is strict adherence to a life-long gluten-free diet.

137 h care provider diagnosis and adherence to a gluten-free diet.

138 accine in patients with coeliac disease on a gluten-free diet.

139 l children develop celiac disease or require gluten-free diets.

140 erization of phenolic fingerprints in common gluten-free flours is still scarce.

141 arch and qualitative comparison of different gluten-free flours.

142 Monitoring the compliance of gluten-free foods to the regulatory threshold of 20mg/kg

143 were as much as 100-fold higher than in most gluten-free foods.

144 Gluten-free labeled foods are available as a safe altern

145 s likely impact on the enforcement of the EU gluten-free legislation.

146 R-Biopharm R5 ELISA, we quantified gluten in gluten-free oatmeal servings from an in-market survey.

147 were determined in healthy C57BL/6 mice on a gluten-free or ATI-free diet and in mice given low-level

148 lour and potato starch in the development of gluten-free pasta for celiac disease patients.

149 A gluten-free pasta was prepared adding chia at rice flour

150 selected 38 different gluten-containing and gluten-free products, either unprocessed (such as wheat,

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

152 Nutritionally improved, gluten-free spaghetti (NIS) showed significantly increas

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

154 Gluten from wheat, rye, and barley can trigger IgE-media

155 , and 10.1 +/- 3.7, respectively, during the gluten, fructan, and placebo challenges (P = .004).

156 SRS-IBS scores differed significantly during gluten, fructan, and placebo challenges; mean values wer

157 roup, until they completed all 3 challenges (gluten, fructan, and placebo).

158 Thus, the gluten grain source and processing conditions should be

159 This microbe-gluten-host interaction may modulate autoimmune risk in

160 and reproducibly digest specific classes of gluten in barley.

161 e higher to deamidated gluten than to native gluten in children and adults.

162 gg, soy or whey protein co-exists with wheat gluten in different food products.

163 ate methods for the quantitative analysis of gluten in flour.

164 assay (ELISA) are commonly used to quantify gluten in foods.

165 -like disorder caused by exposure to dietary gluten in genetically predisposed individuals.

166 Using R-Biopharm R5 ELISA, we quantified gluten in gluten-free oatmeal servings from an in-market

167 bicity, FTIR, SDS-PAGE and thiol content) of gluten in relation to its antigenicity (determined by En

168 hypersensitivity to certain cereal proteins: gluten in wheat, secalin in rye, hordein in barley, and

169 4 to 6 mo of age, with a stepwise and fixed gluten increase until age 10 mo and unrestricted intake

170 Proanthocyanidins (PA) crosslink wheat gluten, increasing its polymer size and strength.

171 DS, dough development time (DDT), LASRC and gluten index (GI) were positively related to polymeric p

172 /E ratio (r=0.745( * *) and r=-0.869( * *)), gluten index (r=0.959( * *) and r=-0.994( * *)), dough d

173 grain quality parameters, except for reduced gluten index in the high-gluten variety PR22D89, as well

174 DS sedimentation volume, dough stability and gluten index were found to have a negative impact on cha

175 ph and were associated with highly increased gluten index, larger amounts of gluten macropolymers, la

176 fferential abundance analysis, we identified gluten-induced clonotypes in each patient that were comp

177 Observations: Celiac disease is a gluten-induced immune-mediated enteropathy characterized

178 uten directed immune activity and identified gluten-induced T-cell clonotypes from total blood and gu

179 BACKGROUND & AIMS: Gluten ingestion leads to symptoms and small intestinal

180 s of the vaccine, similar to those caused by gluten ingestion.

181 roducing gut PCs accumulate in patients upon gluten ingestion.

182 y of the PreventCD trial (www.preventcd.com).Gluten intake was prospectively quantified by using spec

183 ge 10 mo onward on CD development.Mean daily gluten intakes from 10 mo onward were significantly diff

184 gluten toxicity in the diet of patients with gluten intolerance.

185 of undigested peptides, including for those gluten-intolerant.

186 ds to the regulatory threshold of 20mg/kg of gluten is essential for celiac disease patients.

187 ly increased gluten index, larger amounts of gluten macropolymers, larger size distribution for glute

188 dough mixed to peak showed a more continuous gluten matrix in the mutant transgenic lines than the on

189 ics in determining the co-protein effects in gluten mixtures.

190 rmed hypothesis about partial dehydration of gluten network after polysaccharides addition.

191 es were used to investigate their effects on gluten network formation.

192 the effects of the Hofmeister salt series on gluten network formation.

193 DSC results, while the TGA ones showed that gluten network remained thermally stable after polysacch

194 gelatinized wheat starch, gluten, and formed gluten network.

195 he effects of different cations on dough and gluten of different flours mostly followed the Hofmeiste

196 beta-sheets in dough and disulfide groups in gluten of the mut1Ax1 transgenic lines were significantl

197 Foods with gluten often contain fructans, a type of fermentable oli

198 tance for a wide range of food products with gluten or globular proteins as functional agents.

199 antly higher than for participants consuming gluten (P = .049), as was the GSRS bloating score (P = .

200 T-cell responses to different gluten peptides appear to be similar between adults and

201 repertoires directed to some immunodominant gluten peptides have previously been described, but the

202 y disorder mediated by an immune response to gluten peptides in genetically susceptible individuals.

203 ts a novel approach to quantify the digested gluten peptides in human urine with outstanding sensitiv

204 and tested proliferative response to various gluten peptides.

205 cells from adults only recognize deamidated gluten peptides.

206 d the way for the development of an ultralow gluten phenotype.

207 These contaminants are like gluten 'pills', shown here to skew gluten analysis resul

208 r level of gliadin was incorporated into the gluten polymer and dough layers tended to 'slide' apart

209 6.25Jcm(-2)) on selected properties of wheat gluten powder and aqueous suspension (absorbance, partic

210 ced structure modifications were observed in gluten powder, pulsed light induced the development of b

211 psin bi-functional inhibitors (ATIs) are non-gluten protein components of wheat and other cereals tha

212 Barley contains four gluten protein families, and the existence of barley gen

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

214 nd two polyclonal antibodies to well-defined gluten protein types (GPT) isolated from wheat, rye and

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

216 The results showed significant changes to gluten proteins after GF treatment; cross-reactivity tow

217 y were used to study changes in structure of gluten proteins and their thermal properties influenced

218 ze exclusion chromatography fractionated the gluten proteins apparently into five peaks.

219 odies recognizing almost the entire range of gluten proteins as well as the antigenic epitopes throug

220 romoted partial depolymerisation of hydrated gluten proteins by disulphide exchange.

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

222 ubjects triggered by the ingestion of cereal gluten proteins for which the only treatment is strict a

223 Gluten proteins functionality during pastry production w

224 Complete digestion of gluten proteins is of critical importance during quantit

225 Gluten proteins of certain cereals (wheat, rye and barle

226 ize molecular weight distribution pattern of gluten proteins of four Indian commercial wheat varietie

227 ees C) or by the solvent WSB, which affected gluten proteins.

228 is influenced by changes in the structure of gluten proteins.

229 in the structure and antigenic properties of gluten proteins.

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

231 The ELISA kits exhibited variations in gluten quantitation depending on the gluten-containing g

232 The source of gluten can influence gluten quantitation due to variability in protein profil

233 various non-assay related factors can affect gluten quantitation.

234 DQ-gluten tetramer-based assays that detects gluten-reactive T cells identifies patients with and wit

235 It has been proposed that gluten-reactive T cells in children recognize deamidated

236 lthy subjects versus 79% in CD patients were gluten-reactive upon tetramer restaining.

237 Acceptable gluten recoveries were obtained in 200mg/kg wheat, rye,

238 10) did not differ between participants with gluten-related conditions and those without.

239 population-based study, we analyzed data on gluten-related conditions from the National Health and N

240 l and nutritional markers based on status of gluten-related conditions.

241 ss, it is possible to differentiate specific gluten-related disorders from other conditions, based on

242 The treatment of gluten-related disorders is based on a lifelong, and str

243 The prevalence of gluten-related disorders is rising, and increasing numbe

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

245 Oats are easily contaminated with gluten-rich kernels of wheat, rye and barley.

246 strain hardening behaviour of both dough and gluten samples.

247 Celiac disease and nonceliac gluten sensitivity are common.

248 The mechanisms of non-celiac gluten sensitivity are unclear, and there are no biomark

249 inguish between celiac disease and nonceliac gluten sensitivity by symptoms, as they are similar in b

250 BACKGROUND & AIMS: Non-celiac gluten sensitivity is characterized by symptom improveme

251 Nonceliac gluten sensitivity is diagnosed in individuals who do no

252 uishing between celiac disease and nonceliac gluten sensitivity is important for long-term therapy.

253 e lack of validated biomarkers for nonceliac gluten sensitivity make establishing the prevalence, rea

254 "Gluten sensitivity" has become commonplace among the pub

255 of individuals with self-reported non-celiac gluten sensitivity, we found fructans to induce symptoms

256 A third entity is nonceliac gluten sensitivity, which has been created because of th

257 separately in individuals with self-reported gluten sensitivity.

258 d treatment for celiac disease and nonceliac gluten sensitivity.

259 ions such as coeliac disease and non-coeliac gluten sensitivity.

260 eliac disease on a GFD [due to self-reported gluten sensitivity], 10 subjects with celiac disease on

261 corn, the highest TA was in small grits and gluten slurry in dry-milling and wet-milling coproducts,

262 Proanthocyanidins reduced gluten solubility in urea and decreased surface hydropho

263 39(+) Treg cell frequency within circulating gluten-specific CD4(+) T cells after oral gluten challen

264 prised a major proportion of all circulating gluten-specific CD4(+) T cells but had impaired suppress

265 We now show that gluten-specific CD4(+) T cells isolated from CD duodenal

266 approximately 80% of the ex vivo circulating gluten-specific CD4(+) T cells were FOXP3(+)CD39(+) Treg

267 esting the involvement of HLA-DQ2-restricted gluten-specific CD4(+) T cells.

268 To comprehensively measure the gluten-specific CD4(+) T-cell response, we paired tradit

269 The vaccine is intended to engage and render gluten-specific CD4-positive T cells unresponsive to fur

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

271 celiac disease have a dysfunction or lack of gluten-specific forkhead box protein 3 (FOXP3)(+) Treg c

272 sease, after a short in vitro expansion, the gluten-specific FOXP3(+)CD39(+) Treg cells exhibited sig

273 LA-DQ-gluten tetramers can be used to detect gluten-specific T cells in blood of patients with celiac

274 heat challenge to stimulate recirculation of gluten-specific T cells.

275 Numbers of circulating gluten-specific Treg cells and effector T cells both inc

276 Gluten strength indicators such as DS, dough development

277 Protein content and gluten strength parameters like SDS sedimentation volume

278 influence of different cationic salts on the gluten structure formation during dough mixing, compared

279 that HLA class I molecules restrict the anti-gluten T cell response in CD patients.

280 orally administered mixture of 2 recombinant gluten-targeting proteases, to reduce mucosal morphometr

281 and characterize the distribution of 0.25-g gluten test results for kernel contaminated oats, twelve

282 ntrols with positive results from the HLA-DQ-gluten tetramer test, 2 had unrecognized celiac disease

283 We investigated whether an HLA-DQ-gluten tetramer-based assay accurately identifies patien

284 For the HLA-DQ-gluten tetramer-based assay, we combined flow-cytometry

285 An HLA-DQ-gluten tetramer-based assays that detects gluten-reactiv

286 We found that gluten tetramer-binding memory cells were rare in blood

287 We produced HLA-DQ-gluten tetramers and added them to peripheral blood mono

288 HLA-DQ-gluten tetramers can be used to detect gluten-specific T

289 T cells that bound HLA-DQ-gluten tetramers were quantified by flow cytometry.

290 orth or greater have celiac disease or avoid gluten than persons living south of this latitude, indep

291 f T-cell responses were higher to deamidated gluten than to native gluten in children and adults.

292 al dietary products for people intolerant to gluten, their amount must not exceed the regulatory thre

293 ts sample grinding may inadequately disperse gluten to allow a single accurate gluten assessment.

294 velopment of innovative strategies to reduce gluten toxicity in the diet of patients with gluten into

295 except for reduced gluten index in the high-gluten variety PR22D89, as well as for the sensorial pro

296 ur reconstituted from wheat starch and wheat gluten was mixed with the polysaccharides in five concen

297 is the strict lifelong exclusion of dietary gluten, which is difficult to accomplish.

298 wheat shares homologous proteins (including gluten) with barley and rye and can also be processed wi

299 s characterized by symptom improvement after gluten withdrawal in absence of celiac disease.

300 ac disease and 1.1% of participants to avoid gluten without celiac disease.