ライフサイエンスコーパス: peanut

1 nvoke a mental simulation (e.g., "grasping a peanut").

2 peanut-allergic child reacts when exposed to peanut).

3 sitization to specific foods (milk, egg, and peanut).

4 he severity of a future allergic reaction to peanut.

5 ons as to the state of thermal processing of peanut.

6 ant factor determining allergic responses to peanut.

7 discontinuation, or low-dose maintenance, of peanut.

8 are more efficiently extracted from roasted peanut.

9 eads were mapped to the diploid ancestors of peanut.

10 who were neither sensitized nor allergic to peanut.

11 AD with the history of clinical reactions to peanut.

12 function during acute allergic reactions to peanut.

13 en, including seven to hazelnut and three to peanut.

14 absence of cholera toxin and react on OFC to peanut.

15 is transferrable and expressed in tetraploid peanut.

16 y an acclimation mechanism to heat stress in peanut.

17 elivery of RNAi in controlling aflatoxins in peanut.

18 eactions or low dose threshold during OFC to peanut.

19 revent aflatoxin accumulation in transformed peanuts.

20 ntify the most salient peptide biomarkers in peanuts.

21 draining lymph nodes and produced IgE Abs to peanuts.

22 therapy (OIT) in children highly allergic to peanuts.

23 rea under the ROC curve (AUROC) was 0.98 for peanut, 0.97 for cashew, 0.92 for hazelnut, 0.95 for pis

24 21 (35%) of peanut-0 group participants and one (4%) placebo group p

25 received 52 weeks of placebo (PLB), Viaskin Peanut 100 mug (VP100) or 250 mug (VP250), and then cros

26 Participants who became reactive to 4 g of peanut 13 weeks off active OIT exhibited higher peanut-i

27 /L) varied by food: milk 5.7%, egg 4.0%, and peanut 7.9%.

28 beta-chain (TCRbeta) usage and phenotypes of peanut-activated, CD154(+) CD4(+) memory T cells using f

29 cone-specific glycocalyx stained by the PNA (peanut agglutinin) lectin marker.

30 gen, using the lectin from Arachis hypogaea (peanut agglutinin, PNA) as the recognition element.

31 -MNA was packaged with a mixture of powdered peanut allergen (PNA), 1,25-dihydroxyvitamin D(3) (VD3),

32 ng two commercial ELISA kits: Veratox(R) for peanut allergen and peanut ELISA from Morinaga.

33 and linear IgE-binding epitopes of the major peanut allergen Ara h 2 and to produce a hypoallergenic

34 In mice, recombinant TI variants of the peanut allergen Ara h 2, but not the canonical allergen

35 ityof intact and post-translationallycleaved peanut allergen Ara h 6 in relation to IgE-binding.

36 ted the immunological mechanisms involved in peanut allergen sensitization by using mouse models.

37 some non-specific proteases in reducing raw peanut allergenicity was investigated.

38 Synthetic overlapping 15-mer peptides of peanut allergens (Ara h 1-11) were spotted onto microarr

39 of nonhomologous allergens, as shown for the peanut allergens Ara h 1 and 2.

40 The residues of major peanut allergens Ara h 1, Ara h 2 and Ara h 6 were deter

41 We discovered 2 peanut allergens, which we believe to be previously unre

42 mpared with specific IgE to peanut and other peanut allergens.

43 Key features of clinical peanut allergic are increased frequency of activated B c

44 and may improve the quality of life for many peanut allergic children.

45 IgE-mediated peanut allergic is common, often serious, and usually li

46 res of reaction severity (ie, how severely a peanut-allergic child reacts when exposed to peanut).

47 Participants included peanut-allergic children (aged 4-11 years [n = 356] with

48 llowed by incubation with sera from 55 Dutch peanut-allergic children and (125) I-labelled anti-IgE.

49 rated transcriptomic and epigenomic study of peanut-allergic children as they reacted in vivo during

50 In peanut-allergic children, the sIgE reactivity was direct

51 LARI profoundly blocked cat- and peanut-allergic IgE-mediated basophil activation, inhibi

52 and 17% of the sequences were shared between peanut-allergic individuals, suggesting strong convergen

53 Peanut-allergic participants (4-25 years) received 52 we

54 Peanut-allergic patients appear to demonstrate higher ab

55 he peanut-specific CD4(+) T-cell response in peanut-allergic patients that correlate with high clinic

56 volunteers (n = 6, healthy controls; n = 14, peanut-allergic patients) at various time-points followi

57 lls were isolated from blood bank donors and peanut-allergic patients.

58 chanisms underlying the variable severity of peanut-allergic reactions remain unclear.

59 Interestingly, in peanut-allergic subjects, Ara h 6 could be detected foll

60 rapy (OIT) can successfully desensitize many peanut-allergic subjects, but clinical tolerance diminis

61 differences in absorption in healthy versus peanut-allergic volunteers.

62 acy of epicutaneous immunotherapy (EPIT) for peanut allergy (250 mug, daily epicutaneous peanut prote

63 Peanut allergy (PA) is a common, potentially life-threat

64 of children with atopic dermatitis (AD) with peanut allergy (PA) is associated with increased transep

65 Peanut allergy (PA) is associated with marked quality-of

66 Limited research has examined the impact of peanut allergy (PA) on children using validated instrume

67 vey that highlighted the negative impacts of peanut allergy (PA) on quality of life.

68 ge (OFC) is the criterion standard to assess peanut allergy (PA), but it involves a risk of allergic

69 ermine whether antibody profiles can predict peanut allergy after age 4 years.

70 randomized controlled study of children with peanut allergy and 4 to 11 years old, previously reporte

71 atterns of total IgE from individuals with a peanut allergy and from non-atopic individuals without a

72 IT) may be a relevant and safe treatment for peanut allergy and may improve the quality of life for m

73 We identified a strong association between peanut allergy and the MALT1 locus in LEAP participants

74 ffective and safer immunotherapies to manage peanut allergy are in great demand despite extensive inv

75 ance group with 58.6% of carriers developing peanut allergy at 60 months as compared to 12.7% of non-

76 osis of peanut allergy, it is important that peanut allergy be accurately diagnosed so that an approp

77 ts demonstrate that daily EPIT treatment for peanut allergy beyond 1 year leads to continued response

78 content on total IgE from individuals with a peanut allergy compared with non-atopic individuals.

79 vants relative to peanut is a determinant of peanut allergy development.

80 Peanut allergy history rates and peanut- and Ara h 2-spe

81 Peanut allergy imposes an adverse psychosocial impact on

82 Ara h 2 is the dominant conglutin in peanut allergy in the United Kingdom, despite a degree o

83 Peanut allergy is a growing public concern; however, lit

84 gen-specific immunotherapy for patients with peanut allergy is available.

85 Peanut allergy is characterized by the development of Ig

86 Individuals with peanut allergy range in clinical sensitivity: some can c

87 tance of Oral Tolerance to Peanut study, and Peanut Allergy Sensitization study participants by admin

88 We assessed Learning Early about Peanut Allergy study, Persistance of Oral Tolerance to P

89 Peanut allergy was more common in London, cashew and pis

90 he Addendum Guidelines for the Prevention of Peanut Allergy were published with recommendations on ea

91 Most patients with peanut allergy were sensitized to both Ara h 2 and Ara h

92 showed the greatest diagnostic accuracy for peanut allergy when compared with specific IgE to peanut

93 uman PBMC culture platform, a mouse model of peanut allergy, and various experimental readouts to ass

94 eter addresses the diagnosis of IgE-mediated peanut allergy, both in children and adults, as pertaini

95 The cohort included chidren who had peanut allergy, children who were sensitized to but tole

96 In patients with peanut allergy, high-certainty evidence shows that avail

97 sease and the consequences of a diagnosis of peanut allergy, it is important that peanut allergy be a

98 ss various studies of OIT for egg, milk, and peanut allergy, strong levels of desensitization have be

99 nistic understanding of reaction severity in peanut allergy.

100 l requirements for an IgE recall response in peanut allergy.

101 o date the best serologic marker to diagnose peanut allergy.

102 elative importance of Ara h 2 and Ara h 6 in peanut allergy.

103 he clinician who is evaluating a patient for peanut allergy.

104 opment, IgE Ab production, and initiation of peanut allergy.

105 reatments will be introduced, especially for peanut allergy.

106 changes with long-term SLIT in children with peanut allergy.

107 iving eliciting doses in the population with peanut allergy.

108 iagnosis and lead to novel means of treating peanut allergy.

109 gE provide the greatest accuracy to diagnose peanut allergy.

110 era from 48 Ara h 2-sensitized patients with peanut allergy.

111 genetic architecture of reaction severity in peanut allergy.

112 hods for determination of boron in hazelnut, peanut, almond, raisin, prune and date samples were desc

113 al anaphylaxis were identified, 2 because of peanut and 1 of wasp allergy.

114 -specific IgE will react upon consumption of peanut and can eat the food without adverse reactions, k

115 Levels of specific (s)IgE and sIgG(4) to peanut and component proteins, and 50 esIgE and esIgG(4)

116 Levels of specific IgE to peanut and individual allergens were quantified by using

117 egrating BAT results for 10 and 100 ng/mL of peanut and individual tree nut extracts was optimal.

118 ed and clinically reactive) to milk, egg, or peanut and nonallergic controls for stimulation with end

119 t allergy when compared with specific IgE to peanut and other peanut allergens.

120 peanut from a solid model food incurred with peanut and subjected to processing was evaluated using t

121 Peanut and tree nut allergies are the most important cau

122 eptable measures of fit (r(2) = 94%-56%) for peanut and tree nut sIgE testing at the extract and mole

123 test can predict allergic clinical status to peanut and tree nuts in multi-nut-sensitized children an

124 ed patients aged 0.5-17 years with confirmed peanut and/or tree nut (almond, cashew, hazelnut, pistac

125 nsisted of sera from 18 subjects allergic to peanut and/or tree nuts but tolerant to almond.

126 eact with allergens in natural rubber latex, peanuts and grass and tree pollens.

127 ldren who were sensitized to but tolerant of peanut, and children who were neither sensitized nor all

128 contaminated with four allergens (egg, milk, peanut, and hazelnut), the concatemer approach was found

129 s are robust to food processing, specific to peanuts, and satisfy sequence-based criteria.

130 ons of whole and chopped almonds, hazelnuts, peanuts, and walnuts.

131 Peanut allergy history rates and peanut- and Ara h 2-specific immunoglobulin E (sIgE) tit

132 Significant increases in peanut- and Ara h2-specific IgG(4) observed at week 52 p

133 racterized by the development of IgE against peanut antigen.

134 with epitopes of allergenic 2S albumins from peanut (Ara h 2 and 6) and Brazil nut (Ber e 1).

135 Understanding the changes in peanut (Arachis hypogaea L.) anther lipidome under heat

136 Like many other crops, the cultivated peanut (Arachis hypogaea L.) is of hybrid origin and has

137 Unexpected allergic reactions to peanut are the most common cause of fatal food-related a

138 e-blind placebo-controlled food challenge to peanut as part of a clinical trial.

139 the MALT1 locus in LEAP participants in the peanut avoidance group with 58.6% of carriers developing

140 The peanut B subgenome has more genes and general expression

141 cells in regulating Ag-specific IgE using a peanut-based food allergy model in mice.

142 nical sensitivity: some can consume grams of peanut before experiencing any symptoms, whereas others

143 red lines (RILs) developed by the Australian peanut breeding program.

144 ncurred in different food matrices (cookies, peanut butter and chocolate dessert).

145 rds) of participants who underwent OFC using peanut butter for the first time at Miyagi Children's Ho

146 d peanuts were compared to that of untreated peanuts by western blot.

147 subject based on symptoms experienced during peanut challenge and the eliciting dose.

148 anges were reproduced at a subsequent repeat peanut challenge in 26 participants, and could be revers

149 ns had allergic reactions to intraperitoneal peanut challenge, whereas only CC027/GeniUnc mice reprod

150 vivo during double-blind, placebo-controlled peanut challenges.

151 tion produced significantly fewer IgE Abs to peanuts compared with control mice.

152 ith recommendations on early introduction of peanut-containing foods based on infants' clinical histo

153 Roasting of peanut contaminants influenced ELISA results, with raw p

154 IgE sensitization and allergic reactions to peanut could facilitate diagnosis and lead to novel mean

155 We examined the performance of peanut detection methods in cumin and garlic, focusing o

156 and threshold dose of allergic reactions to peanut during OFC.

157 gests that independent domestications formed peanut ecotypes.

158 ISA kits: Veratox(R) for peanut allergen and peanut ELISA from Morinaga.

159 tcomes from a randomized controlled trial of peanut epicutaneous immunotherapy, observing modest and

160 tic parameters following extended open-label peanut epicutaneous immunotherapy.

161 The PEPITES (Peanut EPIT Efficacy and Safety) trial, a 12-month rando

162 A peanut extract prepared at pH 4 was fractionated by phys

163 lenge of mice sensitized intragastrically to peanut extract.

164 in humans, naive BALB/c mice were exposed to peanut flour by inhalation without any exogenous adjuvan

165 When exposed to peanut flour, naive mice developed T follicular helper (

166 rce of IL-13 when naive mice were exposed to peanut flour.

167 albumins are the most important allergens in peanuts for inducing an allergic effector response.

168 efficacy of different buffers in extracting peanut from a solid model food incurred with peanut and

169 olyploidy constrained genetic variation, the peanut genome sequence aids mapping and candidate-gene d

170 A multi-seasonal phenotypic analysis of 10 peanut genotypes revealed C76-16 (C-76) and Valencia-C (

171 for the fast and accurate identification of peanut genotypes.

172 ilt virus (TSWV) is a devastating disease to peanut growers in the South-eastern region of the United

173 spice containing products due to undeclared peanut have highlighted the importance of analytical met

174 ainability of these materials suggested that peanut hulls can be valorized via thermochemical convers

175 on the characterization and valorization of peanut hulls through the generation of green composites.

176 Peanut hulls were pyrolyzed at 500 degrees C and analyze

177 No studies have been conducted on peanut hydrolysates that are crosslinked with TGase.

178 Peanuts hydrolyzed by the three selected enzymes (200 Az

179 (<2 years, >=5 kUA/L, otherwise >=14 kUA/L, peanut IgE)] among 511 participants (median follow-up, 7

180 Allergy to Peanuts ImPacting Emotions And Life (APPEAL-1) was a rec

181 The Allergy to Peanuts imPacting Emotions And Life 1 (APPEAL-1) survey,

182 Allergy to Peanuts imPacting Emotions And Life study 1 (APPEAL-1) w

183 Allergy to Peanuts imPacting Emotions And Life study 1 was an onlin

184 ng a cornerstone for functional genomics and peanut improvement.

185 ly suitable for the qualitative detection of peanut in cumin and garlic.

186 djuvants to promote sensitization to inhaled peanut in mice.

187 sensitized tolerance and clinical allergy to peanut in the first year of life.

188 reactivity had higher basophil activation to peanut in vitro.

189 integrity', was conceived to prepare low-fat peanuts in response to health-conscious consumer demands

190 following ingestion of increasing levels of peanut incurred in different food matrices (cookies, pea

191 Assessments of peanut-induced basophil activation and peanut-specific i

192 nut 13 weeks off active OIT exhibited higher peanut-induced basophil activation ex vivo and higher pe

193 anut introduction, with a 3-fold increase in peanut introduction by age 1 year in 2018 compared with

194 ere has been a striking shift toward earlier peanut introduction, with a 3-fold increase in peanut in

195 osure to environmental adjuvants relative to peanut is a determinant of peanut allergy development.

196 Peanut is a potent inducer of proallergenic T(H)2 respon

197 Peanut kernels were treated by Alcalase, papain, Neutras

198 We show that chemometric analysis of peanut leaflet spectra provides accurate identification

199 Processed peanut matrices were prepared and analyzed using an unta

200 he now Food and Drug Administration-approved peanut OIT product Palforzia (Aimmune Therapeutics, Bris

201 Peanut OIT significantly decreased basophil activation,

202 ind, randomized, placebo-controlled, phase 2 peanut OIT study.

203 With egg and peanut OIT, a limited remission, or sustained unresponsi

204 maintain long-term clinical tolerance after peanut OIT.

205 c immunoglobulins, are useful biomarkers for peanut OIT.

206 by successful phase 2 and phase 3 studies of peanut OIT.

207 The BAT outperformed sIgE testing for peanut or hazelnut and was comparable for walnut (AUROC

208 Consumption of peanuts or tree nuts significantly decreased HOMA-IR and

209 ) and egg (OR 1.4, 95% CI 1.01-1.9), but not peanut (OR 0.98, 95% CI 0.8-1.2).

210 ally reactive and those who were tolerant to peanut oral challenges.

211 high-certainty evidence shows that available peanut oral immunotherapy regimens considerably increase

212 taminants influenced ELISA results, with raw peanut over-detected (3.9-fold) and roasted peanut under

213 nt allergen LFIAs (two for hazelnut, one for peanut) over 0.075-3500 ppm, LFIAs with C only, surface

214 utritional composition with antioxidant-rich peanut phenotype and could yield commercial profits.

215 ut, coconut, hazelnut, Macadamia nut, pecan, peanut, pine nut, pistachio and walnut) as well as nut p

216 2 duplicate sRNA libraries of in-vitro-grown peanut plants, 24 and 48 h after exogenous application o

217 o compare exogenous RNAi delivery methods on peanut plants, and to analyze the efficacy of molecular

218 "Winter rapeseed + " replanting peanuts, potatoes, rice, seed melons and other crops gen

219 Drought is one of the main constraints in peanut production in West Texas and eastern New Mexico r

220 We sought to detect peanut protein (PN)-induced changes in gene expression i

221 d shortly after ingestion (<=5 minutes); the peanut protein concentration peaks between 1 and 4 hours

222 es were also decreased as compared to intact peanut protein extracts.

223 , allergenicity and functional properties of peanut protein hydrolysate cross-linked by TGase were te

224 od-grade enzymes for the kinetic analysis of peanut protein hydrolysis that lead to high reduction ra

225 ne the absorption kinetics of immunoreactive peanut protein in relation to the allergic response in h

226 Ingested peanut protein is absorbed systemically and retains its

227 essful in demonstrating that: immunoreactive peanut protein was absorbed shortly after ingestion (<=5

228 , placebo-controlled food challenge (5044 mg peanut protein), and adherence, safety, and mechanistic

229 olunteers following ingestion of 300-1000 mg peanut protein, although variations in the kinetics of p

230 ge at an eliciting dose of 300 mg or less of peanut protein.

231 peanut allergy (250 mug, daily epicutaneous peanut protein; DBV712 250 mug).

232 Small, basic peanut proteins are often poorly extracted in pH-neutral

233 ncentration peaks between 1 and 4 hours; and peanut proteins can circulate for at least 48 hours in t

234 processing could reduce the allergenicity of peanut proteins while may lose the functional properties

235 bsorption kinetics of immunologically intact peanut proteins.

236 traction buffers provides better recovery of peanut residues from a processed solid food matrix.

237 uHCl recovered 65% +/- 4% and 77% +/- 10% of peanut, respectively from unprocessed samples with the V

238 Peanut RIL p27-362 presents a superior nutritional compo

239 ts obtained from spectroscopic signatures of peanut seeds.

240 However, a test that indicates there is peanut sensitization present (eg, a "positive" test) is

241 ival, and loss of GC dark zone B cells after peanut sensitization.

242 Another set of peanut-sensitized mice treated by EPIT or OIT were sacri

243 evaluate the efficacy of this novel EPIT in peanut-sensitized mice.

244 ional epitopes did not induce anaphylaxis in peanut-sensitized mice.

245 r parents at the start of OIT for milk, egg, peanut, sesame, or tree nuts, at the end of up-dosing, a

246 ted interaction networks with the identified peanut severity genes and CpGs.

247 nd 3 groups of interacting key node CpGs and peanut severity genes encompassing immune response, chem

248 In contrast, peanut sIgE level was significantly lower in the Toleran

249 duced basophil activation ex vivo and higher peanut sIgE levels and sIgE/total IgE, but lower sIgG(4)

250 An algorithm combining esIgEs with peanut sIgE outperformed different clinically relevant I

251 significantly decreased basophil activation, peanut sIgE, Ara h 1, Ara h 2, and Ara h 3 IgE levels, a

252 of apples (a-PAC), cranberries (c-PAC), and peanut skins (p-PAC) were determined by matrix-assisted

253 ore A-type bonds, whereas in cranberries and peanut skins, 96% of the PAC oligomers contain one or mo

254 ydrolysis, the IgE-binding properties of the peanut soluble extracts were decreased (by 85%-95%); and

255 Six allergenic ingredients (milk, egg, peanut, soybean, hazelnut, and almond) were incurred int

256 Transcripts from peanut, soybean, sesame, and mite allergens contained a

257 y aggregates showed significant reduction in peanut specific plasma Immunoglobulin E (IgE).

258 rofessionals, mostly by clinical history and peanut-specific allergy testing.

259 We sought to identify characteristics of the peanut-specific CD4(+) T-cell response in peanut-allergi

260 Peanut-specific CD8(+) T cells in nonallergic individual

261 Furthermore, the ratio of peanut-specific clones in the effector versus regulatory

262 s, suggesting strong convergent selection of peanut-specific clones.

263 Expansion of the peanut-specific effector T-cell repertoire is correlated

264 vivo in response to peanut stimulation, and peanut-specific IgE (sIgE) and peanut-specific IgG(4) (s

265 Early epitope-specific plus peanut-specific IgE is predictive of allergy status at a

266 of T(H)2 cytokines strongly correlated with peanut-specific IgE levels.

267 aling by B cells led to a severely curtailed peanut-specific IgE response, decreased GCB cell surviva

268 Peanut-specific IgE titers and anaphylaxis responses wer

269 s 5 days posttransplantation, newly acquired peanut-specific IgE were transiently detected from 1 don

270 Not all individuals who produce peanut-specific IgE will react upon consumption of peanu

271 of Arachis hypogaea 2-specific IgE, level of peanut-specific IgE, and IgG4/IgE ratio also had 100% se

272 prick test (SPT) and measuring the levels of peanut-specific IgE, Arachis hypogaea 2-specific IgE, an

273 cell responses had markedly higher levels of peanut-specific IgE, revealing an active helper function

274 d mediator from human mast cells, suppressed peanut-specific IgE-mediated passive cutaneous anaphylax

275 mulation, and peanut-specific IgE (sIgE) and peanut-specific IgG(4) (sIgG(4)), in a large, single-sit

276 ic IgE, Arachis hypogaea 2-specific IgE, and peanut-specific IgG4, and we analyzed the utility of the

277 We compared basophil responsiveness and peanut-specific immunoglobulins between those who were c

278 ts of peanut-induced basophil activation and peanut-specific immunoglobulins can help to predict trea

279 ivation in whole blood, and plasma levels of peanut-specific immunoglobulins, are useful biomarkers f

280 ction of TNFalpha and increased frequency of peanut-specific memory CD4 T cells.

281 by single-cell RNA sequencing, expanded with peanut stimulation and maintained their pathogenic pheno

282 vation in whole blood ex vivo in response to peanut stimulation, and peanut-specific IgE (sIgE) and p

283 ffers that are optimal for the extraction of peanut storage proteins such as Ara h 1.

284 ergy study, Persistance of Oral Tolerance to Peanut study, and Peanut Allergy Sensitization study par

285 icate cohort of adult AD patients with FA to peanut, suggesting a unique STS proteomic endotype for A

286 terpart seems to be important in established peanut tolerance.

287 Peanut, tree nut, and sesame allergies are responsible f

288 Overall, the rate of coexistent peanut, tree nut, and sesame seed allergy was 60.7% (n =

289 sing the challenge-proven rate of coexistent peanut, tree nut, and/or sesame seed allergy.

290 Allergies to peanuts, tree nuts, and sesame seeds are among the most

291 icochemical properties of the 2S albumins in peanuts, tree nuts, and sesame seeds will enhance our ab

292 explain much of the observed coallergy among peanuts, tree nuts, and sesame seeds.

293 line values) of legumes, fish and shellfish, peanuts, tree nuts, vegetables, soy foods, and soy drink

294 ical integration of allergen-specific IgE to peanut/tree nut allergens from three IgE test platforms.

295 adian and Austrian children/adolescents with peanut/tree nut sensitization and a cohort of sensitized

296 peanut over-detected (3.9-fold) and roasted peanut under-detected (3.5-fold).

297 requencies of sensitization to legumins from peanut, walnut, hazelnut, and cashew were similar in bot

298 litate selective breeding of polyphenol-rich peanuts, we looked for mass spectrometry-based proteomic

299 SDS-PAGE, and the allergenicities of treated peanuts were compared to that of untreated peanuts by we

300 om children allergic to milk or egg, but not peanut, were significantly lower compared to controls in