ライフサイエンスコーパス: peanut

1 t is 1.5 mg of peanut protein (6 mg of whole peanut).

2 state of coregulated networks in response to peanut.

3 blind, placebo-controlled oral challenges to peanut.

4 which recommended a delayed introduction of peanut.

5 nylated stilbenoids and their derivatives in peanut.

6 derivatives in different parts of germinated peanut.

7 -blind, placebo-controlled food challenge to peanut.

8 xperienced no reaction to the single dose of peanut.

9 ied, 16 compounds were unique to the roasted peanuts.

10 gic reactions are in connection with roasted peanuts.

11 obtained from both raw and in-shell roasted peanuts.

12 fruit or vegetable (0.7%), dairy (0.5%), and peanut (0.5%).

13 were treated with placebo (n = 25), Viaskin Peanut 100 mug (VP100; n = 24) or Viaskin Peanut 250 mug

14 1), with the most common food triggers being peanut, 2.7% (95% CI, 2.3-3.2), and tree nut, 2.3% (95%

15 ood allergy was 5.5% (95% CI, 4.9-6.2), with peanut, 2.8% (95% CI, 2.3-3.3), and tree nut, 2.3% (95%

16 in Peanut 100 mug (VP100; n = 24) or Viaskin Peanut 250 mug (VP250; n = 25; DBV Technologies, Montrou

17 ipaensis, the wild progenitors of cultivated peanut (A. hypogaea).

18 nt evidence on how environmental exposure to peanut affects the development of peanut allergy.

19 1 pathway is involved in the Tfh response to peanut allergen exposure.

20 Previous studies could detect peanut allergen in house dust.

21 results show marked differences in specific peanut allergen profiles in peanut butter and flour and

22 igate the immunologic mechanisms involved in peanut allergen sensitization.

23 The extraction of Ara h 6 (a peanut allergen) from a complex chocolate-based food mat

24 that present various epitopes from the major peanut allergen, Ara h2, we directly determined the immu

25 rogenic dendritic cells pulsed with the main peanut allergens [pea-T10 cells]).

26 with PA and HC subjects pulsed with the main peanut allergens of Arachis hypogaea, Ara h 1 and 2, and

27 In most cases specific peanut allergens were not detected in tree nut butters o

28 e profile the dynamic transcriptome of acute peanut allergic reactions using serial peripheral blood

29 red by peanut, but not placebo, during acute peanut allergic reactions.

30 Analyses in 21 additional peanut allergic subjects replicate major findings.

31 ipheral blood mononuclear cells (PBMCs) from peanut-allergic (PA) and nonallergic subjects were stimu

32 BAT, HR, and passive HR were performed on 11 peanut-allergic and 14 nonallergic subjects.

33 ere analyzed by immunoblot with sera from 52 peanut-allergic individuals displaying different clinica

34 led, dose-ranging trial of a peanut patch in peanut-allergic patients (6-55 years) from 22 centers, w

35 In this dose-ranging trial of peanut-allergic patients, the 250-mug peanut patch resul

36 tion to oleosins was observed exclusively in peanut-allergic subjects suffering from severe systemic

37 elayed introduction is beneficial to prevent peanut allergies in infants.

38 ssed their abilities to reverse ovalbumin or peanut allergies in mouse models, as well as their opera

39 acebo-controlled study, 74 participants with peanut allergy (ages 4-25 years) were treated with place

40 In the Learning Early About Peanut Allergy (LEAP) study, early peanut introduction i

41 t 5 years of age in the Learning Early About Peanut Allergy (LEAP) study.

42 Peanut allergy (PA) is a complex disease with both envir

43 Peanut allergy (PA) is a life-threatening condition that

44 3 infants with challenge-proven IgE-mediated peanut allergy against 148 non-allergic infants (all 1

45 The reported prevalence of peanut allergy among children in the United States has i

46 he anaphylaxis associated with ovalbumin and peanut allergy and affects the epigenome of T cells, the

47 We used a model of peanut allergy and anaphylaxis, various knockout mice, a

48 revious findings for the association between peanut allergy and HLA-DRB1 in this Australian populatio

49 t various risk levels for the development of peanut allergy and is intended for use by a wide variety

50 study aimed to develop a new mouse model for peanut allergy and to investigate the immunologic mechan

51 Genetic variants for IgE-mediated peanut allergy are yet to be fully characterized and to

52 evere eczema, egg allergy, or both prevented peanut allergy at 5 years of age in the Learning Early A

53 Late-onset peanut allergy at age 4 years was rare (0.2%).

54 mmunotherapy may have potential for treating peanut allergy but has been assessed only in preclinical

55 l trial and other emerging data suggest that peanut allergy can be prevented through introduction of

56 Young adults with peanut allergy face challenges when moving from the safe

57 We pooled data from 104 children with peanut allergy from 3 peanut OIT studies.

58 About 20% of patients with reported peanut allergy had a radioallergosorbent test/ImmunoCAP

59 Observations: The prevalence of peanut allergy has increased despite the publication of

60 The prevalence of peanut allergy has increased over the years and still re

61 Consecutive eligible children with peanut allergy in 3 centers were prospectively invited t

62 Genetic determinants for challenge-proven peanut allergy include alleles at the HLA-DRB1 locus.

63 umption of peanut in infants at high risk of peanut allergy is allergen specific and does not prevent

64 Peanut allergy is common, life-threatening, and without

65 Peanut allergy is one of the most common and most severe

66 c mice develop normal humoral responses in a peanut allergy oral sensitization model.

67 house dust, and their levels correlate with peanut allergy prevalence.

68 -maximally sensitized mice with ovalbumin or peanut allergy reduced anaphylactic responses to oral al

69 Omalizumab allows subjects with peanut allergy to be rapidly desensitized over as little

70 ts (AEs), and efficacy of a peanut patch for peanut allergy treatment.

71 notherapy (EPIT) by using Viaskin Peanut for peanut allergy treatment.

72 lergic reactions to food in 22 patients with peanut allergy undergoing double-blind, placebo-controll

73 from 46 healthy donors and 120 patients with peanut allergy was collected into EDTA or heparin tubes,

74 Tfh cells play a key role in peanut allergy, and the IL-1 pathway is involved in the

75 tion, both BALB/c and C57BL/6 mice developed peanut allergy, as demonstrated by the presence of peanu

76 ral immunotherapy is a promising approach to peanut allergy, but reactions are frequent, and some pat

77 s perceived by adolescents/young adults with peanut allergy, their families, and their friends.

78 strates that association of the HLA locus is peanut allergy-specific whereas the other four loci incr

79 eanut exposure influences the development of peanut allergy.

80 lease assay (passive HR) in the diagnosis of peanut allergy.

81 chanistic study and therapeutic targeting of peanut allergy.

82 ic variants associated with challenge-proven peanut allergy.

83 , when available, for patients with reported peanut allergy.

84 es to specifically address the prevention of peanut allergy.

85 protein and prevention of the development of peanut allergy.

86 fewer than the predicted 5% of patients with peanut allergy.

87 diets of infants at various risk levels for peanut allergy.

88 xposure to peanut affects the development of peanut allergy.

89 ema and/or egg allergy have a higher risk of peanut allergy.

90 aged 9 to 36 months with suspected or known peanut allergy.

91 nologic effects of EPIT for the treatment of peanut allergy.

92 a significantly decreased risk of developing peanut allergy.

93 peanuts during infancy increases the risk of peanut allergy; however, these studies did not address m

94 species (canola, soybean, sunflower, maize, peanut and coconut) and showed high sensitivity in a bro

95 ntified five candidate prenyltransferases in peanut and confirmed that two of them are stilbenoid-spe

96 prenylated phenolics were made from lupine, peanut and soybean seedlings.

97 Peanut and tree nuts were the most common food triggers.

98 usion of new genetic diversity in cultivated peanut and will inform the development of high-resolutio

99 muM trolox equivalents 100g(-1)) followed by peanuts and pistachios (3169.6 and 2990.1muM trolox equi

100 between specific types of nuts, specifically peanuts and walnuts, and cardiovascular disease remain u

101 Peanut skin prick test responses and peanut- and Ara h 2-specific IgE levels were not associa

102 ffinity anti-IgE mAbs profoundly block human peanut- and cat-allergic IgE-mediated basophil CD63 indu

103 ot nematode was introgressed into cultivated peanut Arachis hypogaea from a wild peanut relative, A.

104 The clinical importance of peanut (Arachis hypogaea) allergies demands standardized

105 immobilization of beta-amylase (bamyl) from peanut (Arachis hypogaea) onto Graphene oxide-carbon nan

106 Defense responses of peanut (Arachis hypogaea) to biotic and abiotic stresses

107 Peanut (Arachis hypogaea; 2n = 4x = 40) is a nutritious

108 Medical guidelines on the introduction of peanut as well as other allergenic foods have evolved wi

109 ion was associated with IgE sensitization to peanut at age 4 years (adjusted odds ratio, 1.88; 95% CI

110 Feeding high doses of peanut before sensitization decreased percentages of CD3

111 while breast-feeding and directly introduced peanuts before 12 months.

112 ternative isoform was not only identified in peanut but also in soybean and Arabidopsis.

113 tion is associated with IgE sensitization to peanut but not to other allergens.

114 enes with changes in expression triggered by peanut, but not placebo, during acute peanut allergic re

115 pared with those who did not consume nuts or peanut butter [lowest category of consumption (C0)], par

116 nces in specific peanut allergen profiles in peanut butter and flour and peanut preparations for clin

117 en the highest and lowest intakes of nuts or peanut butter and the risk of gastric cardia adenocarcin

118 This inverse association was also seen for peanut butter consumption [C3 compared with C0, HR: 0.75

119 to evaluate the associations between nut and peanut butter consumption and the risk of esophageal and

120 ma.Among older American adults, both nut and peanut butter consumption were inversely associated with

121 ional Institute for Standards and Technology Peanut Butter Standard Reference Material 2387.

122 Intakes of nuts and peanut butter were assessed through the use of a validat

123 Roasting can increase Ara h 1 levels in peanut butter.

124 Roasted peanut butters contained 991 to 21,406 mug/g Ara h 1 and

125 d peanuts themselves but directly introduced peanuts by 12 months (17.6%).

126 tive of anaphylactic degranulation; suppress peanut-, cat-, and dansyl-specific IgE-mediated passive

127 +) T cell, and macrophage populations during peanut challenge.

128 consumption while breast-feeding and infant peanut consumption by 12 months were protective in combi

129 Furthermore, peanut consumption does not hasten the resolution of ecz

130 Breast-feeding and maternal and infant peanut consumption were captured by repeated questionnai

131 p and maternal atopy confirmed that maternal peanut consumption while breast-feeding and infant peanu

132 In this secondary analysis, maternal peanut consumption while breast-feeding paired with dire

133 nvestigate the relationship between maternal peanut consumption while breast-feeding, timing of direc

134 in LEAP participants and was not affected by peanut consumption.

135 ever, these studies did not address maternal peanut consumption.

136 ll other combinations of maternal and infant peanut consumption.

137 rgy can be prevented through introduction of peanut-containing foods beginning in infancy.

138 he timing and approaches for introduction of peanut-containing foods in the health care provider's of

139 ave been developed for early introduction of peanut-containing foods into the diets of infants at var

140 is study, sequences and transcript levels of peanut CSD1 isoforms (AhCSD1-1, AhCSD1-2.1, and AhCSD1-2

141 valuate whether omalizumab facilitated rapid peanut desensitization in highly allergic patients.

142 The median peanut dose tolerated on the initial desensitization day

143 treated subjects were exposed to much higher peanut doses.

144 low-molecular-weight compound composition of peanuts due to dry-roasting.

145 Qualifying subjects reacted to peanut during an entry food challenge and were block-ran

146 Recent trials have shown that avoiding peanuts during infancy increases the risk of peanut alle

147 We sought to validate the predicted peanut ED05 (1.5 mg) with a novel single-dose challenge.

148 not associated with objective reactivity to peanut ED05.

149 tionships between peanut tolerance, baseline peanut/egg sensitization, eczema severity/duration, age

150 We evaluated peanut epicutaneous immunotherapy (EPIT) by using Viaski

151 Peanut EPIT administration was safe and associated with

152 levels and IgG4/IgE ratios were observed in peanut EPIT-treated participants, along with trends towa

153 with filaggrin mutations) and environmental peanut exposure influences the development of peanut all

154 allergy induction, using either ovalbumin or peanut extract as allergens for sensitization and challe

155 Blood was incubated with peanut extract or anti-IgE and tests were performed as f

156 rgic subjects were stimulated (14-16 h) with peanut extract to detect peanut-specific CD4(+) CD154(+)

157 High or low doses of peanut extract were administered to pups every day for 2

158 Foxp3 methylation was increased in peanut extract-sensitized and challenged mice, whereas i

159 eanut (n = 16) and tree nut (n = 16) butter, peanut flour (n = 11), oils (n = 8), extracts used for d

160 nmental exposure, naive mice were exposed to peanut flour by inhalation for up to 4 weeks.

161 When exposed to peanut flour by inhalation, both BALB/c and C57BL/6 mice

162 Furthermore, peanut flour exposure increased lung levels of IL-1alpha

163 Ara h 2, and Ara h 6 in peanut foods and in peanut flour extracts used for allergy diagnosis and OIT

164 In contrast, peanut flours contained 787 to 14,631 mug/g Ara h 2 and

165 surement of Ara h 1, Ara h 2, and Ara h 6 in peanut foods and in peanut flour extracts used for aller

166 aneous immunotherapy (EPIT) by using Viaskin Peanut for peanut allergy treatment.

167 chools self-designate as peanut-free or have peanut-free areas, but the impact of policies on clinica

168 nuts from home, served in schools, or having peanut-free classrooms did not affect epinephrine admini

169 Some schools self-designate as peanut-free or have peanut-free areas, but the impact of

170 public school nurse survey reports of school peanut-free policies from 2006 to 2011 and whether schoo

171 uired before decisions can be made regarding peanut-free policies in schools.

172 We sought to determine the effect of peanut-free policies on rates of epinephrine administrat

173 Both self-designated peanut-free schools and schools banning peanuts from bei

174 Schools with peanut-free tables, compared to without, had lower rates

175 2011 and whether schools self-designated as "peanut-free" based on policies.

176 policies used by schools self-designated as peanut-free.

177 ated peanut-free schools and schools banning peanuts from being served in school or brought from home

178 Policies restricting peanuts from home, served in schools, or having peanut-f

179 ogical activity and chemical constituents of peanuts germinated for 0-9days.

180 prenyltransferase genes in elicitor-treated peanut hairy root cultures.

181 der investigation, but early introduction of peanut has been advised as a public health measure based

182 the years, guidelines on the introduction of peanut have evolved, and recent literature suggests that

183 Early introduction of dietary peanut in high-risk infants with severe eczema, egg alle

184 Early consumption of peanut in infants at high risk of peanut allergy is alle

185 effect persisted after 12 months of avoiding peanuts in the 12-month extension of the LEAP study (LEA

186 t-feeding paired with direct introduction of peanuts in the first year of life was associated with th

187 Raw peanuts in the USA are subjected to thermal processing,

188 contained within the vesicular bodies of the peanut increased after roasting.

189 Peanut-induced allergic reactions resulted in a signific

190 emonstrated the efficacy of EPIT in treating peanut-induced EGIDs.

191 Peanut introduction between 6 and 11 months of age was a

192 successful OFC was significantly higher with peanut introduction between 6 and 11 months than at 4-6

193 updated their guidelines in 2008 to promote peanut introduction during infancy.

194 rly About Peanut Allergy (LEAP) study, early peanut introduction in high-risk 4- to 11-month-olds was

195 that have led to the evolving guidelines on peanut introduction in infants.

196 ption while breast-feeding, timing of direct peanut introduction, and peanut sensitization at age 7 y

197 The predicted ED05 for peanut is 1.5 mg of peanut protein (6 mg of whole peanut

198 Peanut is a potent natural source of phytochemical compo

199 g (nod-) and nodulating (nod+) sister inbred peanut lines, E4/E5 and E7/E6, and their nod+ parents, F

200 Peanut skin (PS) and meal from dry-blanched peanuts (MDBP) were evaluated as sources of phenolic com

201 h 6 were used to compare allergen levels in peanut (n = 16) and tree nut (n = 16) butter, peanut flo

202 Peanut nut and tree nut allergy are characterised by IgE

203 /day, 28h) in extra-virgin olive oil (EVOO), peanut oil (PO) and canola oil (CO), and compared for di

204 while the total tocopherols were greatest in peanut oils with darker colors.

205 rapeseed, sunflower, sesame, cottonseed and peanut oils, it was superior to the widely utilized anal

206 ens were not detected in tree nut butters or peanut oils.

207 Peanut OIT is associated with frequent AEs, with rates d

208 T trials, comprising the largest analysis of peanut OIT safety to date.

209 from 104 children with peanut allergy from 3 peanut OIT studies.

210 was conducted, pooling data from 3 pediatric peanut OIT trials, comprising the largest analysis of pe

211 o assess the effect of early introduction of peanut on the development of allergic disease, food sens

212 ren aged 4-12 years undergoing OIT for milk, peanut, or egg allergy, at the beginning and after 4 mon

213 Though peanut oral immunotherapy (OIT) is a promising investiga

214 Probiotic and peanut oral immunotherapy has a sustained beneficial eff

215 Peanut oral immunotherapy is a promising approach to pea

216 Probiotic and peanut oral immunotherapy was associated with significan

217 ly desensitized over as little as 8 weeks of peanut oral immunotherapy.

218 patients (1:1:1:1) received an epicutaneous peanut patch containing 50 mug (n = 53), 100 mug (n = 56

219 ose, adverse events (AEs), and efficacy of a peanut patch for peanut allergy treatment.

220 placebo-controlled, dose-ranging trial of a peanut patch in peanut-allergic patients (6-55 years) fr

221 ial of peanut-allergic patients, the 250-mug peanut patch resulted in significant treatment response

222 s, acidic buffers, and thermal processing of peanuts perturbed allergen quantification in ELISAs, pro

223 isins) and edible seeds (almonds, hazelnuts, peanuts, pine nuts, pistachios, and walnuts) using a QuE

224 Concurrent sensitization to peanut (PN) and tree nuts (TN), the most dangerous food

225 The impact of peanut (PN) feeding and IgE neutralization on the develo

226 rgen profiles in peanut butter and flour and peanut preparations for clinical use.

227 andardization and provide accurate dosing of peanut preparations that are being used for OIT.

228 (OIT) are strengthened by using standardized peanut preparations with defined doses of major allergen

229 The predicted ED05 for peanut is 1.5 mg of peanut protein (6 mg of whole peanut).

230 ts underwent an open challenge to 4000 mg of peanut protein 12 weeks after stopping study drug.

231 andomized to omalizumab tolerated 2000 mg of peanut protein 6 weeks after stopping omalizumab versus

232 hanisms underlying induction of tolerance to peanut protein and prevention of the development of pean

233 tolerated, subjects continued on 4000 mg of peanut protein daily.

234 A single administration of 1.5 mg of peanut protein elicited objective reactions in fewer tha

235 ized by three intra-peritoneal injections of peanut protein extract (PPE) with adjuvant, and then giv

236 3), 100 mug (n = 56), or 250 mug (n = 56) of peanut protein or a placebo patch (n = 56).

237 times increase and/or reaching >/=1000 mg of peanut protein) in each group vs placebo patch after 12

238 pid 1-day desensitization of up to 250 mg of peanut protein, followed by weekly increases up to 2000

239 es to an eliciting dose of 300 mg or less of peanut protein.

240 doses of peanut to pups induced tolerance to peanut protein.

241 tinued, and subjects continued on 2000 mg of peanut protein.

242 Notably, peanut proteins have been detected in house dust, and th

243 els of IgE antibody and challenged mice with peanut proteins.

244 ltivated peanut Arachis hypogaea from a wild peanut relative, A. cardenasii and previously mapped to

245 sis-related genes in a genome-wide manner in peanut representative of the 'crack entry' species.

246 on were compared for schools with or without peanut-restrictive policies.

247 Peanuts roasted to equivalent surface colors at differen

248 applied for the analysis of AFB1 in rice and peanut samples.

249 Runner and virginia-type peanut seeds were characterized using several analytical

250 her vegetable oils (canola, safflower, corn, peanut, seeds, grapeseed, palm, linseed, sesame and soyb

251 play an important role in the regulation of peanut sensitivity and maintenance of immune homeostasis

252 Patients (n = 221) had peanut sensitivity and positive double-blind, placebo-co

253 istered to pups every day for 2 weeks before peanut sensitization and challenge.

254 This review aims to explore routes of peanut sensitization and the current evidence on how env

255 g, timing of direct peanut introduction, and peanut sensitization at age 7 years.

256 The way in which peanut sensitization occurs has been explored, such as v

257 Skin prick testing for peanut sensitization was performed at age 7 years.

258 life was associated with the lowest risk of peanut sensitization, compared with all other combinatio

259 large animal model of gastric eosinophil in peanut-sensitized piglets.

260 Peanut skin (PS) and meal from dry-blanched peanuts (MDB

261 Peanut skin prick test responses and peanut- and Ara h 2

262 se identifiable by using routinely available peanut skin prick test responses or specific IgE levels,

263 ck and purple bean, black lentil (BL), black peanut, sorghum (SH), black rice, and blue wheat.

264 At age 3, sensitization to foods (milk, egg, peanut, soy, wheat, walnut) was assessed.

265 ated (14-16 h) with peanut extract to detect peanut-specific CD4(+) CD154(+) T cells.

266 r, costaining of CD161 and CD200R identified peanut-specific highly differentiated IL-4(+) IL-5(+) Th

267 allergy, as demonstrated by the presence of peanut-specific IgE antibodies and manifestation of acut

268 Peanut-specific IgE levels significantly declined in E-O

269 than matched standard-care controls, in whom peanut-specific IgE levels significantly increased (rela

270 Increases in peanut-specific IgG4 levels and IgG4/IgE ratios were obs

271 Peanut-specific immune responses were serially analyzed.

272 ic and had high TH2 cytokine production upon peanut-specific restimulation.

273 In PA subjects, the peanut-specific Th2 (CD154(+) CRTh2(+) ) cells expressed

274 rends toward reduced basophil activation and peanut-specific TH2 cytokines.

275 We sought to determine whether peanut-specific TR1 cells can be generated in vitro from

276 Peanut-specific TR1 cells can be induced from HC subject

277 nd whether they are functional compared with peanut-specific TR1 cells induced from healthy control (

278 These results suggest that the peanut sprout exerts high anti-inflammatory effects that

279 Baseline allergic rhinitis (AR) and peanut SPT wheal size were significant predictors of hig

280 and are significantly associated with AR and peanut SPT wheal size, respectively.

281 more likely to successfully consume dietary peanut than matched standard-care controls, in whom pean

282 ond 12 months (15.1%), or if mothers avoided peanuts themselves but directly introduced peanuts by 12

283 Feeding high doses of peanut to pups induced tolerance to peanut protein.

284 while breast-feeding but delayed introducing peanuts to their infant beyond 12 months (15.1%), or if

285 ity had limited impact on the probability of peanut tolerance in the early introduction arm.

286 The probability of peanut tolerance in the early introduction group was 83%

287 Odds of peanut tolerance were lower with increasing peanut wheal

288 EAP dataset, exploring relationships between peanut tolerance, baseline peanut/egg sensitization, ecz

289 age was associated with the highest rates of peanut tolerance, questioning the 'urgency' of introduct

290 rees C for a quite long time (24-36h), while peanuts undergo a roasting process at 160-180 degrees C

291 San Francisco, Calif) might allow more rapid peanut updosing and decrease reactions.

292 The overall flavor of roasted peanuts was found to be optimized at 177 degrees C/15min

293 ty of oleosins derived from in-shell roasted peanuts was increased as shown by immunoblot analysis an

294 milk, soy flour, ground hazelnut and ground peanut were prepared at laboratory scale.

295 Jumbo-size runner-type peanuts were systematically roasted at 5 temperatures (1

296 Dried prunes and peanuts were the only samples appreciably contaminated,

297 peanut tolerance were lower with increasing peanut wheal size (OR 0.58, P < 0.001, 95% CI 0.46-0.74)

298 served among children whose mothers consumed peanuts while breast-feeding and directly introduced pea

299 icantly higher (P < .05) if mothers consumed peanuts while breast-feeding but delayed introducing pea

300 ecular mechanisms of symbiosis in cultivated peanut with a 'crack entry' infection process are largel