ライフサイエンスコーパス: anaphylactic

1 ergy or intolerance patients) and 15.9% were anaphylactic.

2 tions that were potentially IgE-mediated and anaphylactic.

3 hat in the murine model, the serum level and anaphylactic activity of IgE may be downregulated by gly

4 er a mechanistic explanation for the reduced anaphylactic activity.

5 nse to rituximab as well as infusion-related anaphylactic adverse events is the development of antidr

6 No investigator-assessed anaphylactic allergic reactions or reactions requiring e

7 RasGRP1-deficient mice failed to mount anaphylactic allergic reactions.

8 ctivation of p110delta protects mice against anaphylactic allergic responses.

9 Their discovery ended the belief that an anaphylactic/allergic reaction was caused by poisons, bu

10 ng, and ultimately preventing these emerging anaphylactic and other vector-borne diseases.

11 their in vivo ability to induce Ber-specific anaphylactic antibodies and the role of invariant natura

12 eutral and common phospholipids, induced Ber anaphylactic antibodies in mice.

13 iNKT-deficient mice produced lower levels of anaphylactic antibodies than WT mice.

14 th Ber e 1 and specific lipid fractions, and anaphylactic antibodies were measured by enzyme-linked i

15 novel and alternative treatment strategy for anaphylactic attacks.

16 e robust and ultrasensitive detection of the anaphylactic beta-conglutin allergen using Apta-PCR achi

17 Five NMBA-related anaphylactic deaths occurred during P0 and P1 and, howev

18 ated with the morphologic continuum of PMD-->anaphylactic degranulation (characterized by extrusion o

19 the high-affinity anti-IgE mAbs that trigger anaphylactic degranulation at low concentration.

20 he cell surface-bound IgE without triggering anaphylactic degranulation even at high concentration, a

21 diated basophil CD63 induction indicative of anaphylactic degranulation; suppress peanut-, cat-, and

22 Last, the effect of anaphylactic-derived high-density lipoprotein (HDL) part

23 ropod vectors have been involved in emerging anaphylactic diseases.

24 phopoietin) at 3 time points (ie, during the anaphylactic episode and in convalescent samples 7 and 3

25 etermine an unfavorable outcome of the acute anaphylactic episode and should be addressed during indi

26 After treatment of an anaphylactic episode, follow-up with a physician, prefer

27 All patients recovered from the anaphylactic episode.

28 f allergic symptoms and prevention of future anaphylactic episodes are clinically important.

29 after immunotherapy was associated with more anaphylactic episodes before treatment and a lower start

30 ear-old girl who presented with a history of anaphylactic episodes on three occasions, that developed

31 a need of more knowledge about work-related anaphylactic episodes.

32 fied from human studies due to the rarity of anaphylactic events and their unpredictability.

33 um discriminated between nonanaphylactic and anaphylactic events in a perioperative setting when acut

34 The primary end point was anaphylactic events in the 6 months after baseline.

35 istory-guided treatment: if history excludes anaphylactic features, give cefazolin (Hx-Cefaz); and (3

36 for the rapid and sensitive detection of the anaphylactic food allergen Lup an 1 (beta-conglutin) exp

37 immune responses, mast cell homeostasis, and anaphylactic food allergy was assessed in these animals.

38 ut sensitization (PS) and (ii) differentiate anaphylactic from nonanaphylactic PA.

39 re unaltered, while ApoA1 was reduced in the anaphylactic group.

40 constitute a central pathogenetic element of anaphylactic (IgE-dependent) and anaphylactoid (IgE-inde

41 egranulation resulting in a life-threatening anaphylactic-like response in mice.

42 ig model of immediate type hypersensitivity, anaphylactic mast cell degranulation in bronchial rings

43 We found a reduction of both lipoproteins in anaphylactic mice as well as in orally challenged food a

44 mine release, in an in vivo passive systemic anaphylactic model, is exacerbated by a single dose and

45 eutic efficacy while exhibiting virtually no anaphylactic off-target effects.

46 All 14 patients with anaphylactic or anaphylactoid reactions survived.

47 otentially serious events, such as seizures, anaphylactic or anaphylactoid reactions, serum sickness,

48 sitized children, 55 nonanaphylactic, and 53 anaphylactic PA cases from the Chicago Food Allergy Stud

49 We therefore assessed anaphylactic patients seen by emergency physicians in th

50 ns are the receptors for the chemotactic and anaphylactic peptides, C5a and C3a, which are the most-p

51 n driving fluid extravasation and the severe anaphylactic phenotype are not fully elucidated.

52 are thought to lead to the life-threatening anaphylactic phenotype.

53 were associated with a 38% increased risk of anaphylactic reaction (40.7 per 100,000 person-years vs.

54 ema (n=69, 20.9%), asthma (n=65, 19.7%), and anaphylactic reaction (n=19, 5.8%).

55 ive patients with a convincing history of an anaphylactic reaction after a hymenoptera sting were tes

56 ort we describe a patient who experienced an anaphylactic reaction after the injection of fluorescein

57 OcAn, both confirmation of the diagnosis of anaphylactic reaction and identification of the trigger

58 ced a serious infusion reaction (one grade 4 anaphylactic reaction and one grade 3 stridor) during th

59 history of allergy to contrast agents had an anaphylactic reaction and recovered without sequelae.

60 ing patients after complete resolution of an anaphylactic reaction and to dispense with prolonged mon

61 We suspected an anaphylactic reaction and treated him with intramuscular

62 tide-induced EAE models led to a rapid-onset anaphylactic reaction characterized by respiratory distr

63 An anaphylactic reaction due to a Hymenoptera sting is a cl

64 Anaphylactic reaction following contrast agent administr

65 veloping anaphylaxis or failure to treat the anaphylactic reaction made up the majority of allegation

66 sis lesions, and clinical characteristics of anaphylactic reaction might be useful for differential d

67 This anaphylactic reaction required a human CD32a transgene b

68 activation of mast cells is a hallmark of an anaphylactic reaction to allergen.

69 E-dependent effector mechanisms, and a local anaphylactic reaction to an unrelated antigen can enhanc

70 with the ingestion of only Citrus unshiu, an anaphylactic reaction was induced by additional acetyl-s

71 associated with a modestly increased risk of anaphylactic reaction when compared with DPP-4 inhibitor

72 Such an anaphylactic reaction would also limit potential therape

73 ears [n = 356] without a history of a severe anaphylactic reaction) developing objective symptoms dur

74 hycardia, upper gastrointestinal hemorrhage, anaphylactic reaction, acute kidney injury, and acute my

75 was conducted with the MeSH of anaphylaxis, anaphylactic reaction, anaphylactic shock, refractory an

76 Urticaria, anaphylactic reaction, and angioneurotic edema were only

77 ated (four cases of haematoma expansion, one anaphylactic reaction, and one ischaemic stroke) and two

78 decrease in body temperature, reflecting the anaphylactic reaction, is substantially enhanced by the

79 No serious complications such as blindness, anaphylactic reaction, or terminal disease transmission

80 ltuximab (lower respiratory tract infection, anaphylactic reaction, sepsis).

81 8) generated a modest increase in the HR for anaphylactic reaction, with a wide 95% CI (36.9 per 100,

82 7.7% (95% CI, 5.7% to 9.7%) reported a prior anaphylactic reaction.

83 cted to oral challenge, which resulted in an anaphylactic reaction.

84 The patient developed an anaphylactic reaction.

85 cur with fluorescein angiography, such as an anaphylactic reaction.

86 ent was also observed in an active cutaneous anaphylactic reaction.

87 ng signals can dominate to initiate a severe anaphylactic reaction.

88 95.4%) and in all patients with a history of anaphylactic reaction.

89 symptoms ranging from oral pruritus to fatal anaphylactic reaction.

90 4 toxicities included acne-like rash (6.1%), anaphylactic reactions (1.5%), and diarrhea (1.5%).

91 dren with higher esIgD had decreased odds of anaphylactic reactions (OR =0.48, P = .038).

92 s (0.6%) who received pemivibart experienced anaphylactic reactions (serious in 2).

93 2)=0%, RD 5.7%, moderate-certainty), and non-anaphylactic reactions (vomiting: RR 1.79 [95%CI 1.35-2.

94 Allergic and anaphylactic reactions after the first and second doses

95 uced anaphylaxis (WDEIA) is characterized by anaphylactic reactions after wheat ingestion and physica

96 gy to peanut is one of the leading causes of anaphylactic reactions among food allergic patients.

97 o beta-lactams are the most common causes of anaphylactic reactions and can be life-threatening.

98 pture, as in case of misdiagnosis, may cause anaphylactic reactions and dissemination.

99 HalphaT(+) patients were more likely to have anaphylactic reactions and less likely to have cutaneous

100 Elicitors of anaphylactic reactions are any sources of protein with a

101 Severe IgE-mediated, food-induced anaphylactic reactions are characterized by pulmonary ve

102 ate that the vast majority of food-triggered anaphylactic reactions are not life-threatening.

103 Anaphylactic reactions are not uncommon and are often fa

104 Although anaphylactic reactions are potentially life-threatening,

105 Anaphylactic reactions associated with the Food and Drug

106 city while reducing their potential to cause anaphylactic reactions by essentially eliminating IgE-me

107 ) disease that can lead to potentially fatal anaphylactic reactions caused by excessive MC mediator r

108 Systemic anaphylactic reactions did not occur.

109 he scientific evidence on self-medication of anaphylactic reactions due to Hymenoptera stings, to inf

110 The underlying mechanisms of anaphylactic reactions due to occupational exposure are

111 The effects on anaphylactic reactions following PN challenge and the as

112 We identified 213 anaphylactic reactions in 192 children (97 male patients

113 teria monocytogenes (HKLM) as an adjuvant on anaphylactic reactions in a mouse model of PN allergy.

114 The prevalence and incidence of anaphylactic reactions in Germany are unknown.

115 roles in initiating and amplifying allergic/anaphylactic reactions in humans.

116 IIA may therefore contribute to allergic and anaphylactic reactions in humans.

117 xtravasation in the severity of IgE-mediated anaphylactic reactions in mice.

118 ast to non-PEGylated rMETase, which elicited anaphylactic reactions in monkeys.

119 antibody production in mice and monkeys and anaphylactic reactions in monkeys.

120 inhibitors have been associated with severe anaphylactic reactions in patients with hymenoptera veno

121 s of pathogenic antibody or life-threatening anaphylactic reactions in protein replacement therapy fo

122 c response to infused VWF concentrates up to anaphylactic reactions in rare cases.

123 early-phase and severely blunted late-phase anaphylactic reactions in response to antigen challenge

124 carrying btk mutations exhibited diminished anaphylactic reactions in response to IgE and antigen.

125 ontrast media, the major cause of iatrogenic anaphylactic reactions in the hospital, is explored.

126 s referred to our hospital owing to repeated anaphylactic reactions induced by exercise after meals.

127 Monitoring after complete resolution of anaphylactic reactions is recommended.

128 She experienced anaphylactic reactions just after the inhalation of Inav

129 Anaphylactic reactions may occur among 1%-2% of botulinu

130 Anaphylactic reactions occurred in 6 of the 149 treated

131 Grade 3 severe anaphylactic reactions occurred in seven cases of nine.

132 oducing Treg cells, without causing allergic/anaphylactic reactions or generalized immunosuppression.

133 We performed a review of PED records for anaphylactic reactions over 5 years.

134 regimens considerably increase allergic and anaphylactic reactions over avoidance or placebo, despit

135 Moreover, this treatment eliminated fatal anaphylactic reactions that occurred after four to six e

136 on of pork kidney proteins mediating delayed anaphylactic reactions through specific IgE to alpha-Gal

137 Although anaphylactic reactions to blood products are rare, the i

138 nd distress commonly feature in survivors to anaphylactic reactions to drug.

139 (iii) The anaphylactic reactions to food derived from non-primate

140 ) is the major cause of fatal and near-fatal anaphylactic reactions to foods.

141 d to treat the few patients who present with anaphylactic reactions to Hymenoptera stings, as well as

142 Anaphylactic reactions to immunoglobulin infusions in im

143 Among the most frequent anaphylactic reactions to insects are those attributed t

144 Anaphylactic reactions to neuromuscular blocking agents

145 as to evaluate mortality rate in France from anaphylactic reactions to NMBAs, to identify risk factor

146 f parenteral penicillins, and because severe anaphylactic reactions to oral amoxicillin are rare.

147 tructure and described as major elicitors of anaphylactic reactions to peanut (allergens Ara h 2 and

148 eggs, or occurrence of Sampson Grade 3 to 5 anaphylactic reactions upon egg ingestion.

149 nses compared to free allergen in mice while anaphylactic reactions were essentially abolished.

150 ited Kingdom, Canada, and the United States, anaphylactic reactions were reported.

151 lls in multiple tissues and displayed robust anaphylactic reactions when passively sensitized with pa

152 ble involvement of augmenting factors; after anaphylactic reactions, always ask for possible augmenta

153 p between serum basal tryptase (sBT) levels, anaphylactic reactions, and clonal mast cell diseases wa

154 peptide 1 receptor agonists (GLP-1 RAs) with anaphylactic reactions, but real-world evidence for this

155 Biphasic anaphylactic reactions, especially clinically important

156 with pathological conditions or allergic and anaphylactic reactions, it may contribute beneficially t

157 (NARA), total number of reports on suspected anaphylactic reactions, number of reactions where NMBAs

158 eaction tryptase level) detected most of the anaphylactic reactions, particularly if baseline levels

159 phasic - and clinically important biphasic - anaphylactic reactions, the number of transfers to inten

160 ll deficient and protected from IgE-mediated anaphylactic reactions, their dramatically different res

161 protein injection of immunized mice induced anaphylactic reactions, which were more severe in multip

162 can range from mild local symptoms to severe anaphylactic reactions.

163 re were 507 uniphasic and 25 (4.5%) biphasic anaphylactic reactions.

164 patients to prevent further life-threatening anaphylactic reactions.

165 ocument a role for cofactors in about 30% of anaphylactic reactions.

166 Symptoms range from mild to anaphylactic reactions.

167 , thereby promoting allergic and potentially anaphylactic reactions.

168 ere, including one moderate reaction and two anaphylactic reactions.

169 developed significantly attenuated cutaneous anaphylactic reactions.

170 allergenic food capable of provoking severe anaphylactic reactions.

171 allergenic foods, which can result in severe anaphylactic reactions.

172 eous tissue, are less likely to give rise to anaphylactic reactions.

173 mice represents a new animal model to study anaphylactic reactions.

174 the most common cause of fatal food-induced anaphylactic reactions.

175 The TWEAK/Fn14 axis participates in anaphylactic reactions.

176 lation of SNAP-23 leads to degranulation and anaphylactic reactions.

177 on of IgG1 Abs and to the risk of triggering anaphylactic reactions.

178 ete Freund's adjuvant has resulted in severe anaphylactic reactions.

179 life of the rMETase apoenzyme and eliminated anaphylactic reactions.

180 diators that cause allergic inflammation and anaphylactic reactions.

181 ths, and no patients experienced allergic or anaphylactic reactions.

182 d minor allergic responses, and 3 (0.7%) had anaphylactic reactions.

183 Drugs are a frequent cause of severe anaphylactic reactions.

184 could also abort ongoing acute IgE-mediated anaphylactic reactions.

185 ot all patients with mastocytosis experience anaphylactic reactions.

186 s organs and severe or even life-threatening anaphylactic reactions.

187 hereas PGE(2) stabilization protects against anaphylactic reactions.

188 rotective immune responses in the absence of anaphylactic reactions.

189 ere confirmed as allergic, including 11 with anaphylactic reactions.

190 the VE IL-4Ralpha and ABL1 pathway in severe anaphylactic reactions.

191 history of anaphylaxis are at risk of future anaphylactic reactions.

192 posed to contain milk proteins, which caused anaphylactic reactions.

193 portantly, CpG/PN-NP treatment did not cause anaphylactic reactions.

194 Two patients in the reslizumab group had anaphylactic reactions; both responded to standard treat

195 AHG2 also significantly inhibited acute anaphylactic reactivity, including the prototypical decr

196 Anaphylactic release of renin, histamine, and beta-hexos

197 deficient MCs was sufficient to drive a full anaphylactic response in mice.

198 free (SPF) mice, and prevented or treated an anaphylactic response to allergen challenge.

199 intestinal epithelium preceded onset of the anaphylactic response to ingested OVA antigen.

200 show that the human alpha-chain restores an anaphylactic response to the nonresponsive alpha-deficie

201 Anaphylactic response was assessed by core body temperat

202 ocker) and ramipril (ACE inhibitor) with the anaphylactic response was determined.

203 ot of apo-Alt a 1, significantly impeded the anaphylactic response, impaired splenic antigen-presenti

204 1, holo-Alt a 1 or RA alone before measuring anaphylactic response, serum antibody levels, splenic cy

205 Ear swelling was assessed to evaluate the anaphylactic response.

206 and cytokine release, as well as the in vivo anaphylactic response.

207 )-BSA) substantially reduced the BSA-induced anaphylactic response.

208 L-10 overexpression reduced the IgE-mediated anaphylactic response.

209 daily without a mucocutaneous, bronchial, or anaphylactic response.

210 vivo as young lyn-/- mice showed an enhanced anaphylactic response.

211 cient mice produce a normal passive systemic anaphylactic response.

212 MC effector response is required for a full anaphylactic response.

213 Anti-IgE (omalizumab) treatment ablated this anaphylactic response.

214 silonRI-dependent late-phase, but not acute, anaphylactic responses and airway inflammation.

215 o vascular hyperpermeability and intensified anaphylactic responses in female mice, providing additio

216 ature, dye extravasation) to assess systemic anaphylactic responses in nonanesthetized wild-type, Fc

217 opment of IgE antibodies, TH2 responses, and anaphylactic responses on challenge.

218 ignificantly reduced severity of MC-mediated anaphylactic responses that emerge prior to puberty and

219 but not CMA, infants were protected against anaphylactic responses to a cow's milk allergen.

220 ial for fluid and electrolyte losses and for anaphylactic responses to luminal antigens.

221 ice with ovalbumin or peanut allergy reduced anaphylactic responses to oral allergen challenge by 84%

222 Anaphylactic responses were more pronounced in female th

223 th either active, or IgG1-dependent passive, anaphylactic responses were significantly greater in Fc

224 oparticles is effective in modulating murine anaphylactic responses, and indicate its prophylactic ut

225 Immunoglobulin E-triggered anaphylactic responses, including elevation of circulati

226 induced airway inflammation and OVA induced anaphylactic responses, including hypothermia and clinic

227 d cultured mast cells (HCMCs) and on in vivo anaphylactic responses.

228 cell function, as revealed by impaired local anaphylactic responses.

229 on to modulate peanut antigen-induced murine anaphylactic responses.

230 mast cell responses and, remarkably, in vivo anaphylactic responses.

231 pendent mast cell degranulation and systemic anaphylactic responses.

232 and IgG levels, and significantly attenuated anaphylactic responses.

233 10 on DCs in the development of allergic and anaphylactic responses.

234 egy for the rapid inhibition of IgE-mediated anaphylactic responses.

235 may lead to improvement of DS treatments for anaphylactic responses.

236 s been reported between 7% and 8.5%, but the anaphylactic risk at the time of introduction is current

237 companying the immune therapy constituted an anaphylactic risk factor only when the autoantigen was n

238 These are (1) anaphylactic sensitivity to peanut, (2) eosinophilic eso

239 addition, purified HDL particles from human anaphylactic sera failed to stabilize and maintain the e

240 Anaphylactic shock (76.6%), severe systemic reactions (1

241 Anaphylactic shock (AS) is an acute, potentially life-th

242 ssociated with a higher risk of mortality of anaphylactic shock (AS), but it is unknown whether this

243 All cases with a diagnosis of anaphylactic shock and 20% of cases with related diagnos

244 S-derived NO is the principal vasodilator in anaphylactic shock and define eNOS and/or PI3K or Akt as

245 tions are life-threatening reactions such as anaphylactic shock and fatal anaphylaxis.

246 release mediators and cytokines that trigger anaphylactic shock and promote allergic inflammation.

247 A 12-year-old girl experienced anaphylactic shock and respiratory failure immediately a

248 After sensitization and induction of anaphylactic shock by ovalbumin, animals received either

249 CPN1(-/-) mice were hypersensitive to lethal anaphylactic shock due to acute complement activation by

250 We studied PAF and anaphylactic shock in conscious mice.

251 Anaphylactic shock is a sudden, life-threatening allergi

252 Anaphylactic shock is associated with severe hypotension

253 Anaphylactic shock is associated with severe impairment

254 e contribution of NO to PAF-induced shock or anaphylactic shock is still ambiguous.

255 Severe hypotension resulting from anaphylactic shock may be refractory to epinephrine and

256 l oxygenation and metabolism contributing to anaphylactic shock morbidity and mortality.

257 event cerebral ischemia and could be used in anaphylactic shock refractory to epinephrine.

258 in the PLP(139-151) model demonstrating that anaphylactic shock resulting in death occurs upon rechal

259 Interestingly, all patients with an anaphylactic shock showed a positive BAT to CLV using CD

260 de 1 reaction and negative skin tests had an anaphylactic shock to the OC.

261 ere sensitized with ovalbumin (1 mg SC), and anaphylactic shock was induced by IV injection of ovalbu

262 so protect primed recipients from Ag-induced anaphylactic shock, and thus does not cause immune devia

263 anti-inflammatory scavenger and is linked to anaphylactic shock, asthma, and allergic reactions.

264 No serious adverse events, such as anaphylactic shock, mortality, and the development of an

265 MeSH of anaphylaxis, anaphylactic reaction, anaphylactic shock, refractory anaphylaxis and subheadin

266 , and two of them provoked the occurrence of anaphylactic shock, which was relieved by the intramuscu

267 e first-line vasoconstrictive agent to treat anaphylactic shock.

268 eutrophils and monocytes to the induction of anaphylactic shock.

269 nulation of mast cells may cause symptoms of anaphylactic shock.

270 Among the 14 patients, 12 presented with anaphylactic shock.

271 a critical role, results in life-threatening anaphylactic shock.

272 counteract the vasodilation associated with anaphylactic shock.

273 that induces rashes, vomiting, diarrhea, and anaphylactic shock.

274 was less susceptible to Ag-induced systemic anaphylactic shock.

275 ish samples was not performed due to risk of anaphylactic shock.

276 ding erythema, abdominal pain, vomiting, and anaphylactic shock.

277 E (FcepsilonRI) underlies type I allergy and anaphylactic shock.

278 ncreases survival in the Wistar rat model of anaphylactic shock.

279 treated rats survived after the induction of anaphylactic shock.

280 ere administered 1 minute after induction of anaphylactic shock.

281 gh basal plasma S1P levels protective during anaphylactic shock.

282 rapeutic approach to treatment of refractory anaphylactic shock.

283 tore blood pressure and increase survival in anaphylactic shock.

284 Despite high Ab titers, anaphylactic side reactions were not observed when MP4 w

285 placebo-controlled food challenge in all but anaphylactic subjects.

286 Anaphylactic symptom scores, core body temperatures, pla

287 -mutant mice with allergen plus CT abrogates anaphylactic symptoms and Ag-specific IgE, and results i

288 N-specific IgE that correlated with systemic anaphylactic symptoms and elevated plasma histamine.

289 c IgE, elevated plasma histamine levels, and anaphylactic symptoms in three different strains of mice

290 modulate an ongoing Th2 response and prevent anaphylactic symptoms in vivo, presenting a novel option

291 th 2'-fucosyllactose and 6'-sialyllactose on anaphylactic symptoms induced by oral ovalbumin (OVA) ch

292 t, their combined administration exacerbated anaphylactic symptoms potently and simultaneously enhanc

293 inth-infected mice, both PN-specific IgE and anaphylactic symptoms were greatly diminished.

294 s to IL-10, the PN-specific IgE response and anaphylactic symptoms were similar to, or greater than,

295 ll mice in the sham-treated groups exhibited anaphylactic symptoms with a median symptom score of 3,

296 t, mice were challenged orally to cashew and anaphylactic symptoms, as well as plasmatic levels of ma

297 its from her diet, she has not developed any anaphylactic symptoms.

298 nt guidelines for the specific management of anaphylactic transfusion reactions are contradictory as

299 st cells at these sites exhibited extensive, anaphylactic-type degranulation.

300 sed evaluation of patients who have suffered anaphylactic vaccine reactions and prospective clinical