1 tions that were potentially IgE-mediated and
anaphylactic.
2 ergy or intolerance patients) and 15.9% were
anaphylactic.
3 er a mechanistic explanation for the reduced
anaphylactic activity.
4 No investigator-assessed
anaphylactic allergic reactions or reactions requiring e
5 RasGRP1-deficient mice failed to mount
anaphylactic allergic reactions.
6 ctivation of p110delta protects mice against
anaphylactic allergic responses.
7 Their discovery ended the belief that an
anaphylactic/
allergic reaction was caused by poisons, bu
8 ng, and ultimately preventing these emerging
anaphylactic and other vector-borne diseases.
9 their in vivo ability to induce Ber-specific
anaphylactic antibodies and the role of invariant natura
10 eutral and common phospholipids, induced Ber
anaphylactic antibodies in mice.
11 iNKT-deficient mice produced lower levels of
anaphylactic antibodies than WT mice.
12 th Ber e 1 and specific lipid fractions, and
anaphylactic antibodies were measured by enzyme-linked i
13 novel and alternative treatment strategy for
anaphylactic attacks.
14 e robust and ultrasensitive detection of the
anaphylactic beta-conglutin allergen using Apta-PCR achi
15 Five NMBA-related
anaphylactic deaths occurred during P0 and P1 and, howev
16 ated with the morphologic continuum of PMD-->
anaphylactic degranulation (characterized by extrusion o
17 the high-affinity anti-IgE mAbs that trigger
anaphylactic degranulation at low concentration.
18 he cell surface-bound IgE without triggering
anaphylactic degranulation even at high concentration, a
19 diated basophil CD63 induction indicative of
anaphylactic degranulation; suppress peanut-, cat-, and
20 ropod vectors have been involved in emerging
anaphylactic diseases.
21 phopoietin) at 3 time points (ie, during the
anaphylactic episode and in convalescent samples 7 and 3
22 After treatment of an
anaphylactic episode, follow-up with a physician, prefer
23 after immunotherapy was associated with more
anaphylactic episodes before treatment and a lower start
24 ear-old girl who presented with a history of
anaphylactic episodes on three occasions, that developed
25 istory-guided treatment: if history excludes
anaphylactic features, give cefazolin (Hx-Cefaz); and (3
26 for the rapid and sensitive detection of the
anaphylactic food allergen Lup an 1 (beta-conglutin) exp
27 immune responses, mast cell homeostasis, and
anaphylactic food allergy was assessed in these animals.
28 ut sensitization (PS) and (ii) differentiate
anaphylactic from nonanaphylactic PA.
29 re unaltered, while ApoA1 was reduced in the
anaphylactic group.
30 constitute a central pathogenetic element of
anaphylactic (
IgE-dependent) and anaphylactoid (IgE-inde
31 egranulation resulting in a life-threatening
anaphylactic-
like response in mice.
32 ig model of immediate type hypersensitivity,
anaphylactic mast cell degranulation in bronchial rings
33 We found a reduction of both lipoproteins in
anaphylactic mice as well as in orally challenged food a
34 mine release, in an in vivo passive systemic
anaphylactic model, is exacerbated by a single dose and
35 eutic efficacy while exhibiting virtually no
anaphylactic off-target effects.
36 All 14 patients with
anaphylactic or anaphylactoid reactions survived.
37 otentially serious events, such as seizures,
anaphylactic or anaphylactoid reactions, serum sickness,
38 sitized children, 55 nonanaphylactic, and 53
anaphylactic PA cases from the Chicago Food Allergy Stud
39 We therefore assessed
anaphylactic patients seen by emergency physicians in th
40 ns are the receptors for the chemotactic and
anaphylactic peptides, C5a and C3a, which are the most-p
41 n driving fluid extravasation and the severe
anaphylactic phenotype are not fully elucidated.
42 are thought to lead to the life-threatening
anaphylactic phenotype.
43 ema (n=69, 20.9%), asthma (n=65, 19.7%), and
anaphylactic reaction (n=19, 5.8%).
44 ive patients with a convincing history of an
anaphylactic reaction after a hymenoptera sting were tes
45 OcAn, both confirmation of the diagnosis of
anaphylactic reaction and identification of the trigger
46 ced a serious infusion reaction (one grade 4
anaphylactic reaction and one grade 3 stridor) during th
47 ing patients after complete resolution of an
anaphylactic reaction and to dispense with prolonged mon
48 We suspected an
anaphylactic reaction and treated him with intramuscular
49 tide-induced EAE models led to a rapid-onset
anaphylactic reaction characterized by respiratory distr
50 An
anaphylactic reaction due to a Hymenoptera sting is a cl
51 sis lesions, and clinical characteristics of
anaphylactic reaction might be useful for differential d
52 This
anaphylactic reaction required a human CD32a transgene b
53 E-dependent effector mechanisms, and a local
anaphylactic reaction to an unrelated antigen can enhanc
54 with the ingestion of only Citrus unshiu, an
anaphylactic reaction was induced by additional acetyl-s
55 Such an
anaphylactic reaction would also limit potential therape
56 ated (four cases of haematoma expansion, one
anaphylactic reaction, and one ischaemic stroke) and two
57 decrease in body temperature, reflecting the
anaphylactic reaction, is substantially enhanced by the
58 ltuximab (lower respiratory tract infection,
anaphylactic reaction, sepsis).
59 7.7% (95% CI, 5.7% to 9.7%) reported a prior
anaphylactic reaction.
60 cted to oral challenge, which resulted in an
anaphylactic reaction.
61 ent was also observed in an active cutaneous
anaphylactic reaction.
62 ng signals can dominate to initiate a severe
anaphylactic reaction.
63 95.4%) and in all patients with a history of
anaphylactic reaction.
64 symptoms ranging from oral pruritus to fatal
anaphylactic reaction.
65 4 toxicities included acne-like rash (6.1%),
anaphylactic reactions (1.5%), and diarrhea (1.5%).
66 uced anaphylaxis (WDEIA) is characterized by
anaphylactic reactions after wheat ingestion and physica
67 o beta-lactams are the most common causes of
anaphylactic reactions and can be life-threatening.
68 pture, as in case of misdiagnosis, may cause
anaphylactic reactions and dissemination.
69 Elicitors of
anaphylactic reactions are any sources of protein with a
70 Severe IgE-mediated, food-induced
anaphylactic reactions are characterized by pulmonary ve
71 ate that the vast majority of food-triggered
anaphylactic reactions are not life-threatening.
72 Although
anaphylactic reactions are potentially life-threatening,
73 city while reducing their potential to cause
anaphylactic reactions by essentially eliminating IgE-me
74 ) disease that can lead to potentially fatal
anaphylactic reactions caused by excessive MC mediator r
75 Systemic
anaphylactic reactions did not occur.
76 he scientific evidence on self-medication of
anaphylactic reactions due to Hymenoptera stings, to inf
77 The underlying mechanisms of
anaphylactic reactions due to occupational exposure are
78 The effects on
anaphylactic reactions following PN challenge and the as
79 We identified 213
anaphylactic reactions in 192 children (97 male patients
80 teria monocytogenes (HKLM) as an adjuvant on
anaphylactic reactions in a mouse model of PN allergy.
81 The prevalence and incidence of
anaphylactic reactions in Germany are unknown.
82 IIA may therefore contribute to allergic and
anaphylactic reactions in humans.
83 xtravasation in the severity of IgE-mediated
anaphylactic reactions in mice.
84 ast to non-PEGylated rMETase, which elicited
anaphylactic reactions in monkeys.
85 antibody production in mice and monkeys and
anaphylactic reactions in monkeys.
86 inhibitors have been associated with severe
anaphylactic reactions in patients with hymenoptera veno
87 s of pathogenic antibody or life-threatening
anaphylactic reactions in protein replacement therapy fo
88 c response to infused VWF concentrates up to
anaphylactic reactions in rare cases.
89 early-phase and severely blunted late-phase
anaphylactic reactions in response to antigen challenge
90 carrying btk mutations exhibited diminished
anaphylactic reactions in response to IgE and antigen.
91 ontrast media, the major cause of iatrogenic
anaphylactic reactions in the hospital, is explored.
92 s referred to our hospital owing to repeated
anaphylactic reactions induced by exercise after meals.
93 Monitoring after complete resolution of
anaphylactic reactions is recommended.
94 She experienced
anaphylactic reactions just after the inhalation of Inav
95 Anaphylactic reactions may occur among 1%-2% of botulinu
96 Anaphylactic reactions occurred in 6 of the 149 treated
97 Grade 3 severe
anaphylactic reactions occurred in seven cases of nine.
98 oducing Treg cells, without causing allergic/
anaphylactic reactions or generalized immunosuppression.
99 We performed a review of PED records for
anaphylactic reactions over 5 years.
100 Moreover, this treatment eliminated fatal
anaphylactic reactions that occurred after four to six e
101 on of pork kidney proteins mediating delayed
anaphylactic reactions through specific IgE to alpha-Gal
102 Although
anaphylactic reactions to blood products are rare, the i
103 nd distress commonly feature in survivors to
anaphylactic reactions to drug.
104 ) is the major cause of fatal and near-fatal
anaphylactic reactions to foods.
105 d to treat the few patients who present with
anaphylactic reactions to Hymenoptera stings, as well as
106 Anaphylactic reactions to immunoglobulin infusions in im
107 Among the most frequent
anaphylactic reactions to insects are those attributed t
108 Anaphylactic reactions to neuromuscular blocking agents
109 as to evaluate mortality rate in France from
anaphylactic reactions to NMBAs, to identify risk factor
110 tructure and described as major elicitors of
anaphylactic reactions to peanut (allergens Ara h 2 and
111 eggs, or occurrence of Sampson Grade 3 to 5
anaphylactic reactions upon egg ingestion.
112 nses compared to free allergen in mice while
anaphylactic reactions were essentially abolished.
113 ble involvement of augmenting factors; after
anaphylactic reactions, always ask for possible augmenta
114 p between serum basal tryptase (sBT) levels,
anaphylactic reactions, and clonal mast cell diseases wa
115 Biphasic
anaphylactic reactions, especially clinically important
116 with pathological conditions or allergic and
anaphylactic reactions, it may contribute beneficially t
117 (NARA), total number of reports on suspected
anaphylactic reactions, number of reactions where NMBAs
118 eaction tryptase level) detected most of the
anaphylactic reactions, particularly if baseline levels
119 phasic - and clinically important biphasic -
anaphylactic reactions, the number of transfers to inten
120 ll deficient and protected from IgE-mediated
anaphylactic reactions, their dramatically different res
121 protein injection of immunized mice induced
anaphylactic reactions, which were more severe in multip
122 re were 507 uniphasic and 25 (4.5%) biphasic
anaphylactic reactions.
123 patients to prevent further life-threatening
anaphylactic reactions.
124 ocument a role for cofactors in about 30% of
anaphylactic reactions.
125 Symptoms range from mild to
anaphylactic reactions.
126 , thereby promoting allergic and potentially
anaphylactic reactions.
127 ere, including one moderate reaction and two
anaphylactic reactions.
128 developed significantly attenuated cutaneous
anaphylactic reactions.
129 allergenic food capable of provoking severe
anaphylactic reactions.
130 allergenic foods, which can result in severe
anaphylactic reactions.
131 eous tissue, are less likely to give rise to
anaphylactic reactions.
132 mice represents a new animal model to study
anaphylactic reactions.
133 the most common cause of fatal food-induced
anaphylactic reactions.
134 lation of SNAP-23 leads to degranulation and
anaphylactic reactions.
135 on of IgG1 Abs and to the risk of triggering
anaphylactic reactions.
136 ete Freund's adjuvant has resulted in severe
anaphylactic reactions.
137 life of the rMETase apoenzyme and eliminated
anaphylactic reactions.
138 diators that cause allergic inflammation and
anaphylactic reactions.
139 ths, and no patients experienced allergic or
anaphylactic reactions.
140 ere confirmed as allergic, including 11 with
anaphylactic reactions.
141 the VE IL-4Ralpha and ABL1 pathway in severe
anaphylactic reactions.
142 rotective immune responses in the absence of
anaphylactic reactions.
143 posed to contain milk proteins, which caused
anaphylactic reactions.
144 portantly, CpG/PN-NP treatment did not cause
anaphylactic reactions.
145 can range from mild local symptoms to severe
anaphylactic reactions.
146 Two patients in the reslizumab group had
anaphylactic reactions; both responded to standard treat
147 AHG2 also significantly inhibited acute
anaphylactic reactivity, including the prototypical decr
148 Anaphylactic release of renin, histamine, and beta-hexos
149 intestinal epithelium preceded onset of the
anaphylactic response to ingested OVA antigen.
150 show that the human alpha-chain restores an
anaphylactic response to the nonresponsive alpha-deficie
151 ocker) and ramipril (ACE inhibitor) with the
anaphylactic response was determined.
152 MC effector response is required for a full
anaphylactic response.
153 and cytokine release, as well as the in vivo
anaphylactic response.
154 Anti-IgE (omalizumab) treatment ablated this
anaphylactic response.
155 )-BSA) substantially reduced the BSA-induced
anaphylactic response.
156 L-10 overexpression reduced the IgE-mediated
anaphylactic response.
157 daily without a mucocutaneous, bronchial, or
anaphylactic response.
158 vivo as young lyn-/- mice showed an enhanced
anaphylactic response.
159 cient mice produce a normal passive systemic
anaphylactic response.
160 Ear swelling was assessed to evaluate the
anaphylactic response.
161 silonRI-dependent late-phase, but not acute,
anaphylactic responses and airway inflammation.
162 o vascular hyperpermeability and intensified
anaphylactic responses in female mice, providing additio
163 ature, dye extravasation) to assess systemic
anaphylactic responses in nonanesthetized wild-type, Fc
164 opment of IgE antibodies, TH2 responses, and
anaphylactic responses on challenge.
165 ial for fluid and electrolyte losses and for
anaphylactic responses to luminal antigens.
166 ice with ovalbumin or peanut allergy reduced
anaphylactic responses to oral allergen challenge by 84%
167 Anaphylactic responses were more pronounced in female th
168 th either active, or IgG1-dependent passive,
anaphylactic responses were significantly greater in Fc
169 oparticles is effective in modulating murine
anaphylactic responses, and indicate its prophylactic ut
170 Immunoglobulin E-triggered
anaphylactic responses, including elevation of circulati
171 induced airway inflammation and OVA induced
anaphylactic responses, including hypothermia and clinic
172 d cultured mast cells (HCMCs) and on in vivo
anaphylactic responses.
173 cell function, as revealed by impaired local
anaphylactic responses.
174 on to modulate peanut antigen-induced murine
anaphylactic responses.
175 mast cell responses and, remarkably, in vivo
anaphylactic responses.
176 pendent mast cell degranulation and systemic
anaphylactic responses.
177 10 on DCs in the development of allergic and
anaphylactic responses.
178 egy for the rapid inhibition of IgE-mediated
anaphylactic responses.
179 may lead to improvement of DS treatments for
anaphylactic responses.
180 s been reported between 7% and 8.5%, but the
anaphylactic risk at the time of introduction is current
181 companying the immune therapy constituted an
anaphylactic risk factor only when the autoantigen was n
182 These are (1)
anaphylactic sensitivity to peanut, (2) eosinophilic eso
183 Anaphylactic shock (76.6%), severe systemic reactions (1
184 Anaphylactic shock (AS) is an acute, potentially life-th
185 ssociated with a higher risk of mortality of
anaphylactic shock (AS), but it is unknown whether this
186 All cases with a diagnosis of
anaphylactic shock and 20% of cases with related diagnos
187 S-derived NO is the principal vasodilator in
anaphylactic shock and define eNOS and/or PI3K or Akt as
188 After sensitization and induction of
anaphylactic shock by ovalbumin, animals received either
189 CPN1(-/-) mice were hypersensitive to lethal
anaphylactic shock due to acute complement activation by
190 We studied PAF and
anaphylactic shock in conscious mice.
191 Anaphylactic shock is a sudden, life-threatening allergi
192 Anaphylactic shock is associated with severe hypotension
193 Anaphylactic shock is associated with severe impairment
194 e contribution of NO to PAF-induced shock or
anaphylactic shock is still ambiguous.
195 Severe hypotension resulting from
anaphylactic shock may be refractory to epinephrine and
196 l oxygenation and metabolism contributing to
anaphylactic shock morbidity and mortality.
197 event cerebral ischemia and could be used in
anaphylactic shock refractory to epinephrine.
198 in the PLP(139-151) model demonstrating that
anaphylactic shock resulting in death occurs upon rechal
199 de 1 reaction and negative skin tests had an
anaphylactic shock to the OC.
200 ere sensitized with ovalbumin (1 mg SC), and
anaphylactic shock was induced by IV injection of ovalbu
201 so protect primed recipients from Ag-induced
anaphylactic shock, and thus does not cause immune devia
202 anti-inflammatory scavenger and is linked to
anaphylactic shock, asthma, and allergic reactions.
203 , and two of them provoked the occurrence of
anaphylactic shock, which was relieved by the intramuscu
204 e first-line vasoconstrictive agent to treat
anaphylactic shock.
205 eutrophils and monocytes to the induction of
anaphylactic shock.
206 nulation of mast cells may cause symptoms of
anaphylactic shock.
207 Among the 14 patients, 12 presented with
anaphylactic shock.
208 a critical role, results in life-threatening
anaphylactic shock.
209 counteract the vasodilation associated with
anaphylactic shock.
210 was less susceptible to Ag-induced systemic
anaphylactic shock.
211 ding erythema, abdominal pain, vomiting, and
anaphylactic shock.
212 E (FcepsilonRI) underlies type I allergy and
anaphylactic shock.
213 ncreases survival in the Wistar rat model of
anaphylactic shock.
214 treated rats survived after the induction of
anaphylactic shock.
215 ere administered 1 minute after induction of
anaphylactic shock.
216 gh basal plasma S1P levels protective during
anaphylactic shock.
217 rapeutic approach to treatment of refractory
anaphylactic shock.
218 tore blood pressure and increase survival in
anaphylactic shock.
219 ish samples was not performed due to risk of
anaphylactic shock.
220 Despite high Ab titers,
anaphylactic side reactions were not observed when MP4 w
221 placebo-controlled food challenge in all but
anaphylactic subjects.
222 Anaphylactic symptom scores, core body temperatures, pla
223 -mutant mice with allergen plus CT abrogates
anaphylactic symptoms and Ag-specific IgE, and results i
224 N-specific IgE that correlated with systemic
anaphylactic symptoms and elevated plasma histamine.
225 c IgE, elevated plasma histamine levels, and
anaphylactic symptoms in three different strains of mice
226 th 2'-fucosyllactose and 6'-sialyllactose on
anaphylactic symptoms induced by oral ovalbumin (OVA) ch
227 t, their combined administration exacerbated
anaphylactic symptoms potently and simultaneously enhanc
228 inth-infected mice, both PN-specific IgE and
anaphylactic symptoms were greatly diminished.
229 s to IL-10, the PN-specific IgE response and
anaphylactic symptoms were similar to, or greater than,
230 ll mice in the sham-treated groups exhibited
anaphylactic symptoms with a median symptom score of 3,
231 its from her diet, she has not developed any
anaphylactic symptoms.
232 nt guidelines for the specific management of
anaphylactic transfusion reactions are contradictory as
233 st cells at these sites exhibited extensive,
anaphylactic-
type degranulation.