ライフサイエンスコーパス: hypersensitivity

1 gnaling defect but does not rescue rapamycin hypersensitivity.

2 inal expansion of E coli leading to visceral hypersensitivity.

3 Pd1 (Pdcd1) exhibited thermal and mechanical hypersensitivity.

4 von Frey filament-evoked punctate mechanical hypersensitivity.

5 all study participants associated with cold hypersensitivity.

6 nd spontaneous withdrawal-induced mechanical hypersensitivity.

7 urons and reversing neuropathic pain-related hypersensitivity.

8 tional Tregs may influence predisposition to hypersensitivity.

9 Pollambda levels counteracted the oxidative hypersensitivity.

10 ulated for treatment of IBS-related visceral hypersensitivity.

11 likely contributes to persistent mechanical hypersensitivity.

12 ere STOML3 inhibitors can reverse mechanical hypersensitivity.

13 and demonstration of leishmanin delayed-type hypersensitivity.

14 h-risk period and exclusion of patients with hypersensitivity.

15 coli during maternal separation and visceral hypersensitivity.

16 are detectable in patients with beta-lactam hypersensitivity.

17 the development of nerve injury-induced pain hypersensitivity.

18 ced baseline sensitivity and the duration of hypersensitivity.

19 c effects in a Balb/c mouse model of Met e 1 hypersensitivity.

20 g lymph nodes following induction of contact hypersensitivity.

21 immunity, regulates the development of pain hypersensitivity.

22 p53 is necessary and sufficient for crowding hypersensitivity.

23 flammation pain model contributes to thermal hypersensitivity.

24 n regions, which could contribute to sensory hypersensitivity.

25 atients with IBS and a rat model of visceral hypersensitivity.

26 on stress as a root causative factor in CHKi hypersensitivity.

27 h as peripheral neuropathy, hypotension, and hypersensitivity.

28 nd spontaneous withdrawal-induced mechanical hypersensitivity.

29 with 10(9) commensal E coli induced visceral hypersensitivity.

30 ory neurons largely contribute to mechanical hypersensitivity.

31 ion and replication stress, attenuating CHKi hypersensitivity.

32 htened anxiety-like behavior and nociceptive hypersensitivity.

33 -evoked dynamic and filament-evoked punctate hypersensitivities.

34 ociceptors to selectively inhibit mechanical hypersensitivity, a major symptom of neuropathic pain.

35 down of Kv4.3 selectively induces mechanical hypersensitivity, a major symptom of neuropathic pain.

36 GF mice displayed visceral hypersensitivity accompanied by increases in Toll-like r

37 hypersensitivity and partially relieved this hypersensitivity after it was established.

38 o re-express Panx1 was sufficient to recover hypersensitivity after nerve injury; this rescue require

39 n the G2A-receptor show decreased mechanical hypersensitivity after oxaliplatin treatment.

40 extend the search to an even broader list of hypersensitivity/allergic disorders.

41 jection of G-CSF exhibit pronounced visceral hypersensitivity, an effect that is abolished by microgl

42 Chromatin state mapping and DNase I hypersensitivity analyses across adult tissues demonstra

43 tion of CXCL13 was sufficient to induce pain hypersensitivity and astrocyte activation via CXCR5 and

44 al cells, we used histone signatures, DNaseI hypersensitivity and ChIP-seq data to identify enhancers

45 ses and reduced inflammation in delayed-type hypersensitivity and clinical disease in EAE mouse model

46 with maternal separation developed visceral hypersensitivity and defects in Paneth cells, as reporte

47 ders most frequently associated with EM were hypersensitivity and eosinophilic granulomatosis with po

48 assessed by means of suppression of contact hypersensitivity and hapten-specific IFN-gamma-producing

49 demonstrated that acupoints show mechanical hypersensitivity and have high electrical conductance.

50 orn rats from their mothers induces visceral hypersensitivity and impaired epithelial secretory cell

51 t alternately biases sound processing toward hypersensitivity and improved behavioral sound detection

52 Xerico2 in Arabidopsis and maize confers ABA hypersensitivity and improved water use efficiency, whic

53 ism-based therapeutic approaches for dentine hypersensitivity and inflammatory tooth pain.

54 blocked development of nerve injury-induced hypersensitivity and partially relieved this hypersensit

55 lations to reveal the underlying chemoreflex hypersensitivity and reduced stability that foretells mo

56 n of efficacy targets and pathways mediating hypersensitivity and resistance relevant to the compound

57 FXS is broadly characterized by sensory hypersensitivity and several developmental alterations i

58 Chromatin immunoprecipitation, DNase I hypersensitivity and transposase-accessibility assays co

59 ing regions were characterized by high DNAse hypersensitivity and unusually broad H3K4me3 signal.

60 ggered by immune (immediate and delayed-type hypersensitivity) and non-immune (intolerance) mechanism

61 increased paw-guarding behaviors, mechanical hypersensitivity, and decreased grip strength.

62 combination of mammalian conservation, DNase hypersensitivity, and histone modification from ENCODE a

63 eract with RNA and DNA, probe regions of DNA hypersensitivity, and measure levels of DNA methylation

64 elements have active chromatin marks, DNase hypersensitivity, and occupancy by multiple transcriptio

65 ctive fear circuits, glucocorticoid receptor hypersensitivity, and response to long-term selective se

66 ies, 4 addressed patients with carotid sinus hypersensitivity, and the remaining 6 addressed vasovaga

67 ve unit may be involved in IBS-like visceral hypersensitivity, and this process is likely initiated b

68 ronal pools innervating regions of secondary hypersensitivity are dominated by descending facilitatio

69 Pathological anxiety and stress hypersensitivity are driven by constitutive increases in

70 in tumors, but the mechanisms accounting for hypersensitivity are poorly understood.

71 of uPA in the CIA model and the delayed-type hypersensitivity arthritis model.

72 itis progression in the CIA and delayed-type hypersensitivity arthritis models.

73 im of this study was to utilize piperacillin hypersensitivity as an exemplar to (i) develop cell cult

74 miR-21 in sensory neurons reduce neuropathic hypersensitivity as well as the extent of inflammatory m

75 sms of action of IgE in pathologic immediate hypersensitivity, as well as its multifaceted roles in p

76 ied in vivo in a mouse model of delayed-type hypersensitivity assay.

77 n chromatin regions identified using DNase I hypersensitivity assays, and are enriched in the promote

78 It is notably associated with hypersensitivity at the site of tissue injury.

79 Sensory hypersensitivity (aversion to certain sounds, touch, etc

80 , and DNA methylation changes in the DNase I hypersensitivity based regulatory network.

81 The eed1 farnesol hypersensitivity can be explained by higher internal con

82 However, tolerance is brief, and allergen hypersensitivity can recur within days following allerge

83 itor often inducing severe delayed-type drug hypersensitivity, can trigger innate immune activation t

84 epithelial neoplasia and increased abdominal hypersensitivity caused by augmented spinal astroglial a

85 th patient discomfort due to cervical dentin hypersensitivity (CDH) and esthetic dissatisfaction.

86 UVB-induced immunosuppression using contact hypersensitivity (CHS) as a model in C3H/HeN mice.

87 ne components that modulate allergic contact hypersensitivity (CHS) responses are poorly defined.

88 during inflammation induced by acute contact hypersensitivity (CHS).

89 209 patients had anaphylaxis and allergic or hypersensitivity comorbidities description.

90 To explore genomic underpinnings of CHKi hypersensitivity, comparative genomic analysis was perfo

91 ox)-vil-Cre mice also had increased visceral hypersensitivity compared with control littermate Sox9(f

92 -glucans or a SYK inhibitor reduced visceral hypersensitivity, compared with controls.

93 letion in GFAP-positive glia cells prevented hypersensitivity completely, whereas deletion of neurona

94 fication model addressed to the allergic and hypersensitivity conditions according to the Internation

95 vement of healthcare system for allergic and hypersensitivity conditions worldwide.

96 e first example of how the new 'Allergic and hypersensitivity conditions' section of the forthcoming

97 in the construction of the new 'Allergic and hypersensitivity conditions' section under the 'Disorder

98 From all 2318 files related to allergic or hypersensitivity conditions, 673 had some of the anaphyl

99 ants, rbk1 insertional mutants display auxin hypersensitivity, consistent with a possible role for RB

100 an, produce decreased mechanical and thermal hypersensitivity, decreased affective pain behaviors, an

101 Delayed-type beta-lactam hypersensitivity develops in subset of patients.

102 ach component in the Kv4 complex, mechanical hypersensitivity develops in the hindlimbs of rats in pa

103 Secondary hypersensitivity develops within undamaged tissue adjace

104 est and best-documented risk factor for drug hypersensitivity (DH) is the history of a previous react

105 patients 180 days after treatment of dentin hypersensitivity (DH) with laser and cyanoacrylate.

106 atory element activities measured by DNase I hypersensitivity (DH).

107 includes a group of common and less frequent hypersensitivity disorders frequently misdiagnosed and n

108 hilic gastrointestinal disorders (EGIDs) are hypersensitivity disorders frequently triggered by food

109 ernal exposure to dLAN dampened delayed type hypersensitivity (DTH) responses in male offspring.

110 ymphocyte reactions, trans-vivo delayed-type hypersensitivity, enzyme-linked immunospot assays, the u

111 ity or tolerability to other PPI after their hypersensitivity episodes.

112 atopoietic cells is necessary for mechanical hypersensitivity following nerve injury.

113 tio of patients without systemic symptoms of hypersensitivity following SC challenge, over the number

114 Module genes were also enriched for DNase I hypersensitivity footprints and binding from four transc

115 (n = 40), with the highest occurrence in the hypersensitivity form (36.1%; p = 0.026).

116 Established mechanical and cold pain-related hypersensitivity generated by the spared nerve injury mo

117 beta-Lactam hypersensitivity has been classified according to the ph

118 Loss of hypersensitivity has been reported for IgE-mediated reac

119 zation in mice with established IgE-mediated hypersensitivity, IgG facilitated tolerance restoration,

120 upstream MAP kinase kinase MKK3 also display hypersensitivity in auxin-responsive cell expansion assa

121 identified mpk1-1 as a mutant that displays hypersensitivity in auxin-responsive cell expansion assa

122 eventive action against transient mechanical hypersensitivity in BMMC-treated rats.

123 (ACD) using an established model of contact hypersensitivity in C57Bl/6 mice utilizing 2,4-dinitrofl

124 reversed established mechanical and thermal hypersensitivity in EAE mice.

125 thresholds and enhanced inflammatory thermal hypersensitivity in females.

126 e injuries are well-described causes of pain hypersensitivity in humans and in rodent animal models,

127 d thousand genomic loci that display DNase I hypersensitivity in one or more ENCODE cell lines.

128 Acid hypersensitivity in patients with NERD might be partiall

129 inal cord ameliorates mechanical and thermal hypersensitivity in peripheral nerve injury models of ne

130 important role for this channel in mediating hypersensitivity in preclinical models of inflammatory o

131 potent in vivo efficacy in the delayed type hypersensitivity in rats.

132 IV neurons was sufficient to induce thermal hypersensitivity in the absence of injury.

133 duced both ongoing pain and evoked cutaneous hypersensitivity in the context of cystitis, but had no

134 ockout mice (Panx1(-/-)) were protected from hypersensitivity in two sciatic nerve injury models.

135 ic rheostats that promote ionizing radiation hypersensitivity in various normal stem cell populations

136 -cell proliferation and control delayed-type hypersensitivity in vivo.

137 d be an indicator of basophil activation and hypersensitivity in vivo.

138 ction, inflammation, glucocorticoid receptor hypersensitivity) in addition to behavioral phenotypes.

139 emory in the form of hapten-specific contact hypersensitivity independent of T and B cells.

140 e could cause mesenteric afferent mechanical hypersensitivity independently, and this effect was syne

141 We reduced dynamic mechanical hypersensitivity induced by nerve injury or inflammation

142 ttenuated pre-established dynamic mechanical hypersensitivity induced by nerve injury, suggesting tha

143 and potentiated the morphine effect on pain hypersensitivity induced by nerve injury.

144 We also find that cold hypersensitivity induced by peripheral nerve injury is r

145 Drug hypersensitivity involves the activation of T cells in a

146 Interstrand cross-link (ICL) hypersensitivity is a characteristic trait of Fanconi an

147 Sensory hypersensitivity is a common symptom in autism spectrum

148 Mechanical hypersensitivity is a debilitating symptom for millions

149 Thus, the propensity to develop hypersensitivity is dependent on other factors, such as

150 -nociceptor inputs associated with secondary hypersensitivity is likely to be at least partly depende

151 BACKGROUND & AIMS: Visceral hypersensitivity is one feature of irritable bowel syndr

152 Given the involvement of p53, compaction hypersensitivity may be widespread among damaged cells a

153 ia-independent to a microglia-dependent pain hypersensitivity mechanism.

154 Using DNase I hypersensitivity methods and ENCODE data, we have identi

155 We developed and used a chronic contact hypersensitivity model in wild-type and MC-deficient mic

156 of 41 participants in the opicinumab group (hypersensitivity [n=2], asymptomatic increase in transam

157 INTERPRETATION: Hypersensitivity of corticostriatal glutamatergic termin

158 BID rats showed hypersensitivity of corticostriatal glutamatergic termin

159 behavior as detected by bilateral mechanical hypersensitivity of hindlimbs, but corpus callosotomy el

160 root developmental defects and latrunculin B hypersensitivity of hlb1, and analyses of ahlb1/ min7/be

161 ss, CDK2 activation, replication stress, and hypersensitivity of HNSCC cells to CHKi monotherapy was

162 n many forms of neural plasticity, including hypersensitivity of nociceptors in the presence of infla

163 The hypersensitivity of TGCTs to cisplatin is a subject of w

164 We found that the HU hypersensitivity of the hem13-1 mutant is caused by oxid

165 OsMTP11 partially rescues the Mn-hypersensitivity of the pmr1 yeast mutant but only sligh

166 by which maternal separation causes visceral hypersensitivity or its relationship with defects in epi

167 those of 39 patients with IBS (with visceral hypersensitivity or normal levels of sensitivity).

168 also followed up the potential risk of cross-hypersensitivity or tolerability to other PPI after thei

169 se (SYK), a SYK inhibitor to reduce visceral hypersensitivity, or vehicle (control).

170 ls who carry HLA risk alleles do not develop hypersensitivity, other parameters must control developm

171 We evaluated NSAID-hypersensitivity over time in NIUA patients.

172 We found that such a hypersensitivity phenotype can also be induced by agents

173 RATIONALE: Current diagnosis of chronic hypersensitivity pneumonitis (cHP) involves considering

174 NSIP; kappaw=0.42 [0.37-0.49]); and fair for hypersensitivity pneumonitis (kappaw=0.29 [0.24-0.40]).

175 [range, 23-86 years]), and 192 with chronic hypersensitivity pneumonitis (men, 76; women, 116; media

176 Occupational hypersensitivity pneumonitis (OHP) is an immunologic lun

177 Nine of 192 (4.7%) had chronic hypersensitivity pneumonitis (P < .001), and 27 of 244 (

178 d son (patient 2) diagnosed with summer-type hypersensitivity pneumonitis (SHP).

179 Patients with hypersensitivity pneumonitis are at risk of developing p

180 critical review of the current knowledge on hypersensitivity pneumonitis caused by the occupational

181 In the combined UCSF and UTSW chronic hypersensitivity pneumonitis cohort, we saw associations

182 Final diagnosis: hypersensitivity pneumonitis in 47.3% (n = 513; exposure

183 and assessed their associations with chronic hypersensitivity pneumonitis risk, survival, and clinica

184 nd reduced survival in patients with chronic hypersensitivity pneumonitis suggest shared pathobiology

185 or MUC5B rs35705950 in patients with chronic hypersensitivity pneumonitis than in healthy controls (2

186 Hypersensitivity pneumonitis was the most common new-ons

187 independent cohorts of patients with chronic hypersensitivity pneumonitis, one from the University of

188 lmonary fibrosis (IPF) or chronic (fibrotic) hypersensitivity pneumonitis, which suggests these disor

189 and reduced survival in people with chronic hypersensitivity pneumonitis.

190 t the mechanisms that regulate this type III hypersensitivity process remain poorly understood.

191 One patient experienced a hypersensitivity reaction and developed non-neutralizing

192 Anaphylaxis is a severe systemic hypersensitivity reaction that is rapid in onset; charac

193 r 1996 and July 2015 for a suspicion of drug hypersensitivity reaction to BLs, with negative ST and p

194 ngs suggest that HORV is caused by a delayed hypersensitivity reaction to vancomycin.

195 re, life-threatening generalized or systemic hypersensitivity reaction'.

196 Anaphylaxis is a life-threatening hypersensitivity reaction.

197 One participant who received TMP-SMX had a hypersensitivity reaction.

198 However, severe delayed-type hypersensitivity reactions (DHR) induced by PPI, such as

199 Drug hypersensitivity reactions (DHRs) represent growing heal

200 HIV-1 antiretroviral with treatment-limiting hypersensitivity reactions (HSRs) associated with multip

201 Hypersensitivity reactions (HSRs) to intravenous iron pr

202 Immediate drug hypersensitivity reactions (IDHR) to moxifloxacin consti

203 ced a case of 10-year-old girl who developed hypersensitivity reactions after eating enokitake.

204 idence that some exanthematous allergic drug hypersensitivity reactions are mediated by drug-specific

205 Hypersensitivity reactions during receipt of antibiotic

206 nd a possible cause of the high incidence of hypersensitivity reactions during the first application

207 Molecules that are necessary for ocular hypersensitivity reactions include the receptors CCR1 an

208 ls through FcepsilonRI and trigger immediate hypersensitivity reactions on antigen encounter.

209 Small immune complexes cause type III hypersensitivity reactions that frequently result in tis

210 ions, whereas three patients developed cross-hypersensitivity reactions to alternative structurally s

211 Patients with an ACS and histories of hypersensitivity reactions to ASA, especially following

212 with stable CIHD and histories of nonsevere hypersensitivity reactions to ASA/NSAIDs, an ASA challen

213 ociations have been discovered for immediate hypersensitivity reactions to beta-lactams, aspirin, and

214 adults in the United States now affected by hypersensitivity reactions to various foods.

215 ding of the role of CCL7 in mediating ocular hypersensitivity reactions will provide insights into ma

216 During IgE-mediated immediate hypersensitivity reactions, vascular endothelial cells p

217 her structurally different PPI without cross-hypersensitivity reactions, whereas three patients devel

218 ent dual-modality to interfere with allergic hypersensitivity reactions.

219 ith wild-type littermates after delayed-type hypersensitivity reactions.

220 ducing ADRs, especially those caused by drug hypersensitivity reactions.

221 cereals (wheat, rye and barley) can trigger hypersensitivity reactions.

222 tors (PPIs) have been known to induce type I hypersensitivity reactions.

223 cause of medical decision and not because of hypersensitivity reactions.

224 thermore, hyperalgesic priming of mechanical hypersensitivity requires both TRPA1 and AKAP.

225 , these microparticles inhibited destructive hypersensitivity responses to subsequent allergen exposu

226 plicated in negative regulation of immediate hypersensitivity responses.

227 ve mice with L. major or testing for contact hypersensitivity results in exacerbated skin inflammator

228 In silico analyses located a DNase I hypersensitivity site to rs7692387 and predicted binding

229 and in particular in tissue-specific DNase I hypersensitivity sites (DHSs).

230 atively correlated with LLD, such as DNase I hypersensitivity sites (DHSs).

231 ants in histone modification peaks and DNase hypersensitivity sites in B cells.

232 ssociation tests, prior knowledge of DNase-I hypersensitivity sites or other relevant biological anno

233 Previously, DNase I hypersensitivity sites were reported to explain 79% of S

234 Chronic contact hypersensitivity skin of Sash mice exhibited elevated le

235 the advances and use of the pioneering "Drug hypersensitivity" subsection of ICD-11 and implementatio

236 in a mouse tissue model of chronic visceral hypersensitivity, suggesting the potential of KOR agonis

237 e immunopathogenesis of T-cell mediated drug hypersensitivity syndromes.

238 tization, there is a sustained state of pain hypersensitivity that is continuously suppressed by the

239 o water avoidance stress (to induce visceral hypersensitivity), then given fungicide and donor cecum

240 ciceptor activation in the area of secondary hypersensitivity to a degree equivalent to that evoked b

241 n in DNA repair in cancer cells that confers hypersensitivity to a LigIIIalpha inhibitor, L67, in com

242 However, a precursor's hypersensitivity to a reduction of the Deltapsi is not l

243 Hypersensitivity to acetylsalicylic acid (ASA) constitut

244 Hus1(neo/Delta1) mice showed hypersensitivity to agents that cause replication stress

245 +) uptake after ammonium shock and conferred hypersensitivity to ammonium and to the transport analog

246 open field, deficits in prepulse inhibition, hypersensitivity to amphetamine, antisocial behaviors, r

247 Immediate hypersensitivity to antivenoms often occurs during the f

248 tability and tumorigenesis but also generate hypersensitivity to cancer therapeutics.

249 CD is a non-IgE hypersensitivity to certain cereal proteins: gluten in w

250 significantly impaired G1 arrest and induced hypersensitivity to chemotherapeutic drugs.

251 The pub13 mutants showed hypersensitivity to chitooctaose-induced rapid responses

252 This indicates that colonic hypersensitivity to distension, rather than excessive ga

253 ers (but not non-handled mycobiome) restored hypersensitivity to distension.

254 ss-of-function mutants showed some degree of hypersensitivity to DNA damage and elevated expression o

255 sposition syndrome characterized by cellular hypersensitivity to DNA interstrand crosslinks (ICLs).

256 n chromatin", which were identified based on hypersensitivity to DNase I digestion and association wi

257 to the alpha-gal epitope are associated with hypersensitivity to equine antivenoms.

258 inflammatory disorder triggered by allergic hypersensitivity to food and associated with genetic var

259 s causes reduced expression of CBF genes and hypersensitivity to freezing, suggesting that the MKK4/5

260 s exhibit altered tactile discrimination and hypersensitivity to gentle touch.

261 mybs1 mutant exhibited hypersensitivity to glucose, whereas mybs2 seedlings wer

262 ation as a consequence of myeloid progenitor hypersensitivity to granulocyte-macrophage colony-stimul

263 ytosis, myelodysplasia, and a characteristic hypersensitivity to granulocyte-macrophage colony-stimul

264 This hypersensitivity to hematopoietic ablation was completel

265 soluble proteins including multiple RPs, and hypersensitivity to imbalances in production of RPs and

266 the role of IKD in damage-triggered painful hypersensitivity to innocuous cold.

267 tor activity, consistent with the behavioral hypersensitivity to light we observed.

268 Depletion of RNF146 caused hypersensitivity to LPS-induced TNF-alpha production in

269 otherapeutic agent paclitaxel (which induces hypersensitivity to mechanical and cold stimulation only

270 pment of ongoing spontaneous pain and evoked hypersensitivity to mechanical and thermal stimuli.

271 Late postoperative complications included hypersensitivity to mechanical shocks (39 of 51 patients

272 artial sciatic nerve ligation (which induces hypersensitivity to mechanical, cold and heat stimulatio

273 In conclusion, immediate hypersensitivity to moxifloxacin might involve mechanism

274 o hypersensitive rats reduced their visceral hypersensitivity to normal levels of sensitivity.

275 anied with decreased DNA repair capacity and hypersensitivity to oxidative stress.

276 ncluding increased endogenous ROS levels and hypersensitivity to oxidizing agents.

277 ch9; hal4 hal5 and trk1 trk2 mutants display hypersensitivity to rapamycin, and reciprocally, TORC1 i

278 levels of spontaneous chromosomal damage and hypersensitivity to replication-blocking lesions than Fa

279 nderdeveloped inhibitory control, and thus a hypersensitivity to reward.

280 Hypersensitivity to sounds is one of the prevalent sympt

281 argeted acetyl-coenzyme A carboxylase, cause hypersensitivity to spectinomycin.

282 o use piperacillin as a model of beta-lactam hypersensitivity to study the nature of the drug-specifi

283 responsive TRAM-dependent TLR4 signaling and hypersensitivity to the TLR4 ligand lipopolysaccharide.

284 e, leading to severe genomic instability and hypersensitivity to Topo-isomerase I inhibitors.

285 12)-driven acquired resistance, resulting in hypersensitivity to translational inhibitors.

286 nvestigated whether fungi can cause visceral hypersensitivity using rats exposed to fungicide (flucon

287 is a non-IgE-mediated gastrointestinal food hypersensitivity usually due to cow's milk or soy.

288 lammation, barrier dysfunction, and visceral hypersensitivity (VH).

289 Long-term hypersensitivity was also observed in tail-resected pigs

290 SNL-evoked mechanical hypersensitivity was attenuated, accompanied by a partia

291 the 381 SPT with reliable results, cutaneous hypersensitivity was found in 201 (53%) participants.

292 cy of ivermectin in ameliorating behavioural hypersensitivity was mirrored at the cellular level by a

293 We show that the delayed hypersensitivity was not mediated by either cell swellin

294 In the mouse model of delayed type hypersensitivity, we have shown an essential role for PL

295 In a mouse model of allergic airway hypersensitivity, we show that rhinovirus infection trig

296 Allergic rhinitis, atopic eczema and food hypersensitivity were covered in 15.7%, 24.5% and 9.0%,

297 of rats, we found fungi to promote visceral hypersensitivity, which could be reduced by administrati

298 ctivation to medication-induced delayed-type hypersensitivity, which may stimulate new concepts for t

299 AIDs) are the most frequent triggers of drug hypersensitivity with NSAIDs-induced urticaria/angioedem

300 that contributes to inflammatory mechanical hypersensitivity, yet little is known as to the post-tra