ライフサイエンスコーパス: eosinophilia

1 oids to manage severe asthma associated with eosinophilia.

2 subjects with elevated serum IgE and airway eosinophilia.

3 ed by EDN as separators of high vs low blood eosinophilia.

4 ring effects and attenuates blood and sputum eosinophilia.

5 ce, PM2.5 + OVA exacerbated OVA-related lung eosinophilia.

6 ILCs, can both effectively reduce intestinal eosinophilia.

7 818, had no significant effect on esophageal eosinophilia.

8 icantly inhibited airway hyperreactivity and eosinophilia.

9 in mice that recovered from allergic airway eosinophilia.

10 severity and lung function and module 2 with eosinophilia.

11 osteroid medications, and presence of airway eosinophilia.

12 4 of 20 patients (20%) developed peripheral eosinophilia.

13 otype control antibody, as well as decreased eosinophilia.

14 ies for patients with significant esophageal eosinophilia.

15 IL-5 is a major therapeutic target to reduce eosinophilia.

16 velopment of papain- or IL-33-induced airway eosinophilia.

17 rotease or IL-33-mediated innate-type airway eosinophilia.

18 eight loss and no sign of histopathology and eosinophilia.

19 as associated with a higher hazard of having eosinophilia.

20 ng candidate for exacerbation of murine lung eosinophilia.

21 rome or chronic myelomonocytic leukemia with eosinophilia.

22 on of benralizumab in patients with COPD and eosinophilia.

23 there are alternative pathways for promoting eosinophilia.

24 proton pump inhibitor-responsive esophageal eosinophilia.

25 res of asthma and increased blood and sputum eosinophilia.

26 ells, a member of ILC2s, which leads to lung eosinophilia.

27 obliterative phlebitis, and mild to moderate eosinophilia.

28 -5, and this correlates with their degree of eosinophilia.

29 proapoptotic pathway for controlling airway eosinophilia.

30 hilia either alone or with concurrent sputum eosinophilia.

31 proton pump inhibitor-responsive esophageal eosinophilia.

32 lls and the development of pronounced airway eosinophilia.

33 or chronic inflammation, crypt distortion or eosinophilia.

34 obliterative phlebitis, and mild to moderate eosinophilia.

35 ases in serum levels of eotaxins and hepatic eosinophilia.

36 4 (IL-4) production, IL-5 transcription, and eosinophilia.

37 racterized by airway hyperresponsiveness and eosinophilia.

38 the genetic basis of myeloid neoplasms with eosinophilia.

39 on, agmatine positively correlated with lung eosinophilia.

40 l-replicated asthma gene and associates with eosinophilia.

41 d sensitization, airway hyperreactivity, and eosinophilia.

42 tients with severe, uncontrolled asthma with eosinophilia.

43 roid-responsive symptoms, but without tissue eosinophilia.

44 , intensive upper airway symptoms, and blood eosinophilia (18.9% of patients); class 2, asthma with a

45 e, with infiltrating leukocytes and a marked eosinophilia (49%).

46 Of 263 patients with esophageal eosinophilia, a total of 179 fulfilled the diagnostic cr

47 210 subjects referred for the evaluation of eosinophilia (absolute eosinophil count [AEC] > 1500/muL

48 ther study on the basis of inducing a robust eosinophilia accompanied by degranulation.

49 umber of patients with persistent peripheral eosinophilia (AEC > 1500/muL) appear to have clinically

50 ncluding humoral response, airway and tissue eosinophilia, AHR, and TH2 and TH17 pulmonary profiles.

51 esenchymal stem cells (MSCs) decrease airway eosinophilia, airway hyperresponsiveness (AHR), and remo

52 2 cell responses, and related events such as eosinophilia, alternative macrophage activation, and imm

53 features of antigen-specific IgE and tissue eosinophilia, although the cellular and molecular circui

54 After exclusion of secondary causes of eosinophilia, an idiopathic hypereosinophilic syndrome (

55 cular adnexal angiolymphoid hyperplasia with eosinophilia, an unusual but often misdiagnosed benign d

56 nstrate a pathogenic role for IL-33-mediated eosinophilia and activation of Th2 immunity in chronic i

57 nts of Th2 cytokines, with associated airway eosinophilia and AHR after a single challenge, and these

58 obial composition was associated with airway eosinophilia and AHR to mannitol but not airway neutroph

59 murine models lacking T and B cells induces eosinophilia and airway hyper-reactivity (AHR), which ar

60 pious amounts of IL-5 and IL-13, which cause eosinophilia and airway hyperreactivity (AHR), a cardina

61 thma approach with assessing the presence of eosinophilia and allergy provides a way for more precise

62 overexpressing mice have increased pulmonary eosinophilia and are more susceptible to C. neoformans i

63 isolone may lead to a prompt amelioration of eosinophilia and associated symptoms.

64 etermine whether CCL26 levels correlate with eosinophilia and asthma severity.

65 e of relevance for optimal control of airway eosinophilia and asthma.

66 ges(-/-) lungs and sharply reduces pulmonary eosinophilia and basal secretion of MC products.

67 nosed on the basis of bronchoalveolar lavage eosinophilia and blood findings.

68 onse to C. neoformans by promoting pulmonary eosinophilia and by inhibiting the activation and antifu

69 acute exacerbations of COPD in patients with eosinophilia and COPD.

70 minant process that drives persistent airway eosinophilia and corticosteroid requirement in severe as

71 nonatopic subjects exhibit peripheral blood eosinophilia and elevated IgE, suggesting that processes

72 Blood eosinophilia and elevated serum creatinine phosphokinase

73 irb(-/-) mice displayed increased esophageal eosinophilia and EoE pathology, including epithelial cel

74 expression of IL-3 receptors, whereas airway eosinophilia and eosinophil peroxidase deposition were b

75 Endogenously generated cysLTs induced eosinophilia and expanded group 2 innate lymphoid cells

76 tly available inflammatory biomarkers sputum eosinophilia and fractional exhaled nitric oxide levels,

77 L-5 is recognized as a critical regulator of eosinophilia and has effects on eosinophil progenitors,

78 f rather than atopy per se contribute to the eosinophilia and IgE elevation observed in the absence o

79 at although both free CpG and NP-CpG reduced eosinophilia and IgE levels to the same extent, NP conju

80 bust relationship was observed between blood eosinophilia and IL-5, IL-13, and eosinophil-derived neu

81 in-4 (IL-4) production, in mediating hepatic eosinophilia and injury during HILI.

82 Eosinophilia and its cellular activation are hallmark fe

83 de of Ccl24 prevented the exaggerated airway eosinophilia and lung inflammation in mice given HDM-pul

84 ry disease (AERD) is characterized by tissue eosinophilia and mast cell activation, including abundan

85 lymphoid cells (ILC2s), which promote tissue eosinophilia and mast cell responses, undergo chemotaxis

86 of allergic airway disease, including airway eosinophilia and methacholine hyper-responsiveness.

87 ls caused a resolution of the papain-induced eosinophilia and mucus production.

88 cells to generate PGD2 and facilitate tissue eosinophilia and nasal polyposis in patients with AERD.

89 d asthma phenotype characterized by elevated eosinophilia and neutrophilia, tissue inflammation, mucu

90 , NOS) is assigned to patients with MPN with eosinophilia and nonspecific cytogenetic/molecular abnor

91 end organ manifestations attributable to the eosinophilia and not otherwise explained in the clinical

92 ction in serum IgE levels, reduced pulmonary eosinophilia and peri-bronchiolar collagen deposition.

93 th CARMA3-deficient AECs have reduced airway eosinophilia and proinflammatory cytokine production in

94 ) category, "Myeloid/lymphoid neoplasms with eosinophilia and rearrangement of PDGFRA, PDGFRB, or FGF

95 In addition, pIL5 treatment could induce eosinophilia and reduce Pneumocystis burden in CD4-deple

96 tial therapeutic target to reduce esophageal eosinophilia and remodeling.

97 of clinical treatable traits, such as airway eosinophilia and risk of infection/exacerbation, that ar

98 demographic data and antibiotic exposures on eosinophilia and subsequent HSRs, including documented r

99 equency and predictors of antibiotic-induced eosinophilia and subsequent hypersensitivity reactions (

100 tivation is well known in drug reaction with eosinophilia and systemic symptom (DRESS), but such a ph

101 Drug reaction with eosinophilia and systemic symptoms (DRESS) is a rare sev

102 Possible drug rash with eosinophilia and systemic symptoms (DRESS) syndrome case

103 Drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome is a

104 ome (DIHS), also known as drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome, is

105 sm in the pathogenesis of drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome.

106 c epidermal necrolysis (TEN), drug rash with eosinophilia and systemic symptoms (DRESS), and acute ge

107 pidermal necrolysis (TEN), or drug rash with eosinophilia and systemic symptoms (DRESS), are rarely r

108 us) were suspected to trigger drug rash with eosinophilia and systemic symptoms or GVHD.

109 ypersensitivity syndrome, drug reaction with eosinophilia and systemic symptoms syndrome, and Stevens

110 chronic GVHD or unrecognized drug rash with eosinophilia and systemic symptoms, the others recovered

111 Traf4 (-/-) mice resulted in blunted airway eosinophilia and Th2 cytokine production.

112 way symptoms had the highest levels of blood eosinophilia and the highest concentrations of urinary L

113 patients who had allergic asthma with sputum eosinophilia and who also had biphasic early and late as

114 with attenuation of allergen-induced sputum eosinophilia and with lower levels of tryptase in sputum

115 rent infections, increased serum IgE levels, eosinophilia, and a high incidence of allergic and autoi

116 endent secretion of type 2 cytokines, airway eosinophilia, and airway hyperresponsiveness in juvenile

117 ted with epithelial IL-25 expression, airway eosinophilia, and beneficial responses to ICS treatment.

118 ric parameters, peak expiratory flows, blood eosinophilia, and corticosteroid doses were assessed on

119 Plgf dampened AHR, reduced inflammation and eosinophilia, and decreased expression of the Th2 cytoki

120 culating eosinophils, bronchoalveolar lavage eosinophilia, and eosinophil peroxidase deposition in br

121 ggs is characterized by increased Th2 cells, eosinophilia, and high serum IgE levels.

122 I-RSV immune mice showed severe weight loss, eosinophilia, and histopathology, and RSV reinfection al

123 cy increased inflammatory cell infiltration, eosinophilia, and IL-5 and IL-13 expression in the lung

124 cells induced marked pulmonary inflammation, eosinophilia, and increased bronchoalveolar lavage fluid

125 inophilic sinusitis with nasal polyps, blood eosinophilia, and increased concentrations of urinary le

126 hyper-IgE syndromes (HIES) regarding eczema, eosinophilia, and increased serum IgE levels.

127 enge models similarly suppressed AHR, airway eosinophilia, and mucus hypersecretion without any reduc

128 nergistic increases in airway Th2 cytokines, eosinophilia, and peribronchial inflammation compared wi

129 ogical assessment of atopy, peripheral blood eosinophilia, and serum IgE concentrations has ever been

130 ave longstanding allergies, peripheral blood eosinophilia, and serum IgE elevation.

131 pathology, allergen-specific IgE production, eosinophilia, and Th2 cytokine production.

132 disease, the later onset of elevated CPK and eosinophilia, and the possibility for relapses.

133 perresponsiveness, mucus hyperplasia, airway eosinophilia, and type 2 pulmonary inflammation.

134 Standard spirometry, atopy traits, blood eosinophilia, and urinary LTE4 concentrations were evalu

135 This response is typified by massive eosinophilia, and we were able to confirm pyroptosis in

136 Pulmonary symptoms with eosinophilia are most common, though 1 case did involve

137 ii) compare its diagnostic value with sputum eosinophilia as gold standard and (iii) validate the mod

138 s the most important distinguisher and blood eosinophilia as second most important identifier in prin

139 ontaneous progressive skin inflammation with eosinophilia, as well as increased levels of thymic stro

140 y for 10 days, a sequence leading to gastric eosinophilia assessed by endoscopy.

141 icance, reclassifying some of these cases as eosinophilia-associated neoplasms.

142 nclusion in the current WHO-defined group of eosinophilia-associated TK fusion-driven neoplasms.

143 IL-13 are reliable biomarkers for the blood eosinophilia asthma phenotype.

144 nts that have been diagnosed with esophageal eosinophilia between 1993 and 2013.

145 In severe asthmatics with persistent airway eosinophilia, blockade of interleukin-5 has significant

146 to SplD led to IL-33 and eotaxin production, eosinophilia, bronchial hyperreactivity, and goblet cell

147 ltr1 blunted LTC4-induced ILC2 expansion and eosinophilia but did not alter IL-33 induction.

148 tly decreased esophageal and bronchoalveolar eosinophilia but only when given as a therapeutic treatm

149 ificantly attenuated allergen-induced sputum eosinophilia by 63 and 61% at 7 hours, respectively, and

150 ase allergens, can induce innate-type airway eosinophilia by activating natural helper (NH) cells, a

151 Esophageal eosinophilia can be proton pump inhibitor (PPI) resistan

152 y, but it is now appreciated that esophageal eosinophilia can respond to proton pump inhibitors.

153 88, in exacerbation of allergen-induced lung eosinophilia caused by urban PM2.5 was investigated.

154 , mostly severe asthma with nasal polyps and eosinophilia characterized cluster 5.

155 with an increase in lung inflammatory cells, eosinophilia, circulating IgE, Th2 cytokine production,

156 milar phenotype resulting in enhanced airway eosinophilia compared to WT mice.

157 d SP-A therapy had significantly less tissue eosinophilia compared with mice receiving vehicle.

158 Although drug-induced peripheral eosinophilia complicates antimicrobial therapy, little i

159 n inflammatory disease characterized by lung eosinophilia controlled by type 2 cytokines.

160 Baseline sputum eosinophilia correlated with a higher leukotriene D4 (LT

161 The severity of epithelial esophageal eosinophilia correlated with epithelial remodeling (basa

162 as seen by decreased airway inflammation and eosinophilia, decreased secretion of the Th2 cytokines I

163 nfections, eczema, bronchiectasis, high IgE, eosinophilia, defective B cell memory, and an impaired a

164 Patients with increased BAL eosinophilia demonstrated worse CLAD-free and overall su

165 ow limitation in asthma patients with airway eosinophilia despite treatment with high-dose inhaled co

166 Although most patients with eosinophilia do not have an HSR, eosinophilia increases

167 Patients suffering from 'EoE without eosinophilia' do not fulfill formally the diagnostic cri

168 nts receiving IL-2 treatment also experience eosinophilia due to an unknown mechanism.

169 had less Th9 cells and developed attenuated eosinophilia during OVA-induced airway inflammation comp

170 neous drug-reaction had higher proportion of eosinophilia during treatment, and higher interleukin (I

171 with inflammatory disorders involving marked eosinophilia (e.g. asthma), were particularly elevated i

172 nd assessed for histopathological indices of eosinophilia, epithelial hyperplasia, and angiogenesis b

173 Periostin did not identify blood or sputum eosinophilia, even after stratification for total IgE, a

174 ated for phenotypic traits, sputum and blood eosinophilia, exhaled NO, serum cytokines and chemokines

175 Familial eosinophilia (FE) is a rare autosomal dominant inherited

176 gic inflammation and showed little pulmonary eosinophilia, few airway TH2 cells, and no rise in serum

177 Patients with eosinophilia frequently develop cardiomyopathies.

178 rks of allergic airway disease, such as lung eosinophilia, goblet cell hyperplasia, Ag-specific Th2 r

179 ling to lung recruited CD4+ T cells enhanced eosinophilia, goblet cell hyperplasia, and overall infla

180 mation, as characterized by increased airway eosinophilia, goblet cell metaplasia, accumulation of IL

181 allergic airway inflammation with increased eosinophilia, goblet cell metaplasia, and TH2 cytokine p

182 BAL eosinophilia >/=2% is associated with poor outcome in ou

183 rized by the presence of lifelong peripheral eosinophilia (>1500/muL).

184 travel to Tioman Island after 1 March 2011, eosinophilia (>5%), clinical or laboratory-supported myo

185 6.2% or more (median in patients with sputum eosinophilia, >3%), eosinophils decreased from a median

186 Liver eosinophilia has been associated with incidences of drug

187 In addition, sputum eosinophilia has been shown to be associated with severe

188 These studies show that pulmonary eosinophilia has dual outcomes: one linked to RSV-induce

189 In this regard, liver eosinophilia has often been associated with DILI, althou

190 She showed peripheral blood eosinophilia, high level of FENO, bronchial hyperrespons

191 , we found that NP-CpG significantly reduced eosinophilia, IgE levels, mucus production and Th2 cytok

192 NP) in Western countries is characterized by eosinophilia, IgE production, and TH2 cytokine expressio

193 Marked eosinophilia in a blood test and sputum, poorly defined

194 ed in a significant diminution of epithelial eosinophilia in addition to basal cell hyperplasia and v

195 rmulation, to reduce symptoms and esophageal eosinophilia in adolescents and adults with EoE.

196 trated efficacy in reducing blood and tissue eosinophilia in all subjects.

197 ivates platelets in vitro and induces airway eosinophilia in allergen-sensitized and -challenged mice

198 ediator in resolving tissue and lavage fluid eosinophilia in allergic mouse models.

199 and dose-dependently counteracted acute lung eosinophilia in an experimental animal model.

200 Using a cutoff of >/=2% eosinophilia in bronchoalveolar lavage (BAL) fluid, chro

201 s a condition characterized by dense mucosal eosinophilia in conjunction with symptoms of esophageal

202 , which assesses the presence of allergy and eosinophilia in each asthmatic patient.

203 are consistent with the hypothesis that the eosinophilia in FE is secondary to dysregulation of IL-5

204 study was to identify the cells driving the eosinophilia in FE.

205 Moreover, the etiology of the eosinophilia in HESs can be primary (myeloid), secondary

206 itized WT mice suppressed the enhancement of eosinophilia in IL-15(-/-) animals to levels observed in

207 respiratory diseases, but the exact role of eosinophilia in lung transplantation has not been thorou

208 hepatic TSLP signaling, type 2 immunity, and eosinophilia in mediating liver injury caused by a drug.

209 cells resulted in a similar degree of airway eosinophilia in miR-155 KO and WT mice.

210 allergen challenge partially restored airway eosinophilia in miR-155 KO mice, and adoptive transfer o

211 tion by BECs might be involved in persistent eosinophilia in patients with severe asthma despite trea

212 This study established a model of gastric eosinophilia in peanut-sensitized piglets to evaluate th

213 xamine FeNO, airway responsiveness and blood eosinophilia in relation to type and degree of IgE sensi

214 ase and obstructive lung disease, and marked eosinophilia in sputum may be one of the useful tools fo

215 tivity and specificity for predicting sputum eosinophilia in the 3 weight groups.

216 V challenge; however, the roles of pulmonary eosinophilia in the antiviral response and in disease pa

217 L5-treated mice had increased serum IL-5 and eosinophilia in the lung, as well as reduced Pneumocysti

218 sing isolate Af5517 induced increased airway eosinophilia in the lungs of recipient mice compared to

219 stomach, crypt distortion in the colon, and eosinophilia in the rectosigmoid distinguished the IBD g

220 tosis, suggesting a pathway for ameliorating eosinophilia in the setting of asthma and other eosinoph

221 To drive eosinophilia in vivo, Rag1(-/-) mice were treated with a

222 d airway inflammation (both neutrophilia and eosinophilia) in a mouse model of severe allergic asthma

223 ory products and described several causes of eosinophilia including asthma, various skin diseases, he

224 exclusion of competing causes of esophageal eosinophilia, including proton pump inhibitor-responsive

225 sequent HSR in 64 (30%) of 210 patients with eosinophilia, including rash (n = 32), renal injury (n =

226 tients with eosinophilia do not have an HSR, eosinophilia increases the hazard rate of having rash an

227 ysiology, including lung function and airway eosinophilia induced by Alternaria.

228 s of recipient mice compared to the level of eosinophilia induced by isolate Af293.

229 mice suppresses Type 2 innate responses and eosinophilia induced by the allergen Alternaria.

230 owing challenge there were reduced pulmonary eosinophilia, inflammation, Th2-type cytokine responses,

231 Eosinophilia is a central feature of the host response t

232 Eosinophilia is a common, but not invariable, feature of

233 Eosinophilia is a feature of the host immune response th

234 Angiolymphoid hyperplasia with eosinophilia is a rare disease that can affect the ocula

235 Airway eosinophilia is associated with exacerbations and has be

236 Eosinophilia is associated with worsening asthma severit

237 Drug-induced eosinophilia is common with parenteral antibiotics.

238 ral circulation to the development of airway eosinophilia is not known.

239 Eosinophilia is promoted by the cytokines interleukin (I

240 Eosinophilia is rare in severe sepsis, even in the tropi

241 is, for which the relationship to peripheral eosinophilia is unclear (hypereosinophilia of unknown si

242 tory diseases, the role of EBI2 in pulmonary eosinophilia is unknown.

243 me, focused on the hypothesis that pulmonary eosinophilia linked with allergic respiratory disease is

244 Lymphopenia, eosinophilia, low numbers of naive CD8(+) T cells and sw

245 ay allergy, with increased airway and tissue eosinophilia, lung inflammation, and IL-4, IL-5, IL-13,

246 Interestingly, increased BAL eosinophilia may be specifically associated with the dev

247 f the DNA-PK inhibitor NU7441 reduced airway eosinophilia, mucus hypersecretion, airway hyperresponsi

248 ase prevented the development of AHR, airway eosinophilia, mucus hypersecretion, and TH2 cytokine pro

249 or evaluation of airway hyperresponsiveness, eosinophilia, mucus production, inflammatory gene expres

250 ntation was dyspnea (59.4%), with peripheral eosinophilia observed in 75.9%.

251 t activation of ILC2 was responsible for the eosinophilia observed with IL-2 therapy.

252 disorders characterized by peripheral blood eosinophilia of 1.5 x 10(9)/L or higher and evidence of

253 t groups or over time with respect to airway eosinophilia or AHR.

254 tient with an angiolymphoid hyperplasia with eosinophilia or Kimura disease.

255 mphocyte subsets to produce this dichotomous eosinophilia or neutrophilia.

256 cytic asthma, which occurs in the absence of eosinophilia or neutrophilia.

257 0.724, 95%-CI 0.324-1.621, P = 0.433), blood eosinophilia (OR 1.532, 95%-CI 0.569-4.118, P = 0.398),

258 On the contrary, eosinophilia (OR, 1.6; P = 0.0002), lymphocytosis (OR, 1

259 rcellular spaces; P < .0001), lamina propria eosinophilia (P < .0001), and fibrosis (P < .0001).

260 axin, and IL-8 identified two separate blood eosinophilia patient clusters linked to asthma severity.

261 Proton-pump inhibitor-responsive esophageal eosinophilia (PPI-REE) refers to patients showing sympto

262 phagitis (EoE) and PPI-responsive esophageal eosinophilia (PPI-REE), respectively.

263 airway hyperresponsiveness, bronchoalveolar eosinophilia, pulmonary inflammation, and Th2 cytokine p

264 eolar lavage fluid cytology to assess airway eosinophilia, pulmonary mechanics and clinical scoring t

265 (H)2 cells were highly correlated with blood eosinophilia (r = 0.78-0.98) and were present in 30- to

266 er, abdominal pain, and diarrhea, along with eosinophilia ranging from 0.9 x 109/L to 6.1 x 109/L.

267 h proton pump inhibitor-resistant esophageal eosinophilia received intravenous QAX576 (6 mg/kg) or pl

268 ice were prone to develop exaggerated airway eosinophilia, release type 2 helper T cell cytokines and

269 mediated disease characterized by esophageal eosinophilia, remodeling, and fibrosis.

270 with impaired pulmonary function and airway eosinophilia, respectively, in non-severe asthma.

271 These mice exhibit lung eosinophilia; smooth muscle cell, collagen, and goblet c

272 ng profound blood and gastrointestinal tract eosinophilia, TH2 immunity, and a conserved gastric tran

273 clusters (T2, T3, and T4) had higher sputum eosinophilia than cluster T1, with no differences in spu

274 -11 and polyclonal B5, inhibited AHR, airway eosinophilia, the increase of cytokines in the lung tiss

275 Conventional EoE, with its prominent eosinophilia, therefore appears to be only one phenotype

276 cins by which their glycans can control lung eosinophilia through engagement of Siglec-F.

277 allergen and compared the effects on airway eosinophilia, type 2 cytokine levels, goblet cell metapl

278 nflammation exemplified by diminished airway eosinophilia, type 2 cytokine production and mucus secre

279 c lung inflammation, characterized by airway eosinophilia, type 2 cytokine release, mucus production,

280 All subjects with eosinophilia underwent yearly evaluation, including a st

281 ian cells has been shown to induce pulmonary eosinophilia upon RSV infection in a mouse model.

282 onide did not reduce allergen-induced sputum eosinophilia versus placebo.

283 mong children with "Difficult asthma"; blood eosinophilia was a significant feature of "Difficult," "

284 Resolution of eosinophilia was also observed in mice lacking IL-4 spec

285 The amplitude of sputum eosinophilia was associated with postbronchodilator FEV(

286 bsence of crypt architectural distortion and eosinophilia was documented.

287 No significant effect on eosinophilia was observed when NCC 2287 was given as a p

288 Airway eosinophilia was similar in GSTM1+ and GSTM1null asthmat

289 epressed consciousness, and peripheral blood eosinophilia were associated with PCR positivity.

290 markers that identify the phenotype of blood eosinophilia were evaluated in adult asthmatics, and the

291 EBI2 ligands and pulmonary eosinophilia were measured in the bronchoalveolar lavage

292 0 years with dysphagia and active esophageal eosinophilia were randomized to receive either BOS 2 mg

293 Patients with eosinophilia were significantly more likely to have rash

294 ) and IRF3/7(-/-) mice presented with airway eosinophilia, whereas only IRF3/7(-/-) mice developed an

295 with acute myeloid leukemia subtype M4 with eosinophilia, which generates a CBFB-MYH11 fusion gene.

296 selectively observed in patients with tissue eosinophilia, whilst no clear relation to smoking histor

297 l phenylalanine was found to identify sputum eosinophilia with 90.5% sensitivity and 91.5% specificit

298 c findings of angiolymphoid hyperplasia with eosinophilia with ocular adnexal involvement are variabl

299 Myeloid neoplasms and eosinophilia with rearrangements of PDGFRB are uncommon

300 an therapy duration, 41 days), 210 (25%) had eosinophilia, with median peak absolute eosinophil count