ライフサイエンスコーパス: asthmatic

1 d bronchial brushings (7 non-asthmatic and 9 asthmatic).

2 tially methylated between asthmatics and non-asthmatics.

3 ted with low BMD in both childhood and adult asthmatics.

4 s associated with their clinical efficacy in asthmatics.

5 d treatment response in persistent childhood asthmatics.

6 oderate allergic asthmatics, and nonallergic asthmatics.

7 and the complex immune response in blood of asthmatics.

8 bundles in endobronchial biopsies in severe asthmatics.

9 igher at 08:00 vs. 20:00 in controls but not asthmatics.

10 in the TAC3 group compared to TAC1 and TAC2 asthmatics.

11 jects were recruited and provided sputum (83 asthmatics; 14 healthy subjects), with 29 also undergoin

12 olation techniques; pronase digestion (9 non-asthmatic, 8 asthmatic) and bronchial brushings (7 non-a

13 omized, crossover, acute feeding study in 23 asthmatic adults (n = 12 nonobese and n = 11 obese subje

14 tudy of nonobese (n = 51) and obese (n = 76) asthmatic adults.

15 Thirty-three nonsevere and 22 severe asthmatic African American children were included in an

16 lood mononuclear cells (PBMCs) from 17 adult asthmatics after a long-term use of oral glucocorticoid.

17 mmortalized B cells (IBCs) from 32 childhood asthmatics after multiple oral glucocorticoid bursts and

18 Increased cholinergic fibers in asthmatic airway biopsies was found, paralleled by incre

19 primary human airway epithelia in vitro and asthmatic airway epithelia in vivo.

20 In vitro studies demonstrated that asthmatic airway fibroblasts are deficient in their pack

21 A role for smooth muscle ARHGEF1 in asthmatic airway hyper-responsiveness is worthy of furth

22 carotid bodies, in parasympathetic-mediated asthmatic airway hyperresponsiveness.

23 n periostin-rich extracellular matrix in the asthmatic airway in an ADAM8-dependent manner, making AD

24 impacts the development of allergen-induced asthmatic airway inflammation and which immune modulatin

25 gest that neutralization of IL-13 may reduce asthmatic airway remodelling.

26 is a characteristic feature of remodeling in asthmatic airways and stems from the imbalance between p

27 anized and fragmented within large and small asthmatic airways compared with control subjects, using

28 fibrils was found to be more disorganized in asthmatic airways compared with control subjects, using

29 eling of the cholinergic neuronal network in asthmatic airways driven by brain-derived neurotrophic f

30 at Sema3E modulates angiogenesis in allergic asthmatic airways via modulating pro- and anti-angiogeni

31 8 asthmatic) and bronchial brushings (7 non-asthmatic and 9 asthmatic).

32 nti-bacterial immune responses in pre-school asthmatic and control children within the EU-wide study

33 In PBMCs of asthmatic and control children, NIP45 mRNA directly corr

34 We studied human blood and lung ILCs from asthmatic and control subjects by flow cytometry, ELISA,

35 linical characteristics and comorbidities in asthmatic and nonasthmatic patients with COVID-19.

36 ximate urban communities, and importantly in asthmatic and nonasthmatic schoolchildren.

37 cing and confirmed by quantitative PCR in 29 asthmatics and 10 healthy individuals.

38 of macrophage subtypes in the sputum of 104 asthmatics and 16 healthy volunteers from the U-BIOPRED

39 As were performed by quantitative PCR in 138 asthmatics and 39 healthy subjects.

40 ease in nitrotyrosine in HBECs in cells from asthmatics and controls.

41 uman bronchial epithelial cells (HBECs) from asthmatics and healthy controls to evaluate: (i) ADMA-me

42 expression differs between eosinophils from asthmatics and healthy subjects.

43 fluid (BALF) levels of SOCS3 were reduced in asthmatics and in allergen-challenged mice.

44 gions were differentially methylated between asthmatics and non-asthmatics.

45 Primary human ASM cells isolated from asthmatics and nonasthmatics were treated with E(2), an

46 AP-1 (P < 0.01, P < 0.05) in ASM cells from asthmatics and nonasthmatics.

47 PP5 were increased in ASM cells from severe asthmatics and PP5 knockdown using siRNA restored flutic

48 ly related with the BMD Z score in childhood asthmatics and tested if these gene modules were preserv

49 X (sPLA(2)-X) is elevated in the airways of asthmatics and that mice lacking the sPLA(2)-X gene (Pla

50 iques; pronase digestion (9 non-asthmatic, 8 asthmatic) and bronchial brushings (7 non-asthmatic and

51 .14) events/10 person-years for intermittent asthmatics, and 0.19 (95% CI, 0.120.49) events/10 person

52 healthy children, mild-to-moderate allergic asthmatics, and nonallergic asthmatics.

53 a few studies involving healthy individuals, asthmatics, and smokers.

54 We hypothesized that persistent asthmatics are at higher risk for developing AF and that

55 Evidence suggests that elderly asthmatics are more likely to be underdiagnosed and unde

56 of the disease, and critically, a subset of asthmatics are resistant to steroid therapy.

57 enotypes, such as obese asthmatics or severe asthmatics, are required.

58 Baseline ISS levels of PGE(2) were higher in asthmatics as compared to HC at baseline (NERD vs HC P =

59 el as well as in nasal epithelial cells from asthmatics as compared with healthy controls.

60 And also, we diagnosed 12 asthmatics as PTE from 33 patients.

61 tly associated with the BMD Z score in adult asthmatics as well.

62 Macrophages were isolated from asthmatic BALF and derived from THP-1 cells and human mo

63 In asthmatics, basophils were positively correlated with sp

64 pithelial inflammatory and resident cells in asthmatic biopsies.

65 involved in carotid body-mediated sensing of asthmatic blood-borne inflammatory mediators.

66 Asthmatic bronchial biopsies were immunostained for CD48

67 In asthmatic bronchial biopsies, mCD48 was expressed predom

68 arc resulting in efferent vagal activity and asthmatic bronchoconstriction.

69 herapeutic target to reduce allergen-induced asthmatic bronchoconstriction.

70 creased at 08:00 vs. 20:00 in basophils from asthmatics but not controls.

71 m basophil numbers are increased in allergic asthmatics, but it is unclear what role airway basophils

72 Remarkably, this molecular profile of non-asthmatic cells after compression recapitulated the prof

73 ter compression recapitulated the profile of asthmatic cells before compression.

74 Three hundred fifty mouse-sensitized/exposed asthmatic children (5-17 years old) were enrolled in a 1

75 re validated in an independent population of asthmatic children (n = 30) by using a shared healthy co

76 A total of 130 asthmatic children aged 4-6 years from the multinational

77 NAm differences between severe and nonsevere asthmatic children and evaluate the impact of environmen

78 This was not the case for asthmatic children as a group, but those receiving stero

79 tify the attitude and practice of mothers of asthmatic children concerning their use of inhalers, com

80 HFEV(1) asthmatic children display distinct lung mechanical prop

81 Furthermore, asthmatic children had more episodes of infection that r

82 Over 89% of asthmatic children in underdeveloped countries demonstra

83 ylated regions, was selectively increased in asthmatic children of asthmatic mothers and was associat

84 ide differential gene expression among obese asthmatic children was enriched for genes, including VAV

85 A sample of 100 consecutive mothers of asthmatic children was enrolled.

86 IL33R-ST2 was found induced in the blood of asthmatic children with additional Gram + bacteria in th

87 lationships between the airway microbiome of asthmatic children, loss of asthma control, and severe e

88 We performed HC in a rich data set from 613 asthmatic children, using 45 clinical variables (Model 1

89 mechanisms explaining the paradox of severe asthmatic children, whom when clinically stable can have

90 apacity over 1 year among sensitized/exposed asthmatic children.

91 function growth in mouse-sensitized/exposed asthmatic children.

92 ls were coupled with regression models in an asthmatic cohort (n = 177) to simulate the impact of sma

93 e and dexamethasone in ASM cells from severe asthmatic compared to that in healthy subjects.

94 use dust mite (HDM) allergy, relative to non-asthmatic control subjects.

95 -16] years), PSW (age 2 [1-5] years) and non-asthmatic controls (age 7 [2-14] years) underwent bronch

96 with FEV(1) <=80% (LFEV(1) ; n = 14) and non-asthmatic controls (n = 10).

97 n between ages 2 and 6 years, and 65,415 non-asthmatic controls, and we replicate findings in 918 chi

98 e last climate change review with a focus on asthmatic disease.

99 to advance our knowledge into the origins of asthmatic disease.

100 features more usually associated with severe asthmatic disease.

101 Neutrophilic, but not eosinophilic, asthmatics display overexpression of IFN-beta, IFN-lambd

102 bronchial epithelial cells derived from non-asthmatic donors and asthmatic donors, we applied a comp

103 In cells from non-asthmatic donors, compression by itself was sufficient t

104 cells derived from non-asthmatic donors and asthmatic donors, we applied a compressive stress and th

105 and lung function was reduced among allergic asthmatics early after rhinovirus inoculation but increa

106 ions closely approximated gene expression in asthmatic epithelial brushings.

107 ene cascade remains highly activated in some asthmatics, even those on high-dose inhaled or oral cort

108 osteroid and biologic therapies, many severe asthmatics exhibit corticosteroid-unresponsive mixed gra

109 d in sera, as miR-185-5p which discriminates asthmatics from healthy subjects.

110 In risk-factor adjusted models, persistent asthmatics had a greater risk of incident AF (hazard rat

111 At baseline, both groups of asthmatics had a lower FEV1 and Pc20 and increased eosin

112 HFEV(1) asthmatics had larger airways (FEV(1) z-scores 1.12 vs -

113 Moreover, HFEV(1) asthmatics had significantly reduced elastic recoil pres

114 Because a large subgroup of asthmatics have associated eosinophilia, often accompani

115 Nevertheless, gene expression studies in asthmatics have so far focused on sex-combined analysis,

116 people worldwide, and nearly ten percent of asthmatics have what is considered "severe" disease.

117 Non-asthmatic healthy controls (N = 17) were used as control

118 ental rhinovirus infection in 24 healthy and asthmatic human volunteers.

119 f administering omalizumab versus placebo to asthmatics in a randomized, double-blind placebo-control

120 ands, it will be critical to include elderly asthmatics in large clinical trials so that therapy may

121 e a unique nationwide panel dataset tracking asthmatic individuals' use of rescue medication and thei

122 exosomal contents between EVs of healthy and asthmatic individuals, which could be employed as potent

123 d sputum (IS) allows to measure mediators of asthmatic inflammation in bronchial secretions.

124 the effect of GM-CSF signaling deficiency on asthmatic inflammation in general and on eosinophils in

125 Elucidating the mechanisms that sustain asthmatic inflammation is critical for precision therapi

126 to elucidate the role of GM-CSF signaling in asthmatic inflammation.

127 a Random Forest model that can even sort the asthmatics into intermittent, mild persistent, moderate

128 These miRNAs can classify asthmatics into two clusters that differed in the number

129 ate from obese asthmatic (OA) patients, lean asthmatic (LA) patients, and obese nonasthmatic (ONA) su

130 This provides additional asthmatic ligands contributing to the previously establi

131 20.49) events/10 person-years for persistent asthmatics (log-rank P=0.008).

132 ic effector type 2 helper T cells (T(H)2) in asthmatic lungs and find evidence for type 2 cytokines i

133 hy lungs to a T(H)2-dominated interactome in asthmatic lungs.

134 chyma in healthy lungs, and lower airways in asthmatic lungs.

135 A 23-year old, asthmatic male with coronavirus pneumonia developed with

136 al/bronchial biopsies from controls and mild asthmatics (MAs) to severe asthmatics (SAs) in relation

137 Additionally, IL-6-deficient asthmatic mice exhibited reduced goblet cell hyperplasia

138 e key changes in the lungs of IL-6-deficient asthmatic mice resulted in dysregulated tight junction p

139 y inflammation in ovalbumin (OVA)-sensitized asthmatic mice.

140 lectively increased in asthmatic children of asthmatic mothers and was associated with childhood asth

141 spiratory computed tomography in a cohort of asthmatic (n = 41) and healthy (n = 11) volunteers to un

142 ological and microbiome alterations in obese asthmatics (n = 50, mean age = 45), non-obese asthmatics

143 sthmatics (n = 53, mean age = 40), obese non-asthmatics (n = 51, mean age = 44) and their healthy cou

144 sthmatics (n = 50, mean age = 45), non-obese asthmatics (n = 53, mean age = 40), obese non-asthmatics

145 D4(+) T-cells were decreased in the lungs of asthmatic NIP45(-/-) mice.

146 mics of exhaled breath condensate from obese asthmatic (OA) patients, lean asthmatic (LA) patients, a

147 ased with farm exposure and increased within asthmatics, opposite to age 4.5 years.

148 tribute to disease phenotypes, such as obese asthmatics or severe asthmatics, are required.

149 breath washout (MBW) are associated with key asthmatic patient-related outcome measures and airways h

150 independent population of white adult atopic asthmatic patients (n = 12) and control subjects (n = 12

151 nflammasome activity in the airways of obese asthmatic patients after macronutrient overload and in i

152 ed from 8:00 am to 10:00 am in 248 pediatric asthmatic patients aged 0-18 years that were under long-

153 in bronchial biopsy specimens from 10 atopic asthmatic patients and 15 nonasthmatic nonatopic control

154 bronchoalveolar lavage (BAL) samples from 39 asthmatic patients and 19 healthy subjects followed by 1

155 RNA sequencing data from 408 asthmatic patients and 405 control subjects were used to

156 al brushings, bronchial biopsy specimens (91 asthmatic patients and 46 healthy control subjects), and

157 ine and after rhinovirus infection in atopic asthmatic patients and control subjects.

158 tterns revealed different topologies between asthmatic patients and healthy control subjects.

159 AECs were obtained from asthmatic patients and healthy subjects and treated with

160 view evidence about symptom misperception in asthmatic patients and how to identify and manage affect

161 EF1 expression was also enhanced in ASMCs of asthmatic patients and in lungs of ovalbumin-sensitized

162 id-insensitive, pathogenic effector cells in asthmatic patients and in mice in a model of experimenta

163 irway inflammation defines a novel subset of asthmatic patients and might drive airway inflammation a

164 miR-1 has therapeutic potential in asthmatic patients and patients with CRS.

165 struction, and number of hospitalizations in asthmatic patients and sinonasal tissue eosinophilia in

166 xpression of eosinophils between healthy and asthmatic patients and to establish a differentially exp

167 predicting future exacerbation frequency in asthmatic patients are required.

168 in controlling non-T2 cytokine responses in asthmatic patients are unclear.

169 he fungal microbiota structure of airways in asthmatic patients associated with T2 inflammation, atop

170 The proportion of asthmatic patients at age 23 to 24 years differed betwee

171 nt knowledge on pathogenic CD4(+) T cells in asthmatic patients by drawing on observations in mouse m

172 inflammatory cell counts in induced sputum, asthmatic patients can be classified into 4 unique pheno

173 Lack of increased absorption permeability in asthmatic patients can further be reconciled with occurr

174 Identifying DNA methylation profiles in asthmatic patients can inform disease pathogenesis.

175 In asthmatic patients CD4(+) T cells in response to TGF-bet

176 ILC2 numbers are increased in asthmatic patients compared with healthy control subject

177 tes/macrophages expressing IFN-alpha/beta in asthmatic patients during infection.

178 -6) were followed up for replication in 1697 asthmatic patients from six European studies.

179 BAL fluid from asthmatic patients had increased TSLP but not IL-7 level

180 Asthmatic patients have been reported to have higher car

181 Reports have shown that some asthmatic patients have decreased levels of one member o

182 Asthmatic patients have higher microbiome diversity and

183 Despite ICS therapy, many asthmatic patients have persistent airway type 2 inflamm

184 d the clinician's approach to characterizing asthmatic patients in the clinic.

185 the bronchial epithelium at 3 time points in asthmatic patients in vivo.

186 r data demonstrate that barrier leakiness in asthmatic patients is induced by TH2 cells, IL-4, and IL

187 the role of IL-6 trans-signaling (IL-6TS) in asthmatic patients is unclear.

188 can contribute to IL-13-driven pathology in asthmatic patients remain unclear.

189 Specific comparison of patients with FA and asthmatic patients revealed differences in the microbiot

190 , which is much higher than the 8% to 10% of asthmatic patients seen in the general population.

191 HBECs from asthmatic patients showed a significantly low TJ integri

192 ronchial hyperresponsiveness in adult stable asthmatic patients taking inhaled corticosteroids.

193 Their frequency was higher in asthmatic patients than in disease controls.

194 icroscopy and then apply it to the sputum of asthmatic patients to find known and novel relationships

195 Sputum cell T2GM values in asthmatic patients were significantly increased and rema

196 rring in the airways of prednisone-dependent asthmatic patients with increased eosinophil activity, r

197 BAL fluid ILC2s from asthmatic patients with increased TSLP levels were stero

198 ght to undertake a deep phenotyping study of asthmatic patients with upregulated IL-17 immunity.

199 gi were present in a large proportion of our asthmatic patients' airways, but their presence was not

200 utum supernatants from 246 participants (206 asthmatic patients) as a novel means of asthma stratific

201 Eosinophils are a therapeutic target in asthmatic patients, and GM-CSF has been suggested to con

202 ood of both allergic and non-allergic severe asthmatic patients, and these cells are recruited to the

203 plasma proteins characteristically occurs in asthmatic patients, being especially pronounced in those

204 Cough is a common and troublesome symptom in asthmatic patients, but little is known about the neuron

205 s and inflammatory bowel disease, but not in asthmatic patients, in whom further study is required.

206 ificantly higher in sputum supernatants from asthmatic patients, notably those with greater than 61%

207 he concept of the environmental epigenome in asthmatic patients, summarize previous publications of r

208 rial airway microbiota is known to differ in asthmatic patients, the fungal and bacterial markers tha

209 tes with variations in the microbiome across asthmatic patients, whereas neutrophilic airway inflamma

210 e peripheral blood CD4(+) T cells from adult asthmatic patients.

211 ed in severe asthmatics when compared to non-asthmatic patients.

212 iated with alveolar macrophage phenotypes in asthmatic patients.

213 ages during infection were both deficient in asthmatic patients.

214 t accompanied by deficient PRR expression in asthmatic patients.

215 mmasome is a potential therapeutic target in asthmatic patients.

216 resumed in concomitant ICS plus LABA-treated asthmatic patients.

217 studies of perception of airway function in asthmatic patients.

218 or 4 (TLR4) and NLRP3 at 4 hours in nonobese asthmatic patients.

219 levels were greater in obese versus nonobese asthmatic patients.

220 ion and molecular and clinical phenotypes in asthmatic patients.

221 on changes in nasal epithelia of adult white asthmatic patients.

222 during experimental rhinovirus infection of asthmatic patients.

223 orticosteroids indicates disease severity in asthmatic patients.

224 from control subjects but not in HBECs from asthmatic patients.

225 patients and in peripheral blood of allergic asthmatic patients.

226 ture compared with both control subjects and asthmatic patients.

227 ted with plasma cortisol levels in pediatric asthmatic patients.

228 of the adrenal cortex function in pediatric asthmatic patients.

229 ysLTs) are potent prophlogistic mediators in asthmatic patients; however, inhibition of CysLT recepto

230 The phylogenetic microbiota composition in asthmatics patients' homes was characteristically differ

231 anical proprieties compared to their LFEV(1) asthmatic peers.

232 The results showed that, among asthmatics, PFASs were positively associated with estrad

233 multi- and trans-generationally transmitted asthmatic phenotype that tends to wane over successive g

234 F0 only and F0/F1 exposure groups showed an asthmatic phenotype, an effect that was more pronounced

235 ilic infiltrate that characterize the severe asthmatic phenotype.

236 demographically and clinically diverse adult asthmatic populations.

237 eripheral Blood mononuclear cells (PMBCs) of asthmatic pre-school children with allergies and in the

238 We thus characterize immune networks of asthmatic predisposition in children at the age of 2, pr

239 The majority of moderate to severe asthmatics present with a "type 2-high" (T2-hi) phenotyp

240 quid interface (ALI) cultures of control and asthmatic primary human bronchial epithelial cells (HBEC

241 y sufficient to cause bronchoconstriction in asthmatic rats.

242 ), daily sputum (1.69 [1.19-2.38]), and late asthmatic reactions (1.52 [1.09-2.08]).

243 -2.98]), atopy (1.49 [1.09-2.05]), and early asthmatic reactions (2.86 [1.98-4.16]).

244 e mainstay of asthma treatment, up to 50% of asthmatics remain uncontrolled.

245 te that systemic PKCepsilon blockade reduces asthmatic respiratory distress in response to allergen a

246 of a PKCepsilon-blocking peptide suppresses asthmatic respiratory distress in response to allergen a

247 Mice with a low asthmatic response colonized with microbiota from Pglyrp

248 ediatric asthma morbidity and may modify the asthmatic response to indoor PM.

249 e feces and oropharynx correlated with lower asthmatic responses in the lungs.

250 results show that Pglyrp1 enhances allergic asthmatic responses primarily through its effect on the

251 sceptibility of children to allergen-induced asthmatic responses.

252 Unlike healthy participants, the asthmatic's post-viral-challenge state resembled more ot

253 controls and mild asthmatics (MAs) to severe asthmatics (SAs) in relation to exacerbation rate.

254 y expressed on eosinophils and mast cells in asthmatic sputum and targeting Siglec-8 with an antibody

255 ls of the bacterial endotoxin protein in the asthmatic state.

256 erential DNA methylation was associated with asthmatic status in AECs, providing further evidence for

257 As a consequence, the effect of asthmatic status on DNA methylation was assessed within

258 e and after rhinovirus challenge in allergic asthmatic subjects (total IgE, 133-4692 IU/mL; n = 28) a

259 lveolar lavage fluid (BALF) macrophages from asthmatic subjects and identify how APOE regulates IL-1b

260 Allergic asthmatic subjects are uniquely susceptible to acute whe

261 asthma heralded the beginning of phenotyping asthmatic subjects based on airways inflammation.

262 Asthmatic subjects displayed a range of significant alte

263 Obese asthmatic subjects have lower cut points for IgE levels

264 2 innate and adaptive responses in allergic asthmatic subjects infected with rhinovirus.

265 ed to delineate eosinophilic inflammation in asthmatic subjects should be approached with caution in

266 s induces robust T(H)1 responses in allergic asthmatic subjects that may promote disease, even after

267 NLPR3 inflammasome in BALF macrophages from asthmatic subjects to secrete IL-1beta.

268 ced an amplified antiviral T(H)1 response in asthmatic subjects versus controls, with synchronized al

269 from peripheral eosinophils from healthy and asthmatic subjects were isolated and analyzed by next-ge

270 Asthmatic subjects were uniquely enriched in members of

271 ast, T(H)2 responses were absent in infected asthmatic subjects who had normal lung function, and in

272 In uninfected asthmatic subjects, higher numbers of circulating virus-

273 erm Extension Safety Study of Mepolizumab in Asthmatic Subjects, NCT01691859) was an open-label exten

274 d enrichment of Rho-GTPase pathways in obese asthmatic Th cells, identifying them as a novel therapeu

275 ces that were more pronounced among allergic asthmatics than among controls by days 2 and 3 after vir

276 ate resembled more other rhinovirus-infected asthmatics than their own pre-viral-challenge state (hyp

277 cohort of sensitized, high-risk, pre-school asthmatics (total n = 166) were measured with three R&D

278 ssing immune responses to COVID-19 in severe asthmatics treated with biologics.

279 Med whole-genome sequencing dataset with 897 asthmatic trios from Costa Rica.

280 th low BMD after glucocorticoid treatment in asthmatics using gene expression profiles of peripheral

281 es and LRTS scores occurred among the atopic asthmatics versus the controls during the resolution of

282 sm with asthma and airway obstruction within asthmatics via multivariate logistic regression.

283 The most common fungus in asthmatics was Aspergillus fumigatus complex and this ta

284 Symptom control in severe asthmatics was not associated with airway tissue inflamm

285 k, together with epidemiologic findings that asthmatics were less likely to suffer from severe influe

286 Asthmatics were more likely to be hospitalized but less

287 Fifty seven times examinations (33 asthmatics) were detected from 304 times of enhanced che

288 CCL27 are significantly increased in severe asthmatics when compared to non-asthmatic patients.

289 Mild asthmatics who smoke cigarettes may develop unstable dis

290 We investigated adult asthmatics who visited our hospital and examined chest c

291 and Pc20 for both mild/ moderate and severe asthmatics with a correlation between the baseline eosin

292 trols, 43 allergic rhinitis patients and 192 asthmatics with different phenotypes and severities), we

293 were evaluated in three groups of children: asthmatics with FEV(1) >=100% (HFEV(1) ; n = 13), asthma

294 atics with FEV(1) >=100% (HFEV(1) ; n = 13), asthmatics with FEV(1) <=80% (LFEV(1) ; n = 14) and non-

295 imental inoculation with rhinovirus-16 among asthmatics with high levels of total IgE was compared to

296 Asthmatics with persistent airflow obstruction had great

297 Adult asthmatics with PTE were high BMI and heavy compared wit

298 l inoculation with rhinovirus-16 in allergic asthmatics with the response in healthy controls and to

299 0.024) heavy weight (p=0.033), compared with asthmatics without PTE.

300 e-bronchodilator lung function compared with asthmatics without sensitization including a lower FEV(1