bluuebunny/crossref_metadata_2025_split huggingface dataset:
Functional equations involving means and their Gauss composition
Authors: Daróczy Zoltán , Maksa Gyula , Páles Zsolt 
Published: October 2005

In this paper the equivalence of the two functional equations\[f(M1(x,y))+f(M2(x,y))=f(x)+f(y)(x,y∈I)f(M_1(x,y))+f(M_2(x,y))=f(x)+f(y) \qquad (x,y\in I)\]and\[2f(M1⊗M2(x,y))=f(x)+f(y)(x,y∈I)2f(M_1\otimes M_2(x,y))=f(x)+f(y) \qquad (x,y\in I)\]is studied, whereM1M_1andM2M_2are two variable strict means on an open real intervalII, andM1⊗M2M_1\otimes M_2denotes their Gauss composition. The equivalence of these equations is shown (without assuming further regularity assumptions on the unknown functionf:I→Rf:I\to \mathbb {R}) for the cases whenM1M_1andM2M_2are the arithmetic and geometric means, respectively, and also in the case whenM1M_1,M2M_2, andM1⊗M2M_1\otimes M_2are quasi-arithmetic means. IfM1M_1andM2M_2are weighted arithmetic means, then, depending on the algebraic character of the weight, the above equations can be equivalent and also non-equivalent to each other.
The von Neumann-Jordan constant, weak orthogonality and normal structure in Banach spaces
Authors: Jiménez-Melado Antonio , Llorens-Fuster Enrique , Saejung Satit 
Published: October 2005

We give some sufficient conditions for normal structure in terms of the von Neumann-Jordan constant, the James constant and the weak orthogonality coefficient introduced by B. Sims. In the rest of the paper, the von Neumann-Jordan constant and the James constant for the Bynum space

ℓ

2
,
∞

\ell _{2,\infty }

are computed, and are used to show that our results are sharp.
Involvement of distal airways in a chronic model of experimental asthma
Authors: Wegmann M. , Fehrenbach H. , Fehrenbach A. , Held T. , Schramm C. , Garn H. , Renz H. 
Published: October 2005

SummaryBackground
Bronchial asthma is characterized by chronic airway inflammation and airway remodelling which occurs in both proximal and distal airways. These changes are associated with development of airway hyper‐responsiveness and airflow limitation.Objective
This study was aimed to analyse whether chronic inhalative allergen challenges in mice lead to morphological and physiological changes comparable with this phenotype.Methods
For this purpose, BALB/c mice were systemically sensitized to ovalbumin (OVA) followed by aerosol allergen challenges on 2 consecutive days per week for 12 weeks.Results
In chronically challenged mice, tissue inflammation in proximal as well as distal airways was observed with a predominance of lymphocytes within the cellular infiltrate. In contrast, inflammation in the airway lumen decreased over time. These changes were associated by a shift in bronchoalveolar lavage–cytokine levels from IL‐4, IL‐5 and TNF‐α production (during the acute phase) towards markedly increased levels of TGF‐β during the chronic phase. Goblet cell hyperplasia and subepithelial fibrosis occurred throughout the airway tree. In terms of lung function, chronically challenged mice developed persistent bronchial hyper‐responsiveness and progressive airflow limitation. Six weeks after OVA aerosol discontinuation, airway inflammation still persisted although lung function was normalized.Conclusion
These data indicate that our model of chronic aerosol allergen challenges leads to a phenotype of experimental asthma with participation of distal airways and persistence of inflammation thereby resembling many morphological and physiological aspects of human bronchial asthma.
Eosinophil chemoattractants in the middle ear of patients with eosinophilic otitis media
Authors: Iino Y. , Kakizaki K. , Katano H. , Saigusa H. , Kanegasaki S. 
Published: October 2005

SummaryBackground
Patients with intractable otitis media associated with bronchial asthma have an extensive accumulation of eosinophils in the effusion and mucosa of the middle ear; this condition is called eosinophilic otitis media (EOM). It remained to be determined how eosinophils accumulate in the middle ear.Objectives
To clarify the pathogenesis of middle ear diseases, we measured the concentration of eosinophil chemoattractants in middle ear effusion (MEE), and carried out immunohistochemical studies of middle ear mucosa specimens to demonstrate the expression of eosinophil chemoattractants.Methods
Middle ear effusion samples were obtained from 15 EOM patients with bronchial asthma and from six controls for the measurement of eosinophil cationic protein (ECP), IL‐5, eotaxin and regulated on activation, normal T expressed and secreted concentrations. Middle ear mucosa samples were also taken from 14 EOM patients and 16 controls for immunohistochemical study. In 10 EOM patients, the numbers of immunoreactive cells as well as apoptotic cells were determined before and after the topical application of triamcinolone acetonide into the middle ear.Results
In EOM, significantly higher ECP and IL‐5 concentrations were detected in MEE than in serum, and ECP, IL‐5 and eotaxin concentrations in MEE were higher in the EOM patients than in the controls. ECP concentration positively correlated with that of IL‐5. Immunohistochemically, the numbers of cells positive for EG2 and ecalectin were significantly higher in the EOM patients than in the controls. After the topical application of triamcinolone acetonide, the numbers of infiltrating cells and immunoreactive cells distinctly decreased, whereas the number of apoptotic cells significantly increased.Conclusion
In EOM, locally produced IL‐5 may play a crucial role in the accumulation of eosinophils in the middle ear. Chemokines such as ecalectin and eotaxin are also produced in the middle ear, and help activate and enhance the survival of eosinophils to induce the intractable condition in the middle ear. The topical application of triamcinolone acetonide induces the apoptosis of not only eosinophils but also eosinophil chemoattractant‐producing cells, thereby improving the middle ear condition.
Mouse allergen‐specific immunoglobulin G and immunoglobulin G4 and allergic symptoms in immunoglobulin E‐sensitized laboratory animal workers
Authors: Matsui E. C. , Diette G. B. , Krop E. J. M. , Aalberse R. C. , Smith A. L. , Curtin‐Brosnan J. , Eggleston P. A. 
Published: October 2005

SummaryBackground
High levels of allergen‐specific IgG have been associated with clinical efficacy in immunotherapy studies, but whether this antibody isotype is associated with clinical tolerance in the setting of environmental exposure remains unclear.Objective
To determine if mouse allergen‐specific IgG (mIgG) and IgG4 (mIgG4) levels are associated with mouse‐related symptoms among IgE‐sensitized laboratory workers.Methods
Fifty‐eight workers with either skin test or serologic evidence of IgE‐mediated mouse sensitization were studied. Symptom data were obtained by a questionnaire. Serum levels of mouse‐specific IgG, IgG4, and IgE were quantified by a solid‐phase antigen‐binding assay (IgG) and RAST (IgG4 and IgE), and the relationships between mouse‐specific serologic responses and mouse‐related symptoms were analysed.Results
Twenty‐three (39.7%) participants reported mouse‐related symptoms. Mouse‐specific IgG and IgG4 levels were not associated with mouse‐related symptoms among the study population as a whole. Among the 29 (50%) participants with detectable mouse‐specific IgE (mIgE), higher mouse‐specific IgG and IgG4 levels were associated with a decreased risk of symptoms, after adjusting for mIgE level (odds ratio (OR) 0.3, 95% confidence interval (CI): 0.1–1.4, and OR 0.3, 95% CI: 0.04–2.6, respectively). Higher levels of mIgG and mIgG4 remained associated with a decreased risk of symptoms after additional adjustment for sex and handling of mice (OR 0.1, 95% CI: 0.02–0.7, and OR 0.2, 95% CI: 0.02–2.1, respectively). Higher mIgG : IgE and mIgG4 : IgE ratios were also associated with a decreased risk of symptoms after adjusting for these confounders (OR 0.1, 95% CI: 0.02–0.7, and OR 0.2, 95% CI: 0.02–0.92, respectively).Conclusion
Among workers with detectable mIgE, higher mIgG and mIgG4 levels are associated with a decreased risk of mouse‐related symptoms. High serum levels of mIgG or mIgG4 may be markers for clinical tolerance among laboratory mouse workers with detectable mIgE, but these findings need to be confirmed in larger, prospective studies.
Bronchial matrix and inflammation respond to inhaled steroids despite ongoing allergen exposure in asthma
Authors: De Kluijver J. , Schrumpf J. A. , Evertse C. E. , Sont J. K. , Roughley P. J. , Rabe K. F. , Hiemstra P. S. , Mauad T. , Sterk P. J. 
Published: October 2005

SummaryBackground
Inflammatory and structural changes of the airway mucosa are chronic features of asthma. The mechanisms underlying these changes and their modulation by steroid prophylaxis have not been clarified.Objective
We postulated that asymptomatic ongoing allergen exposure could drive airway inflammation as well as changes in the extracellular matrix (ECM), and that inhaled steroids could prevent this.Methods
Therefore, we exposed patients with mild asthma to 2 weeks of repeated low‐dose allergen, with concomitant inhaled steroid or placebo treatment. Bronchial biopsies, which were taken before and after this exposure, were stained and digitally analysed. The ECM proteins in asthmatics were also compared with a normal control group.Results
Low‐dose allergen exposure alone resulted in a significant increase of bronchial epithelial macrophages. Despite ongoing allergen exposure, inhaled steroids reduced the numbers of mucosal eosinophils, neutrophils and T lymphocytes. At baseline, the mean density of the proteoglycans (PGS) biglycan and decorin were, respectively, higher and lower in the bronchial mucosa of asthmatics as compared with normal controls. Steroid treatment, during allergen exposure, increased the mean density of the PGS biglycan and versican.Conclusion
We conclude that chronic allergen exposure induces inflammatory changes in the bronchial mucosa. Despite ongoing allergen exposure, steroid treatment decreases mucosal inflammatory cells while altering PG density. The latter observation highlights the need to examine steroid‐induced changes closely in the airway structure in patients with asthma.
Circulating eosinophils in asthma, allergic rhinitis, and atopic dermatitis lack morphological signs of degranulation
Authors: Malm‐Erjefält M. , Greiff L. , Ankerst J. , Andersson M. , Wallengren J. , Cardell L.‐O. , Rak S. , Persson C. G. A. , Erjefält J. S. 
Published: October 2005

SummaryBackground
In allergic diseases, eosinophils in affected tissues release granule proteins with cytotoxic, immunoregulatory, and remodelling‐promoting properties. From recent observations, it may be assumed that eosinophils degranulate already in circulating blood. If degranulation occurs in the circulation, this could contribute to widespread systemic effects and provide an important marker of disease.Objective
To determine the degranulation status of circulating eosinophils in common allergic diseases.Methods
Using a novel approach of whole blood fixation and leucocyte preparation, the granule morphology of blood eosinophils from healthy subjects, non‐symptomatic patients, symptomatic patients with asthma, asthma and Churg–Strauss syndrome, allergic rhinitis, and atopic dermatitis was evaluated by transmission electron microscopy (TEM) and eosinophil peroxidase (TEM) histochemistry. Plasma and serum levels of eosinophil cationic protein were measured by fluoroenzymeimmunoassay. Selected tissue biopsies were examined by TEM.Results
Regardless of symptoms, circulating eosinophils from allergic patients showed the same granule morphology as cells from healthy subjects. The majority of eosinophil‐specific granules had preserved intact electron‐density (96%; range: 89–98%), while the remaining granules typically exhibited marginal coarsening or mild lucency of the matrix structure. Abnormalities of the crystalline granule core were rarely detected. Furthermore, granule matrix alterations were not associated with any re‐localization of intracellular EPO or increase in plasma eosinophil cationic protein. By contrast, eosinophils in diseased tissues exhibited cytolysis (granule release through membrane rupture) and piecemeal degranulation (loss of granule matrix and core structures).Conclusion
In symptomatic eosinophilic diseases, circulating blood eosinophils retain their granule contents until they have reached their target organ.
Long‐term exposure to background air pollution related to respiratory and allergic health in schoolchildren
Authors: Pénard‐Morand C. , Charpin D. , Raherison C. , Kopferschmitt C. , Caillaud D. , Lavaud F. , Annesi‐Maesano I. 
Published: October 2005

SummaryBackground
The impact of air pollution on asthma and allergies still remains a debate.Objective
Our cross‐sectional study was intended to analyse the associations between long‐term exposure to background air pollution and atopic and respiratory outcomes in a large population‐based sample of schoolchildren.Methods
Six thousand six hundred and seventy‐two children aged 9–11 years recruited from 108 randomly schools in six French cities underwent a clinical examination including a skin prick test (SPT) to common allergens, exercise‐induced bronchial reactivity (EIB) and skin examination for flexural dermatitis. The prevalence of asthma, allergic rhinitis (AR) and atopic dermatitis was assessed by a standardized health questionnaire completed by the parents. Three‐year‐averaged concentrations of air pollutants (NO2, SO2, PM10 and O3) were calculated at children' schools using measurements of background monitoring stations.Results
After adjusting for confounders, EIB, lifetime asthma and lifetime AR were found to be positively related to an increase in the exposure to SO2, PM10 and O3. The adjusted odds ratios (aOR) per increase of 5 μg/m3 of SO2 was 1.39 (95% confidence interval (CI)=1.15–1.66) for EIB and 1.19 (1.00–1.41) for lifetime asthma. The aOR for lifetime AR per increase of 10 μg/m3 of PM10 was 1.32 (CI=1.04–1.68). Moreover, SPT positivity was associated with O3 (aOR=1.34; CI=1.24–1.46). Associations with past year symptoms were consistent, even if not always statistically significant. Results persisted in long‐term resident (current address for at least 8 years) children. However, no consistent positive association was found with NO2.Conclusions
A moderate increase in long‐term exposure to background ambient air pollution was associated with an increased prevalence of respiratory and atopic indicators in children.
Bacterial and fungal agents in house dust and wheeze in children: the PARSIFAL study
Authors: Schram‐Bijkerk D. , Doekes G. , Douwes J. , Boeve M. , Riedler J. , Üblagger E. , von Mutius E. , Benz M. R. , Pershagen G. , van Hage M. , Scheynius A. , Braun‐Fahrländer C. , Waser M. , Brunekreef B. ,   on behalf of the PARSIFAL study group
Published: October 2005

SummaryBackground
Growing up on a farm and an anthroposophic lifestyle are associated with a lower prevalence of allergic diseases in childhood. This might be related to increased inhalatory exposure to microbial agents.Objective
To assess the association between microbial agents in house dust and atopic wheeze in farm children, Steiner school children and reference children.Methods
Levels of bacterial endotoxin, fungal β(1,3)‐glucans and fungal extracellular polysaccharides (EPS) in mattress and living room floor dust were measured in a population of 270 atopic (=Phadiatop‐positive) children with self‐reported wheezing, including 168 current atopic wheezers, and 441 non‐atopic, non‐symptomatic controls. These children were selected from a cross‐sectional study in five European countries.Results
In the study population as a whole, average levels of mattress dust endotoxin, EPS and glucans were slightly (1.1–1.2‐fold; P<0.10) higher in control children than in atopic wheezers. Atopic wheeze was related to mattress levels of endotoxin, EPS and glucans in farm and farm‐reference children. However, when adjusting for group (farm vs. farm‐reference children), the associations became non‐significant whereas the group effect remained. No associations between atopic wheeze and microbial agents were observed in Steiner and Steiner‐reference children. For current atopic wheeze, the farm effect became non‐significant after adjustment for microbial agent levels.Conclusion
Not only bacterial endotoxin but also mould components might offer some protection against atopic wheeze in children. However, the protective effect of being raised on a farm was largely unexplained by the mattress microbial agent levels measured in this study.
Nitric oxide synthase polymorphisms and asthma phenotypes in Chinese children
Authors: Leung T. F. , Liu E. K. H. , Tang N. L. S. , Ko F. W. S. , Li C. Y. , Lam C. W. K. , Wong G. W. K. 
Published: October 2005

SummaryBackground
Nitric oxide (NO) is a key factor for balancing T‐helper type 1/T‐helper type 2 immunity. Single nucleotide polymorphisms (SNPs) in nitric oxide synthase (NOS) genes have been associated with atopy and exhaled NO concentrations in Caucasians. We investigated the association between asthma traits and genetic polymorphisms in neuronal NO synthase (NOS1) and endothelial NO synthase (NOS3) in Chinese children.Methods
Asthmatic children between 5 and 18 years of age and non‐allergic controls were recruited. Plasma total IgE was measured by microparticle immunoassay, whereas allergen‐specific IgEs were measured by fluorescent enzyme immunoassay. Fractional exhaled NO concentration (FeNO) was measured by a chemiluminescence analyser. NOS1 C5266T and NOS3 G894T were genotyped by restriction fragment length polymorphism, and (AAT)n polymorphism in intron 20 of NOS1 was determined by GeneScan analysis.Results
The mean (SD) ages of 295 asthmatics and 174 controls were 11.1 (3.8) years and 11.6 (4.0) years, respectively (P=0.162). NOS1 C5266T and NOS3 G894T were not associated with asthma, atopy or FeNO. However, significantly more subjects with T/T in NOS1 C5266T had increased plasma total IgE as compared with those with C/T or C/C (P=0.017). This SNP was also associated with sensitization to Dermatophagoides pteronyssinus (P=0.049). Among asthmatic patients, log‐transformed plasma total IgE levels were significantly higher among those homozygous for 5266T of NOS1 [mean (SD): 2.84 (0.44) for T/T, 2.68 (0.42) for C/T, 2.59 (0.69) for C/C; P=0.021]. This study found a significant inter‐ethnic difference in the allele frequencies of AAT repeats, and this polymorphism was associated with high plasma total IgE levels (P=0.044) but not FeNO (P=0.158). NOS3 G894T was not associated with any asthma or atopy phenotype.Conclusions
NOS1 C5266T and AAT repeats affect plasma IgE concentrations in Chinese children. On the other hand, neither NOS1 nor NOS3 SNP was associated with FeNO or the risk of having asthma.
Double‐blind study of tolerability and antibody production of unmodified and chemically modified allergen vaccines ofPhleum pratense
Authors: Casanovas M. , Sastre J. , Fernández‐Nieto M. , Lluch M. , Carnés J. , Fernández‐Caldas E. 
Published: October 2005

SummaryBackgroundThe physicochemical modification of allergen extracts provides a chance for administering higher doses of allergen vaccines.ObjectiveTo evaluate the safety of a chemically modified (depigmented‐glutaraldehyde polymerized) therapeutic vaccine ofPhleum pratenseadministered at doses that are 10 times higher than those used in clinical practice, in comparison with conventional doses of the corresponding non‐modified alum‐adsorbed vaccine.Materials and methodsThe design of the study was randomized, double‐blind, parallel and included two groups of patients. Twenty‐three patients were treated weekly during nine visits for the build‐up phase, followed by two weekly maintenance doses (a total of 11 injections per patient). Twelve patients received a vaccine containing the standardized unmodified extract, at a maximum concentration of 308.5 mcg of freeze dried material/mL (Group A). Eleven patients received a standardized modified allergen extract (Group B). The maximum dose used was 2400 mcg/mL. Safety was evaluated recording all adverse events. Skin test results and specific antibody levels were evaluated at the beginning and at the end of the study.ResultsGroup A patients experienced three local immediate (two clinically irrelevant and one with a diameter > 5 cm) and 18 delayed reactions (15 irrelevant and three with a diameter > 10 cm), while Group B experienced six local immediate and 12 delayed reactions (all clinically irrelevant). Nine Group A patients experienced 12 systemic reactions (one immediate of grade 1, one of grade 2; and one delayed of grade 1; four of grade 2 and three of grade 3), while Group B patients experienced one immediate systemic reaction of grades 1, and 1 delayed reaction of grade 1.ConclusionsThe modified extract ofP. pratenseis safe to treat sensitive patients, even at concentrations that are 10 times higher than those regularly administered in clinical practice. The majority of the local reactions were clinically irrelevant. No systemic reactions of grade 2, 3 or 4 were reported using the modified extract.
Exposure of the fetus and infant to hens' egg ovalbumin via the placenta and breast milk in relation to maternal intake of dietary egg
Authors: Vance G. H. S. , Lewis S. A. , Grimshaw K. E. C. , Wood P. J. , Briggs R. A. , Thornton C. A. , Warner J. O. 
Published: October 2005

SummaryBackground
Maternally derived allergens may be transferred to the developing infant during pregnancy and lactation. However, it is not known how manipulation of environmental allergen levels might impact on this early‐life exposure.Objective
To measure dietary egg allergen (ovalbumin (OVA)) in gestation‐associated environments, in relation to maternal dietary egg intake.Method
OVA was measured by allergen‐specific ELISA in maternal blood collected throughout pregnancy, infant blood at birth (umbilical cord) and in breast milk at 3 months post‐partum. Samples derived from pregnant women undergoing diagnostic amniocentesis at 16–18 weeks gestation who were not subject to any dietary intervention, and from pregnant women, with personal or partner atopy, randomized to complete dietary egg exclusion or an unmodified healthy diet before 20 weeks gestation as a primary allergy prevention strategy. Maternal dietary egg intake was monitored closely throughout the study period by diary record and serial measurement of OVA‐specific immunoglobulin G concentration.Results
Circulating OVA was detected throughout pregnancy in 20% of women and correlated with both presence (P<0.001) and concentration (r=0.754, P<0.001) of infant OVA at birth (umbilical cord). At 3 months post‐partum OVA was detected in breast milk samples of 35% women, in higher concentrations than measured in blood. Blood and breast milk OVA were not related to maternal dietary intake or atopic pre‐disposition.Conclusions
Rigorous dietary egg exclusion does not eliminate trans‐placental and breast milk egg allergen passage. This early‐life exposure could modulate developing immune responses.