bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of inhaled atrial natriuretic peptide on methacholine bronchoconstriction in asthma
Authors: ANGUS R. M. , McCALLUM M. J. A. , THOMSON N.C. 
Published: April 2006

SummaryWe have previously demonstrated that intravenous and inhaled atrial natriuretic peptide (ANP) significantly inhibits histamine induced bronchoconstriction in asthmatic patients. The current study was designed to determine whether inhaled ANP was also able to inhibit the effects of methacholine. Eight atopic asthmatic patients (five women) were studied: mean (SD) age 38.2 (8.3) years flow expiratory volume per second (FEV1) 2.97 (0.60) litres, equivalent to 92 (13) % of the predicted. Each had demonstrated at least mild bronchial hyperreactivity to inhaled methacholine at screening (geometric mean PC20 l.02mg/ml; range 0.1l–6.54mg/ml). Patients attended for 3 study days and after baseline spirometry received 3.5 ml saline (placebo), 0.1 mg ANP or 1 mg ANP (ANP dissolved in 3.5ml saline) in a randomized, double‐blind manner via a Mizer aerosol conservation device. Aerosolization took approximately 9 min and FEV1 was repeated at 0.5, 1.5 and 3 min after completion. Immediately thereafter each patient received a 2 min inhalation of methacholine at a dose individually calculated to give a 25% fall in FEV1 (as extrapolated at their initial screening visit) and the FEY1 was followed over the next 20 min. Mean (SEM)% FEV1 did not change significantly after ANP being ‐4.3 (1.7), ‐3.2 (2.7) and ‐2.4 (1.2) after placebo, 0.1 mg ANP and 1 mg ANP respectively. The mean (SEM) maximum fall in FEV1 after methacholine was as follows: placebo 26.9 (5.7)%, 0‐1 mg ANP 18.2 (4.3)% and 1.0mg 11.2(2 7)%, (P < 0.05 placebo vs 1 mg ANP). These results demonstrate that ANP offers significant protection against methacholine induced bronchoconstriction in asthmatic patients.
Discrepancies between in vitro and in vivo tests for house dust mite allergy: is domestic exposure a better predictor than sensitization?
Authors: NIGGEMANN B. , KLEINAU I. , SCHOU C. , HANSEN G. N. , WAHN U. 
Published: April 2006

SummaryWe subjected seven asthmatic children to two bronchial allergen challenges, first with an extract from the house dust mite Dermatophagoides pteronyssinus (Derp) and then Dermatophagoides farinae (Der f), or vice versa. All children had elevated specific serum IgE to both species as well as reactions by crossed radioimmuno/electrophoresis (CRIE) to both group I and II allergens from both species. Immunoabsorption and subsequent analysis by CRIE showed a considerable concentration of serum IgE with specificity for epitopes common to the two species of house dust mite. Home dust sampling established that all children were exposed to Der f and only two to Der p. On bronchial provocation tests, all responded to Der f with an immediate reaction and five with a late reaction, only three of seven showed an immediate response to Der p, with four of the seven showing a late reaction. Our data could indicate that the local allergic immune reaction in the respiratory tract is sustained by ongoing exposure, and may thus have a different species specificity than the response reflected in the serum. In conclusion, our data indicates a lack of association between in vitro and in vivo tests for house dust mite allergy, which supports the continuing need for monitoring current clinical sensitization by allergen provocation tests and by measuring domestic exposure to the corresponding allergen. Extended studies are needed to support our findings.
Inhibition by a novel peptide leukotriene receptor antagonist ONO‐1078 of airway wall thickening and airway hyperresponsiveness to histamine induced by leukotriene C4 or leukotriene D4 in guinea‐pigs
Authors: KUROSAWA M. , YODONAWA S. , TSUKAGOSHI H. , MIYACHI Y. 
Published: April 2006

SummaryWe studied the effect of intravenous administration of leukotriene (LT) C4 or LTD., on airway responsiveness to histamine and airway wall thickening in guinea‐pigs. Guinea‐pigs were killed and the lungs were fixed in formalin. Slides from paraffin‐embedded section of the lungs were stained and the airways that were cut in transverse section were measured by tracing enlarged images using a digitizer, Moreover, airway resistance (Raw) was determined by a pulmonary mechanics analyser and we calculated two indices, an index of airway wall thickening and the one of airway hyperresponsiveness to histamine, from changes of baseline‐Raw and peak‐Raw following intravenous administration of histamine before and after the intravenous administration of LTC4 or LTD4. The infusion of LTC4 or LTD4 induced an increase of the relative thickness of the airway wall in peripheral bronchi demonstrable by the histological examination. In analysis of airway function, intravenous administration of LTC4 or LTD4 induced airway hyperresponsiveness to histamine with airway wall thickening. The LTC4 and LTD4 receptor antagonist ONO‐1078 inhibited these effects of LTC4 and LTD4, suggesting LTC4 and LTD4 may induce airway wall thickening and airway hyperresponsiveness through LTC4 and LTD4 receptors in the airways.
Ipratropium bromide nasal spray in non‐allergic rhinitis: efficacy, nasal cytological response and patient evaluation on quality of life
Authors: GEORGITIS J. W. , BANOV C. , BOGGS P. B. , DOCKHORN R. , GROSSMAN J. , TINKELMAN D. , ROSZKO P. , WOOD C. 
Published: April 2006

SummaryIntranasal fluorocarbon anticholinergic agents have been used to treat the nasal hypersecretion of perennial non‐allergic rhinitis, but chronic use has been restricted either due to the potential for systemic anticholinergic adverse events or due to the irritating properties of the fluorocarbon metered dose formulations. This study evaluates a new aqueous nasal formulation of ipratropium bromide (Atrovent Nasal Spray 0.03%) in subjects with perennial non‐allergic rhinitis in a double‐blind, placebo‐controlled trial. Two hundred and twenty‐eight patients were randomized to receive two sprays per nostril of either ipratropium bromide (42μ/nostril) or placebo‐administered three times a day as an aqueous nasal spray over an 8‐week interval. Patients were evaluated bi‐weekly and maintained daily diaries for duration and severity of nasal symptoms. Ipratropium bromide reduced the mean severity and duration of rhinorrhoea within the first week and throughout the 8 weeks of active treatment compared with placebo (P < 0.05). Secondary endpoints of efficacy (patient and physician global assessments and a quality of life assessment) also supported the use of ipratropium bromide nasal spray for rhinitis symptom control. With the reduction in rhinorrhoea by the ipratropium bromide nasal spray, patients reported a marked improvement in daily moods vs placebo (P < 0.01). Both placebo and ipratropium bromide nasal spray induced a modest reduction of nasal congestion, sneezing and postnasal drip. This improvement in these other nasal symptoms was consistent with the known soothing effects of a nasal saline vehicle. There were no drug‐related serious or systemic anticholinergic adverse events. The medication was well tolerated with side‐effects limited to infrequent episodes of epistaxis and nasal dryness of mild intensity. Assessment for nasal rebound for 1 week after discontinuation of treatment showed no increase in nasal symptoms above the original baseline symptoms. These data indicate that ipratropium bromide administered as an 0.03% aqueous nasal spray, 42μg/nostril t.i.d., is a well tolerated and a highly effective medication for controlling the severity and duration of rhinorrhoea in perennial non‐allergic rhinitis. This new aqueous formulation should provide an additional therapeutic agent to utilize for the chronic treatment of non‐allergic rhinitis.
Measurement of airborne rat urinary allergen in an epidemiological study
Authors: GORDON S. , TEE R. D. , NIEUWENHUIJSEN M. J. , LOWSON D. , HARRIS J. , TAYLOR A. J. NEWMAN 
Published: April 2006

SummaryThe suitability of radioallergosorbent test (RAST) inhibition to quantify occupational exposure to rat urinary aeroallergen (RUA) has been assessed. When using a constant pool of rat allergic sera, the reproducibility of the assay over 1 year was comparable to that reported for other immunoassays; at 50% RAST inhibition the inter‐assay coefficient of variation (CV) was 7.0% and the intra‐assay CV was 3.0%. The assay was highly specific for rat urine; mouse urine was 1100‐fold less potent at inhibiting the rat urine RAST system. Significant inter‐assay variation in the ‘high’ control was not due to batch variation and was relatively small when compared with the variation in RUA concentrations in the occupational environment. Measurement of workplace RUA exposure demonstrated that those directly involved in the care of rats experienced the highest RUA exposure of the nine occupational groups studied (animal technicians GM = 23.10/μg/m3) followed in decreasing order by those working with soiled litter (e.g. cage cleaners GM = 4.20 μg/m3), dead animals (e.g. post mortem GM = 1.60 μg/m3, scientists GM = 0.67 μg/m3) and rat tissue (e.g. slide production GM = 0.04μg/m3). In view of the complexity of rat allergens, RAST inhibition is an appropriate method for the quantification of occupational exposure to rats.
Effect of an asthmatic attack on CD23 and CD21 expression on lymphocytes from allergic children during the allergen season
Authors: GAGRO A. , RABATIĆ S. , LOKAR‐KOLBAS R. , MEDAR‐LASIĆ M. , ZIMIĆ L. 
Published: April 2006

SummaryBackground: The overproduction of IgE antibodies by atopic individuals in response to inhaled aeroallergen, forms the basis of an allergic disease. Furthermore, the exposure to allergen might trigger the symptom exacerbation.Objective: In children with bronchial asthma, the possible effects of seasonal, natural exposure to allergen on the expression of CD21 and CD23 antigens on B lymphocytes, and on the expression of HLA‐DR, CD45RA and CD45RO on CD4+ T cells were investigated.Methods: Heparinized blood samples were obtained from 15 children with bronchial asthma allergic to Dermcttophagoides pteronyssimis (Der p) at the time of an acute asthmatic attack and 2–4 weeks after the attack when the peak expiratory flow (PEF) was stabilized. The samples were analysed on a flow cytometer after the three‐colour immunofluorescence staining had been performed.Results: The increased proportion of B cells expressing CD23 antigen was found at the time of attack rather than after stabilization. Serum levels of total and Der p‐specific IgE increased 2–4 weeks after the asthmatic attack. This increase was accompanied by a further increase in the expression of CD23 antigen on CD21−B lymphocytes. In 10 out of 15 tested children, we found CD23 expressed on CD4+ HLA‐DR+ T cells during the asthmatic attack. No significant difference was found in the expression of CD45RA and CD45RO antigens.Conclusion: Since we have previously demonstrated the increased percentage of CD23 on CD21− B cells in allergic children as compared with controls, we speculate that natural exposure to the allergen which caused the increase in total and specific IgE levels might be related to the increased expression of CD23 on CD21− B cells
IL‐5, IL‐8 and GM‐CSF immunostaining of sputum cells in bronchial asthma and chronic bronchitis
Authors: HOSHI H. , OHNO I. , HONMA M. , TANNO Y. , YAMAUCHI K. , TAMURA G. , SHIRATO K. 
Published: April 2006

SummaryBackground: Granulocyte‐macrophage colony stimulating factor (GM‐CSF) and inlerleukin (IL)‐5 or IL‐8 have been .suggested to play an important role in the pathogenesis of eosinophilic airway inflammation in bronchial asthma or neutrophilic airway inflammation in chronic bronchitis, respectively, However, GM‐CSF and IL‐8 have biological activities to either eosinophils or neutrophils.Objective: To investigate the contribution of these cytokines to airway inflammation, we compared the cellular differential and immunolocalization of GM‐CSF, IL‐5 and IL‐8 in sputum cells from patients with bronchial asthma and chronic bronchitis.Methods: Cytospins of sputum cells from 12 patients with bronchial asthma and 12 with chronic bronchitis were subjected to cellular differential counting and immunocytochemistry with antihuman GM‐CSF, IL‐5 and IL‐8 antibody.Results: The predominant cells in bronchial asthma were eosinophils and lymphocytes, while those in chronic bronchitis were neutrophils. All cytokines examined were detected in either bronchial asthma or chronic bronchitis, although the percentage of GM‐CSF and IL‐5 positive cells in bronchial asthma (53.4 ± 6.0 [mean±sfm]% and 9.7 ± 2.8%, respectively) was significantly higher than that in chronic bronchitis (11.4±2.5%; P < 0.001 and 1.7plusmn;0.3%; P < 0.007. respectively). In contrast, the percentage of IL‐8 positive cells in chronic bronchitis (23.8 ± 7.0%) was significantly higher than that in bronchial asthma (7.7 ± 1.9%; P < 0.04). The cells positive for IL‐5 were lymphocytes in bronchial asthma and chronic bronchitis. The cells positive for GM‐CSF in bronchial asthma were predominantly eosinophils. while those in chronic bronchitis were monocytes/macrophages and neutrophils. In contrast, neutrophils are mainly positive for IL‐8 in chronic bronchitis, while monocytes/macrophages and bronchial epithelial cells are positive for IL‐8 in bronchial asthma.Conclusion: The immunochcmical comparison of GM‐CSF and IL‐8 localization in sputum cells between bronchial asthma chronic bronchitis suggests the differential regulation and roles of these cytokines in eosinophilic vs neutrophilic airway inflammation, resulting in the development of different types of airway inflammation.
Increased serum IgE in alcohol abusers
Authors: GONZÁLEZ‐QUINTELA A. , VIDAL C. , GUDE F. , TOMÉ S. , LOJO S. , LORENZO M. J. , BECERRA E. P. , MARTINEZ‐VAZQUEZ J. M. , BARRIO E. 
Published: April 2006

SummaryBackground: It has been reported that total serum IgE is increased in patients with alcoholic cirrhosis, but it is not clear if this fact is related to alcoholic liver disease or to alcohol intake.Objective: To measure serum IgE in a group of chronic alcoholics with different stages of liver injury in order to elucidate if IgE increase is related to alcoholic liver damage.Patients and methods: Total serum IgE was determined by enzyme immunoassay in 186 chronic alcoholic patients (137 male/49 female) and 101 healthy controls. Patients and controls with known reasons for IgE elevation were excluded. Among alcoholic patients, 24 had fatty liver, 28 hepatic fibrosis, 29 alcoholic hepatitis, and 67 liver cirrhosis (38 patients were not evaluable concerning liver injury).Results: Total serum IgE was found to be increased in alcoholics (median 154.5IU/mL, range 1–7329IU/mL) with respect to healthy controls (median 20IU/mL, range < 1–1417 IU/mL) (P < 0.001). IgE increase was moderate (180–1000 IU/mL) in 60 alcoholics (32.3%) and marked (> 1000 IU/mL) in 27 (14.5%). Male alcoholics had higher IgE levels than females (median 191 IU/mL and range 1–7329 IU/mL vs 105IU/mL and range 2–2189IU/mL) (P= 0.009). On logistic regression analysis, alcoholism, male sex and younger age (but not smoking) were independently associated with higher IgE levels. No clear relationship was noted between serum IgE and severity of alcoholic liver disease. Thus, no correlation was observed between IgE and parameters of liver function (serum bilirubin, albumin or prothrombin index). Likewise, IgE concentrations were not significantly different in patients with liver cirrhosis with respect to patients with less severe liver disease. Serum IgE was increased (> 180 IU/mL) in 47.8 % of cirrhotics and in 44% of patients without liver cirrhosis. In contrast, other immunoglobulins (IgG, IgA and IgM) were significantly correlated with liver dysfunction.Conclusion: Chronic alcoholism should be considered as a cause of increased total serum IgE, regardless of the severity of the underlying liver disease.
Is unrecognized anaphylaxis a cause of sudden unexpected death?
Authors: SCHWARTZ H. J. , YUNGINGER J. W. , SCHWARTZ L. B. 
Published: April 2006

SummaryBackground: Serum tryptase levels reflect mast cell activation and correlate with anaphylactic reactions. Elevated post‐mortem serum tryptase levels have been found in witnessed fatal anaphylaxis.Objective: This study was designed to examine whether or not unwitnessed anaphylaxis may be a hitherto unrecognized cause of sudden unexplained death.Methods: Mast cell tryptase was measured by immunoassay in 68 post‐mortem sera remaining from a previous study which reported elevated venom‐specific IgE antibodies in 22 (23%) of 94 victims of sudden unexpected death. Autopsies were performed in all cases. The cause of death was independently reported by pathologists unfamiliar with the nature of this study.Results: Serum tryptase levels were elevated (> 10ng/mL) in nine of 68 cases. The levels could not be predicted from the clinical circumstances surrounding death. Sera from four individuals contained both elevated tryptase and previously reported elevated venom‐specific IgE.Conlusions: We conclude that mast cell activation may accompany up to 13% of sudden unexpected deaths in adults. Measurement of both tryptase and specific IgE antibody levels in post‐mortem sera from persons experiencing sudden, unexpected death may identify a small subset of cases due to clinically unrecognized fatal anaphylaxis, including those due to insect stings.
Crossreactivity between Dermatophagoides siboney and other house dust mite allergens in sensitized asthmatic patients
Authors: FERRÁNDIZ R. , CASAS R. , DREBORG S. , EINARSSON R. , FERNÁNDEZ B 
Published: April 2006

SummaryBackground
The role of Pyroglyphid mites in IgE‐mediated serisitizalion has been well eslahlished. Although mites belonging to the genus Dermatophagoidess dominate in the acarofauna of domestic dust. non‐pyroglyphid mites might also be of clinical importance. In Cuba, Dermatophagoides siboney is found in dust coexisting with D. pteronyssiuus and Blomia tropicalis. Dermatophagoides forinae is not found. Storage mites, such as Acorus siro, Lepidoglyphus destructor and Tyrophagus putrescentiae might also be present.Objective
The aim of this study was to investigate the allergenic relationships among the mites present in the environment of allergic patients in Cuba.Methods
The crossreactivialty between an extract of D. siboney and the above mentioned six mites was studied by specific IgE inhibition, using sera of mite‐sensitive patients after incubation with serial dilutions of D. sibaney.Results
The inhibitory effect of D. sidiney extract was more pronounced against D. farinae. 91%, than against D. pyteronyssinus, 62%. Specific IgE to B. tropicali, A. siro, L. destructor and T. putrescentiae were inhibited to a much lesser extent, i.e. between 47 and 58%. The correlation between IgE to D. siboney and IgE to D. pteronyssinus and D. farinae was of 0.92 and 0.90. respectively. A weaker correlation was found between D. siboney and L. destructor (0.7), A. siro (0.67), B. tropicalis (0.54) and T. putrescentiae (0.51).Conclusion
Thus. D. siboney seems to be most closely related to D. farinae.
Perspectives of identity by descent (IBD) mapping in founder populations
Authors: TE MEERMAN G. J. , VAN DER MEULEN M. A. , SANDKUIJL L. A. 
Published: April 2006

SummaryIn a founder population patients with a genetic disease are likely to share predisposing genes from a common ancestor. We show that, depending on the distance of the relationship, patients are expected to share extended segments of DNA around the disease gene. Because of the size of the shared segment, a genomic search with DNA markers for such shared segments, identity by descent (IBD) mapping, can efficiently find the map position of genes, particularly due to genetic drift leading to reduction of heterogeneity and the large number of meioses that is implicitly observed. The statistical power of this method and the approximate cost are given as a function of the density of the map of tested markers and the number of generations since a common ancestor. Initial marker spacings between 5 and 15 centiMorgans are shown to be optimal. IBD mapping is applicable to many genetic diseases, because it does not presuppose a specific genetic model.
Pollen allergen homologues in barley and other crop species
Authors: ASTWOOD J. D. , MOHAPATRA S. S. , NI H. , HILL R. D. 
Published: April 2006

SummaryPollen from 10 agricultural plant species was surveyed for the presence of proteins crossreactive with group I, group IV and group IX allergens. Barley (Hordeum vulgare), maize (Zea mays), rye (Secale cerale), triticale (xTriticosecale cereale), oats (Avena saliva), Canola (Brassica napus) and sunflower (Helianthus annux) pollens contained numerous allergen cognate proteins. Northern blot analysis of barley pollen RNA revealed the presence of group I and group IX allergen transcripts. The barley pollen cDNA hvp9742, and three other cloned allergens: phlenum protense (Phip) V, Phl p Va and Lolium perenne (Lol p) 1b, were demonstrated to have extensive nucleotide and amino acid sequence similarity to the Poa p IX isoallergens. It was concluded that hvp9742 represents a Poa p IX isoallergen homologue expressed by barley pollen, and was therefore designated Hor v IX. It is further shown that the most highly conserved domains of all seven proteins, including Hor v IX, map to previously defined Poa p IX antibody binding epitopes.
Blood inflammatory response to inhaled endotoxin in normal subjects
Authors: MICHEL O. , DUCHATEAU J. , PLAT G. , CANTINIEAUX B. , HOTIMSKY A. , GERAIN J. , SERGYSELS R. 
Published: April 2006

SummaryPreviously we have reported that in asthmatics an inhalation of 20 μg lipopolysaccharide (LPS) produces a bronchial obstruction associated with an inflammatory blood response. The aim of the present study was to evaluate this response in normal subjects. Eight normal non‐atopic subjects were challenged by inhalation of a solution containing 20 μg LPS (from Escherichia coli 026:B6) a week after bronchial challenge with control solution. The lung function response was evaluated by the changes in forced expiratory volume in one second (FEV1), in specific conductance and in airway resistance while the blood inflammatory response was evaluated by serial measures of total white blood cells (WBC) and polymorphonuclear neutrophils (PMN) count, luminol enhanced‐chemiluminescence (luminol‐CL, as a marker of the PMN degree of activation), C‐reactive protein (CRP), haptoglobin, complement fraction C3, tumour necrosis factor‐α (TNF‐α) and adrenocorticotropic hormone (ACTH). No response in lung function was observed for 6 h after the LPS inhalation. The count in WBC and PMN increased 300 (P < 0.01) and 360 (P < 0.01) min after the LPS challenge associated with an increase in the level of luminol‐CL (P < 0.001). This rise in luminol‐CL level was significant at 120 min (P < 0.05) before any change in the PMN count. After 24 and 48 h the acute‐phase protein CRP raised significantly (P < 0.01), the other proteins C3 and haptoglobin being unchanged. A slight increase in ACTH was observed 240 and 360 min (P < 0.05) after the LPS challenge while the TNFα detectable level was not modified. In conclusion, in normal subjects, inhalation of a pro‐inflammatory agent is able to induce a systemic inflammatory response in the absence of any effect on lung mechanics, while in asthmatics the same bronchial challenge has been reported to induce a similar blood inflammation associated with a significant response in lung function.