***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: During the ragweed season of 1984 we studied 120 patients with hay fever ; 58 had a history of asthma during the ragweed season the year before . They were divided into four treatment groups to receive nasal sprays of placebo , cromolyn sodium , flunisolide , or beclomethasone . In controlling hay fever symptoms all medications were superior to placebo ; the glucocorticoids were more effective than was cromolyn sodium .  Chest symptoms in the 58 patients with a history of asthma were also relieved by the topical nasal treatment . Various explanations for the beneficial effect of topical nasal treatment in asthma symptoms are conceivable . We consider the most likely to be improvement of nasal airway function . With restoration of the filtering action of the nose , less allergen would penetrate to the intrathoracic airways because of reduction in mouth breathing BACKGROUND We compared the effect of nasal azelastine ( 0.56 mg/day ) , nasal beclomethasone dipropionate ( BDP , 200 micrograms/day ) and matched placebo on seasonal symptoms , nasal cytology , and the increase in bronchial responsiveness occurring during pollen season in a group of subjects with history of allergic rhinitis to grass pollens only . METHODS The study was completed by nine subjects in the azelastine group , 13 subjects in the BDP group , and 13 subjects in the placebo group . Treatments were r and omly administered for 6 weeks . Each subject recorded daily nasal , eye and chest symptoms and additional treatment requirement for the entire pollen season . Each subject performed nasal lavage 4 weeks into the pollen season . Bronchial responsiveness to methacholine was measured before and 4 weeks into the pollen season . Response was expressed as provocative dose causing a 20 % fall in forced expiratory volume in 1 second in micromoles . RESULTS Azelastine-treated subjects had significantly fewer nasal symptoms during week 4 ( p < 0.05 ) , and BDP-treated subjects had fewer nasal symptoms during week 4 ( p < 0.05 ) and week 5 ( p < 0.05 ) compared with subjects given placebo . Both treatments significantly reduced the need for additional medications .  BDP , but not azelastine , treatment significantly reduced the percent of eosinophils recovered in nasal lavage ( p < 0.05 ) . Neither azelastine nor BDP protected against the increase in bronchial responsiveness to methacholine occurring during the pollen season . CONCLUSION We demonstrated that both azelastine and BDP are effective treatments for nasal symptoms of seasonal allergic rhinitis after 4 weeks of therapy . However , we were not able to demonstrate an antiinflammatory activity of nasally administered azelastine . Nasal therapy with azelastine and BDP did not block the increase in bronchial responsiveness to methacholine caused by seasonal allergen exposure BACKGROUND It has been reported that intranasal corticosteroids can influence bronchial hyperresponsiveness ( BHR ) in asthmatic subjects with seasonal rhinitis . The purpose of the present study was to evaluate the effect of intranasal fluticasone propionate and beclomethasone dipropionate on BHR and bronchial calibre ( forced expiratory volume in one second , FEV1 ) in children and young adults with seasonal rhinitis and mild asthma during two consecutive grass pollen seasons . METHODS In the first pollen season 25 patients aged 8–28 years were included in a double blind , placebo controlled study . The active treatment group used fluticasone aqueous spray 200 μg once daily . In the second pollen season 72 patients aged 8–28 years participated in a double blind , placebo controlled study of a similar design to that of the previous year except that an additional treatment group of patients using beclomethasone 200 μg twice daily was included . FEV1 was measured before and after three and six weeks of treatment ; BHR to methacholine ( PD20 ) was measured before and after six weeks of treatment . RESULTS In the first season the mean ( SD ) logPD20 of the patients decreased significantly both in the fluticasone group ( from 2.43 ( 0.8 ) μg to 1.86 ( 0.85 ) μg ) and in the placebo group ( from 2.41 ( 0.42 ) μg to 1.87 ( 0.78 ) μg ) without any intergroup difference in the change in logPD20 . In the second pollen season the mean logPD20 in the fluticasone , beclomethasone , and placebo groups did not change significantly . CONCLUSIONS Intranasal steroids did not influence BHR during two grass pollen seasons in children and young adults with seasonal rhinitis and mild asthma Background Seasonal allergic rhinitis ( SAR ) is a risk factor for asthma in affected individuals .  Nasal allergic inflammation enhances bone‐marrow eosinophil production , mainly via IL‐5 , and rhinitis patients have increased airway inflammation during the pollen season BACKGROUND Exhaled nitric oxide ( eNO ) is a noninvasive test that measures airway inflammation . Insufficient information is available concerning correlations between eNO and biologic , physiologic , and clinical characteristics of asthma in children currently not taking controller medications . OBJECTIVE The aim of this study was to find correlations between eNO and other characteristics of children with mild to moderate asthma currently not taking medications . METHODS Children aged 6 to 17 years with mild to moderate persistent asthma , taking only albuterol as needed , were characterized during 2 visits 1 week apart before being r and omly assigned into a clinical trial . At the screening visit , online measurements of  eNO  ,  spirometry  before and after bronchodilator , and biomarkers of peripheral blood eosinophils , serum eosinophil cationic protein , total serum IgE , and urinary leukotriene E4 were obtained . During a week characterization period before r and omization , symptoms were recorded on a diary and peak expiratory flows were measured twice daily using an electronic device . At the r and omization visit , eNO was repeated followed by a methacholine challenge and aeroallergen skin testing . Correlations and rank regression analyses between eNO and clinical characteristics , pulmonary function , and biomarkers were evaluated . RESULTS eNO was significantly correlated with peripheral blood eosinophils ( r = .51 , P < .0001 ) , IgE ( r = .48 , P < .0001 ) , and serum eosinophil cationic protein ( r = .31 , P = .0003 ) but not with urinary leukotriene E4 ( r = .16 , P = .08 ) . A moderate correlation was found between eNO and the number of positive aeroallergen skin tests ( r = .45 , P < .0001 ) . eNO did not correlate with FEV1 % predicted but was weakly correlated with FEV1/forced vital capacity ( r = -.19 , P = .032 ) , bronchodilator response ( r = .20 , P = .023 ) , and FEV1 PC20 methacholine ( r = -.31 , P = .0005 ) . No significant correlations were found between eNO and clinical characteristics or morning or evening peak expiratory flow measurements . The rank regression analysis demonstrated that 5 variables accounted for an R square of.52 ( eosinophils [ P < .0001 ] , IgE [ P = .0023 ] , age [ P < .0001 ] , months of inhaled corticosteroid use in the year before study entry [ P = .01 ] , and FEV1 PC20 [ P = .0061 ] ) . CONCLUSIONS These findings suggest that eNO provides information about the asthmatic state consistent with information from other markers of inflammation . It is a noninvasive technique that could be used in decisional management of children with asthma Nasopulmonary bronchomotor reflexes elicited by mechanical or irritant stimulation of the nose have been described in animals and asthmatic patients . However , few studies were devoted to the consequences of nasal breathing of cold and dry air or of only dry or only moist air on the bronchomotor control in normal individuals . The present study reported changes in interruption resistance ( Rint ) measured during eupneic breathing of moderately cold ( -4 or -10 degrees C ) and dry [ 0.3 % relative humidity ( RH ) ] air or of room air at 23 degrees C that is either dry ( 0.3 % RH ) or moist ( 97 % RH ) . Nasal inhalation of cold ( -4 degrees C ) dry air or of only dry air significantly increased baseline Rint value ( 17 and 21 % , respectively ) throughout the 15-min test periods . The response to cold was significantly accentuated when the air temperature was lowered to -10 degrees C ( 42 % ) . After nasal anesthesia or inhalation of a cholinergic antagonist , cold air did not induce a change in Rint . Nasal inhalation of moist room air had no effect . No Rint changes were measured during oral breathing of the three test agents . It is concluded that the activation of cold receptors or osmoreceptors in the nasal mucosa induces protective bronchoconstrictor responses in normal individuals BACKGROUND Although there is a recognized association between upper and lower allergic airways disease , it is unknown how seasonal allergic rhinitis ( SAR ) therapy will effect sensitive markers of airway function in patients with no history of asthma . OBJECTIVE To prospect ively evaluate subjective and objective markers of treatment response in 26 patients with SAR who have been screened to exclude a diagnosis of asthma . METHODS The patients ' usual treatment , with antihistamine alone ( n = 13 ) or in combination with intranasal corticosteroid ( n = 13 ) , was withheld for 1 week to achieve a baseline and then resumed . Measurements were made after baseline and after 2 and 4 weeks of treatment for nasal peak inspiratory flow rate ( nPIFR ) ; airways resistance ( Raw ) and specific conductance ( sGaw ) ; and nasal nitric oxide ( NO ) .  Patients reported their symptom ( nasal , throat and eye ) scores , daily activity scores , and ocular sodium cromoglycate usage over the preceding 24 hours . RESULTS Compared with baseline , there were significant ( P < .05 ) improvements with nPIFR , symptom scores and cromoglycate usage at 2 and 4 weeks of treatment . There was no significant suppression for NO at 2 or 4 weeks . There was a significant correlation between nPIFR and nasal symptoms ( r = -0.52 , P < .001 ) . After 4 weeks of treatment there were significant ( P < .05 ) improvements in sGaw ( 143.3 % predicted ) and Raw ( 91.6 % predicted ) compared with baseline ( sGaw : 111.8 % , Raw : 104.2 % predicted ) . CONCLUSION Treatment of SAR improves upper and lower airway parameters but not NO . Nasal PIFR correlates significantly with nasal symptoms To test the hypothesis that nasal antiinflammatory treatment can modify both upper and lower airway responses to allergen exposure , 12 cat-allergic subjects underwent 1 h cat  exposure challenges at baseline , with nasal occlusion , and after 1 wk of treatment with either intranasal triamcinolone acetonide or placebo in a double-blind crossover trial . Challenges were performed in a room containing two cats with airborne Fel d I levels ranging from 35 to 37,525 ng/m3 . Overall , nasal symptoms were moderately reduced by treatment ( p = 0.06 ) , with the greatest reduction occurring in the first 15 and 30 min of the challenge ( p < 0.01 and p < 0.05 , respectively ) . Mean lower respiratory symptoms were also diminished by treatment ( p = 0.02 ) , although those effects were most evident during the last 15 min of the challenge . Maximum changes in FEV1 were slightly reduced by the nasal therapy ( p = 0.07 ) , reaching statistical significance only at the 30-min intervals ( p < 0.05 ) . There were no significant differences in nasal histamine or TAME esterase levels . When challenges were repeated with nasal occlusion , no significant differences were detected in chest symptoms or FEV1 changes . We conclude that treatment with an intranasal corticosteroid led to significant reductions in both upper and lower airway responses to intense cat exposure The effect of intranasally administered corticosteroid ( budesonide ) on nasal symptoms , mode of respiration ( nasal versus mouth breathing ) , and asthma was investigated in 37 asthmatic children who were mouth breathers because of chronic nasal obstruction . After a 2-wk run-in period , the children were allocated r and omly to 4 wk of intranasal therapy with either budesonide ( 400 micrograms/day ) or placebo spray . A double-blind , parallel design was used . Diaries for peak expiratory flow , asthma , and rhinitis symptom scores and degree of mouth breathing were recorded at home . Nasal eosinophilia , nasal airway resistance at a flow of 0.2 L/s ( NAR0.2 ) , and lung function at rest and after exercise challenge were assessed at the clinic immediately before and at end of the 4-wk treatment . Budesonide , when compared with placebo , significantly decreased nasal obstruction ( p less than 0.05 ) , secretion ( p less than 0.01 ) , and eosinophilia ( p less than 0.02 ) , as well as NAR0.2 ( 
    Output:
    
Common mucosal inflammatory responses occur in CARAS .