• Tuberculosis and Respiratory Diseases
• /
• v.54 no.4
• /
• pp.386-394
• /
• 2003

Background : ATS(American Thoracic Society) defined new guidelines for COPD(chronic obstructive lung disease) in April 2001, following the results of the global initiative for chronic obstructive lung disease. The most important concept of COPD is an airflow limitation which is not fully reversible compared to bronchial asthma(BA). The criteria for COPD are postbronchodilator $FEV_1$ less than 80% of the predicted value and an $FEV_1$ per FVC ratio less than 70%. The global initiative for asthma(GINA) study defined asthma, which included immune-mediated chronic airway inflammatory airway disease, and found that airflow limitation was wide spread, variable and often completely reversible. Taken together COPD and BA may be combined in airflow limitation. This study was designed to evaluate the prevalence of BA in patients with COPD of moderate to severe airflow limitation. Methods : COPD was diagnosed by symptoms and spirometry according to ATS guidelines. Enrolled subjects were examined for peak flow meters(PFM), sputum eosinophils and eosinophil cationic protein(ECP) levels, serum total IgE with allergy skin prick test, and methacholine bronchial provocation test(MBPT). Results : About 27% of COPD patients with moderate to severe airflow limitation were combined with BA. There was significantly decreased response to PFM in severe COPD. However, there was no significant relationship between BA and COPD according to the degree of severity. The BA combined with COPD group showed significantly high eosinophil counts and ECP level in induced sputum. However, neutrophil counts in induced sputum showed significant elevation in the pure COPD group. Conclusion : Twenty-seven percent of COPD patients with moderate to severe ventilation disorder were combined with BA, but there were no significant differences according to the degree of severity.

• Tuberculosis and Respiratory Diseases
• /
• v.42 no.6
• /
• pp.813-822
• /
• 1995

Background: Bronchial hyperresponsiveness and abnormal response such as a loss of distensibility are pathophysiologic characteristics if bronchial asthma. The only means of direct in vivo measurement of airway size had been a tantalium bronchography, until high-resolution computed tomography(HRCT) enabled to measure noninvasively two dimensional airway area more accurately and reliably. Method: To investigate airway area responses to bronchial provocation with methacholine and evaluate the major sites of bronchial constriction in patients with bronchial asthma. We examined HRCT scans in five patients with bronchial asthma who had significant bronchoconstriction(20% or more decrease in $FEV_1$) using CT scanner(5,000T CT, Shimadzu Co, Japan) before and in 3~5 min. after methacholine inhalation. Airways which were matched by parenchymal anatomic landmarks in each patient before and after methacholine inhalation were measured using film scanner(TZ-3X scanner; Truvel Co. Chatsworth CA, USA) and a semiautomated region growing method. Results: 1) We identified 9 to 12 airways in each patient which were matched by parenchymal anatomic landmarks before and after methacholine inhalation. 2) Airway responses to methacholine are quite different even in a patient. 3) The constriction of small airways(average diameter <2 mm; area < $3.14mm^2$) was 48.7%(8.3; SEM, n=43), being more prominant than that of large airways(average diameter >2 mm; area > $3.14mm^2$), 53.8% (4.4;SEM, n=10), but not significantly different(p>0.05). 4) There was no significant difference in the degree of constriction between upper(44.3% +5.8; mean + SEM, n=30) and lower lung regions(56.7% +4.5, n=23). Conclusions: Thus airway responses to methacholine bronchoprovocation is quite variable in a patient with bronchial asthma and has no typical pattern in patients with bronchial asthma.

• Journal of Distribution Research
• /
• v.17 no.4
• /
• pp.29-53
• /
• 2012

As so many marketers get to use diverse sales promotion methods, manufacturer and retailer in a channel often use them too. In this context, diverse issues on sales promotion management arise. One of them is the issue of unplanned buying. Consumers' unplanned buying is clearly better off for the retailer but not for manufacturer. This asymmetric influence of unplanned buying should be dealt with prudently because of its possibility of provocation of channel conflict. However, there have been scarce studies on the sales promotion management strategy considering the unplanned buying and its asymmetric effect on retailer and manufacturer. In this paper, we try to find a better way for a manufacturer in a channel to promote performance through the retailer's sales promotion efforts when there is potential of unplanned buying effect. We investigate via game-theoretic modeling what is the optimal cost sharing level between the manufacturer and retailer when there is unplanned buying effect. We investigated following issues about the topic as follows: (1) What structure of cost sharing mechanism should the manufacturer and retailer in a channel choose when unplanned buying effect is strong (or weak)? (2) How much payoff could the manufacturer and retailer in a channel get when unplanned buying effect is strong (or weak)? We focus on the impact of unplanned buying effect on the optimal cost sharing mechanism for sales promotions between a manufacturer and a retailer in a same channel. So we consider two players in the game, a manufacturer and a retailer who are interacting in a same distribution channel. The model is of complete information game type. In the model, the manufacturer is the Stackelberg leader and the retailer is the follower. Variables in the model are as following table. Manufacturer's objective function in the basic game is as follows: ${\Pi}={\Pi}_1+{\Pi}_2$, where, ${\Pi}_1=w_1(1+L-p_1)-{\psi}^2$, ${\Pi}_2=w_2(1-{\epsilon}L-p_2)$. And retailer's is as follows: ${\pi}={\pi}_1+{\pi}_2$, where, ${\pi}_1=(p_1-w_1)(1+L-p_1)-L(L-{\psi})+p_u(b+L-p_u)$, ${\pi}_2=(p_2-w_2)(1-{\epsilon}L-p_2)$. The model is of four stages in two periods. Stages of the game are as follows. (Stage 1) Manufacturer sets wholesale price of the first period($w_1$) and cost sharing level of channel sales promotion(${\Psi}$). (Stage 2) Retailer sets retail price of the focal brand($p_1$), the unplanned buying item($p_u$), and sales promotion level(L). (Stage 3) Manufacturer sets wholesale price of the second period($w_2$). (Stage 4) Retailer sets retail price of the second period($p_2$). Since the model is a kind of dynamic games, we try to find a subgame perfect equilibrium to derive some theoretical and managerial implications. In order to obtain the subgame perfect equilibrium, we use the backward induction method. In using backward induction approach, we solve the problems backward from stage 4 to stage 1. By completely knowing follower's optimal reaction to the leader's potential actions, we can fold the game tree backward. Equilibrium of each variable in the basic game is as following table. We conducted more analysis of additional game about diverse cost level of manufacturer. Manufacturer's objective function in the additional game is same with that of the basic game as follows: ${\Pi}={\Pi}_1+{\Pi}_2$, where, ${\Pi}_1=w_1(1+L-p_1)-{\psi}^2$, ${\Pi}_2=w_2(1-{\epsilon}L-p_2)$. But retailer's objective function is different from that of the basic game as follows: ${\pi}={\pi}_1+{\pi}_2$, where, ${\pi}_1=(p_1-w_1)(1+L-p_1)-L(L-{\psi})+(p_u-c)(b+L-p_u)$, ${\pi}_2=(p_2-w_2)(1-{\epsilon}L-p_2)$. Equilibrium of each variable in this additional game is as following table. Major findings of the current study are as follows: (1) As the unplanned buying effect gets stronger, manufacturer and retailer had better increase the cost for sales promotion. (2) As the unplanned buying effect gets stronger, manufacturer had better decrease the cost sharing portion of total cost for sales promotion. (3) Manufacturer's profit is increasing function of the unplanned buying effect. (4) All results of (1),(2),(3) are alleviated by the increase of retailer's procurement cost to acquire unplanned buying items. The authors discuss the implications of those results for the marketers in manufacturers or retailers. The current study firstly suggests some managerial implications for the manufacturer how to share the sales promotion cost with the retailer in a channel to the high or low level of the consumers' unplanned buying potential.

• Tuberculosis and Respiratory Diseases
• /
• v.49 no.4
• /
• pp.486-494
• /
• 2000

Background : The dominant innervation of airway smooth muscle is parasympathetic fibers which are carried in the vagus nerve. Activation of these cholinergic nerves releases acetylcholine which binds to $M_3$ muscarinic receptors on the smooth muscle causing bronchocontraction. Acetylcholine also feeds back onto neuronal $M_2$ muscarinic receptors located on the postganglionic cholinergic nerves. Stimulation of these receptors further inhibits acetylcholine release, so these $M_2$, muscarinic receptors act as autoreceptors. Loss of function of these $M_2$ receptors, as it occurs in animal models of hyperresponsiveness, leads to an increase in vagally mediated hyperresponsiveness. However, there are limited data pertaining to whether there are dysfunctions of these receptors in patients with asthma. The aim of this study is to determine whether there are dysfunction of $M_2$ muscarinic receptors in asthmatic patients and difference of function of these receptors according to severity of asthma. Method : We studied twenty-seven patients with asthma who were registered at Pulmonology Division of Korea University Hospital. They all met asthma criteria of ATS. Of these patients, eleven patients were categorized as having mild asthma, eight patients moderate asthma and eight patients severe asthma according to severity by NAEPP Expert Panel Report 2(1997). All subjects were free of recent upper respiratory tract infection within 2 weeks and showed positive methacholine challenge test ($PC_{20}$<16mg/ml). Methacholine provocation tests were performed twice on separate days allowing for an interval of one week. In the second test, pretreatment with the $M_2$ muscarinic receptor agonist pilocarpine($180{\mu}g$) through inhalation was performed be fore the routine procedures. Results : Eleven subjects with mild asthma and eight subjects with moderate asthma showed significant increase of $PC_{20}$ from 5.30$\pm$5.23mg/ml(mean$\pm$SD) to 20.82$\pm$22.56mg/ml(p=0.004) and from 2.79$\pm$1.51mg/ml to 4.67$\pm$3.53mg/ml(p=0.012) after pilocarpine inhalation, respectively. However, in the eight subjects with severe asthma significant increase of $PC_{20}$ from l.76$\pm$1.50mg/ml to 3.18$\pm$4.03mg/ml(p=0.161) after pilocarpine inhalation was not found. Conclusion : In subjects with mild and moderate asthma, function of $M_2$ muscarinic receptors was normal, but there was a dysfunction of these receptors in subjects with severe asthma. ηlese results suggest that function of $M_2$ muscarinic receptors is different according to severity of asthma.

• Tuberculosis and Respiratory Diseases
• /
• v.52 no.1
• /
• pp.24-36
• /
• 2002

Background: Bronchial reactivity is known to be a component of airway hyperresponsiveness, a cardinal feature of asthma, with bronchial sensitivity, and is increments in response to induced doses of bronchoconstrictors as manifested by the steepest slope of the dose-response curve. However, there is some controversy regarding methods of measuring bronchial reactivity and clinical impact of such measurements. The purpose of this study was to evaluate the clinical significance and assess the clinical use by analyzing the relationship of the bronchial sensitivity, the clinical severity and the changes in pulmonary function with bronchial reactivity. Method: A total of 116 subjects underwent a methacholine bronchial provocation test. They were divided into 3 groups : mild intermittent, mild persistent, moderate and cough asthma. Severe patients were excluded. Methacholine PC20 was determined from the log dose-response curve and PC40 was determined by one more dose inhalation after PC20. The steepest slope of log dose-response curve, connecting PC20 with PC40, was used to calculate the bronchial reactivity. Body plethysmography and a single breath for the DLCO were done in 43 subjects before and after methacholine test. Results: The average bronchial reactivity was 38.0 in the mild intermittent group, 49.8 in the mild persistent group, 61.0 in the moderate group, and 41.1 in the cough asthma group. There was a weak negative correlation between PC20 and bronchial reactivity. A heightened bronchial reactivity tends to produce an increased clinical severity in patients with a similar bronchial sensitivity and basal spirometric pulmonary function. There were significant correlations between the bronchial reactivity and the initial pulmonary function before the methacholine test in the order of sGaw, Raw, $FEV_1$/FVC, MMFR. There were no correlations between the bronchial sensitivity and the % change in the pulmonary function parameters after the methacholine test. However, there were significant correlations between the bronchial reactivity and the PEF, $FEV_1$, DLCO. Conclusion: There was weak significant negative correlation between the bronchial reactivity and the bronchial sensitivity, and the bronchial reactivity closely reflected the severity of the asthma. Accordingly, measuring both the bronchial sensitivity and the bronchial reactivity can be of assistance in assessing of the ongoing disease severity and in monitoring the effect of therapy.