• Journal of the Korea Academia-Industrial cooperation Society
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• v.15 no.5
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• pp.2713-2723
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• 2014

This study adopts an ecological perspective to empirically navigate the issues surrounding the impact of parental abuse on the emotional development of adolescents. The data is used from the Korean Children and Youth Panel Survey 2011 (KCYPS 2011), which was conducted by the National Youth Policy Institute (n=2,270). Path models were constructed in which adolescents' environmental mediators (i.e., the relationship with parents, friends, and teachers; and school life) control their negative emotions (i.e., aggressiveness, negative physical symptoms, social weakness and depression); in turn to compare the difference between two groups based on parental abuse by using Structural Equation Modeling (SEM). As with the non-abused group (n=1,644), all the environmental mediators remained significant to control their negative emotion; whereas, the abused group (n=626) showed no significant pathway from their relationship with teachers and school life to negative emotion. This indicates that the abused group have limited number of the mediators to control their negative emotion than those of the non-abused group. For the non-abused group, the mediator with the highest total effect to control their negative emotion was the relationship with their friends; on the other hand, the abused group's mediator that showed the highest total effect to control their negative emotion was the relationship with their parents. Although the relationship with teachers remained significant as a mediator to affect school life for the both groups, teachers were not significant to control the negative emotion of the abused group. These findings suggest that the negative relationship with teachers in the abused group is a factor to threat the school adaptation of adolescents, which also leads to problems that are related to the emotional development of adolescents.

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