• Tuberculosis and Respiratory Diseases
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• v.44 no.2
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• pp.290-297
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• 1997

Background : Despite remarkable progress of understanding the pathophysiology and therapy of bronchial asthma, asthma morbidity and mortality are on the rise. Also hospitalization and attending rates of emergency department for asthma have been increasing gradually. We analyzed clinical characteristics and prognosis of patients who visited emergency room due to asthma attack in order to define clinical characteristics of these group of patients. Method : We reviewed 105 adult asthmatic patients who attended emergency department of Korea University Hospital between August 1995 and July 1996, retrospectively. Results : 103 patients(56 female, 47 males, mean age : 48.6 years) attended-68 self referral, 18 practitioner referral and 17 OPD transfer- and 86 patients(83.5%) were admitted. Attending emergncy department was clearly more frequent in December(13.6%) and May(12.6%). Time lag between onset of asthmatic attack and arrival at the hospital was $14.2{\pm}15.5$ hour and initial peak expiratory flow rate was $166.7{\pm}68.3L/min$.(43.3% predicted) The commonest cause for visiting emergency room was aggravation of asthma due to upper respiratory tract infection in mild asthmatics. About half of them had history of previous ER visits. Their prognosis was not bad, but after discharge, about half of patients escaped from OPD follow-up. Conclusion : As a group they merit detailed attention and follow up arrangement. Clinician need to monitor and review the treatment plans, the medications, the patient's management technique, and the level of asthma control. For this group, plans for longer term treatment, including asthma education program and adjustment of overall treatment plan should be made.

• Applied Microscopy
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• v.39 no.1
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• pp.1-7
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• 2009

Experimental induction of polycystic ovary (PCO) resembling some aspects of human PCO syndrome was produced using the long-acting compound estradiol valerate (EV). Our previous study on the role of Korean red ginseng total saponins (GTS) in a steroid-induced PCO rat model demonstrated that electro-acupuncture modulates nerve growth factor (NGF) concentration in the ovaries. In fact, the involvement of a neurogenic component in the pathology of PCO-related ovarian dysfunction is preceded by an increase in sympathetic outflow to the ovaries. In the present study, we tested the hypothesis that therapeutic GTS administration modulates sympathetic nerve activity in rats with PCO. This was done by analyzing NGF protein and NGF mRNA expression involved in the pathophysiological process underlying steroid-induced PCO. EV injection resulted in significantly higher ovarian NGF mRNA expression in PCO rats compared to control rats, and PCO ovaries were counteracted by GTS administration with significantly lower expression of NGF mRNA compared to EV treated ovaries. However, NGF protein was unaffected in both EV and GTS treated ovaries compared to control rats. These results indicate that EV modulates the neurotrophic state of the ovaries, which may be a component of the pathological process by which EV induces cyst formation and anovulation in rodents.

• Tuberculosis and Respiratory Diseases
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• v.50 no.2
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• pp.196-204
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• 2001

Background : Bronchial asthma is characterized by a reversible airway obstruction, airway hyperresponsiveness, and eosinophilic airway inflammation. The bronchodilator response(BDR) after short acting beta agonist inhalation and PC20 with methacholine inhalation are frequently used for diagnosing bronchial asthma. However, the relationship between the presence of a bronchodilator response and the degree of airway hyperresponsiveness is uncertain. Therefore, the availability of a eosinophil cationic protein (ECP) and a correlation ECP with a bronchodilator response and airway hyperresponsiveness was investigated. Method : A total 71 patients with a moderate to severe degree of bronchial asthma were enrolled and divided into two groups. 31 patients with a positive bronchodilator response and 38 patients with a negative bronchodilator response were evaluated. In both groups, the serum ECP, peripheral blood eosinophil counts, and total IgE level were measured and the methacholine bronchial provocation test was examined. Results : There were no differences observed in age, sex, atopy, and baseline spirometry in both groups. The peripheral eosinophil counts showed no difference in both groups, but the ECP level in group 1 (bronchodilator responder group) was higher than in group 2(non-bronchodilator responder group) ($22.4{\pm}20.7$ vs $14.2{\pm}10.4$, mean$\pm$SD). The PC20 in group 1 was significantly lower than in group 2 ($1.14{\pm}1.68$ vs $66{\pm}2.98$). There was a significant positive correlation between the BDR and ECP, and a negative correlation between the bronchial hyperresponsiveness and ECP. Conclusion : The bronchodilator response significantly correlated with the bronchial hyperresponsiveness and serum ECP in the moderate to severe asthma patients. Hence, the positive bronchodilator response is probably related with active bronchial inflammation and may be used as a valuable index in treatment, course and prognosis of bronchial asthma.

• Tuberculosis and Respiratory Diseases
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• v.40 no.3
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• pp.213-222
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• 1993

Background : Bronchial asthma has been known as an inflmmatory disease. There have been many evidences that polymorphonuclear leukocytes (PMN) might play an important role in the pathogrnesis of asthma. Although many investigators suggested that pneumocyte injury by PMN-derived oxygen radicals may contribute to the pathogenesis of asthma, there has been few report for a direct evidence of oxygen radicals-mediated pneumocyte injury in bronchial asthma. Furthermore the exact mechanism of oxygen radicals-mediated pneumocyte injury is still controversy. This study was designed to establish a direct in vitro evidence and its clinical significance of pneumocyte injury by PMN-derived superoxide anion in bronchial asthma and to elucidate the main mechanism of superoxide anion-mediated pneumocyte injury. Methods : 12 stable asthmatics and 5 healthy volunteers were participated in this study. PMN was separated from peripheral venous blood samples by using dextran sedimentation and Ficoll-Hypaque density gradient separation method. Superoxide anion productions by PMN and plasma SOD activities were measured by spectrophotometric assay using the principle of SOD inhibitable cytochrome c reduction. PMN-mediated pneumocyte injuries were measured by $^{51}Cr$-release assay using A549 pneumocytes and were expressed as percent lysis and percent detachment. Results: 1) PMN from asthmatics produced more amount of superoxide anion compared to PMN from normal subjects ($6.65{\pm}0.58$ vs $2.81{\pm}0.95\;nmol/1{\times}10^6$ cells, p<0.05), and showed an inverse correlation with $FEV_1$(R=-0.63, p<0.05), but no correlation with $PC_{20}$ histamine in asthmatics. 2) Plasma SOD activities were decreased in asthmatics compared to normal subjects but not significant, and showed a positive correlation with $FEV_1$(R=0.63, p<0.05) but no correlation with $PC_{20}$ histamine in asthmatics. 3) There were a positive correlation between plasma SOD activity and superoxide anion production by PMN in normal subjects (R=0.88, p<0.05) but not in asthmatics. 4) PMN-mediated pneumocyte injury was predominantly expressed as cell detachment rather than cell lysis in both groups, and PMN from asthmatics showed more potent cytotoxic effect on A549 pneumocytes compated to PMN from normal subjects. PMN-mediated detachment rather than lysis of A549 pneumocytes was significantly inhibited by in vitro SOD but not by diluted serum. 5) PMN-mediated detachment rather than lysis of A549 pneumocytes showed a good correlation with superoxide anion production by PMN (R=0.90 in normal subjects, R=0.82 in asthmatics, p<0.05) but no correlation with plasma SOD activity. PMN-mediated pneumocyte injuries were not correlated with $FEV_1$ or $PC_{20}$ histamine in asthmatics. 6) There were no significant differences in PMN-mediated pneumocyte injuries between allergic and nonallergic asthmatics. Conclusion : Our results suggest that pneumocyte injury by PMN-derived superoxide anion may partially contribute to the pathogenesis of asthma and that cell detachment rather than cell lysis may be the mechanism of superoxide anion-mediated pneumocyte injury.

• Journal of the Korean Chemical Society
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• v.51 no.3
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• pp.251-257
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• 2007

The Tumor necrosis factor-α, (TNF-α), is involved in the pathogenesis of multiple sclerosis and contributes to the degeneration of oligodendrocytes as well as neurons. Nicotine has been found to have immunosuppressive and inflammation-suppressing effects. Astrocytes, the major glial cells in the CNS, are capable of producing TNF-α at both the mRNA and protein levels in response to interleukin-1 (IL-1) or TNF-α. Nicotine has been shown to influence glial cell functions. To order to explore the role of astrocytes in the production of TNF-α, astrocytes were pretreated with nicotine and are stimulated with IL-1β to determine their effects on TNF-α production. The results are as follows. Cytotoxic effects of nicotine on human fetal astrocytes were noted above 10 μg/ml of nicotine. The effect of IL-1β on TNF-α mRNA expression in primary cultured human fetal astrocytes was maximal at 2 h after IL- 1β(100 pg/ml) treatment. Human fetal astrocytes were pretreated with 0.1, 1, and 10 μg/ml of nicotine and then stimulated with IL-1β (100 pg/ml) for 2 h. The inhibitory effect of nicotine on expressions of TNF-α mRNA in human fetal astrocytes with pretreated 0.1 μg/ml of nicotine is first noted at 8 hr, and the inhibitory effect is maximal at 12 h. The inhibitory effect at 1 μg/ml of nicotine is inhibited maximal at 24 h. Nicotine at 0.1, 1 and 10 μg/ml concentrations significantly inhibits IL-1β-induced NF-κB activation. Collectively, this study indicates that nicotine might inhibit the expression of TNF-α in activated human fetal astrocytes.

• Radiation Oncology Journal
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• v.5 no.1
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• pp.31-36
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• 1987

Radiobiological and clinical evidences indicate that hyperthermia combined with ionizing radiation produces a significant improvement in therapeutic effect of cancer. In general, malignant cells are more sensitive to heat than normal cells in the heat range of $41\~45^{\circ}C$. We report the experiences obtained from 42 patients with advanced malignant neoplasms managed with 2,450MHz microwave-induced local hyperthermia and ionizing radiation at the Department of Radiology, Kangnam St. Mary's Hospital, Catholic University Medical College. A clinical analysis of 42 thermoirradiated patients showed result of 11(26\%),\;15(36\%),\;11(26\%)\;and\;5(12\%)$ patients with complete response (CR), partial response (PR), minor response (MR) and no response (NR), respectively. Histologically there were $17(40.2\%)$ squamous cell carcinomas, $12(28.6\%)$ adenocarcinomas and $6(14.3\%)$ miscellaneous cancers. Eleven patients with CR consisted of five squamous cell carcinomas, five adenocarcinomas, and one chloroma. Among 15 patients with PR were five squamous cell carcinomas, five adenocarcinomas, three unknown primary tumors, and one poorly differentiated, and miscellaneous tumor each.

• Tuberculosis and Respiratory Diseases
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• v.48 no.3
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• pp.347-356
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• 2000

Background : Patients with obstructive sleep apnea syndrome are known to have high long-term mortality compared to healthy subjects because of their cardiovascular dysfunction. The observation of hemodynamic changes by obstructive apneas is helpful when attempting to understand the pathophysiological mechanism of the development of cardiovascular dysfunction in those patients. Therefore, we studied the changes in cardiovascular function with an animal model and tried to obtain the basic data for an ideal experimental model (this phrase is unclear), a requirement for a more advanced study. Methods : Sixteen anesthetized dogs with ${\alpha}$-chloralose delete were divided into two groups : 8 dogs of room air breathing group and 8 dogs of oxygen breathing group. We measured $PaO_2$, $PaCO_2$, heart rate, cardiac output, mean femoral artery pressure, and mean pulmonary artery pressure at specified times during the apnea-breathing cycle before endotracheal tube occlusion (baseline), 25 seconds after endotracheal tube occlusion (apneic period), 10 seconds (early phase of postapneic period, EPA) and 25 seconds (late phase of postapneic period, LPA) after spontaneous breathing. Results : In room air breathing group, the heart rate significantly decreased during the apneic period compared to that at baseline (P<0.01) and increased at EPA and LPA compared to that during the apneic period (P<0.01). But, the heart rate showed no significant changes during apneic and postapneic periods in the oxygen breathing group. Cardiac output tended to decrease during apneic period compared to that at baseline, but was statistically significant. Cardiac output significantly decreased at LP A compared to at baseline (P<0.01). Mean femoral artery pressure was significantly decreased at during apneic period compared to that at baseline (P<0.05). Conclusion : Through this experiment, we were partially able to understand the changes of cardiovascular function indirectly, but delete new experimental animal model displaying physiological mechanism close to natural sleep should be established, and the advanced study in the changes of cardiovascular function and their causes should be continued.

• Journal of Yeungnam Medical Science
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• v.18 no.2
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• pp.215-225
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• 2001

Background: There are many evidences that inflammation is an important determinant of the development of atherosclerosis and one of the systemic markers of inflammation, C-reactive protein(CRP), is associated with extent of coronary artery disease and risk of coronary events. We assessed the time response of CRP response after coronary angioplasty and it's influence on the clinical restenosis in angina patients. Materials and Methods: Patients included 36 angina patients undergoing single vessel angioplasty. Levels of CRP were measured before and 12, 24, 48, and 72 hours after angioplasty. Clinical restenosis was assessed at 6 months after procedure. Results: Baseline CRP level was $0.30{\pm}0.01$ mg/dL in stable and $0.46{\pm}0.28$ mg/dL in unstable angina patients(p<0.05). After angioplasty, CRP level was increased with peak at 24 hour and persisted to 72 hours after angioplasty. At 24 hour after angioplasty, the magnitude of CRP change was $0.32{\pm}0.31$ mg/dL in stable and $0.79{\pm}0.73$ mg/dL in unstable angina patient(p<0.05). The change of CRP level was not associated with troponin-T after angioplasty. In unstable angina patients, clinical restenosis was developed in 8% of patients with low baseline CRP levels and in 50% of those with high baseline CRP levels more than 0.6 mg/dL(p<0.05). Conclusion: In unstable angina patients, inflammatory response is more increased than stable angina patients, and increased inflammatory response effects on the restenosis after coronary angioplasty.

• Clinical and Experimental Pediatrics
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• v.52 no.7
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• pp.766-771
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• 2009

Purpose : The objective of this study was to compare the levels of adipocytokines in obesity group with those in control group and examine their correlation with insulin resistance. Methods : We enrolled 36 obese children (male:female [M:F]=17:19; age, $9.3{\pm}1.9yrs$) with ${\geq}95^{th}$ percentile body mass indexes (BMIs) (obesity group) and 35 healthy children (M:F=16:19; age, $9.1{\pm}2.1yrs$) with $25^{th}-75^{th}$ percentile BMIs (control group). We measured the serum leptin, adiponectin, and resistin levels and insulin resistance in both the groups. Results : The weights, heights, BMIs, fasting sugar levels, insulin levels, and homeostasis model assessment for insulin resistance (HOMA-IR) values were higher in the obesity group than in the control group. As compared to the control group, the obesity group showed significantly higher leptin levels and lower adiponectin levels; no significant difference was observed in the resistin levels. The leptin/adiponectin (L/A) ratio was higher in the obesity group than in the control group. In the obesity group, HOMA-IR showed significant positive correlations with weight, height, BMI, and leptin level. However, it was not correlated with age and adiponectin and resistin levels. In the obesity group, leptin level showed significant positive correlations with age, weight, height, and BMI, while adiponectin and resistin levels showed no such correlations with the other variables. Conclusion : We suggest that adiponectin plays an important protective role against weight gain in obese children. Further, L/A ratio can be used as a parameter for predicting the prognosis of obese children.

• Applied Microscopy
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• v.41 no.4
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• pp.235-248
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• 2011

Traumatic brain injury (TBI) is one of the leading causes of death and disability in children and adults and is a major risk factor for the development of posttraumatic epilepsy (PTE). Recent studies have provided significant insight into the pathophysiological mechanisms underlying the development of epilepsy. Although the link between brain trauma and epilepsy is well recognized, the complex biological mechanisms that result in PTE following TBI have not been fully elucidated. Therefore, this study investigated in order to identify whether or not the abnormal expression of calcium-binding proteins in the lesioned hippocampus plays a role in neuronal damage by brain trauma and whether or not the expressions may change in the contralateral hippocampus during the adaptive stage as early time point following TBI. During early time point following TBI, both parvalbumin (PV) and calbindin D-28k (CB) immunoreactivities were decreased with in the lesioned hippocampus. However, these expressions were recovered to control levels as depend on time courses. On the other hand, PV immunoreactivity in contralateral hippocampus was transiently reduced as compared to the control levels, whereas CB expression was unchanged. These findings indicate that the alterations of the calcium-binding proteins, especially PV and CB, may contribute to the neuronal death and/or damage induced by abnormal inhibitory neurotransmission at early time period following brain trauma and the development of epileptogenesis in patients with traumatic brain injury.