• Journal of Physiology & Pathology in Korean Medicine
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• v.21 no.4
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• pp.921-933
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• 2007

This experiment was designed to investigate the effects of the KBCMT hot water extract & ultra-fine powder on Alzheimer's Disease Model Induced by ${\beta}A$. The effects of the KBCMT hot water extract on expression of $IL-1{\beta}$, IL-6, $TNF-{\alpha}$, NOS-II, COX-2 mRNA and production of $IL-1{\beta}$, IL-6, $TNF-{\alpha}$, NO in BV2 microglial cell line treated by lipopolysacchaide(LPS). The effects of the KBCMT hot water extract & ultra-fine powder on (1) the behavior (2) expression of $IL-1{\beta}$, $TNF-{\alpha}$, MDA, CD68 and CD11b; (3) AChE in serum (4) the infarction area of the hippocampus, and brain tissue injury in Alzheimer's diseased mice induced with ${\beta}A$ were investigated. The KBCMT hot water extract suppressed the expression of $IL-1{\beta}$, IL-6 and $TNF-{\alpha}$ mRNA in BV2 microglia cell line treated with LPS. The KBCMT hot water extract suppressed the production of $IL-1{\beta}$, IL-6, $TNF-{\alpha}$, NO in BV2 microglial cell line treated with LPS. The KBCMT hot water extract & ultra-fine powder a significant inhibitory effect on the memory deficit was shown for the mice with Alzheimer's disease induced by ${\beta}A$ in the Morris water maze experiment, which measured stop-through latency and distance movemet-through latency The KBCMT ultra-fine powder suppressed the expression of TNF-a protein significantly in the microglial cell of mice with Alzheimer's disease induced by ${\beta}A$. The KBCMT hot water extract & ultra-fine powder reduced the MDA and suppressed the over-expression of CD68, CD11b in the mice with Alzheimer's disease induced by ${\beta}A$. The KBCMT hot water extract & ultra-fine powder decreased AChE significantly in the serum of the mice with Alzheimer's disease induced by ${\beta}A$. The KBCMT hot water extract & ultra-fine powder reduced infarction area of hippocampus, and controlled the injury of brain tissue in the mice with Alzheimer's disease induced by ${\beta}A$. The KBCMT hot water extract & ultra-fine powder reduced the tau protein, GFAP, and presenilin1, 2 of hippocampus in the mice with Alzheimer's disease induced by ${\beta}A$. These results suggest that the KBCMT hot water extract & ultra-fine powder may be effective for the prevention and treatment of Alzheimer's disease. Investigation into the clinical use of the KBCMT hot water extract & ultra-fine powder for Alzheimer's disease is suggested for future research.

• Journal of Physiology & Pathology in Korean Medicine
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• v.20 no.5
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• pp.1159-1165
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• 2006

This study was done to investigate the effects of Gamisojaganggi-tang(GSGT) on immunopathologic changes in OVA-induced asthma model of mice. Pathologic indicators associated with this immune disease, which include cytokines, the number of immune-cells, immunoglobin E (IgE), were examined, and histological changes of bronchial tissues were also examined. The administration of GSGT significantly reduced the lung weight compared with control mice of OVA-induced asthma model. The administration of GSGT significantly reduced the number of total cells in BALF compared with control mice of OVA-induced asthma model. The administration of GSGT significantly reduced the number of eosinophil in BALF compared with control mice of OVA-induced asthma model. The administration of GSGT insignificantly increased the number of monocyte in BALF compared with control mice of OVA-induced asthma model. The administration of GSGT significantly reduced the number of lymphocyte in BAL compared with control mice of OVA-induced asthma model. The administration of GSGT significantly reduced the gene expression of eotaxin in lung tissue compared with control mice of OVA-induced asthma model. The administration of GSGT insignificantly reduced the IL-4 and IL-5 production in BALF compared with control mice of OVA-induced asthma model. The administration of GSGT insignificantly reduced the levels of total IgE and ovalbumin-specific IgE in BALF. The administration of GSGT significantly reduced the levels of ovalbumin-specific IgE whereas the serum levels of total IgE were insignificantly reduced compared with control mice of OVA-induced asthma model. The administration of GSGT moderately reduced bronchial alveolar narrowing, bronchiovascular edema and increase in the size of alveolar space, which shown in control mice of OVA-induced asthma model, in a dose dependent manner. Furthermore, GSGT reduced invasion of inflammatory cells, and proliferation of smooth muscle cells in bronchial tissue. These results suggested that GSGT has suppressive effects on pathologic changes associated with disease progression in asthma through the modulation of immune system. GSGT has potential to use as an anti-asthmatic agents.

• Journal of Physiology & Pathology in Korean Medicine
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• v.21 no.3
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• pp.688-699
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• 2007

This experiment was designed to investigate the effect of the SST hot water extract & ultra-fine Powder on Alzheimer's Disease Model Induced by ${\beta}$A. The effects of the SST hot water extract on expression of IL-1${\beta}$, IL-6, TNF-${\alpha}$, NOS-II, COX-2 mRNA and production of IL-l${\beta}$, IL-6, TNF-${\alpha}$, NO in BV2 microglial cell line treated by lipopolysacchaide(LPS). The effects of the SST hot water extract & ultra-fine powder on (1) the behavior (2) expression of IL-1${\beta}$, TNF-${\alpha}$, MDA, (3) Glucose, AChE in serum (4) the infarction area of the hippocampus, and brain tissue injury in Alzheimer's diseased mice induced with ${\beta}$A were investigated. The SST hot water extract suppressed the expression of IL-1${\beta}$, IL-6 and TNF-a mRNA ${\alpha}$in BV2 microglia cell line treated with LPS. The SST hot water extract suppressed the production of IL-1${\beta}$, IL-6, TNF-${\alpha}$, NO in BV2 microglial cell line treated with LPS. The SST hot water extract & ultra-fine powder a significant inhibitory effect on the memory deficit was shown for the mice with Alzheimer's disease induced by ${\beta}$A in the Morris water maze experiment, which measured stop-through latency. The SST ultra-fine powder suppressed the expression of TNF-a protein significantly in the microglial cell of mice with Alzheimer's disease induced by ${\beta}$A. The SST hot water extract & ultra-fine powder reduced the MDA and suppressed the over-expression of CD68, CD11b in the mice with Alzheimer's disease induced by ${\beta}$A. The SST hot water extract & ultra-fine powder decreased AChE significantly in the serum of the mice with Alzheimer's disease induced by ${\beta}$A. The SST hot water extract & ultra-fine powder reduced infarction area of hippocampus, and controlled the injury of brain tissue in the mice with Alzheimer's disease induced by ${\beta}$A. The SST hot water extract & ultra-fine powder reduced the tau protein, GFAP, and presenilin1, 2 of hippocampus in the mice with Alzheimer's disease induced by ${\beta}$A. These results suggest that the SST hot water extract & ultra-fine powder may be effective for the prevention and treatment of A1zheimer's disease. Investigation into the clinical use of the SST hot water extract & ultra-fine powder for Alzheimer's disease is suggested for future research.

• Journal of Life Science
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• v.32 no.2
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• pp.142-147
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• 2022

Oxysterols are known to be involved in the physiopathology of atherosclerosis. Since 7-ketocholesterol (7-KC) is found in large amounts in oxysterols and in atherosclerotic plaque, the study on how 7-KC may affect monocyte differentiation induced by phorbol myristate acetate (PMA) in the monocytic cell line, THP-1, is essential. 7-KC induced a dose-dependent reduction in cell proliferation without inducing cytotoxicity, and the substantial staining of Nile red demonstrates the increased absorption of intracellular lipids. Although 7-KC itself did not increase cell adhesion, it markedly decreased the adhesion of cells treated with PMA. Furthermore, by observing the effect of 7-KC on phagocytosis using fluorescent-labeled latex beads, 7-KC's ability to abolish phagocytosis in PMA-stimulated macrophages was illustrated. The effect of 7-KC on the expression of selected protein markers on the process of differentiation induced by PMA in THP-1 cells was also examined. 7-KC inhibited expression of ICAM-1, CD11a, SR-A1, and SR-B2 (CD36) in PMA-stimulated THP-1 cells. Conversely, 7-KC drastically increased the expression of SR-D1 (CD68)in PMA-stimulated THP-1 cells. In conclusion, these results suggest that 7-KC modulates monocyte differentiation and activation via the intracellular accumulation of lipid droplets.

• Tuberculosis and Respiratory Diseases
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• v.44 no.4
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• pp.729-741
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• 1997

Background : We have recently reported that airway epithelial cells can produce RANTES and IL-8 in response to the stimulation of tubercle bacilli suggesting a certain role of airway epithelial cells in the pathogenesis of pulmonary tuberculosis. The pathogenesis of tuberculosis is determined by several factors including phagocytosis, immunological response of host, and virulence of tubercle bacilli. Interestingly, there have been reports suggesting that difference in immunological response of host according to the virulence of tubercle bacilli may be related with the pathogenesis of tuberculosis. We, therefore, studied the expressions and productions of RANTES and IL-8 in airway epithelial cells in response to tubercle bacilli(H37Rv, virulent strain and H37Ra, avirulent strain), in order to elucidate the possible pathophysiology of pulmonary tuberculosis. Methods : Peripheral blood monocytes were isolated from normal volunteers. Peripheral blood monocytes (PBM) were stimulated with LPS($10{\mu}g/ml$), H37Rv, or H37Ra($5{\times}10^5$ bacilli/well) along with normal control for 24 hours. A549 cells were stimulated with supernatants of cultured PBM for 24 hours. ELISA kit was used for the measurement of $TNF{\alpha}$ and IL-$1{\beta}$ production in supernatants of cultured PBM and for the measurement of RANTES and IL-8 in supernatants of cultured A549 cells. Northern blot analysis was used for the measurement of RANTES and IL-8 mRNA expression in cultured A549 cells. Results : $TNF{\alpha}$ and IL-$1{\beta}$ productions were increased in cultured PBM stimulated with LPS or tubercle bacilli(H37Rv or H37Ra) compared with the control. There was, however, no difference in $TNF{\alpha}$ and IL-$1{\beta}$ production between cultured PBM stimulated with H37Rv and H37Ra. RANTES and IL-8 expressions and productions were also increased in cultured A549 cells stimulated with LPS or tubercle bacilli compared with the control. RANTES and IL-8 mRNA expressions were significantly increased in cultured A549 cells stimulated with H37Ra-conditioned media(CM) compared with A549 cells stimulated with H37Rv-CM (p<0.05). However, there was no difference in RANTES and IL-8 productions between A549 cells stimulated with H37Rv-CM and H37Ra-CM. Conclusion : Airway epithelial cells can produce the potent chemokines such as RANTES and IL-8, in response to the stimulation of tubercle bacilli. These results suggest that airway epithelial cells may play a certain role in the pathogenesis of pulmonary tuberculosis. However, the role of airway epithelial cells in the pathogenesis of tuberculosis according to the virulence of tubercle bacilli was not clear in this study.

• Tuberculosis and Respiratory Diseases
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• v.43 no.4
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• pp.600-612
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• 1996

Background : Recent studies deported that untreated patients with obstructive sleep apnea syndrome had high long-term mortality rates, and cardiovascular complications of these patients clad a major effect on mortality. Several data indicates that obstructive sheep apnea syndrome contributes to the development of diurnal systemic hypertension. But the pathophysiological mechanism of the development of systemic hypertension in these patients is still uncertain. This study was performed to evaluate the possible role of sympathetic nervous system activity for the development of systemic hypertension in patients with obstructive sleep apnea syndrome. Method : 35 patients with obstructive sleep apnea syndrome(OSAS) and 13 Control subjects(control) were included in this study. 21 patients of OSAS were normotensives(OSAS-NBP), and 14 patients of OSAS were hypertensives(OSAS-HBP). Full night polysomnography was undertaken to all subjects. We measured plasma norepinephrine(NE) and epinephrine(EP) concentrations during waking and sleep, using high performance liquid chromatography, in all patients and control subjects. Results : In OSAS, OSAS-NBP and control, plasma NE and EP concentrations during sleep were lowed than during waking(p<0.01). But, in OSAS-HBP, these was no difference between during waking and sleep. Plasma NE concentrations during sleep of OSAS, OSAS-NBP and OSAS-HBP were higher than Control(p<0.05). In OSAS-HBP, daytime systolic blood pressure correlated with plasma NE concentration during sleep(r=0.7415, p<0.01), arid correlated inversely with mean arterial oxygen saturation(r=-0.6465, p<0.05) or arterial oxygen saturation nadir(r=-0.6) 14, p<0.05) during sleep. Conclusion : The sympathetic activity during sleep of obstructive sleep apnea syndrome patients was higher than control subjects. In obstructive sleep apnea syndrome patients with systemic hypertension, there was no diurnal variation of sympathetic activity, and there was correlation between daytime systolic blood pressure and sympathetic activity during sleep. These data suggests that chronic hyperactivity of sympathetic nervous system may contribute to the development of diurnal systemic hypertension in patients with obstructive sleep apnea syndrome.

• Tuberculosis and Respiratory Diseases
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• v.42 no.2
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• pp.206-217
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• 1995

Background: In patients with obstructive sleep apnea syndrome(OSAS), there are several factors increasing upper airway resistance and there is a predisposition to compromised respiratory function during waking and sleep related to constitutional factors including a tendency to obesity. Several recent studies have suggested a possible relationship between sleep apnea(SA) and systemic hypertension. But the possible pathophysiologic link between SA and hypertension is still unclear. In this study, we have examined the relationship among age, body mass index(BMI), pulmonary function parameters and polysomnographic data in patients with OSAS. And also we tried to know the difference among these parameters between hypertensive OSAS and normotensive OSAS patients. Methods: Patients underwent a full night of polysomnography and measured pulmonary function during waking. OSAS was diagnosed if patients had more than 5 apneas per hour(apnea index, AI). A careful history of previously known or present hypertension was obtained from each patient, and patients with systolic blood pressure $\geq$ 160mmHg and/or diastolic blood pressure $\geq$ 95mmHg were classified as hypertensives. Results: The noctural nadir of arterial oxygen saturation($SaO_2$ nadir) was negatively related to AI and respiratory disturbance index(RDI), and the degree of noctural oxygen desaturation(DOD) was positively related to AI and RDI. BMI contributed to AI, RDI, $SaO_2$ nadir and DOD values. And also BMI contributed to $FEV_1,\;FEV_1/FVC$ and DLco values. There was a correlation between airway resistance(Raw) and AI, and there was a inverse correlation between DLco and DOD. But there was no difference among these parameters between hypertensive OSAS and normotensive OSAS patients. Conclusion: The obesity contributed to the compromised respiratory function and the severity of OSAS. AI and RDI were important factors in the severity of hypoxia during sleep. The measurement of pulmonary function parameters including Raw and DLco may be helpful in the prediction and assessment of OSAS patients. But we could not find clear difference between hypertensive and normotensive OSAS patients.

• Clinical and Experimental Pediatrics
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• v.50 no.11
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• pp.1097-1103
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• 2007

Purpose : Acute symptomatic seizure is defined as a temporary seizure together with acute systemic, metabolic, or toxic insult in association with an acute central nervous system insult. And unprovoked seizure is defined as seizure without provocating factors. We studied the risk factors of unprovoked seizures after acute symptomatic seizure in children. Methods : We retrospectively reviewed the records of one hundred and ten children with acute symptomatic seizures who were admitted to the pediatric department of Chungbuk National University Hospital between January, 1998 and December, 2003. We analyzed overall risk factors of unprovoked seizures after acute symptomatic seizures involving etiology, incidence, type of seizure, duration and neuroimaging. Results : We analyzed records of 110 children with acute symptomatic seizures aged from 1 month to 17 years. 24 children had unprovoked seizures (21.8%) after acute symptomatic seizures. Causes in order of frequency were encephalopathy, central nervous system infection, brain tumor, cerebrovascular disease. The risk of unprovoked seizure was significantly greater for those with status epilepticus (68.4%) than without status epilepticus, with partial seizure (64.7%) than generalized seizure. And the risk of unprovoked seizure was strongly associated with abnormal finding of electroencephalogram (79.1%) and neuroimaging (41.6%). Conclusion : In conclusion, the leading cause of subsequent unprovoked seizure in children with acute symptomatic seizure was encephalopathy and age specific incidence was high in the group aged 24-72 months. The risk for subsequent unprovoked seizure was greater for those with partial seizure, status epilepticus, abnormal finding of neuroimaging and electroencephalography.

• 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.

• Tuberculosis and Respiratory Diseases
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• v.42 no.3
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• pp.342-350
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• 1995

Background: Although there are improvements of clinical symtoms after bronchodilator inhalation in COPD patients, it has been noted that there was no increase of $FEV_1$ in some cases. $FEV_1$ did not reflect precisely the improvement of ventilatory mechanics after bronchodilator inhalation in these COPD patients. The main pathophysiology of COPD is obstruction of airway in expiratory phase but in result, the load of respiratory system is increased in inspiratory phase. Therefore the improvement of clinical symptoms after bronchodilator inhalation may be due to the decrease of inspiratory load. So we performed the study which investigated the effect of bronchodilator on inspiratory response of vetilatory mechanics in COPD patients. Methods: In 17 stable COPD patients, inspiratory and expiratory forced flow-volume curves were measured respectively before bronchodilator inhalation. 10mg of salbutamol solution was inhaled via jet nebulizer for 4 minutes. Forced expiratory and inspiratory flow-volume curves were measured again 15 minutes after bronchodilator inhalation. Results: $FEV_1$, FVC and $FEV_1$/FVC% were $0.92{\pm}0.34L$($38.3{\pm}14.9%$ predicted), $2.5{\pm}0.81L$($71.1{\pm}21.0%$ predicted) and $43.1{\pm}14.5%$ respectively before bronchodilator inhalation. The values of increase of $FEV_1$, FVC and PIF(Peak Inspiratory Flow) were $0.15{\pm}0.13L$(relative increase: 17.0%), $0.58{\pm}0.38\;L$(29.0%) and $1.0{\pm}0.56L$/sec(37.5%) respectively after bronchodilator inhalation. The increase of PIF was twice more than $FEV_1$ in average(p<0.001). The increase of PIF in these patients whose $FEV_1$ was not increased after bronchodilator inhalation were 35.0%, 44.0% and 55.5% respectively. Conclusion: The inspiratory parameter reflected improvement of ventilatory mechanics by inhaled bronchodilater better than expiratory parameters in COPD patients.