• Tuberculosis and Respiratory Diseases
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• v.46 no.1
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• pp.17-24
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• 1999

Background : A sizable percentage of tuberculous pleurisy patients are known to have residual pleural thickening(RPT) despite adequate anti-tuberculous chemotherapy. But, the predictive factors related to the development of RPT is not well known. Therefore, we studied to determine which factors are related to the development of RPT after completion of therapy. Methods: By retrospective review of medical records, fifty-eight patients initially diagnosed as having tuberculous pleurisy between March 1995 and January 1998 were separated into two groups : 27 patients in group 1 had RPT on simple chest radiography, while 31 patients in group 2 had no RPT after 6 month of anti-tuberculous chemotherapy. The clinical characteristics, radiologic findings and pleural fluid findings of the two group were compared at the time of diagnosis and during the course of therapy. Results: 47% of patients had RPT after 6 month of chemotherapy, and RPT was more common in man than in women(54% vs 29%, p=0.092). In group 2 patients, complete resorption of pleural lesion occurred rather late stage of therapy(1-2 month: 26%, 3-4 month: 29%, 5-6 month: 45%). Group 1 patients had increased percentage of loculated pleural lesion(26 % vs 19%) and increased white blood cell and lymphocyte count, lactate dehydrogenase level in pleural fluid ($3527\pm5652$ vs $2467\pm2201$/ml, $2066\pm2022$ vs $1698\pm1835$/ml and $1636\pm1143$ vs $1441\pm923$IU/mL respectively) than group 2 at the time of diagnosis, but statistically insignificant. Duration of symptom prior to treatment, size of pleural effusion, presence of parenchymal lung lesion, level of total protein, glucose and adenosine deaminase(ADA)activity in pleural fluid were similar in both group. Conclusion: 53% of tuberculous pleurisy patients showed slow but complete resorption of pleural lesion after 6 month of chemotherapy. But, no clinical, radiological and pleural fluid findings are predictive for the development of RPT.

• Journal of Aquaculture
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• v.6 no.2
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• pp.107-123
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• 1993

To define the effects of various levels $(0\~1.5\%)$ of dietary n-3HUFA on the physiological changes in the Korean rockfish, variations in blood variables and hepatocytes were studied. Biochemical serum analyses, lactate dehydrogenase (LDH) activity of the liver cytosol and ATPase activity of the liver microsomal membrane were also studied. The haematological values (red blood cell, hemoglobin, hematocrit, MCHC, MCV and MCH) were not significantly different in the experimental groups $(P\geq0.05)$. The total protein and glucose levels in the serum were affected by dietary n-3HUFA levels. These levels in groups fed n-3HUFA insufficient diets were significantly lower than those of n-3HUFA sufficient groups (P<0.05). Serum levels of total cholesterol, free cholesterol, glutamic pyruvic transaminase (GPT) and glutamic oxaloacetatic transaminase (GOT) showed significantly higher values in the fish fed n-3HUFA deficient diets (P<0.05). The LDH in the serum was dropped with increasing dietary n-3HUFA levels, but the LDH activity of the liver cytosol was elevated. Histologically, the hepatic cell in the fish fed n-3HUFA free diet was abnormal and showed a necrotic condition. $Ca^{2+}-ATPase$ activities of the liver microsomal membrane were significantly lower in the fish fed n-3HUFA deficient diets than in those fed n-3HUFA sufficient diets (p<0.005). These results suggested that the liver cell membrane was affected by dietary fatty acid compositions and cell membrane of the fish fed n-3HUFA insufficient diets showed abnormalities.

• Journal of Life Science
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• v.19 no.8
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• pp.1152-1158
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• 2009

For the toxicological pathologic study of amanita muscaria, we have investigated single and repeated dose toxicity in Sprague-Dawley (SD) rats. Single dose toxicity study was identified as catalepsy, incline and tail pinch methods (control 0 mg/kg, low 3.3 mg/kg, middle 16.5 mg/kg, high 33.0 mg/kg). Repeated dose toxicity study was carried out in blood tests, serum tests and histopathological methods. Neurotoxicity - muscle paralysis, and convulsion and loss of movement - was observed at 33.0 mg/kg group in the single dose toxicity study. Dysfunction of liver and kidney were shown in the repeated oral administration of the amanita muscaria at 3${\sim}$4 weeks. Serum chemistry results revealed a marked increase of LDH [Lactate Dehydrogenase (3181.5 IU/L; normal 230-460 IU/l)], ALT [Alanine transaminase (124.0 IU/l; normal <40 IU/l)] but the kidney was normal. Histopathological results show interstitial edema and tubular epithelial necrosis in the kidney. These results suggest that amanita muscaria has a neurotoxic effect and causes dysfunction of liver and kidney in the SD rat.

• Journal of the Korean Society of Food Science and Nutrition
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• v.32 no.2
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• pp.278-286
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• 2003

Alcohol is well known agent which can damage the human tissues such as liver via stimulating lipid peroxidation. On the other hand, carotenoids in addition to vitamins A, C and I play important roles in protecting these oxidative damages as well as preventing the production of free radicals. This study was carried out to investigate the effect of dietary vitamin A on lipid peroxidation and antioxidants status in ethanol-treated rats. In the experiment, male Sprague-Dawley rats weighing 160~180 g were given a liquid diet containing 36% of total calories as ethanol for 7 weeks. The pair-fed control rats received an isocaloric amount of diet containing sucrose instead of ethanol on the following day Additionally, the liquid diet contained adequate amount of $\beta$-carotene, retinyl acetate or 13-sis-reinoic acid except vitamin A-deficient diet. The results obtained are as follows. The levels of plasma and hepatic lipid peroxide were increased after chronic ethanol feeding in rats. Retinyl acetate supplementation significantly reduced lipid peroxidation induced by ethanol feeding Glucose 6-phosphatase activity was significantly reduced in rats fed vitamin A-deficient diet with ethanol and alkaline phosphatase activity was significantly induced in rats fed 13-cis-reinoic acid diet with ethanol. Catalase and alcohol dehydrogenase activities did not show a consistent tendency in experiment groups. The hepatic antioxidant enzyme activities did not significantly changed by chronic ethanol feeding groups. The striking decrease in conversion of $\beta$-carotene to retinol was observed in rats fed a $\beta$-carotene diet with ethanol feeding The level of retinol and retinoic acid in plasma and liver was decreased after chronic ethanol administration Based on this result, these data suggest that ethanol feeding enhances oxidative stress especially in those fed a vitamin A-deficient diet, and vitamin A supplementation, especially, retinyl acetate intake can prevent enhanced lipid peroxidation and related damage to some extent.

• Journal of the Korean Society of Food Science and Nutrition
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• v.32 no.2
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• pp.238-243
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• 2003

The effects of Paecilomyes japonica on weight gains, food intakes, food efficiency ratios, serum and hepatic lipid concentrations, serum protein levels and serum enzyme activities, were studied in adult male rats. Sprague-Dawley rats,35 weeks old, were given four different types of diets for a succeeding period of five weeks: either a normal diet (5% corn oil), a control diet (high fat; 5% corn oil + 15% lard), a PF diet (control diet + 3% fruiting body of Paecilomyes japonica), or a PM diet (control diet+.3% mycelium of Paecilomyes japonica). The body weight gains, hepatic weights and food efficiency ratios of rats fed the PF or PM diets were significantly lower than those fed the control diet, but were similar to those fed the normal diet. The concentrations of hepatic total lipids, cholesterol and triglyceric, and serum triglyceride, of rats given the PF or PM diets were significantly lower than those given the control diet. Hut the concentrations of total cholesterol, HDL-cholesterol, LDL-cholesterol and phospholipid in the serum of rats fed the control, PF or PM diets were significantly higher than those fed the normal diet. In the serum of rats fed the PF diet, the HDL-cholesterol/total cholesterol ratio was significantly higher and the atherogenic index was significantly lower than those fed the control diet, while such effect was not observed in rats fed the PM diet. The alkaline phosphatase activity in the serum of rats fed the control and PM diets was more significantly decreased compared to rats fed the PF and normal diet. No differences were noted in the weights of the pancreas, kidney and heart, the serum concentrations of glucose, hemoglobin and albumin, and the activities of GOT, GPT and ${\gamma}$-GTP, among the rats on all the experimental diets. In conclusion, the rats fed the PF or PM diets maintained normal body and hepatic weights. Despite of the high intake of fats in the PF and PM diets, the concentrations of hepatic total lipids, cholesterol and triglyceride, and serum triglyceride were decreased.

• Journal of Ginseng Research
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• v.1 no.1
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• pp.59-78
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• 1976

In order to investigate the influences of Panax ginseng (white ginseng and red ginseng) on the anesthetic effect and toxic effect of alcohol, experimental studies .had been carried out with albino rabbits, mongolian dogs and mice. The anesthetic effect of alcohol was observed by measuring the induction time, .anesthetic time, recovery time and duration from the beginning of induction to , the recovery of anesthesia (total time), respectively. and toxic effect ($LD_{50}$) of alcohol was measured. In addition to these experiments, al cohol concentration in .blood, blood sugar level, serum transaminase (GOT and GPT) activities and serum alkaline phosphatase activity were measured. Also in order to study the clinical effect of alcohol in healthy students, code .substitution, response time and muscle coordination were tested. The results were obtained as follows. 1. In the rabbits and mongolian Jags, the induction time of anesthesia by the administration of alcohol was delayed by the pretreatment of ginseng but recovery time and total time of anestksia were markedly shortend. 2. The bleed alcohol concentration was decreased by the pretreatment of ginseng , but not affected in mongolian dogs. 3. The blood sugar level, serum transaminase (GOT and GPT) activities and alkaline phoshatase activity in rabbits and dogs induced by the administration of alcohol were affected by the Pretreatment of ginseng. Because those were included within normal ranges, the differnces have no remarkable significance. 4. Liver alcohol dehydrogenase activity of rabbit was increased by the treatment of ginseng, especially it was markedly increased by the treatment of red ginseng 5. The average lethal dose of alcohol to mice was increased by the pretreatment. of ginseng, especially it was markedly increased by the pretreatment of red .ginseng. 6. In the clinical experiments, the blood alcohol concentration induced by alcohol administration was not affected by the pretreatment of ginseng whereas the bleed sugar level was increased. Blood alcohol concentration and bleed sugar level were measured after three hours alcohol administration. 7. The response time of healthy students administered with alcohol was markedly shortened by the pretreatment of ginseng but the experiments on the code substitution and muscle coordination were not affected.

• Journal of the Korean Society of Food Science and Nutrition
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• v.46 no.4
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• pp.417-425
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• 2017

Cnidium monnieri (L.) Cusson is distributed in China and Korea, and the fruit of C. monnieri is used as traditional Chinese medicine to treat carbuncle and pain in female genitalia. In this study, we examined the anti-proliferation and cell cycle arrest effects of ethanol extracts from C. monnieri (CME) in AGS gastric cancer cells. Our results show that CME suppressed cell proliferation and induced release of lactate dehydrogenase (LDH) in AGS cells by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide assay and LDH assay. Cell morphology was altered by CME in a dose-dependent manner. In order to identify the cell cycle arrest effects of CME, we investigated cell cycle analysis after CME treatment. In our results, CME induced cell cycle arrest at G1 phase. Protein kinase B (Akt) plays a major role in cell survival mechanisms such as growth, division, and metastasis. Akt protein regulates various downstream proteins such as glycogen synthase kinase-$3{\beta}$ (GSK-$3{\beta}$) and tumor protein p53 (p53). Expression levels of p-Akt, p-GSK-$3{\beta}$, p53, p21, cyclin E, and cyclin-dependent kinase 2 (CDK2) were determined by Western blot analysis. Protein levels of p-Akt, p-GSK-$3{\beta}$, and cyclin E were reduced while those of p53, p21, and p-CDK2 (T14/Y15) were elevated by CME. Moreover, treatment with CME, LY294002 (phosphoinositide 3-kinase/Akt inhibitor), BIO (GSK-$3{\beta}$ inhibitor), and Pifithrin-${\alpha}$ (p53 inhibitor) showed that cell cycle arrest effects were mediated through regulation of the Akt/GSK-$3{\beta}$/p53 signaling pathway. These results suggest that CME induces cell cycle arrest at G1 phase via the Akt/GSK-$3{\beta}$/p53 signaling pathway in AGS gastric cancer cells.

• Tuberculosis and Respiratory Diseases
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• v.41 no.3
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• pp.222-230
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• 1994

Background: Paraquat, a widely used herbicide, is extremely toxic, causing multiple organ failure in humans. Paraquat especially leads to irreversible progressive pulmonary fibrosis, which is related to oxygen free radicals. However, its biochemical mechanism is not clear. Natural mechanisms that prevent damage from oxygen free radicals include changes in glutathione level, G6PDH, superoxide dismutase(SOD), catalase, and glutathione peroxidase. The authors think catalase is closely related to paraquat toxicity in the lungs Method: The effects of 3-amino-1,2,4-triazole(aminotriazole), a catalase inhibitor, on mice administered with paraquat were investigated. We studied the effects of aminotriazole on the survival of mice administered with paraquat, by comparing life spans between the group to which paraquat had been administered and the group to which a combination of paraquat and aminotriazole had been administered. We measured glutathion level, glucose 6-phosphate dehydrogenase(G6PDH), superoxide dismutase(SOD), catalase, and glutathione peroxidase(GPx) in the lung tissue of 4 groups of mice: the control group, group A(aminotriazole injected), group B(paraquat administered), group C(paraquat and aminotriazole administered). Results: The mortality of mice administered with paraquat which were treated with aminotriazole was significantly increased compared with those of mice not treated with aminotriazole. Glutathione level in group B was decreased by 20%, a significant decrease compared with the control group. However, this level was not changed by the administration of aminotriazole(group C). The activity of G6PDH in all groups was not significantly changed compared with the control group. The activities of SOD, catalase, and glutathione peroxidase(GPx) in the lung tissue were significantly decreased by paraquat administration(group B); catalase showed the largest decrease. Catalase and GPX were significantly decreased by aminotriazole treatment in mice administered with paraquat but change in SOD activity was not significant(group C). Conclusion: Decrease in catalase activity by paraquat suggests that paraquat toxicity in the lungs is closely related to catalase activity. Paraquat toxicity in mice is enhanced by aminotriazole administration, and its result is related to the decrease of catalase activity rather than glutathione level in the lungs. Production of hydroxyl radicals, the most reactive oxygen metabolite, is accelerated due to increased hydrogen peroxide by catalase inhibition and the lung damage probably results from nonspecific tissue injury of hydroxyl radicals.

• Tuberculosis and Respiratory Diseases
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• v.45 no.6
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• pp.1214-1222
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• 1998

Background : The intrapleural hypofibrinolysis is caused by mainly excessive concentration of pleural plasminogen activator inhibitor-1 antigen(PAI-1 Ag), which binds tissue type plasminogen activator. In pleural inflammation induced by sclerosing agents for pleurodesis, levels of pleural PAI-1 antigen increase in relation to decreasing D-dimer levels. It has been known that the pleural mesothelial cells have the capability of secreting PAI-1 Ag in response to inflammation in vivo. Therefore, we estimated whether pleural inflammation changes the balance between fibrinolytic and coagulative properties in exudative pleural effusions. Method : The thirty cases was included in our study. We determined the pleural levels of glucose, lactic dehydrogenase(LDH), pH and the counts of white blood cell(WBC), polymorpho leukocyte(PMN), lymphocyte as the parameters of pleural inflammation and cellular components of pleural fluid. The plasma level of fibrinogen in fluid and the neutrophil count in blood were determined. The levels of D-dimer, PAI-1 Ag and thrombinantithrombin III complex(TAT) were determined by ELISA(Behring, Marburg, Germany). Result : The causes of pleural effusion were as following : tuberculous in 14 cases, malignant in 10 cases and parapneumonic in 6 cases. The levels of pleural D-dimer, PAI-1 Ag and TAT was significantly higher than that of plasma(p<0..001). The severity of pleural inflammation did not correlated with pleural D-dimer, PAI-1 Ag, TAT and their plasma levels. But the level of pleural TAT correlated with pleural WBC and lymphocyte count. Conclusion : We found that the severity of pleural inflammations did not correlated with pleural D-dimer, PAI-1 Ag, TAT and the possibility of local production of PAI-1 antigen is present.

• Tuberculosis and Respiratory Diseases
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• v.50 no.5
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• pp.540-548
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• 2001

Backgrounds : Because ventilator-induced lung injury is partly dependent on the intensity of vascular flow, we hypothesized that hypothermia may attenuate the degree of such an injury through a reduced cardiac output. Methods : Twenty-seven male Sprague-Dawley rats were randomly assigned to normothermia ($37{\pm}1^{\circ}C$)-injurious ventilation (NT-V) group (n=10), hypothermia ($27{\pm}1^{\circ}C$)-injurious ventilation (HT-V) group (n=10), or nonventilated control group (n=7). The two thermal groups were subjected to injurious mechanical ventilation for 20 min with peak airway pressure 30 cm $H_2O$ at zero positive end-expiratory pressure, which was translated to tidal volume $54{\pm}6\;ml$ in the NT-V group and $53{\pm}4\;ml$ in the HT-V group (p>0.05). Results : Pressure-volume (P-V) curve after the injurious ventilation was almost identical to the baseline P-V curve in the HT-V group, whereas it was shifted rightward in the NT-V group. On gross inspection, the lungs of the HT-V group appeared smaller in size, and showed less hemorrhage especially at the dependent regions, than the lungs of the NT-V group. [Wet lung weight (g)/body weight (kg)] ($1.6{\pm}0.1$ vs $2.4{\pm}1.2$ ; p=0.014) and [wet lung weight/dry lung weight] ($5.0{\pm}0.1$ vs $6.1{\pm}0.8$ ; p=0.046) of the HT-V group were both lower than those of the NT-V group, while not different from those of the control group($1.4{\pm}0.4$, $4.8{\pm}0.4$, respectively). Protein concentration of the BAL fluid of the HT-V group was lower than that of the NT-V group($1,374{\pm}726\;ug/ml$ vs $3,471{\pm}1,985\;ug/ml$;p=0.003). Lactic dehydrogenase level of the BAL fluid of the HT-V group was lower than that of the NT-V group ($0.18{\pm}0.10\;unit/ml$ vs $0.43{\pm}0.22\;unit/ml$;p=0.046). Conclusions : Hypothermia attenuated pulmonary hemorrhage, permeability pulmonary edema, and alveolar cellular injuries associated with injurious mechanical ventilation, and preserved normal P-V characteristics of the lung in rats.