Lim, Byung Sung;Sohn, Jang Won;Yang, Seok Chul;Yoon, Ho Joo;Shin, Dong Ho;Park, Sung Soo
Tuberculosis and Respiratory Diseases
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v.52
no.4
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pp.395-404
/
2002
Background : Surfactant protein A (SP-A) is important for regulating surfactant secretion, synthesis and recycling. However, It's regulation in vivo is unclear. SP-A has important roles in regulating surfactant metabolism as well as determining its physical properties. Glucocorticoid accelerates the morphologic differentiation of epithelial cells into type II cells and increase the rate of phosphatidylcholine synthesis. Methods : The authors investigated the effects of glucocorticoid on the accumulation of mRNA encoding SP-A and SP-A protein content. Adult rats were given various doses of subcutaneous dexamethasone and sacrificed after 24 hours and one week. SP-A mRNA was measured using a filter hybridization method. The lung SP-A protein content was determined using a double sandwich ELISA assay with polyclonal antiserum raised in rabbits against purified rat SP-A. Results : 1) The accumulation of SP-A mRNA in the dexamethasone treated group 24 hours after 0.2 mg/kg dexamethasone treatment was increased 38.8% compared to the control group. 2) The accumulation of SP-A mRNA in the dexamethasone treated group 1 week after 2 mg/kg dexamethasone treatment was 49.7% higher than the control group(P<0.01). 3) The total lung SP-A level was not altered after 24 hours by the 0.2mg/kg treatment. The total lung SP-A content one week after 2mg/kg dexamethasone administration was 373.7% higher than the control group(P<0.005). Conclusion : Dexamethasone treatment results in an increase in the SP-A mRNA and SP-A protein levels, suggesting that the pretranslational events in vivo may in part contribute to this process.
Bang, Jun Suck;Lim, Si Hong;Lee, Kyung Hwa;Bae, Eun Joo;Park, Won Il;Lee, Hong Jin
Clinical and Experimental Pediatrics
/
v.49
no.3
/
pp.258-267
/
2006
Purpose : We have done this retrospective study to know the relative incidence and clinical manifestations of organic acidopathies in Korea during 8 years(from Jul. 1997 to May 2005). This results of organic acid analysis of 1,787 patients were compared with the results of organic acid analysis that were published three years ago. Methods : The results of quantitative organic acid analysis of samples of 1788 patients, referred from Jul. 1997 to May 2005, were analyzed retrospectively according to four age group(-2 mon, 3 mon-2 years, 3-12 years) and major clinical manifestations. Quantification of 83 organic acids was done with gas chromatography and mass spectometry. Results : We diagnosed 470 patients with 27 diseases of organic acid metabolism during this study period. Diseases found more than 10 cases are cytosolic 3-ketothiolase deficiency, mitochondrial respiratory chain disorders, PDHC deficiency, mitochondrial 3-ketothiolase deficiency, glutaric aciduria type II, biotinidase deficiency, methylmalonic aciduria and propionic aciduria. Other diseases were diagnosed in less than 10 cases. Conclusion : Though the incidence of individual organic acidemia is low, the overall incidence of organic acidemia as a whole seems to be relatively high in Korea. Compared with the results of organic acid analysis that were reported three years ago, we couldn't find a new disease and the difference of the relative incidences of high incident diseases. We were apprehensive of the errors that was owing to the short study period(3 years), but the relative incidences of our study(8 years) were similar to the results of organic acid analysis that were reported three years ago.
Background: The alveolar macrophage may metabolize arachidonic acid through cyclooxygenase- and lipoxygenase- catalyzed pathways to produce a variety of metabolites of arachidonic acid. The production of these metabolites of arachidonic acid may enhance the defensive ability of the challenged lung. However, continued stimulation with the consequent production of proinflammtory metabolites of arachidonic acid, may ultimately enhance the disease process by contributing to chronic bronchoconstriction, fibrosis, and the persistent release of toxic oxygen species. Silicosis is an example of a disease process resulting from chronic exposure of the lung to foreign particles. This study was carried out to evaluate the changes of arachidonic acid metabolites from macrophages in experimental silicosis. Methods: We measured $PGE_2$, and $LTB_4$ in cultured macrophages taken from rats by radioimmunoassay at 24 and 48 hours after stimulation by silica dust, natural carbon dust, lipopolysaccharide, calcium ionophore (A23187) and medium (RPMI) as a control. For the experimental silicosis, 50 mg silica in 0.5 ml saline was administered intratracheally into the rat and grown to 20 weeks and measured $PGE_2$, and $LTB_4$ in the cultured macrophages lavaged from that rat. The used stimulants were the same as above. Results: 1) The amount of $PGE_2$ in the cultred macrophages from normal rat was significantly decreased in the group which was stimulated with silica dust for 48 hours compare with control non-stimulated group. 2) In the experimental silicosis group, $PGE_2$, release in cultured macrophages after 48 hours incubation with silica and natural carbon dust tended to be lower than those of non-stimulated group. 3) There were marked changes of $LTB_4$ in the groups of normal rats which were incubated with silica for 24, 48 hours and natural carbon for 48 hours compared with non-stimulated group. 4) In the experimental silicosis group, the release of $LTB_4$ was significantly increased macrophages cultured with silica and natural carbon dust after 24 and 48 hours incubation compared with non-stimulated group. Conclusion: The results of these studies suggest that the in vitro exposure of rat alveolar macrophge to silica and coal dust results in an alteration in alveolar macrophage metabolism of arachidonic acid that may promote an inflammatory reaction in lung tissue.
Park, I-Nae;Hong, Sang-Bum;Oh, Yeon-Mok;Lim, Chae-Man;Lee, Sang Do;Koh, Younsuck;Kim, Woo Sung;Kim, Dong Soon;Kim, Won Dong;Shim, Tae Sun
Tuberculosis and Respiratory Diseases
/
v.60
no.1
/
pp.44-48
/
2006
Background : Isoniazid (INH) is one of the most effective anti-tuberculosis (TB) drugs. In Korea, the dose of INH normally used in patients over 50 kg is 400 mg/day, which differs from the dose recommended by other countries. Indeed, the metabolism of INH shows ethnic variations, and Koreans are predominantly rapid acetylators. However, two reports suggested 300 mg of INH might be sufficient to reach an ideal peak level in Korean patients over 50 kg. Therefore, the aim of this study was to compare the effectiveness and adverse reactions between INH 300 mg and 400 mg in Korean TB patients. Method : Patients who were culture-positive, susceptible to all 1st-line drugs, initially on HREZ, and weighed over 50 kg were selected from patients with pulmonary TB between April 2003 and March 2005. The treatment results and adverse reactions in the INH 300 mg and 400 mg group were compared. Since April 2004, most TB patients at Asan Medical Center were administered INH 300 mg irrespective of the body weight. Results : The study included 123 patients in the 300 mg INH group and 128 in the 400 mg INH group. There were no significant differences between the groups in terms of age, gender, weight, history of TB treatment, initial smear strength, and frequency of cavitary lesions. There was no difference in the treatment duration between the groups. One hundred eleven (90%) patients in the INH 300 mg group and 102 (80%) in the INH 400 mg group completed treatment (p>0.05). There were no differences in the frequency of modification of the initial regimen between groups due to any adverse reactions (300 mg : 9.0%, 400 mg : 13.7%) and hepatotoxicity (300 mg : 2.7% ; 400 mg : 7.8%). Conclusion : Considering treatment results and adverse reactions of two groups, 300mg of INH may be sufficient for treating Korean TB patients. Further studies comparing the frequency of relapse will be needed.
Background : Lung cancer is frequently cited as an example of a disease caused solely by exposure to environmental carcinogens. However, there is a growing realization that the genetic constitution is also important in determining individual's susceptibility to lung cancer. This genetic susceptibility may result from functional polymorphims of the genes involved in carcinogen metabolism. In this study, the association between GSTM1 and CYP1A1 polymorphisms and the lung cancer risk in Korean males was investigated. Materials and Method : The study population consisted of 153 male lung cancer patients and 143 healthy male controls. The GSTM1 and CYP1A1 genotypes were determined by multiplex PCR and PCR-RFLP analysis. Result : There were no significant differences in the frequency of the GSTM1 null genotype between the cases and the controls. When the cases were categorized by their histologic type, the frequency of the GSTM1 null genotype in the small cell carcinoma group was higher than those of the controls(67.2% vs 55.9%), but the difference was not statistically significant(OR=1.772 ; 95% CI=0.723-4.340). The distribution of the CYP1A1 MspI genotypes among the cases were similar to those among the controls. When the cases were grouped by their histologic type, the ml/m1, ml/m2, m2/m2 genotypes frequencies among the small cell carcinomas(23.0%, 38.5%, and 38.5%, respectively) were significantly different from those of the controls(36.4%, 46.2%, and 7.4%, respectively, p<0.05). When the m1/m1 genotype was used as a reference, the ml/m2 and m2/m2 genotypes were associated with an increased risk for small cell lung cancer(ml/m2 genotype : OR=1.337, 95% CI=0.453-3.947 ; m2/m2 genotype : OR=3.374, 95% CI=1.092-10.421). Conclusion : These results suggest that the GSTM1 and CYP1A1 genotypes may be a genetic determinant of the risk for lung cancer, particlulary small cell carcinoma. Further investigation is needed to confirm these results.
Background : Vitamin C has been reported to have a role in the decrease of airway hyperresponsiveness in animal models. This data is based on some metabolic actions of vitamin C, such as promotion of histamine degradation, producing more $PGE_2$ than $PGF_{2\alpha}$ in cyclooxygenase pathway, decrease of smooth muscle contraction, and acting as reducing agent of oxidant. It has been also known that heavy smokers have lower blood levels of vitamin C than nonsmokers and this deficiency in heavy smokers have been explained by several mechanisms, such as increased oxidation by oxidants and free radicals, increased biosynthesis of catecholamine and serotonin released by nicotine, and inadequate dietary intake. In this study, We attempted to assess effect of vitamin C on bronchial hyperresponsiveness in heavy smokers who have bronchial hyperresponsiveness and role of vitamin C on bronchial hyperresponsiveness. Method: To assess acute effect of vitamin C on airway hyperresponsiveness, blood sample for vitamin C level and spirometry, methacholine challenge test were done in 17 smokers and 8 nonsmokers, and one hour after oral administration of vitamin C 3 g, blood sample for vitamin C level and spirometry, methacholine challenge test were repeated. To assess chronic effect of vitamin C on airway hyperresponsiveness, after daily administration of vitamin C 1 g for one week in 17 smokers, blood sample for vitamin C level and spirometry, methacholine challenge test were done. To assess role of vitamin C, after oral administration of vitamin C 3 g plus indomethacin 100 mg in 12 of 15 smokers who were reactive to methacholine challenge test, spirometry and methacholine challenge test were done and after oral intake of indomethacin 100 mg in 12 smokers who were reactive to methacholine challenge test, spirometry and methacholine challenge test were repeated. Result: There were no significant differences in whole blood vitamin C levels between smokers($1.17{\pm}0.22$ mg/dL) and nonsmcikers($1.14{\pm}0.19$ mg/dL) (p>0.05). Fifteen of the 17 smokers(88.2%) were reactive to methacholine challenge test and 10 of the 15 smokers who were reactive to methacholine challenge test were less than 8 mg/dL in $PC_{20}FEV-2$, and 7 of the 8 nonsmokers(87.5%) were nonreactive to methacholine challenge test There were significant decrease in bronchial responsiveness after oral administration of vitamin C 3 g in 13 of the 15 smokers who were reactive to methacholine challenge test This significant decrease persisted with maintenance daily administration of 1 g for one week. $PC_{20}FEV-2$ were not correlated to vitamin C levels in smokers. After oral administration of indomethacin 100 mg, significant reduction of bronchial responsiveness that occured after oral administration of vitamin C 3 g in smokers were attenuated. Conclusion: Although there were no significant differences in whole blood vitamin C levels between smokers and nonsmokers. heavy smokers have significant increase in bronchial responsiveness than nonsmokers. This bronchial hyperresponsiveness of heavy smokers can be attenuated by vitamin C supplement. Disappearance of vitamin C effect by indomethacin supplement may suggest that vitamin C exert its effect via alteration of arachidonic acid metabolism.
Kim, Seung Soo;Lee, In Kyu;Ko, Jung Ho;Oh, Myung Ho;Bae, Chong Woo
Clinical and Experimental Pediatrics
/
v.48
no.4
/
pp.376-379
/
2005
Purpose : Mycoplasama pneumoniae is a leading cause of pneumonia and exacerbates other respiratory conditions such as asthma. Surfactant protein A(SP-A) is involved in surfactant physiology and surfactant structure, and plays a major role in innate host defense and inflammatory processes in the lung. In this study, SP-A mediated mycoplasma cidal activity. The candidate-gene approach was used to study the association between the SP-A gene locus and Mycoplasama pneumoniae pneumonia in the genetically homogeneous Korean population. Methods : PCR-cRFLP-based methodology was used to detect SP-A genotype. The forty nine children with Mycoplasama pneumoniae pneumonia were matched to 50 nomal neonates. Results : The specific frequencies for the alleles of the SP-A1 and SP-A2 gene in the study population were : $6A^2=21$ percent, $6A^3=45$ percent, $6A^4=11$ percent, $6A^8=9$ percent, $6A^{14}=8$ percent, 1A=11.3 percent, $1A^0=38$ percent, $1A^1=12.7$ percent, $1A^2=9.2$ percent, $1A^5=15.5$ percent, $1A^7=2.9$ percent, $1A^8=4.9$ percent, $1A^9=2.2$ percent, others=3.3 percent. The frequencies of specific genotypes such as $1A^2$ was higher than control group, significantly. Conclusion : $1A^2$ are susceptible factors for Mycoplasama pneumoniae pneumonia. We conclude that the SP-A gene locus($1A^2$) is an important determinant for predisposition to Mycoplasama pneumoniae pneumonia in children.
Kim, Yumi;Oh, Jong-Min;Jung, Hea-Yeon;Lee, Seung Yeop;Roh, Yul
Economic and Environmental Geology
/
v.47
no.4
/
pp.431-439
/
2014
The purposes of this research were to investigate the enrichment of metal-reducing bacteria from KURT groundwater and the identification of the microbial diversity by 16S rRNA as well as to examine microbial Fe(III)/Mn(IV) reduction and to analyze morphological features of interactions between microbes and precipitates and their mineralogical composition. To cultivate metal-reducing bacteria from groundwater sampled at the KURT in S. Korea, different electron donors such as glucose, acetate, lactate, formate, pyruvate and Fe(III)-citrate as an electron accepter were added into growth media. The enriched culture was identified by 16S rRNA gene sequence analysis for the diversity of microbial species. The effect of electron donors (i.e., glucose, acetate, lactate, formate, pyruvate) and electron acceptors (i.e., akaganeite, manganese oxide) on microbial iron/manganese reduction and biomineralization were examined using the 1st enriched culture, respectively. SEM, EDX, and XRD analyses were used to determine morphological features, chemical composition of microbes and mineralogical characteristics of the iron and manganese minerals. Based on 16S rRNA gene analysis, the four species, Fusibacter, Desulfuromonas, Actinobacteria, Pseudomonas sp., from KURT groundwater were identified as anaerobic metal reducers and these microbes precipitated metals outside of cells in common. XRD and EDX analyses showed that Fe(III)-containing mineral, akaganeite (${\beta}$-FeOOH), reduced into Fe(II)/Fe(III)-containing magnetite ($Fe_3O_4$) and Mn(IV)-containing manganese oxide (${\lambda}-MnO_2$) into Mn(II)-containing rhodochrosite ($MnCO_3$) by the microbes. These results implicate that microbial metabolism and respiratory activities under anaerobic condition result in reduction and biomineralization of iron and manganese minerals. Therefore, the microbes cultivated from groundwater in KURT might play a major role to reduce various metals from highly toxic, mobile to less toxic, immobile.
Tissue homogenates of 12 kinds of human cancer tissues were incubated separately in medium containing $C^{14}-1-glucose$ and $C^{14}-6-glucose$ as a substrate in order to observe the oxidative pathway of glucose in the tumor tissues. At the end of 3 hours incubation in the Dubnuff metabolic shaking incubator, respiratory $CO_2$ samples trapped by alkaling which was placed in the center well of incubation flask were analysed for total $CO_2$ production rates and their radioactivities. The tissue homogenate samples after incubation were analyzed for their concentrations of glucose, lactate and pyruvate. Calculations were made on the glucose consumption rate and accumulation rates of lactate and pyruvate. Fractionation of oxidative pathway of glucose was carried out by calculating $C^{14}O_2 yields from C-1 and C-6 carbon of glucose. The following results were obtained. 1. In 12 kinds of human cancer, total $CO_2$ production rates were less than $8{\mu}M/gm$ except 2 cases. These lower values impressed that oxidative metabolism in the tumor tissues generally inhibited as compared with that in normal tissues. On the other hand, fractions of $CO_2$ derived from glucose to total $CO_2$ production rates (RSA) were less than 10% in every case. These facts showed that oxidation of glucose into $CO_2$ was remarkably inhibited in the tumor tissues. 2. Factions of glucose disappeared into $CO_2\;(RGD_{CO_2})$, lactate $(RGD_L)$, pyruvate $(RGD_P)$ to glucose consumption rates were as follows. $RGD_{CO_2}$ were less than 2% in cases of in this experiment and $RGD_L$ showed more than 5% except in 2 cases. These facts showed that anaerobic degradation of glucose into 3 carbon compounds was easily proceeded but further degradation into $CO_2$ via the TCA cycle was greatly inhibited resulting in accumulation of lactate. There are large variation in values of $RGD_P$ in different kinds of tumor tissue but relatively higher values in $RGD_{CO_2}$ were obtained in the tumor tissues as compared with those of normal tissues. 3. The oxidative pathway of glucose in tumor tissues were analyzed from the values of RSA which were obtained in $C^{14}-1\;and\;C^{14}-6-glucose$ incubation experiments. It was found that 3% of $CO_2$ derived from glucose were oxidized via the principal EMP-TCA cycle and the remainder were via alternate pathway such as HMP in the liver cancer and values in other cancer tissues were as follows; 4% in the tongue cancer, 6% in the colon cancer, 6% in the lung cancer, 9% in the stomach cancer, 11% in the ovarian cancer, 12% in the neck tumor, 22% in the uterine cancer, 22% in the bladder tumor, 32% in the spindle cell sarcoma and 65% in the brain tumor. These values except later 2 cases showed less than 30% which is the lowest value among the normal tissues. Even in the brain tumor in which showed highest value in the tumor group. It is reasonable to suppose that this fraction was remarkably decreased because values in normal brain tissue was more than 90%. From the above data, it was concluded that in tumor tissues, oxidation of glucose via TCA cycle was greatly inhibited but correlation between degree of inhibited oxidation of glucose via TCA cycle and malignancy of tumor were not clarified in this experiments.
Seo, Hyobin;Nam, Ju-Ock;Jeon, Byung-Duk;Kim, Pan-Gi;Ryu, Sungpil
Journal of Korean Society of Forest Science
/
v.101
no.4
/
pp.626-634
/
2012
The purpose of this study was to investigate the potential of persimmon vinegar as a functional beverage by analyzing the effects of persimmon vinegar ingestion on the energy substrate during endurance exercise. The healthy male adolescents (n=8) drunk persimmon vinegar ingested trial (PSV) or purified water ingested trial as the control trial (CON) 1 h prior to the exercise with the 60% of maximal oxygen uptake ($\dot{V}O_{2max}$) for 1 h. The exercise intensity was increased to the 80% of $\dot{V}O_{2max}$ and remained until exhaustion. And, the physiological variables, blood components, and amounts of energy oxidation were analyzed. There was no significant difference between trials in physiological variables, and the heart rates after exhaustion were higher in PSV compared to CON. There was no significant difference between trials in blood glucose level, while the blood lactic acids decreased significantly in PSV 30 and 60 minutes after onset of exercise. The free fatty acids concentration increased significantly in PSV from 15 minutes to 60 minutes after onset of exercise. The carbohydrate oxidation decreased significantly in PSV from 45 minutes after exercise and, on the contrary, the fatty acids oxidation increased significantly for the same period. And, fatty acids oxidation was higher in PSV compared to CON even after exhaustion. The respiratory exchange ratio was lower significantly in PSV compared to CON from 30 minutes to 60 minutes after exercise, whereas lower in CON after total exhaustion. The exercise time to exhaustion was 41% longer in PSV compared to CON. These results showed that the persimmon vinegar increase the level of lipids metabolism and decrease sense of fatigue by inhibiting carbohydrate oxidation during moderate intensity exercise, suggesting the possibility of using of persimmon vinegar as exercise functional beverage when ingested 1 h prior to the endurance exercise performance.
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