• Journal of environmental and Sanitary engineering
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• v.7 no.2
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• pp.95-110
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• 1992

Much progress has been made in understanding the subcellular events of the human lung injuries after acute exposure to environmental air pollutants. Host of those events represent oxidative damages mediated by reactive oxygen species such as superoxide, hydrogen peroxide, and the hydroxy, free radical. Recently, nitric oxide (NO) was found to be endogenously produced by endothelial cells and cells of the reticulo-endothelial system as endothelialderived relaxation factor (EDRF) which is a vasoactive and neurotransmitter substance. Together with superoxide, NO can form another strong oxidant, peroxonitrite. The relative importance of exogenous sources of $N0/N0_2$ and endogenous production of NO by the EDRF producing enzymes in the oxidative stresses to the heman lung has to be elucidated. The exact events leading to chronic irreversible damage are still yet to be known. From chronic exposure to oxidant gases, progressive epithelial and interstitial damages develop. Type I epithelial cells become thicker and cover a smaller average alveolar surface area while thee II cells proliferate instead. Under acute damages, the extent of loss of the alveolar epithelial cell lining, especially type II cells appears to be a good predictor of the ensuing irreversible damage to alveolar compartment. Interstitial matrix undergo remodeling during chronic exposure with increased collagen fibers and interstitial fibroblasts. However, Inany of these changes can be reversed after cessation of exposure. Among chronic lung injuries, genetic damages and repair responses received particular attention in view of the known increased lung cancer risks from exposure to several air pollutants. Heavy metals from foundry emission, automobile traffics, and total suspended particulate, especially polycystic aromatic hydrocarbons have been positively linked with the development of lung cancer. Asbestos in another air pollutant with known risk of lung cancer and mesothelioma, but asbestos fibers are nonauthentic in most bioassays. Studies using the electron spin resonance spin trapping method show that the presence of iron in asbestos accelerates the production of the hydroxy, radical in vitro. Interactions of these reactive oxygen species with particular cellular components and disruption of cell defense mechanisms still await further studies to elucidate the carcinogenic potential of asbestos fibers of different size and chemical composition. The distribution of inhaled pollutants and the magnitude of their eventual effects on the respiratory tract are determined by pollutant-independent physical factors such as anatomy of the respiratory tract and level and pattern of breathing, as well as by pollutant-specific phyco-chemical factors such as the reactivity, solubility, and diffusivity of the foreign gas in mucus, blood and tissue. Many of these individual factors determining dose can be quantified in vitro. However, mathematical models based on these factors should be validated for its integrity by using data from intact human lungs.

• KSBB Journal
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• v.11 no.6
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• pp.663-668
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• 1996

In the production of recombinant protein using E. coli, phage lysogen system can be usefully applied for simultaneously achieving protein production at high cell concentration and recovery by cell disruption in the same bioreactor. A major drawback of this system is that the intracellular product and complex broth components are mixed together in culture broth and hence purification efficiency is reduced. With the E. coli double-lysogen system, the expanded bed adsorption is very useful because the pretreatment processes in a routine bioseparation process can be done in a single column operation, and therefore may contribute towards lowering the operating cost of overall recovery/purification process. In the operation of EBA, it has been observed that the change in broth feed volume does not influence much the protein recovery in a tested range. The amount of protein adsorption per mL of resin was increased from $3.44{\times}106unit to 5.28{\times}106unit$ by doubling the column length. By two-fold increase of the column diameter, the ratio of protein concentration in eluent to that in feed was increased from 0.8 to 2.1. It is concluded from the present investigation that the increase of column length and diameter is necessary to enhance the protein adsorption amount per volume of resin and protein concentration in the eluent. The development of resins with various physical properties will be necessary for more extensive application of EBA.

• Journal of Life Science
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• v.29 no.3
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• pp.376-381
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• 2019

To construct useful yeast strain for bioethanol production, we improved yeast harboring various phenotypes by using yeast protoplast fusion method. In this study, S. cerevisiae BYK-F11 strain which have ethanol tolerance, thermotolerance and ${\beta}-glucanase$ activity and P. $stipitis{\Delta}ura$ strain which has xylose metabolism pathway were fused by genome shuffling. P. $stipitis{\Delta}ura$ strain was constructed for protoplast fusion by URA3 gene disruption, resulting in uracil auxotroph. By protoplast fusion, several fused cells were selected and BYKPS-F8 strain (fused cell) showing both karyotypes from two parent strains (S. cerevisiae BYK-F11 and P. $stipitis{\Delta}ura$ strain) among 22 fused cells was finally selected. Sequentially, various phenotypes such as ${\beta}-glucanase$ activity, xylose utility, ethanol tolerance, thermotolerance and ethanol productivity were analyzed. The BYKPS-F8 strain obtained ${\beta}-glucanase$ activity from BYK-F11 strain and 1.2 fold increased xylose utility from P. $stipitis{\Delta}ura$ strain. Also, the BYKPS-F8 strain showed thermotolerance at $40^{\circ}C$ and increased ethanol tolerance in medium containing 8% ethanol. In this fused cell, 7.5 g/l ethanol from 20 g/l xylose was produced and the multiple phenotypes were stably remained during long term cultivation (260 hr). It was proved that novel biological system (yeast strains) is easily and efficiently bred by protoplast fusion among yeasts having different genus.

• Journal of Life Science
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• v.28 no.11
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• pp.1268-1276
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• 2018

The cytidine analog decitabine (DEC) acts as a nucleic acid synthesis inhibitor, whereas ammonium pyrrolidine dithiocarbamate (PDTC) is an inhibitor of nuclear factor-${\kappa}B$. The aim of this study was to investigate the possible synergistic inhibitory effect of these two inhibitors on proliferation of human gastric cancer AGS cells. The inhibitory effect of PDTC on AGS cell proliferation was significantly increased by DEC in a concentration-dependent manner, and this inhibition was associated with cell cycle arrest at the G2/M phase and the induction of apoptosis. This induction of apoptosis by the co-treatment with PDTC and DEC was related to the induction of DNA damage, as assessed by H2AX phosphorylation. Further studies demonstrated that co-treatment with PDTC and DEC induced the disruption of mitochondrial membrane potential, increased the generation of intracellular reactive oxygen species (ROS) and the expression of pro-apoptotic Bax, and down-regulated the expression of anti-apoptotic Bcl-2, ultimately resulting in the release of cytochrome c from the mitochondria into the cytoplasm. Co-treatment with PDTC and DEC also activated caspase-8 and caspase-9, which are representative caspases of the extrinsic and intrinsic apoptosis pathways. Co-treatment also activated caspase-3, which was accompanied by proteolytic degradation of poly (ADP-ribose) polymerase. Taken together, these data clearly indicated that co-treatment with PDTC and DEC suppressed the proliferation of AGS cells by increasing DNA damage and activating the ROS-mediated extrinsic and intrinsic apoptosis pathways.

• Journal of Korean Neurosurgical Society
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• v.62 no.1
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• pp.106-113
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• 2019

Objective : The efficacy of preoperative embolization for hypervascular metastatic spine disease (MSD) such as renal cell and thyroid cancers has been reported. However, the debate on the efficacy of preoperative embolization for non-hypervascular MSD still remains unsettled. The purpose of this study is to determine whether preoperative embolization for non-hypervascular MSD decreases perioperative blood loss. Methods : A total of 79 patients (36 cases of preoperative embolization and 43 cases of non-embolization) who underwent surgery for metastatic spine lesions were included. Representative hypervascular tumors such as renal cell and thyroid cancers were excluded. Intraoperative and perioperative estimated blood losses (EBL), total number of transfusion and calibrated EBL were recorded in the embolization and non-embolization groups. The differences in EBL were also compared along with the type of surgery. In addition, the incidence of Adamkiewicz artery and complications of embolization were assessed. Results : The average age of 50 males and 29 females was $57.6{\pm}13.5$ years. Lung (30), hepatocellular (14), gastrointestinal (nine) and others (26) were the primary cancers. The demographic data was not significantly different between the embolization and the non-embolization groups. There were no significant differences in intraoperative EBL, perioperative EBL, total transfusion and calibrated EBL between two groups. However, intraoperative EBL and total transfusion in patients with preoperative embolization were significantly lower than in non-embolization in the corpectomy group (1645.5 vs. 892.6 mL, p=0.017 for intraoperative EBL and 6.1 vs. 3.9, p=0.018 for number of transfusion). In addition, the presence of Adamkiewicz artery at the index level was noted in two patients. Disruption of this major feeder artery resulted in significant changes in intraoperative neuromonitoring. Conclusion : Preoperative embolization for non-hypervascular MSD did not reduce perioperative blood loss. However, the embolization significantly reduced intraoperative bleeding and total transfusion in corpectomy group. Moreover, the procedure provided insights into the anatomy of tumor and spinal cord vasculature.

• Journal of Life Science
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• v.32 no.6
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• pp.482-490
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• 2022

Sarcopenia, a geriatric and multifactorial syndrome characterized by progressive systemic skeletal muscle disorder, may be associated with many comorbidities. Sarcopenia caused by a decrease in muscle mass and muscle strength is accompanied by the aggravation of various pathological conditions, and as life expectancy increases, its prevalence will continue to increase in the future. During the aging process, chronic oxidative stress and increased inflammatory responses act as major contributors to skeletal muscle loss. In addition, disruption of autophagy and apoptosis signals associated with dysfunction of mitochondria, which are essential for energy metabolism, accelerates the loss of muscle proteins. The pharmacological effect of cordycepin, a major physiologically active substance in the genus Cordyceps, which has been widely used for the prevention and treatment of various diseases for a long time, is directly related to its antioxidant and anti-inflammatory actions. In this review, we present the correlation between apoptosis, autophagy, protein catabolism, and satellite cell activity important for muscle regeneration using cordycepin for the prevention and treatment of sarcopenia. Although there have been few studies so far on the use of cordycepin for sarcopenia, previous studies suggest that cordycepin may contribute to inhibiting the age-related weakening of mitochondrial function and blocking the breakdown of muscle proteins. In addition, the protective effect of cordycepin on muscle cell damage is considered to be closely related to its antioxidant and anti-inflammatory activities. Therefore, it is considered that more continuous basic research is needed, focusing on the molecular biological mechanism of cordycepin, which is involved in the anti-aging of muscle cells.

• Journal of Plant Biotechnology
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• v.38 no.4
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• pp.285-292
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• 2011

In plants, heteroblasty reflects the morphological adaptation during leaf development according to the external environmental condition and affects the final shape and size of organ. Among parameters displaying heteroblasty, leaf index is an important and typical one to represent the shape and size of simple leaves. Leaf index factor is eventually determined by cell proliferation and cell expansion in leaf blades. Although several regulators and their mechanisms controlling the cell division and cell expansion in leaf development have been studied, it does not fully provide a blueprint of organ formation and morphogenesis during environmental changes. To investigate genes and their mechanisms controlling leaf index during leaf development, we carried out molecular-genetic and physiological experiments using an Arabidopsis mutant. In this study, we identified macrophylla (mac) which had enlarged leaves. In detail, the mac mutant showed alteration in leaf index and cell expansion in direction of width and length, resulting in not only modification of leaf shape but also disruption of heteroblasty. Molecular-genetic studies indicated that mac mutant had point mutation in ROTUDIFOLIA3 (ROT3) gene involved in brassinosteroid biosynthesis and was an allele of rot3-1 mutant. We named it mac/rot3-5 mutant. The expression of ROT3 gene was controlled by negative feedback inhibition by the treatment of brassinosteroid hormone, suggesting that ROT3 gene was involved in brassinosteroid biosynthesis. In dark condition, in addition, the expression of ROT3 gene was up-regulated and mac/rot3-5 mutant showed lower response, compare to wild type in petiole elongation. This study suggests that ROT3 gene has an important role in control of leaf index during leaf expansion process for proper environmental adaptation, such as shade avoidance syndrome, via the control of brassinosteroid biosynthesis.

• KSBB Journal
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• v.23 no.6
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• pp.513-518
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• 2008

This paper described the extraction/purification of $\beta$-carotene from recombinant E.coli and evaluation of anti-wrinkle activity of purified $\beta$-carotene. No significant differences in extraction yields were observed when hexane or isobutyl acetate was used. However, extraction from wet-cell cake resulted in 2-fold higher amount of $\beta$-carotene than that from dry cells. Disruption of 5 g-wet cells by ultrasonic homogenizer, acetone dehydration, extraction with isobutyl acetate resulted in 36 mg of $\beta$-carotene corresponding to 61.2% of recovery. The formation and separation of $\beta$-carotene crystal improved the purity. 633 mg of $\beta$-carotene crystal with 93% purity was obtained from 223 g/L of wet-cell cake harvested from 2.5-L fed-batch culture broth. The cultures of normal human primary fibroblast were performed to investigate the effect of $\beta$-carotene on cytotoxicity as MTT assay and anti-wrinkle activity as collagen synthesis assays. $1.7{\mu}M$ of $\beta$-carotene was found to be optimal concentration at which 1.4-fold higher amount of collagen was synthesized than that in absence of $\beta$-carotene. This indicates that highly purified $\beta$-carotene can be obtained from recombinant E.coli by applying simple method with less toxic solvent and can be used in functional cosmetics as anti-wrinkle agent.

• Korean Journal of Clinical Laboratory Science
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• v.51 no.3
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• pp.360-369
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• 2019

Cadherins are essential transmembrane proteins that promote cell-cell adhesion and maintain the corpus luteum structure in the ovary. This study examined the influence of prostaglandin F2 alpha ($PGF2{\alpha}$) on E-cadherin, N-cadherin, and adhesion in luteal theca cells (LTCs). The luteal cells were isolated from the mid-phase corpus luteum, and the LTCs were cultured separately from the luteal heterogeneous cells according to the morphology of the mesenchymal cells and to determine if steroidogenic and endothelial cells of LTCs, 3beta-hydroxysteroid dehydrogenase ($3{\beta}$-HSD), and vascular endothelial growth factor receptor 2 (VEGFR2) mRNA were used. The LTCs were then incubated in the culture medium supplemented with 0.01, 0.1, and 1.0 mM $PGF2{\alpha}$ for 24 h, and the E-cadherin and N-cadherin proteins in the LTCs were detected by confocal laser scanning microscopy. The results revealed $3{\beta}$-HSD mRNA expression in the LTC but no VEGF2R mRNA expression. The E-cadherin and N-cadherin proteins of the LTCs were damaged in the 0.01, 0.1, and 1.0 mM $PGF2{\alpha}$ treatment groups, and the expression of the N-cadherin protein was reduced significantly in 0.01 mM $PGF2{\alpha}$ compared to the 0 mM $PGF2{\alpha}$ treatment groups (P<0.05). In addition, the number of attached LTCs were significantly lower in the 0.01 mM $PGF2{\alpha}$ treatment group than in the 0 mM $PGF2{\alpha}$ treatment group (P<0.05). In conclusion, $PGF2{\alpha}$ affected the disruption of cadherin proteins and cell adhesion in LTCs. These results may help better understand the cadherin and adhesion mechanism during corpus luteum regression in the ovary.

• Korean Journal of Microbiology
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• v.41 no.2
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• pp.99-104
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• 2005

Corynebacterial clones which exert regulatory effects on the expression of the glyoxylate bypass genes were isolated using a reporter plasmid carrying the enteric lacZ fused to the aceB promoter of Corynebacterium glutamicum. Some clones carried common fragments as turned out by DNA mapping technique. Subcloning analysis followed by the measurement of $\beta-galactosidase$ activity in Escherichia coli identified the region responsible for the aceB-repressing activity. Sequence analysis of the DNA fragment identified two independent ORFs of ORF1 and ORF2. Among them, ORF2 was turned out to be responsible for the aceB-repressing activity. ORF1 encoded a 23,216 Da protein composed of 206 amino acids. Sequence similarity search indicated that the ORF may encode a ECF-type $\sigma$ factor and designated sigH. To identify the function of sigH, C. glutamicum sigH mutant was constructed by gene disruption technique and the sigH mutant showed growth retardation as compared to the wild type strain. In addition, the mutant strain showed sensitivity to oxidative-stress generating agent plumbagin. This result imply that sigH is probably involved in the stress response occurring during normal cell growth.