• Membrane and Water Treatment
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• v.8 no.3
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• pp.225-244
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• 2017

A novel thin-film nanocomposite (TFN) reverse osmosis (RO)/non-woven fabric (NWF) membrane was prepared by adding zinc oxide (ZnO) nanospheres ($30{\pm}10nm$) during the interfacial polymerization process of m-phenylenediamine (MPD) and trimesoyl chloride (TMC) on self-made polysulfone (PSF) membrane/polyester (PET) non-woven fabric support. The improved performance of TFN RO membrane was verified in terms of water contact angle (WCA), water flux, salt rejection, antifouling properties and chlorine resistance. The results showed that the WCA value of TFN RO surface had a continuous decrease with the increasing of ZnO content in MPD aqueous solution. The water flux of composite TFN RO membranes acquired a remarkable increase with a stable high solute rejection (94.5 %) in $1g{\cdot}L^{-1}$ NaCl aqueous solution under the optimized addition amount of ZnO (1 wt%). The continuous testing of membrane separation performance after the immersion in sodium hypochlorite solution indicated that the introduction of ZnO nanospheres also dramatically enhanced the antifouling properties and the chlorine resistance of composite RO membranes.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.6
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• pp.2911-2916
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• 2014

Oxaliplatin is a first-line therapy for colorectal cancer, but cancer cell resistance to the drug compromises its efficacy. To explore mechanisms of drug resistance, we treated colorectal cancer cells (HCT116 and SW620) long-term with oxaliplatin and established stable oxaliplatin-resistant lines (HCT116-OX and SW620-OX). Compared with parental cell lines, $IC_{50}$s for various chemotherapeutic agents (oxaliplatin, cisplatin and doxorubicin) were increased in oxaliplatin-resistant cell lines and this was accompanied by activation of nuclear factor erythroid-2 p45-related factor 2 (Nrf2) and NADPH quinone oxidoreductase 1 (NQO1). Furthermore, luteolin inhibited the Nrf2 pathway in oxaliplatin-resistant cell lines in a dose-dependent manner. Luteolin also inhibited Nrf2 target gene [NQO1, heme oxygenase-1 (HO-1) and $GST{\alpha}1/2$] expression and decreased reduced glutathione in wild type mouse small intestinal cells. There was no apparent effect in Nrf2-/- mice. Luteolin combined with other chemotherapeutics had greater anti-cancer activity in resistant cell lines (combined index values below 1), indicating a synergistic effect. Therefore, adaptive activation of Nrf2 may contribute to the development of acquired drug-resistance and luteolin could restore sensitivity of oxaliplatin-resistant cell lines to chemotherapeutic drugs. Inhibition of the Nrf2 pathway may be the mechanism for this restored therapeutic response.

• Journal of Microbiology and Biotechnology
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• v.25 no.12
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• pp.2082-2089
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• 2015

Avian beta-defensin 9 (AvBD9) is a small cationic peptide consisting of 41 amino acids that plays a crucial rule in innate immunity and acquired immunity in chickens. Owing to its wide antibacterial spectrum, lack of a residue, and failure to induce bacterial drug resistance, AvBD9 is expected to become a substitute for conventional antibiotics in the livestock and poultry industries. Using the preferred codon of Pichia pastoris, the mature AvBD9 peptide was designed and synthesized, based on the sequence from GenBank. The P. pastoris constitutive expression vector pGHKα was used to construct a pGHKα-AvBD9 recombinant plasmid. Restriction enzyme digestion was performed using SacI and BglII to remove the ampicillin resistance gene, and the plasmid was electrotransformed into P. pastoris GS115. High-expression strains with G418 resistance were screened, and the culture supernatant was analyzed by Tricine-SDS-PAGE and western blot assay to identify target bands of about 6 kDa. A concentrate of the supernatant containing AvBD9 was used for determination of antimicrobial activity. The supernatant concentrate was effective against Escherichia coli, Salmonella paratyphi, Salmonella pullorum, Pseudomonas aeruginosa, Enterococcus faecalis, and Enterobacter cloacae. The fermentation product of P. pastoris carrying the recombinant AvBD9 plasmid was adjusted to 1.0 × 10⁸ CFU/ml and added to the drinking water of white feather broilers at different concentrations. The daily average weight gain and immune organ indices in broilers older than 7 days were significantly improved by the AvBD9 treatment.

• Clinical and Experimental Pediatrics
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• v.60 no.5
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• pp.151-157
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• 2017

Purpose: Macrolide resistance rate of Mycoplasma pneumoniae has rapidly increased in children. Studies on the clinical features between macrolide susceptible-M. pneumoniae (MSMP) and macrolide resistant-M. pneumoniae (MRMP) are lacking. The aim of this study was to identify the macrolide resistance rate of M. pneumoniae in Korean children with M. pneumoniae penupmonia in 2015 and compare manifestations between MSMP and MRMP. Methods: Among 122 children (0-18 years old) diagnosed with M. pneumoniae pneumonia, 95 children with the results of macrolide sensitivity test were included in this study. Clinical manifestations were acquired using retrospective medical records. Results: The macrolide resistant rate of M. pneumoniae was 87.2% (82 of 94 patients) in children with M. pneumoniae pneumonia. One patient showed a mixed type of wild type and A2063G mutation in 23S rRNA of M. pneumoniae. There were no significant differences in clinical, laboratory, and radiologic findings between the MSMP and MRMP groups at the first visit to our hospital. The time interval between initiation of macrolide and defervescence was significantly longer in the MRMP group ($4.9{\pm}3.3$ vs. $2.8{\pm}3.1days$, P=0.039). Conclusion: The macrolide resistant rate of M. pneumoniae is very high in children with M. pneumoniae pneumonia in Korea. The clinical manifestations of MRMP are similar to MSMP except for the defervescence period after administration of macrolide. Continuous monitoring of the occurrence and antimicrobial susceptibility of MRMP is required to control its spread and establish strategies for treating second-line antibiotic resistant M. pneumoniae infection.

• Proceedings of the KSME Conference
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• 2002.08a
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• pp.9-10
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• 2002

Human circulatory system between heart and tissue is not directly connected in normal condition but mandatory to go through the capillary system in order to fulfill its physiologic aim to deliver oxygen and nutrients, etc. to the tissue and retrieve used blood together with waste products from the tissue properly. When abnormal connection between arterial and venous system (AV fistula), these two circulatory systems respond differently to the hemodynamic impact of this abnormal connection between high pressure (artery) and low pressure (vein) system. Depending upon the location and/or degree (e.g. size and flow) of fistulous condition, each circulatory system exerts different compensatory hemodynamic response to this newly developed abnormal inter-relationship between two systems in order to minimize its hemodynamic impact to own system of different hemodynamic characteristics. Pump action of the heart can assist the failing arterial system directly to maintain arterial circulation against newly established low peripheral resistance by the AV fistula during the compensation period, while it affects venous system in negative way with increased venous loading. However, the negative impact of increased heart action to the venous system is partly compensated by the lymphatic system which is the third circulatory system to assist venous system independently with different hemodynamics. The lymphatic system with own unique Iymphodynamics based on peristaltic circulation from low resistance to high resistance condition, also increases its circulation to assist the compensation of overloaded venous system. Once these compensation mechanisms should fail to fight to newly established hemodynamic condition due to this abnormal AV connection, each system start to show different physiologic ${\underline{de}compensation}$ including heart and lymphatic system. The vicious cycle of decompensation between arterial and vein, two circulatory system affecting each other by mutually negative way steadily progresses to show series of hemodynamic change throughout entire circulation system altogether including heart. Clinical outcome of AV fistula from the compensated status to decompensated status is closely affected by various biological and mechanical factors to make the hemodynmic status more complicated. Proper understanding of these crucial biomechanical factors iii particular on hemodyanmic point of view is mandatory for the advanced assessment of biomechanical impact of AV fistula, since this new advanced concept of AY fistula based on blomechanical information will be able to improve clinical control of the complicated AV fistula, either congenital or acquired.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.20
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• pp.8617-8622
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• 2014

The goal of this study was to establish paclitaxel resistant MCF-7 cells, as in vitro model, to identify the molecular mechanisms leading to acquired chemoresistance in breast cancer cells. Resistant cells were developed by stepwise increasing exposure to paclitaxel. Gene expression levels of Bax and Bcl-2 along with protein levels of caspase-8 and caspase-9 were evaluated in two resistant cell lines (MCF-7/Pac64 and MCF-7/Pac5 nM). Morphological modifications in paclitaxel resistance cells were examined by light microscopy and fluorescence activated cell sorting (FACS). As an important indicator of resistance to chemotheraputic agents, the Bcl-2/Bax ratio showed a significant increase in both MCF-7/Pac5nM and MCF-7/Pac 64nM cells (p<0.001), while caspase-9 levels were decreased (p<0.001) and caspase-8 was increased (p<0.001). FACS analysis demonstrated that MCF-7/Pac64 cells were smaller than MCF-7 cells with no difference in their granularity. Our results support the idea that paclitaxel induces apoptosis in a mitochondrial-dependent manner. Identifying breast cancer patients with a higher Bcl-2/Bax ratio and caspase 9 level and then inhibiting the activity of these proteins may improve the efficacy of chemotheraputic agents.

• Clinical and Experimental Pediatrics
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• v.60 no.6
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• pp.167-174
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• 2017

Mycoplasma pneumoniae pneumonia (MPP) is one of the most common forms of community-acquired pneumonia in children and adolescents. Outbreaks of MPP occur in 3- to 7-year cycles worldwide; recent epidemics in Korea occurred in 2006-2007, 2011, and 2015-2016. Although MPP is known to be a mild, self-limiting disease with a good response to macrolides, it can also progress into a severe and fulminant disease. Notably, since 2000, the prevalence of macrolide-resistant MPP has rapidly increased, especially in Asian countries, recently reaching up to 80%-90%. Macrolide-resistant Mycoplasma pneumoniae (MRMP) harbors a point mutation in domain V of 23S rRNA with substitutions mainly detected at positions 2063 and 2064 of the sequence. The excessive use of macrolides may contribute to these mutations. MRMP can lead to clinically refractory pneumonia, showing no clinical or radiological response to macrolides, and can progress to severe and complicated pneumonia. Refractory MPP is characterized by an excessive immune response against the pathogen as well as direct injury caused by an increasing bacterial load. A change of antibiotics is recommended to reduce the bacterial load. Tetracyclines or quinolones can be alternatives for treating MRMP. Otherwise, corticosteroid or intravenous immunoglobulin can be added to the treatment regimen as immunomodulators to downregulate an excessive host immune reaction and alleviate immune-mediated pulmonary injury. However, the exact starting time point, dose, or duration of immunomodulators has not been established. This review focuses on the mechanism of resistance acquisition and treatment options for MRMP pneumonia.

• Journal of Life Science
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• v.19 no.12
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• pp.1705-1711
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• 2009

Carcinoma cells that had acquired resistance to a chemotherapeutic drug often show cross-resistance to various other cytotoxic drugs. In the present study, we explored the effect of heat shock in cisplatin-resistant gastric cancer cells SNU601/Cis2 to figure out the efficacy of hyperthermia in drug-resistant carcinoma. While SNU601/WT cells showed a high-sensitivity response to heat shock by dying through apoptosis, SNU601/Cis2 cells were considerably resistant to mild heat shock, but died by necrosis upon treatment with harsh heat shock. The occurrence of necrosis in SNU601/Cis2 cells was linked to the suppression of both JNK1/2 activation and HSP27 induction in response to heat shock. Since necrosis is closely associated with tumor malignancy and poor prognosis through inflammatory responses, our result suggests that hyperthermic treatment should be carefully applied when it is combined with chemotherapy.

• Molecules and Cells
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• v.39 no.2
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• pp.129-135
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• 2016

Eukaryotic translation initiation factor 2 alpha ($eIF2{\alpha}$), which is a component of the eukaryotic translation initiation complex, functions in cell death and survival under various stress conditions. In this study, we investigated the roles of $eIF2{\alpha}$ phosphorylation in cell death using the breast cancer cell lines MCF-7 and MCF-7/ADR. MCF-7/ADR cells are MCF-7-driven cells that have acquired resistance to doxorubicin (ADR). Treatment of doxorubicin reduced the viability and induced apoptosis in both cell lines, although susceptibility to the drug was very different. Treatment with doxorubicin induced phosphorylation of $eIF2{\alpha}$ in MCF-7 cells but not in MCF-7/ADR cells. Basal expression levels of Growth Arrest and DNA Damage 34 (GADD34), a regulator of $eIF2{\alpha}$, were higher in MCF-7/ADR cells compared to MCF-7 cells. Indeed, treatment with salubrinal, an inhibitor of GADD34, resulted in the upregulation of $eIF2{\alpha}$ phosphorylation and enhanced doxorubicin-mediated apoptosis in MCF-7/ADR cells. However, MCF-7 cells did not show such synergic effects. These results suggest that dephosphorylation of $eIF2{\alpha}$ by GADD34 plays an important role in doxorubicin resistance in MCF-7/ADR cells.

• Journal of Biomedical Engineering Research
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• v.23 no.1
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• pp.73-79
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• 2002

The goals of this study are twofold: To investigate non-phobics'and Phobics'Physiological response in virtual environments. and to analyze the trend of phobics' Physiology during virtual reality treatment. As a measure of Physiology. heart rate, skin resistance. and skin temperature were acquired. The data of two group subjects were analyzed: twenty-two non-Phobic subjects (M=32.94 years). thirty-six subjects with fear of flying (M=40.12 yearn) who met the DSM-lV criteria for a fear of flying. As a result. skin resistance showed significant differences between non-Photics and phobics. T(56) =2.978, P〈0.01 And the physiological responses of 33 subjects among the Phobics. who succeed to fly without medicine after virtual reality treatment, showed a gradual trend toward the non-Phobics Physiological responses as therapy sessions went on. In this study. Physiological monitoring. skin resistance appeared to be useful both in understanding the Physiological state of Phobic individuals and in evaluating the results of treatment in virtual reality Psychotherapy.