Se Jin Kim

Korea Advanced Institute of Science and Technology, Sŏul, Seoul, South Korea

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Publications (9)19.35 Total impact

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    ABSTRACT: This study examined the prevalence of cerebral palsy (CP) in South Korea, and the attributable lifetime medical cost according to physiological types and extent of involvement. The number of medical service use and medical cost of CP were obtained from the national health insurance review and assessment (HIRA) service. The prevalence was calculated from the number of five-year-old patients who used medical services between 2004 and 2008. The lifetime medical cost of CP was calculated from the data and discount rate of 3%. The prevalence of CP in South Korea was 2.6 per 1000 children. The attributable lifetime medical cost of CP in South Korea was calculated to be 26,383 US dollars, which is 1.8 times the basic lifetime medical cost of the general population (14,579 US dollars). Spastic CP showed the highest attributable medical cost, followed by dyskinetic and ataxic CP. Spastic diplegia showed 1.4 times of the attributable lifetime medical cost of spastic hemiplegia. The prevalence of CP in South Korea is comparable to that in other countries. CP is a disease with wide range of clinical features, and the medical cost according to the physiological types and extent of involvement should be considered.
    Health Policy 10/2010; 100(2-3):234-8. DOI:10.1016/j.healthpol.2010.09.010 · 1.73 Impact Factor
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    ABSTRACT: Inflammation plays a role in the response to metabolic stress in type 2 diabetes. However, the effects of rosiglitazone on inflammation of skeletal muscle have not been fully examined in type 2 diabetes. We investigated the effects of the insulin-sensitizing anti-diabetic agent, rosiglitazone, on the progression of skeletal muscle inflammation in Otsuka Long-Evans Tokushima Fatty (OLETF) type 2 diabetic rats. We examined the expression of serologic markers (serum glucose, insulin and free fatty acid) and inflammatory cytokines (tumor-necrosis factor-alpha, interleukin [IL]-1beta and IL-6) in OLETF rats from early to advanced diabetic stage (from 28 to 40 weeks of age). Serum glucose and insulin concentrations were significantly decreased in rosiglitazone-treated OLETF rats compared to untreated OLETF rats. Rosiglitazone treatment significantly decreased the concentrations of serum inflammatory cytokines from 28 to 40 weeks of age. The mRNA expression of various cytokines in skeletal muscle was reduced in rosiglitazone-treated OLETF rats compared with untreated OLETF rats. Furthermore, rosiglitazone treatment resulted in the downregulation of ERK1/2 phosphorylation and NF-kappaB expression in the skeletal muscle of OLETF rats. These results suggest that rosiglitazone may improve insulin sensitivity with its anti-inflammatory effects on skeletal muscle.
    Korean Diabetes Journal 06/2010; 34(3):191-9. DOI:10.4093/kdj.2010.34.3.191
    This article is viewable in ResearchGate's enriched format
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    ABSTRACT: Here we present telomerase activity screening using a capillary electrophoretic (CE) microdevice for human cancer diagnostics. The telomerase enzyme, a contributor to the maintenance of telomere length in cancer cells, was extracted from various human cells including MCF-7 (Human breast cancer cells), A549 (Human lung cancer cells), and SK-N-SH (Human neuroblastoma cells), and then telomeric repeat amplification protocol (TRAP)-based genetic analysis was performed to evaluate the activity of telomerase enzyme. The resultant 6-bp tandem repeat PCR amplicons derived from cancer cells were separated and detected on the 6 cm-long CE microdevice within 5 min. A limit of detection of 5 cells was achieved to analyze the telomerase activity on a CE microchip. In comparison with a conventional PAGE method, micro-fabricated CE-based analysis has many advantages in terms of high speed, low sample consumption, and high sensitive detection. The successful demonstration of telomerase activity screening on a chip implies great potential of a complete integration of a sample preparation and PCR unit in a single format for high-performance cancer diagnostics in a clinical arena. KeywordsTelomerase-Telomeric repeat amplification-Polymerase chain reaction-Capillary electrophoretic microdevice-Cancer diagnostics
    BioChip journal 03/2010; 4(1):42-48. DOI:10.1007/s13206-010-4107-y · 1.05 Impact Factor
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    ABSTRACT: Rapid and simple analysis for the multiple target pathogens is critical for patient management. CE-SSCP analysis on a microchip provides high speed, high sensitivity, and a portable genetic analysis platform in molecular diagnostic fields. The capability of separating ssDNA molecules in a capillary electrophoretic microchannel with high resolution is a critical issue to perform the precise interpretation in the electropherogram. In this study, we explored the potential of poly(ethyleneoxide)-poly(propyleneoxide)-poly(ethyleneoxide) (PEO-PPO-PEO) triblock copolymer as a sieving matrix for CE-SSCP analysis on a microdevice. To demonstrate the superior resolving power of PEO-PPO-PEO copolymers, 255-bp PCR amplicons obtained from 16S ribosomal RNA genes of four bacterial species, namely Proteus mirabilis, Haemophilus ducreyi, Pseudomonas aeruginosa, and Neisseria meningitidis, were analyzed in the PEO-PPO-PEO matrix in comparison with 5% linear polyacrylamide and commercial GeneScan gel. Due to enhanced dynamic coating and sieving ability, PEO-PPO-PEO copolymer displayed fourfold enhancement of resolving power in the CE-SSCP to separate same-sized DNA molecules. Fivefold input of genomic DNA of P. aeruginosa and/or N. meningitidis produced proportionally increased corresponding amplicon peaks, enabling correct quantitative analysis in the pathogen detection. Besides the high-resolution sieving capability, a facile loading and replenishment of gel in the microchannel due to thermally reversible gelation property makes PEO-PPO-PEO triblock copolymer an excellent matrix in the CE-SSCP analysis on the microdevice.
    Electrophoresis 03/2010; 31(6):1108-15. DOI:10.1002/elps.200900651 · 3.16 Impact Factor
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    Korean Diabetes Journal 01/2009; 33(5). DOI:10.4093/kdj.2009.33.5.375
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    ABSTRACT: Background.Cisplatin causes the impairment of inner ear functions, including hearing and balance, through the involvement of a number of mechanisms. However, no laboratory studies have been performed on involvement of inflammation-related events in cisplatin-mediated vestibular dysfunction.Methods.We evaluated the secretion of proinflammatory cytokines and nuclear factor-κB (NF-κB) activation in cisplatin-treated UB/UE-1 utricular epithelial cells. We also employed immunohistochemistry to detect proinflammatory cytokines and NF-κB expression in cisplatin-injected mice.Results.Productions of proinflammatory cytokines significantly caused the death of UB/UE1 cells by cisplatin. Pharmacologic inhibition of mitogen-activated protein (MAP) kinase/ERK kinase-1 (MEK1) or extracellular signal-regulated kinase (ERK) significantly attenuated the death of UB/UE1 cells caused by cisplatin and proinflammatory cytokines. Immunohistochemical studies revealed an increase in the expression of proinflammatory cytokines and NF-κB in both the cristae ampullae and utricle of cisplatin-injected mice.Conclusions.These results suggest that proinflammatory cytokines may play an important role in the pathogenesis of cisplatin-mediated vestibulotoxicity. © 2008 Wiley Periodicals, Inc. Head Neck, 2008
    Head & Neck 10/2008; 30(11):1445 - 1456. DOI:10.1002/hed.20892 · 2.83 Impact Factor
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    ABSTRACT: In the present study, crosslinked poly(vinyl alcohol) (PVA) membranes were prepared using poly(styrene sulfonic acid-co-maleic acid) (PSSA_MA) at different crosslinking temperatures. The crosslinked PVA membranes were prepared by varying the content of PSSA_MA (5–11 wt%). The PSSA_MA was used both as a crosslinking agent and as a donor of the hydrophilic group (–SO3H and/or –COOH). The crosslinked PVA/PSSA_MA membranes were characterized using FT-IR spectroscopy, thermogravimetric analysis (TGA) and investigated in relation to proton conductivity and methanol permeability. The proton and methanol transport decreased with increasing the PSSA_MA content. The effect of crosslinking may be more dominant than that of the increase of the number of ionic exchange sites in this system. The proton conductivities and the methanol permeabilities of all the membranes were in the range of 10−3 to 10−2 S/cm and 10−7 to 10−6 cm2/s, respectively, in the temperature range of 25–90 °C, depending on the crosslinking conditions.
    Journal of Membrane Science 09/2006; 281(1-2-281):156-162. DOI:10.1016/j.memsci.2006.03.025 · 4.91 Impact Factor
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    ABSTRACT: Samul extract, containing Radix Rehmanniae, Radix Angelicae Gigantis, Radix Paeoniae, and Rhizoma Cnidii, has been traditionally used for treatment of ischemic heart and brain damages in Oriental medicine. However, little is known about the mechanism by which Samul rescues cells from cytotoxic damage. This study was designed to investigate the protective mechanisms of Samul on H(2)O(2)-induced death of H9c2 cells. Treatment with H(2)O(2) markedly decreased the viability of H9c2 cells in a dose- and time-dependent manner, which was significantly prevented by pre-treatment with Samul. The nature of death of H9c2 cells by H(2)O(2) was demonstrated by apoptotic features, including ladder-pattern fragmentation of genomic DNA and chromatin condensation, which were markedly abolished by pretreatment of Samul in H(2)O(2)-treated cells. We further demonstrated that MEK inhibitor, PD98059, dose-dependently attenuated the protective effects of Samul against H(2)O(2), whereas inhibitors of Jnk and p38 did not. Consistently, Samul induced the early phosphorylation of Erk, p44, in H(2)O(2)-treated cells. In addition, treatment with Samul also resulted in an increase of expression of anti-apotogenic Bcl2 protein, which was decreased by H(2)O(2). However, it inhibited the expression of apotogenic Bax protein in H(2)O(2)-treated cells. Taken together, these results suggest that the protective effects of Samul against oxidative damage may be achieved via activation of MAP kinase, Erk as well as Bcl2 family proteins.
    The American Journal of Chinese Medicine 02/2006; 34(4):695-706. DOI:10.1142/S0192415X06004211 · 2.63 Impact Factor
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    ABSTRACT: Polycyclic aromatic hydrocarbons, such as benzo(a)pyrene (BaP), are widespread in the environment and cause untoward effects, including carcinogenesis, in mammalian cells. However, the molecular mechanism of apoptosis by BaP is remained to be elusive. Pharmacological inhibition of p38 kinase markedly inhibited the BaP-induced cytotoxicity, which was proven as apoptosis characterized by an increase in sub-G(0)/G(1) fraction of DNA content, ladder-pattern fragmentation of genomic DNA, and catalytic activation of caspase-3 with PARP cleavage. Our data also demonstrated that activation of caspase-3 was accompanied with activation of caspase-9 and mitochondrial dysfunction, which was also apparently suppressed by pretreatment with p38 kinase inhibitors. Also, pharmacological inhibition of p38 markedly inhibited the phosphorylation, accumulated expression, and transactivation activity of p53 in BaP-treated cells. Adenoviral overexpression of human p53 (wild-type) further augmented in increase of PARP cleavage and the sub-G(0)/G(1) fraction of DNA content. Furthermore, p53 mediated apoptotic activity in BaP-treated cells was inhibited by p38 kinase inhibitor. The current data collectively indicate that BaP induces apoptosis of Hepa1c1c7 cells via activation of p53-related signaling, which was, in part, regulated by p38 kinase.
    Archives of Biochemistry and Biophysics 01/2006; 444(2):121-9. DOI:10.1016/ · 3.04 Impact Factor

Publication Stats

125 Citations
19.35 Total Impact Points


  • 2010
    • Korea Advanced Institute of Science and Technology
      • Department of Chemical and Biomolecular Engineering
      Sŏul, Seoul, South Korea
  • 2009–2010
    • Ulsan University Hospital
      Urusan, Ulsan, South Korea
  • 2006
    • Wonkwang University School of Medicine and Hospital
      Riri, North Jeolla, South Korea
    • Hannam University
      Eidō, North Chungcheong, South Korea