• Journal of Haehwa Medicine
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• v.16 no.1
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• pp.81-91
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• 2007

Objective : We wished to examine closely effect that Kami-KangHwalSan medicines used to atopy dermatitis disease patient get in atopy eruption control experimentally. Materials and Methods : Atopic dermatitis (AD) usually develops in patients with an individual or family history of allergic diseases, and is characterized by chronic relapsing inflammation seen specially in childhood, association with IgE hyperproduction and precipitation by environmental factors. However, the exact etiology of AD has been unclear. To further explore the pathogenesis and treatment of AD, a suitable animal model is required. We found that skin lesions, which were chnically and histologically very simlar to human AD, mite antigen-induced dermatitis on the face, neck, ears and dorsal skin of inbred NC/Nga mice. Results and Conclusion : Kami-KangHwalSan medicines controlled CD3+/CD69+, CD4+/CD25+, B220+/IgE+, and B220+/CD23+ revelation that an experiment that motive allergy immune reponse because an in vitro experiment stimulates splenocytes of a NC/Nga mouse same t1me by PWM, and interleukin-4, eotaxin 2, CCR3, TARC mRNA outturn that bear in splenocytes decreased remarkably by Kami-KangHwalSan medicines. Th1 cell and Th2 cell observe to be shifted by secretion amount of IL-4 and IFN-$\gamma$ by Kami-KangHwalSan medicines could know that Kami-KangHwalSan medicines can use usefully in allergy autoimmnune diease.

• Journal of Haehwa Medicine
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• v.16 no.1
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• pp.93-105
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• 2007

Objective : We wished to examine closely effect that Kami-JeSeubUilYeongTang medicines used to atopy dermatitis disease patient get in atopy eruption control experimentally. Materials and Methods : Atopic dermatitis (AD) usually develops in patients with an individual or family history of allergic diseases, and is characterized by chronic relapsing inflammation seen specially in childhood, association with IgE hyperproduction and precipitation by environmental factors. However, the exact etiology of AD has been unclear. To further explore the pathogenesis and treatment of AD, a suitable animal model is required. We found that skin lesions, which were clinically and histologically very similar to human AD, mite antigen-induced dermatitis on the face, neck, ears and dorsal skin of inbred NC/Nga mice. Result and Conclusion : Kami-jeseupwiryeongtang(JWRTK) medicines controlled CD3+/CD69+, CD4+/CD25+, B220+/IgE+, and B220+/CD23+ revelation that an experiment that motive allergy immune reponse because an in vitro experiment stimulates splenocytes of a NC/Nga mouse same time by PWM, and interleukin-4, eotaxin 2, CCR3, TARC mRNA outturn that bear in splenocytes decreased remarkably by Jeseupwiryeongtang-Kamibang(JWRTK) medicines. Th1 cell and Th2 cell observe to be shifted by secretion amount of IL-4 and IFN-$\gamma$ by Jeseupwiryeongtang-Kamibang(JWRTK) medicines could know that Jeseupwiryeongtang-Kamibang(JWRTK) medicines can use usefully in allergy autoimmnune diease.

• BMB Reports
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• v.38 no.2
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• pp.151-160
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• 2005

By a cDNA array representing 2308 signal transduction related genes, we studied the expression profiles of HeLa cells stably transfected by Hepatitis C virus nonstructural protein 4B (HCV-NS4B). The alterations of the expression of four genes were confirmed by real-time quantitative RT-PCR; and the aldo-keto reductase family 1, member C1 (AKR1C1) enzyme activity was detected in HCV-NS4B transiently transfected HeLa cells and Huh-7, a human hepatoma cell line. Of the 2,308 genes we examined, 34 were up-regulated and 56 were down-regulated. These 90 genes involved oncogenes, tumor suppressors, cell receptors, complements, adhesions, transcription and translation, cytoskeletion and cellular stress. The expression profiling suggested that multiple regulatory pathways were affected by HCV-NS4B directly or indirectly. And since these genes are related to carcinogenesis, host defense system and cell homeostatic mechanism, we can conclude that HCV-NS4B could play some important roles in the pathogenesis mechanism of HCV.

• Journal of Korean Neurosurgical Society
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• v.52 no.4
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• pp.417-419
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• 2012

Tumors of the central nervous system are common in the pediatric population and constitute the second most prevalent tumor type in children. Within this group, spinal cord tumors are relatively rare and account for 1 to 10% of all pediatric central nervous system tumors. We describe a very rare case of an intradural extramedullary spinal cord tumor with a subcutaneous mass and discuss its clinical presentation, pathogenesis, and treatment. A male infant was delivered normally, with uneventful development. At 16 days post-delivery, his family took him to a pediatrician because of a mass on his upper back. Magnetic resonance imaging of the thoracic spine revealed a well-demarcated soft-tissue mass with central cystic change or necrosis at the subcutaneous layer of the posterior back (T2-7 level). Another mass was found with a fat component at the spinal canal of the T1-3 level, which was intradural extramedullary space. After six weeks, the spinal cord tumor and subcutaneous mass were grossly total resected; pathologic findings indicated an atypical myxoid spindle cell neoplasm, possibly nerve sheath in type. The final diagnosis of the mass was an atypical myxoid spindle cell neoplasm. The postoperative course was uneventful, and the patient was discharged after nine days without any neurological deficit. We report a rare case of an intradural extramedullary spinal tumor with subcutaneous mass in a neonate. It is necessary to monitor the patient's status by examining consecutive radiologic images, and the symptoms and neurological changes should be observed strictly during long-term follow-up.

• Applied Biological Chemistry
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• v.48 no.4
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• pp.301-310
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• 2005

Foot-and-mouth disease (FMD) is a highly contagious disease of mammals and has a great potential for causing severe economic loss in susceptible cloven-hoofed animals, such as cattle, pigs, sheep, goats and buffalo. FMDV, a member of the Aphthovirus genus in the Picornaviridae family, is a non-enveloped icosahedral virus that contains a positive sense RNA of about 8.2 kb in size. The genome carries one open reading frame consisting of 3 regions: capsid protein coding region P1, replication related protein coding region P2, and RNA-dependent RNA polymerase coding region P3. FMDV infects pharynx epithelial cell in the respiratory tract and viral replication is active in lung epithelial cell. Morbidity is extremely high. A FMD outbreak in Korea in 2002 caused severe economic loss. Although intense research is undergoing to develop appropriate drugs to treat FMDV infection, there is no specific therapeutic for controlling FMDV infection. Moreover, there is an increasing demand for the development of vaccine strategies against FMDV infection in many countries. In this report, more effective prevention strategies against FMDV infection were reviewed.

• CELLMED
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• v.3 no.2
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• pp.10.1-10.8
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• 2013

Cancer is one of the major dreaded diseases causing high mortality. Lung cancer is second in position of all cancer related deaths and mainly divided into two morphologic sub-types: small-cell lung cancer and non-small cell lung cancer (NSCLC). NSCLC is an aggressive neoplasm which hardly responds to any conventional chemotherapy. Epidermal growth factor receptor (EGFR) belongs to the ErbB family of receptor tyrosine kinase that is mainly over-expressed in NSCLC. EGFR is mainly involved in the pathogenesis and progression of different carcinoma. In vivo and in vitro studies suggest that EGFR and EGF like peptides are often over-expressed in human NSCLC and these proteins are able to induce cell transformation. The conventional therapies mostly inhibit the EGFR activity and expression level in human NSCLC with the use of some EGFR-inhibitors like HKI-272, EKB569, CL-387785 etc. and some synthetic chemotherapeutic drugs like erlotinib, gefitinib, plumbagin, docetaxel, cisplatin etc., alone or in combination of two or more drugs. These therapies selectively act by competitive inhibition of the binding of adenosine triphosphate to the tyrosine kinase domain of the EGFR, resulting in inhibition of the EGFR signaling pathway. But these chemotherapeutic drugs have some cytotoxic activities to the normal cells and have some adverse side-effects. Recent studies on some traditional alternative therapies including some herbal and plant extracts, active ingredients like curcumin, different homeopathic drugs, etc. can target EGFR-signalling in NSCLC with less toxic side-effects are being currently developed.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.3
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• pp.1171-1176
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• 2014

Objective: The tumor suppressor gene, Ras-association domain family (RASSF)2A, is inactivated by promoter hypermethylation in many cancers. The current study was performed to evaluate the methylation status of RASSF2A in epithelial ovarian cancer (EOC) tissues and plasma, and correlations with gene expression and clinicopathologic characteristics. Method: We detected methylation of the RASSF2A gene in tissues and corresponding plasma samples from 47 EOC patients and 14 patients with benign ovarian tumors and 10 with normal ovarian tissues. The methylation status was determined by methylation-specific PCR while gene expression of mRNA was examined by RT-PCR. The EOC cell line, SKOV3, was treated with 5-aza-2'-deoxycytidine (5-azadC). Results: RASSF2A mRNA expression was significantly low in EOC tissues. The frequency of aberrant methylation of RASSF2A was 51.1% in EOC tissues and 36.2% in corresponding plasma samples, whereas such hypermethylation was not detected in the benign ovarial tumors and normal ovarian samples. The expression of RASSF2A mRNA was significantly down-regulated or lost in the methylated group compared to the unmethylated group (p<0.05). After treatment with 5-aza-dC, RASSF2A mRNA expression was significantly restored in the Skov3 cell line. Conclusion: Epigenetic inactivation of RASSF2A through aberrant promoter methylation may play an important role in the pathogenesis of EOC. Methylation of the RASSF2A gene in plasma may be a valuable molecular marker for the early detection of EOC.

• Journal of Periodontal and Implant Science
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• v.39 no.sup2
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• pp.231-237
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• 2009

Purpose: Cytolethal distending toxin (CDT) is a family of heat-labile cytotoxins produced by several gram-negative mucosa-associated pathogens, including Aggregatibacter actinomycetemcomitans. CDT is well known to be capable of inducing growth arrest, morphological alterations, and eventually death in various cells. CDT belongs to a tripartite $AB_2$ toxin (CdtB: the enzymatic A subunit; CdtA and CdtC: the heterodimeric B subunit). Previous studies proposed that CdtA and CdtC together bind to a cell surface receptor and glycolipids act as a receptor for A. actinomycetemcomitans CDT (AaCDT). In this study, recombinant CdtA and CdtC proteins of AaCDT were co-expressed in a bacterial expression system and tested for their affinity for $GM_1$ ganglioside. Methods: The genes for CdtA and CdtC from A. actinomycetemcomitans Y4 were utilized to construct the expression vectors, pRSET-cdtA and pET28a-cdtC. Both CdtA and CdtC proteins were expressed in Escherichia coli BL21(DE3) and then purified using hexahistidine (His6) tag. The identity of purified protein was confirmed by anti-His6 antibody and monoclonal anti-CdtA antibody. Furthermore, the affinity of recombinant protein to $GM_1$ ganglioside was checked through ELISA. Results: Recombinant CdtA and CdtC proteins were expressed as soluble proteins and reacted to anti-His6 and monoclonal anti-CdtA antibodies. ELISA revealed that purified soluble CdtA-CdtC protein bound to $GM_1$ ganglioside, while CdtA alone did not. Conclusions: Co-expression of CdtA and CdtC proteins enhanced the solubility of the proteins in E. coli, leading to convenient preparation of active CdtA-CdtC, a critical material for the study of AaCDT pathogenesis.

• Biomolecules & Therapeutics
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• v.24 no.6
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• pp.650-658
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• 2016

Chronic alcohol consumption causes alcoholic liver disease, which is associated with the initiation of dysregulated lipid metabolism. Recent evidences suggest that dysregulated cholesterol metabolism plays an important role in the pathogenesis of alcoholic fatty liver disease. Ecklonia stolonifera (ES), a perennial brown marine alga that belongs to the family Laminariaceae, is rich in phlorotannins. Many studies have indicated that ES has extensive pharmacological effects, such as antioxidative, hepatoprotective, and antiinflammatory effects. However, only a few studies have investigated the protective effect of ES in alcoholic fatty liver. Male Sprague-Dawley rats were randomly divided into normal diet (ND) (fed a normal diet for 10 weeks) and ethanol diet (ED) groups. Rats in the ED group were fed a Lieber-DeCarli liquid diet (containing 5% ethanol) for 10 weeks and administered ES extract (50, 100, or 200 mg/kg/day), silymarin (100 mg/kg/day), or no treatment for 4 weeks. Each treatment group comprised of eight rats. The supplementation with ES resulted in decreased serum levels of triglycerides (TGs), total cholesterol, alanine aminotransferase, and aspartate aminotransferase. In addition, there were decreases in hepatic lipid and malondialdehyde levels. Changes in liver histology, as analyzed by Oil Red O staining, showed that the ES treatment suppressed adipogenesis. In addition, the ES treatment increased the expression of fatty acid oxidation-related genes (e.g., PPAR-${\alpha}$ and CPT-1) but decreased the expression of SREBP 1, which is a TG synthesis-related gene. These results suggest that ES extract may be useful in preventing fatty acid oxidation and reducing lipogenesis in ethanol-induced fatty liver.

• Genomics & Informatics
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• v.8 no.1
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• pp.19-27
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• 2010

To discover genetic markers for autism spectrum disorder (ASD), we previously applied genome-wide BAC array comparative genomic hybridization (array-CGH) to 28 autistic patients and 62 normal controls in Korean population, and identified that chromosomal losses on 8p23.1 and on 17p11.2 are significantly associated with autism. In this study, we developed an 8.5K ASD-specific BAC array covering 27 previously reported ASD-associated CNV loci including ours and examined whether the associations would be replicated in 8 ASD patient cell lines of four different ethnic groups and 10 Korean normal controls. As a result, a CNV-loss on 8p23.1 was found to be significantly more frequent in patients regardless of ethnicity (p<0.0001). This CNV region contains two coding genes, DEFA1 and DEFA3, which are members of DEFENSIN gene family. Two other CNVs on 17p11.2 and Xp22.31 were also distributed differently between ASDs and controls, but not significant (p=0.069 and 0.092, respectively). All the other loci did not show significant association. When these evidences are considered, the association between ASD and CNV of DEFENSIN gene seems worthy of further exploration to elucidate the pathogenesis of ASD. Validation studies with a larger sample size will be required to verify its biological implication.