• 대한한방내과학회지
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• 제23권2호
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• pp.306-312
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• 2002

Systemic Lupus Erythematosus(SLE) is a autoimmune disease characterized by combined symtoms of malar rash, discoid rash, neuropsychiatric disorder, renal disorder, hematologic disorder, photosensitivity immunologic disorder, oral ulcer, anti-nuclear antibody, arthritis, pleuritis and pericarditis, etc. Multiple genetic or environmental causes are supposed to facilitate antiboby production to autoantigen such as ds-DNA, histone, phospholipid, red blood cell, platelet, etc. And defective complementary system fail to remove autoantigen-antibody complex, which deposit in multiple organs and result in inflammatory damages. SLE does not correctly correspond to any specific category of oriental medicine. But, accoring to previous reports, it can be controlled by herb medications used differently patients-to-patients. So we are to report this one SLE case being successfully controlled by classic corticosteroids with herb medications based on oriental diffrential diagnosis of symptoms and signs.

• Pediatric Infection and Vaccine
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• 제21권3호
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• pp.219-224
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• 2014

Streptococcus bovis에 의한 신생아 침습감염을 보고한 사례는 많지 않으며, 지금까지 보고된 증례는 대부분 Streptococcus pasteurianus가 원인이었다. 저자들은 생후 28일에 열이 나서 온 환자의 혈액과 뇌척수액에서 분리된 균주를 16S rRNA와 tuf 유전자 염기서열분석을 통해 Streptococcus lutetiensis로 동정할 수 있었다. 환자의 혈액에서 배양된 균주는 자동화 장비(VITEK 2)에서 Streptococcus infantarius로 동정되었고 뇌척수액에서 자란 균주는 동정되지 않았다. 환자는 항균제 투여 2일째부터 열이 떨어지고 전신상태가 호전되었으며, 14일간 항균제 사용 후 신경학적 합병증 없이 퇴원하였다. 저자들은 S. bovis군에 의한 침습 감염 환자에서 정확한 균주 동정을 위해 분자유전학적 검사기법이 도움이 될 수 있음을 확인하였고 본 증례의 원인 균주가 신생아 침습감염의 원인으로 알려진 사례가 없어 보고하는 바이다.

• Journal of the Korean Academy of Child and Adolescent Psychiatry
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• 제6권1호
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• pp.34-42
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• 1995

청소년기의 경계선 인격장애는 충동조절의 결여, 타인에 대한 평가절하와 자신보다는 대상에 대하여 만족감을 얻으려는 욕구, 분리 방어기제를 특징으로 하는 인격장애로서 성인의 경계선 인격장애와 비슷한 양상으로 나타난다. 청소년기의 경계선 인격장애의 주요한 증상은 우울, 불안, 정체성 위기와 이러한 정체성 위기로 인한 반사회적인 행동을 흔히 볼 수 있다. 따라서 이들 증상들과 정상 청소년들이 보일 수 있는 질풍노도의 양상과 구별이 힘든 경우가 있다. 경계선 인격장애에서는 대상관계의 불안정, 정동의 불안정, 분리 등 미숙한 방어기제로 인해서 심한 스트레스하에서 정신병적 삽화가 나타날 수 있으며, 이로인해 정신분열증, 정동장애, 분열형 인격장애, 편집형 인격장애등과 감별진단이 필요하다. 청소년기 경계선 인격장애의 원인으로는 정신역동적 요소, 유전적 요인을 포함한 생물학적 요소, 가족역동적인 요소등을 복합적으로 고려해야 한다. 치료는 개인정신치료, 그룹치료, 가족치료, 약물치료 등이 있다. 소아 청소년기 경계선 인격장애가 성인기 경계선 인격장애로 될 것인가에 대해서는 논란이 되고 있다.

• Journal of Korean Neurosurgical Society
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• 제63권2호
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• pp.153-162
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• 2020

Spinal cord injury (SCI) is one of the most devastating conditions and many SCI patients suffer neurological sequelae. Stem cell therapies are expected to be beneficial for many patients with central nervous system injuries, including SCI. Adult stem cells (ASCs) are not associated with the risks which embryonic stem cells have such as malignant transformation, or ethical problems, and can be obtained relatively easily. Consequently, many researchers are currently studying the effects of ASCs in clinical trials. The environment of transplanted cells applied in the injured spinal cord differs between the phases of SCI; therefore, many researchers have investigated these phases to determine the optimal time window for stem cell therapy in animals. In addition, the results of clinical trials should be evaluated according to the phase in which stem cells are transplanted. In general, the subacute phase is considered to be optimal for stem cell transplantation. Among various candidates of transplantable ASCs, mesenchymal stem cells (MSCs) are most widely studied due to their clinical safety. MSCs are also less immunogenic than neural stem/progenitor cells and consequently immunosuppressants are rarely required. Attempts have been made to enhance the effects of stem cells using scaffolds, trophic factors, cytokines, and other drugs in animal and/or human clinical studies. Over the past decade, several clinical trials have suggested that transplantation of MSCs into the injured spinal cord elicits therapeutic effects on SCI and is safe; however, the clinical effects are limited at present. Therefore, new therapeutic agents, such as genetically enhanced stem cells which effectively secrete neurotrophic factors or cytokines, must be developed based on the safety of pure MSCs.

• The Korean Journal of Physiology and Pharmacology
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• 제9권1호
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• pp.1-8
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• 2005

Myotonic Dystrophies type 1 and 2 (DM1/2) are neuromuscular disorders which belong to a group of genetic diseases caused by unstable CTG triplet repeat (DM1) and CCTG tetranucleotide repeat (DM2) expansions. In DM1, CTG repeats are located within the 3' untranslated region of myotonin protein kinase (DMPK) gene on chromosome 19q. DM2 is caused by expansion of CCTG repeats located in the first intron of a gene coding for zinc finger factor 9 on chromosome 3q. The CTG and CCTG expansions are located in untranslated regions and are expressed as pre-mRNAs in nuclei (DM1 and DM2) and as mRNA in cytoplasm (DM1). Investigations of molecular alterations in DM1 discovered a new molecular mechanism responsible for this disease. Expansion of un-translated CUG repeats in the mutant DMPK mRNA disrupts biological functions of two CUG-binding proteins, CUGBP and MNBL. These proteins regulate translation and splicing of mRNAs coding for proteins which play a key role in skeletal muscle function. Expansion of CUG repeats alters these two stages of RNA metabolism in DM1 by titrating CUGBP1 and MNBL into mutant DMPK mRNA-protein complexes. Mouse models, in which levels of CUGBP1 and MNBL were modulated to mimic DM1, showed several symptoms of DM1 disease including muscular dystrophy, cataracts and myotonia. Mis-regulated levels of CUGBP1 in newborn mice cause a delay of muscle development mimicking muscle symptoms of congenital form of DM1 disease. Since expansion of CCTG repeats in DM2 is also located in untranslated region, it is predicted that DM2 mechanisms might be similar to those observed in DM1. However, differences in clinical phenotypes of DM1 and DM2 suggest some specific features in molecular pathways in both diseases. Recent publications suggest that number of pathways affected by RNA CUG and CCUG repeats could be larger than initially thought. Detailed studies of these pathways will help in developing therapy for patients affected with DM1 and DM2.

• Asian Pacific Journal of Cancer Prevention
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• 제16권2호
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• pp.457-463
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• 2015

The pathogenesis of mantle cell lymphoma, a special subtype of lymphoma that is invasive and indolent and has a median survival of 3 to 4 years, is still partially unexplained. Much research about genes and miRNAs has been conducted in recent years, but interactions and regulatory relations of genetic elements which may play a vital role in genesis of MCL have attracted only limited attention. The present study concentrated on regulatory relations about genes and miRNAs contributing to MCL pathogenesis. Numerous experimentally validated raw data were organized into three topology networks, comprising differentially expressed, associated and global examples. Comparison of similarities and dissimilarities of the three regulating networks, paired with the analysis of the interactions between pairs of elements in every network, revealed that the differentially expressed network illuminated the carcinogenicity mechanism of MCL and the related network further described the regulatory relations involved, including prevention, diagnosis, development and therapy. Three kinds of regulatory relations for host genes including miRNAs, miRNAs targeting genes and genes regulating miRNAs were concluded macroscopically. Regulation of the differentially expressed miRNAs was also analyzed, in terms of abnormal gene expression affecting the MCL pathogenesis. Special regulatory relations were uncovered. For example, auto-regulatory loops were found in the three topology networks, key pathways of the nodes being highlighted. The present study focused on a novel point of view revealing important influencing factors for MCL pathogenesis.

• Asian Pacific Journal of Cancer Prevention
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• 제16권7호
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• pp.2793-2800
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• 2015

In molecular-targeted cancer therapy, acquired resistance to gemcitabine is a major clinical problem that reduces its effectiveness, resulting in recurrence and metastasis of cancers. In spite of great efforts to reveal the overall mechanism of acquired gemcitabine resistance, no definitive genetic factors have been identified that are absolutely responsible for the resistance process. Therefore, we performed a cross-platform meta-analysis of three publically available microarray datasets for cancer cell lines with acquired gemcitabine resistance, using the R-based RankProd algorithm, and were able to identify a total of 158 differentially expressed genes (DEGs; 76 up- and 82 down-regulated) that are potentially involved in acquired resistance to gemcitabine. Indeed, the top 20 up- and down-regulated DEGs are largely associated with a common process of carcinogenesis in many cells. For the top 50 up- and down-regulated DEGs, we conducted integrated analyses of a gene regulatory network, a gene co-expression network, and a protein-protein interaction network. The identified DEGs were functionally enriched via Gene Ontology hierarchy and Kyoto Encyclopedia of Genes and Genomes pathway analyses. By systemic combinational analysis of the three molecular networks, we could condense the total number of DEGs to final seven genes. Notably, GJA1, LEF1, and CCND2 were contained within the lists of the top 20 up- or down-regulated DEGs. Our study represents a comprehensive overview of the gene expression patterns associated with acquired gemcitabine resistance and theoretical support for further clinical therapeutic studies.

• Molecules and Cells
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• 제37권7호
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• pp.540-546
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• 2014

Several types of genetic and epigenetic regulation have been implicated in the development of drug resistance, one significant challenge for cancer therapy. Although changes in the expression of non-coding RNA are also responsible for drug resistance, the specific identities and roles of them remain to be elucidated. Long non-coding RNAs (lncRNAs) are a type of ncRNA (> 200 nt) that influence the regulation of gene expression in various ways. In this study, we aimed to identify differentially expressed lncRNAs in 5-fluorouracil-resistant colon cancer cells. Using two pairs of 5-FU-resistant cells derived from the human colon cancer cell lines SNU-C4 and SNU-C5, we analyzed the expression of 90 lncRNAs by qPCR-based profiling and found that 19 and 23 lncRNAs were differentially expressed in SNU-C4R and SNU-C5R cells, respectively. We confirmed that snaR and BACE1AS were down-regulated in resistant cells. To further investigate the effects of snaR on cell growth, cell viability and cell cycle were analyzed after transfection of siRNAs targeting snaR. Down-regulation of snaR decreased cell death after 5-FU treatment, which indicates that snaR loss decreases in vitro sensitivity to 5-FU. Our results provide an important insight into the involvement of lncRNAs in 5-FU resistance in colon cancer cells.

• BMB Reports
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• 제36권2호
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• pp.237-242
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• 2003

Hepatic lipase is a key enzyme that is involved in HDL-C metabolism. The goal of this study was to find out the frequency of the hepatic lipase C514T polymorphism, and evaluate its relationship with plasma HDL-C levels and coronary artery disease (CAD) in Koreans. Two hundred and twenty four subjects with no previous history of lipid-lowering therapy, 118 patients with significant CAD, and 106 controls were examined with respect to their genotypes, lipid profiles, and other risk factors for CAD. The frequency of the -514T allele was 0.37 in men and 0.35 in women, which were higher than the frequency that was reported in Caucasians, but lower than the frequency that was reported in African-Americans. The -514T allele was associated with significantly higher HDL-C levels in women. After controlling for age, gender, BMI, DM, and smoking, the non-CC genotype was significantly associated with HDL-C levels, and explained 6% of the HDL-C variation in this study. When the genotypes-distribution was compared between the CAD and non-CAD patients, the hepatic lipase C-514T polymorphism was not associated with the presence of CAD. Koreans have a higher frequency of the hepatic lipase gene 514T allele than Caucasians, and the -514T allele is associated with higher plasma HDL-C levels in Korean women, and perhaps non-smoking men. However, our data does not suggest an association between the polymorphism and an increased risk of CAD.

• BMB Reports
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• 제39권5호
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• pp.492-501
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• 2006

Since differentiation therapy is one of the promising strategies for treatment of leukemia, universal efforts have been focused on finding new differentiating agents. In that respect, we used guanosine 5'-triphosphate (GTP) to study its effects on K562 cell line. GTP, at concentrations between 25-200 ${\mu}M$, inhibited proliferation (3-90%) and induced 5-78% increase in benzidine-positive cells after 6-days of treatments of K562 cells. Flow cytometric analyses of glycophorine A (GPA) showed that GTP can induce expression of this marker in more mature erythroid cells in a time- and dose-dependent manner. These effects of GTP were also accompanied with inhibition of DNA synthesis (measured by [$^3H$]-thymidine incorporation) and early S-phase cell cycle arrest by 96 h of exposure. In contrast, no detectable effects were observed when GTP administered to unstimulated human peripheral blood lymphocytes (PBL). However, GTP induced an increase in proliferation, DNA synthesis and viability of mitogen-stimulated PBL cells. In addition, growth inhibition and differentiating effects of GTP were also induced by its corresponding nucleotides GDP, GMP and guanosine (Guo). In heat-inactivated medium, where rapid degradation of GTP via extracellular nucleotidases is slow, the anti-proliferative and differentiating effects of all type of guanine nucleotides (except Guo) were significantly decreased. Moreover, adenosine, as an inhibitor of Guo transporter system, markedly reduced the GTP effects in K562 cells, suggesting that the extracellulr degradation of GTP or its final conversion to Guo may account for the mechanism of GTP effects. This view is further supported by the fact that GTP and Guo are both capable of impeding the effects of mycophenolic acid. In conclusion, our data will hopefully have important impact on pharmaceutical evaluation of guanine nucleotides for leukemia treatments.