• Journal of Chest Surgery
• /
• v.37 no.7
• /
• pp.578-584
• /
• 2004

Sinus of Valsalva aneurysm is a rare cardiac anomaly and a long-term survival after surgical treatment has not been well established. This study was designed to evaluate the long-term surgical results after the repair of sinus Valsalva aneurysm. Material and Method: From April 1991 to November 2003, 35 patients (23 male, 12 female, mean age 35.2 years, range 11∼64) underwent operation for sinus of Valsalva aneurysm. Twenty six patients (74.3%) were in the New York Heart Association (NYHA) class III∼IV before surgery. In preoperative echocardiogram, mean EF was 63.32 $\pm$ 11.43% and nine patients (25.7%) were in AR grade III∼IV. Direct closure, patch closure of ruptured sinus Valsalva were performed in fourteen patients (46.7%), sixteen patients (53.3%) respectively. Aortic valve replacement, valvuloplasty were performed in five patients (14.3%), three patients (8.6%) respectively. Three patients (8.6%) underwent the Bentall procedure. Concomitant procedures were performed in 15 patients (42.9%), which were closure of VSD and ASD. Mean CPB time and ACC time were 116.79 $\pm$ 38.79 and 81.2 $\pm$ 28.97 minutes. Result: There was no operative mortality. One patient (2.9%) developed complete heart block that required a permanent pacemaker implantation. Three patients (8.6%) required reoperation due to a recurred rupture of the sinus Valsalva aneurysm and developed aortic insufficiency. Mean follow-up time was 58.55 $\pm$ 38.38 months. There was one late death. Actuarial 5 year freedom rate from reoperation was 87.1 $\pm$ 7%. Conclusion: Surgical treatment for sinus of Valsalva aneurysm is safe and has satisfactory long-term results.

• Journal of Chest Surgery
• /
• v.33 no.1
• /
• pp.32-37
• /
• 2000

Background: Reconstruction surgery of mitral valve regurgitation is now considered as an effective operative technique and has shown good long-term results. Although reconstructive surgery of mitral valve has been performed since 1970s, we have started only in early 1990s in full scale because of small number of the mitral regurgitation compared to mitral stenosis and lack of knowledge from the viewpoint of patients and physicians. Material and Method: From January 1992 to December 1996, 100 patients underwent repair of the mitral valve for mitral regurgitation with or without mitral stenosis in Seoul National University Hospital. 45(45%) of the patients were men and 55(55%) were women. The mean age was 39.9$\pm$14.4 years. The causes of the mitral regurgitation were rheumatic in 61, degenerative in 28 and others in 11. According to the Carpentier's pathological classification of mitral regurgitation 5 patients were type I. 55 patients were type II and 40 patients were type III. 7 patients underwent concomitant aortic valvuloplasty and 8 patients underwent aortic valve replacement. 7 patients underwent Maze operation or pulmonary vein isolation. Result: There were no operative death but 3 major operative complications: 2patients were postoperative low cardiac output syndrome(needed intra-aortic ballon pump support) and 1 patient was postoperative bleeding. There was one late death(1.0%) The cause of death was sepsis secondary to acute bacterial endocarditis. 3 patients required reoperation for recurred mitral regurgitation. There were no statistically significant risk factors for reoperation. The other 96 patients showed no or mild degree of mitral regurgitation 99 survivors were in NYHA functional class I or II. There were two throumboembolisms but no anticoagulation-related complications. Conclusion: We concluded that mitral valve repair could be performed successfully in most cases of mitral regurgitation even in the rheumatic and combined lesions with very low operative mortality and morbidity. The early results are very promising.

• Journal of the Korean Society of Food Science and Nutrition
• /
• v.33 no.1
• /
• pp.1-6
• /
• 2004

$\beta$-Sitosterol is the major phytosterol in higher plants, including fruits and vegetables. The molecule has been shown to have the potential for prevention and therapy for human cancer. We investigated the effects of $\beta$-sitosterol on the cell proliferation of HCT116 human colon cancer cells in order to understand its anti-proliferative mechanism. $\beta$-Sitosterol treatment resulted in the inhibition of cell proliferation in a concentration-dependent manner. The anti-proliferative effect of HCT116 cells by $\beta$-sitosterol was associated with formation of apoptotic bodies and degradation of $\beta$-catenin protein. In addition, $\beta$-sitosterol-treatment induced a marked accumulation of tumor suppressor p53 and a concomitant induction of cyclin-dependent kinase (Cdk) inhibitor p21 without alteration in the levels of cyclins and Cdks. Taken together, these findings provide important new insights into the possible molecular mechanisms of the anti-cancer activity of $\beta$-sitosterol.

• IMMUNE NETWORK
• /
• v.12 no.2
• /
• pp.58-65
• /
• 2012

Background: A cell line with transfected Wilms' tumor protein 1 (WT1) is has been used for the preclinical evaluation of novel treatment strategies of WT1 immunotherapy for leukemia due to the lack of appropriate murine leukemia cell line with endogenous WT1. However, silencing of the transgene occurs. Regarding the effects of hypomethylating agents (HMAs) on reactivation of silenced genes, HMAs are considered to be immune enhancers. Methods: We treated murine WT1- transfected C1498 (mWT1-C1498) with increasing doses of decitabine (DAC) and azacitidine (AZA) to analyze their effects on transgene reactivation. Results: DAC and AZA decreased the number of viable cells in a dose- or time-dependent manner. Quantification of WT1 mRNA level was analyzed by real-time polymerase chain reaction after mWT1-C1498 treated with increasing dose of HMA. DAC treatment for 48 h induced 1.4-, 14.6-, and 15.5-fold increment of WT1 mRNA level, compared to untreated sample, at 0.1, 1, and $10{\mu}M$, respectively. Further increment of WT1 expression in the presence of 1 and $10{\mu}M$ DAC was evident at 72 h. AZA treatment also induced up-regulation of mRNA, but not to the same degree as with DAC treatment. The correlation between the incremental increases in WT1 mRNA by DAC was confirmed by Western blot and concomitant down-regulation of WT1 promoter methylation was revealed. Conclusion: The in vitro data show that HMA can induce reactivation of WT1 transgene and that DAC is more effective, at least in mWT1-C1498 cells, which suggests that the combination of DAC and mWT1-C1498 can be used for the development of the experimental model of HMA-combined WT1 immunotherapy targeting leukemia.

• KSBB Journal
• /
• v.27 no.2
• /
• pp.75-85
• /
• 2012

Although, microbial arsenic mobilization by dissimilatory arsenate-reducing bacteria (DARB) and the practical use to the removal technology of arsenic from contaminated soil are expected, most previous research mainly has been focused on the geochemical circulation of arsenic. Therefore, in this review we summarized the previously reported DARB to grasp the characteristic for bioremediation of arsenic. Evidence of microbial growth on arsenate is presented based on isolate analyses, after which a summary of the physiology of the following arsenate-respiring bacteria is provided: Chrysiogenes arsenatis strain BAL-$1^T$, Sulfurospirillum barnesii, Desulfotomaculum strain Ben-RB, Desulfotomaculum auripigmentum strains OREX-4, GFAJ-1, Bacillus sp., Desulfitobacterium hafniense DCB-$2^T$, strain SES-3, Citrobacter sp. (TSA-1 and NC-1), Sulfurospirillum arsenophilum sp. nov., Shewanella sp., Chrysiogenes arsenatis BAL-$1^T$, Deferribacter desulfuricans. Among the DARB, Citrobacter sp. NC-1 is superior to other dissimilatory arsenate-reducing bacteria with respect to arsenate reduction, particularly at high concentrations as high as 60 mM. A gram-negative anaerobic bacterium, Citrobacter sp. NC-1, which was isolated from arsenic contaminated soil, can grow on glucose as an electron donor and arsenate as an electron acceptor. Strain NC-1 rapidly reduced arsenate at 5 mM to arsenite with concomitant cell growth, indicating that arsenate can act as the terminal electron acceptor for anaerobic respiration (dissimilatory arsenate reduction). To characterize the reductase systems in strain NC-1, arsenate and nitrate reduction activities were investigated with washed-cell suspensions and crude cell extracts from cells grown on arsenate or nitrate. These reductase activities were induced individually by the two electron acceptors. Tungstate, which is a typical inhibitory antagonist of molybdenum containing dissimilatory reductases, strongly inhibited the reduction of arsenate and nitrate in anaerobic growth cultures. These results suggest that strain NC-1 catalyzes the reduction of arsenate and nitrate by distinct terminal reductases containing a molybdenum cofactor. This may be advantageous during bioremediation processes where both contaminants are present. Moreover, a brief explanation of arsenic extraction from a model soil artificially contaminated with As (V) using a novel DARB (Citrobacter sp. NC-1) is given in this article. We conclude with a discussion of the importance of microbial arsenate reduction in the environment. The successful application and use of DARB should facilitate the effective bioremediation of arsenic contaminated sites.

• Journal of the korean academy of Pediatric Dentistry
• /
• v.38 no.3
• /
• pp.296-302
• /
• 2011

Idiopathic gingival fibromatosisrarely occurs, but frequently recurred after surgical removal. It usually occurs in generalized symmetrical pattern but sometimes in localized unilateral pattern. The localized pattern usually affects the maxillary molar and tuberosity area. This disease usually causes tooth migration, malocclusion, and problems in eating, speech, and esthetics. A boy showed dense gingival fibromatosis localized at primary maxillary right lateral incisor area at the age of 5 years, and his maxillary right lateral incisor become severely displaced at the age of 9 years. He had no medical and hereditary factors relevant to the gingival fibromatosis. However, the dense fibrous tissue was dominant in his labial gingiva of maxillary right incisors. In order to realign the displaced incisors by orthodontic treatment, the dense fibrous tissue covered the defect space between the central incisor and the displaced lateral incisor was surgically removed. The removed specimen was examined by simple immunohistochemical(IHC) array method. IHC array showed increased expression of CTGF, HSP-70, MMP-1, PCNA, CMG2, and TNF-${\alpha}$ in keratinocytes, fibroblasts, endothelial cells, and macrophages of gingival fibromatosis tissue. Therefore, it was suggested that the gingival fibromatosis be caused by the concomitant overexpression of CTGF, HSP-70, MMP-1, PCNA, CMG2, and TNF-${\alpha}$, and resulted in the fibroepithelial proliferation and the inflammatory reaction of gingival tissue.

• Molecules and Cells
• /
• v.40 no.9
• /
• pp.667-676
• /
• 2017

Abnormal differentiation of muscle is closely associated with aging (sarcopenia) and diseases such as cancer and type II diabetes. Thus, understanding the mechanisms that regulate muscle differentiation will be useful in the treatment and prevention of these conditions. Protein lysine acetylation and methylation are major post-translational modification mechanisms that regulate key cellular processes. In this study, to elucidate the relationship between myogenic differentiation and protein lysine acetylation/methylation, we performed a PCR array of enzymes related to protein lysine acetylation/methylation during C2C12 myoblast differentiation. Our results indicated that the expression pattern of HDAC11 was substantially increased during myoblast differentiation. Furthermore, ectopic expression of HDAC11 completely inhibited myoblast differentiation, concomitant with reduced expression of key myogenic transcription factors. However, the catalytically inactive mutant of HDAC11 (H142/143A) did not impede myoblast differentiation. In addition, wild-type HDAC11, but not the inactive HDAC11 mutant, suppressed MyoD-induced promoter activities of MEF2C and MYOG (Myogenin), and reduced histone acetylation near the E-boxes, the MyoD binding site, of the MEF2C and MYOG promoters. Collectively, our results indicate that HDAC11 would suppress myoblast differentiation via regulation of MyoD-dependent transcription. These findings suggest that HDAC11 is a novel critical target for controlling myoblast differentiation.

• Communications of Mathematical Education
• /
• v.32 no.3
• /
• pp.341-362
• /
• 2018

The purpose of this study is to develop a STEAM education model on the basis of mathematics curriculum using real life context, and to analyze the effect of the class based on developed model to make applicable pedagogical discussion. For this purpose, STEAM class materials that can be used in terms of recognition, connection, extension, and application of mathematical concepts, principles and laws are considered, taking into consideration the ways in which real life contexts and mathematical learning could be harmonized. As a results of using these materials, it was empirically confirmed that students' cognitive thinking and affective aspects abilities were improved. The STEAM instruction centered on the mathematics curriculum and the mathematics class based on the data developed in this study have a unique identity compared to the conventional general mathematics teaching methods using the textbooks. And it is pursuing the future class model which could present desirable creativity and personality education. The result of this study would provide preliminary data and meaningful implications to the researchers for next curriculum and concomitant instructional materials as well as the mathematics teachers.

• Molecules and Cells
• /
• v.37 no.12
• /
• pp.899-906
• /
• 2014

Prostaglandin $E_2$ ($PGE_2$) promotes tumor-persistent inflammation, frequently resulting in cancer. Curcumin is a diphenolic turmeric that inhibits carcinogenesis and induces apoptosis. $PGE_2$ inhibits curcumin-induced apoptosis; however, the underlying inhibitory mechanisms in colon cancer cells remain unknown. The aim of the present study is to investigate the survival role of $PGE_2$ and whether addition of exogenous $PGE_2$ affects curcumininduced cell death. HCT-15 cells were treated with curcumin and $PGE_2$, and protein expression levels were investigated via Western blot. Reactive oxygen species (ROS) generation, lipid peroxidation, and intracellular glutathione (GSH) levels were confirmed using specific dyes. The nuclear factor-kappa B ($NF-{\kappa}B$) DNA-binding was measured by electrophoretic mobility shift assay (EMSA). $PGE_2$ inhibited curcumin-induced apoptosis by suppressing oxidative stress and degradation of PARP and lamin B. However, exposure of cells to the EP2 receptor antagonist, AH6809, and the PKA inhibitor, H89, before treatment with $PGE_2$ or curcumin abolished the protective effect of $PGE_2$ and enhanced curcumin-induced cell death. $PGE_2$ activates PKA, which is required for cAMP-mediated transcriptional activation of CREB. $PGE_2$ also activated the Ras/Raf/Erk pathway, and pretreatment with PD98059 abolished the protective effect of $PGE_2$. Furthermore, curcumin treatment greatly reduced phosphorylation of CREB, followed by a concomitant reduction of $NF-{\kappa}B$ (p50 and p65) subunit activation. $PGE_2$ markedly activated nuclear translocation of $NF-{\kappa}B$. EMSA confirmed the DNA-binding activities of $NF-{\kappa}B$ subunits. These results suggest that inhibition of curcumin-induced apoptosis by $PGE_2$ through activation of PKA, Ras, and $NF-{\kappa}B$ signaling pathways may provide a molecular basis for the reversal of curcumin-induced colon carcinoma cell death.

• Journal of Life Science
• /
• v.19 no.10
• /
• pp.1484-1488
• /
• 2009

Familial hypokalemic periodic paralysis (HOKPP) is an autosomal dominant muscle disorder characterized by episodic attacks of muscle weakness with concomitant hypokalemia. Mutations in either a calcium channel gene (CACNA1S) or a sodium channel gene (SCN4A) have been shown to be responsible for this disease. The combination of sarcolemmal depolarization and hypokalemia has been attributed to abnormalities of the potassium conductance governing the resting membrane potential. To understand the pathophysiology of this disorder, we examined both mRNA and protein levels of delayed rectifier potassium channel genes, KCNQ3 and KCNQ5, in skeletal muscle fibers biopsied from patients with HOKOur results showed an increase in the cytoplasmic level of KCNQ3 protein in patients' cells exposed to 50 mM external concentration of potassium. However, mRNA levels of both channel genes did not show significant change in the same condition. Our results suggest that long term exposure of skeletal muscle cells in HOKPP patients to high extracellular potassium alters the KCNQ3 localization, which could possibly hinder the normal function of this channel protein. These findings may provide an important clue to understanding the molecular mechanism of familial hypokalemic periodic paralysis.