• Journal of Chest Surgery
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• v.21 no.2
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• pp.254-269
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• 1988

52 cases of ventricular septal defect [VSD] associated with aortic insufficiency [Al] were found among 1271 patients with simple VSD operated during 27-year period [1959, August-1987, June] at Seoul National University Hospital. Their preoperative data, intraoperative findings and postoperative short-term and long-term follow-up data were evaluated to find the proper timing and method of surgical treatment. The result of this survey shows as follows: 1. To obtain the proper surgical indication, cardiac catheterization and angiography, especially root aortography, was essential. 2. Of all 52 patients, the VSD were type I in 40 patients [77%], type II in 8 [15%] and combination of type I and II in 4 [3%]. Patch closure of VSD were performed in 46 patients and direct suture closure of small VSD in 6. Most common pathologic findings of Al were prolapse of right coronary cusp [40 cases, 77%]. Aortic valve reconstruction were performed in 19 patients, aortic valve replacement in 6 and VSD closure alone in 27. 3. There were 3 surgical deaths [mortality 5.8%], and the long-term follow-up shows that VSD closure alone might have been sufficient to arrest progression of Al in younger patients [less than 10-year old], particularly in those with mild insufficiency. Valve reconstructions, when necessary, were more effective when done at an early age [less than 15-year old]. In a conclusion, we could recommend followings: 1. If patient at any age having VSD with Al is diagnosed, prompt operation is recommended. As for the surgical method, VSD closure only may be fit for mild degree of Al when patient is less than 10-year old, but the management of valve itself may be needed for moderate to severe degree of Al, especially when patient is over 10 year old. The management of valve itself may be variable, but valve reconstruction should be considered as a first choice in less than 15-year old patient. If patient is diagnosed less than 5-year old without evidence of Al, close follow-up observation is recommended. But if Al evidences of clinical findings and/or echocardiography during follow-up examination are notified, corrective operation should be accomplished while the Al is mild. If cusp prolapse and/or even type I VSD of significant size is demonstrated on aortogram, without Al, it should be corrected as early as possible before the patient is about 5 years old.

• Journal of Chest Surgery
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• v.30 no.1
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• pp.17-26
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• 1997

Objeitives. The surgical mortality of congenital heart defects has been reduced (or the very young age group. Especially, young age at repair is an important risk factor for mortality after repair of tetralogy of Falloff. Some risk factors were analyzed Methods. Three hundred and sixty six patients underwent surgical Intervention. Ages ranged from 5 days to 64 years, and 80 patients were adults(over 15 years of age). The defects consisted of 313(84.2%) acyanotic and 53(15.8%) cyanotic anomalies. The surgical mortalities were evaluated by univariate and multivariate analysis. Results. The overall surgical mortality was 10.4%. Mos deaths occurred in the infant group younger than 6 months(20/38 deaths) and in cyanotic group(21/38 deaths). Surgical infant mortality younger than 12 months was 24.8%(25/101). Risk factors of mortality in open heart surgery were age(p< 0.0001), body weight(p< 0.0001), pump time(p< 0.0001), aortic cross clamp time(p< 0.0001), use of total circulatory arrest(p<0.0001) and cyanotic disease(p<0.0001) by univariate analysis. But by multivariate analysis, the risk factor of mortality in open heart surgery was disease entity(p=0.002) only. A disease group with the highest risk was a cyanotic group(odds ratio was 15.3 relative to ventricular septal defect) excluding tetralogy of Falloff(odds ratio=0.27). Conclusions. Even though the most important risk factor was disease entity, we should conentrate our efforts on the technically improvable factors affecting surgical mortality indicated by univarlate analysis.

• Journal of Chest Surgery
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• v.45 no.2
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• pp.110-115
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• 2012

Background: Pneumonectomy remains the ultimate curative treatment modality for destroyed lung caused by tuberculosis despite multiple risks involved in the procedure. We retrospectively evaluated patients who underwent pneumonectomy for treatment of sequelae of pulmonary tuberculosis to determine the risk factors of early and long-term outcomes. Materials and Methods: Between January 1980 and December 2008, pneumonectomy or pleuropneumonectomy was performed in 73 consecutive patients with destroyed lung caused by tuberculosis. There were 48 patients with empyema (12 with bronchopleural fistula [BPF]), 11 with aspergilloma and 7 with multidrug resistant tuberculosis. Results: There were 5 operative mortalities (6.8%). One patient had intraoperative uncontrolled arrhythmia, one had a postoperative cardiac arrest, and three had postoperative respiratory failure. A total of 29 patients (39.7%) suffered from postoperative complications. Twelve patients (16.7%) were found to have postpneumonectomy empyema (PPE), 4 patients had wound infections (5.6%), and 7 patients required re-exploration due to postoperative bleeding (9.7%). The prevalence of PPE increased in patients with preoperative empyema (p=0.019). There were five patients with postoperative BPF, four of which occurred in right-side operation. The only risk factor for BPF was the right-side operation (p=0.023). The 5- and 10-year survival rates were 88.9% and 76.2%, respectively. The risk factors for late deaths were old age (${\geq}50$ years, p=0.02) and low predicted postoperative forced expiratory volume in one second (FEV1) (< 1.2 L, p=0.02). Conclusion: Although PPE increases in patients with preoperative empyema and postoperative BPF increases in right-side operation, the mortality rates and long-term survival rates were found to be satisfactory. However, the follow-up care for patients with low predicted postoperative FEV1 should continue for prevention and early detection of pulmonary complication related to impaired pulmonary function.

• Journal of Life Science
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• v.18 no.6
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• pp.884-890
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• 2008

Genistein, an isoflavone in soybean products, is a potential chemopreventive agent against various types of cancer. There are several studies documenting molecular alterations leading to cell cycle arrest at G2/M phase and induction of apoptosis; however, its mechanism of action and its molecular targets on the prostaglandin $E_2$ ($PGE_2$) production and telomere length regulation in human cancer remain unclear. In this study, we investigated the effect of genistein on the levels of cyclooxygenases (COXs) and telomere regulatory components of several human cancer cell lines (T24, human bladder carcinoma cells; U937, human leukemic cells; AGS, human stomach adenocarcinoma cells and SK-MEL-2, human skin melanoma cells). Genistein treatment resulted in the inhibition of cancer cell proliferation in a concentration-dependent manner. It was found that genistein treatment markedly decreased the levels of COX-2 mRNA and protein expression without significant changes in the expression of COX-1, which was correlated with a decrease in $PGE_2$ synthesis. Genistein treatment also partly inhibited the levels of human telomerase reverse transcriptase (hTERT) as well as human telomerase RNA (hTR) and telomerase-associated protein (TEP)-1, and the activity of telomerase. Taken together, these findings provide important new insights into the possible molecular mechanisms of the anti-cancer activity of genistein.

• Journal of Life Science
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• v.21 no.6
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• pp.851-857
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• 2011

Sulforaphane (SFN) is an isothiocyanate, isolated from glucoraphanin in broccoli and other cruciferaous vegetables. Recent studies have revealed that SFN induces anti-proliferation and apoptosis by cell cycle arrest in various cancer cells. In this study, we investigated the effect of SFN induced apoptosis in chondrosarcoma HTB-94 cells. SFN caused suppression of proliferation and apoptosis in a dose-dependent manner as determined by cell phenotype, MTT assay and FACS analysis in HTB-94 cells. Treatment of SFN led to caspase-3 activation and p53 accumulation as determined by Western blot analysis. Also, SFN significantly induced DNA fragmentation and nuclear degradation though activation of caspase-3, as detected by DNA electrophoresis and immunostaining, respectively. Our results indicate that SFN-induced apoptosis was regulated by p53 and caspase-3 dependent pathways. Furthermore, SFN may act as a potent anti-proliferation agent, and as a promising candidate for molecular-targeting chemotherapy against human chondrosarcoma cells.

• Journal of Life Science
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• v.19 no.12
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• pp.1787-1793
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• 2009

To investigate whether caffeic acid phenethyl ester (CAPE) could affect cancer cell viabilities and gene expression, human colorectal HCT116 cells were incubated with CAPE. CAPE decreased cancer cell viabilities and induced apoptosis in a dose-dependent manner. To analyse differently expressed genes by CAPE, we performed oligo DNA microarray analysis. We found that 266 genes were up-regulated more than twofold, whereas 143 genes were down-regulated more than twofold by 24 hr of treatment with $20{\mu}M$ CAPE. Among the up-regulated genes, we selected 3 genes (NSAID activated gene-1 [NAG-1], cyclin-dependent kinase inhibitor 1A [CDKN1A, p21] and growth arrest and DNA-damage-inducible alpha [GADD45A]) and performed reverse-transcription PCR to confirm microarray data. In addition, we found that CAPE increased NAG-1 gene and NAG-1 protein expression in a dose-dependent manner. And, several other phytochemicals (resveratrol, genistein, daidzein and capsaicin) also could induce NAG-1 expression in human colorectal HCT116 cells. However, CAPE was the highest inducer of NAG-1, even in low concentrations. Overall, these results imply that cancer cell death by CAPE is closely related with over-expression of NAG-1.

• Molecules and Cells
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• v.37 no.8
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• pp.605-612
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• 2014

The p73 gene contains an extrinsic P1 promoter and an intrinsic P2 promoter, controlling the transcription of the pro-apoptotic TAp73 isoform and the anti-apoptotic ${\Delta}Np73$ isoform, respectively. The DNA methylation status of both promoters act equally in the epigenetic transcriptional regulation of their relevant isoforms. The aim of this study was to analyze the different effects of these p73 isoforms in 5-aza-2'-deoxycytidine (5-aza-dC)-induced apoptosis in breast cancer cells. We investigated the effects of the DNA demethylation agent, 5-aza-dC, on the T-47D breast cancer cell line, and evaluated the methylation status of the p73 promoters and expression of TAp73 and ${\Delta}Np73$. Furthermore, we assessed the expression of p53 and p73 isoforms in 5-aza-dC-treated T-47D cells and p53 knockout cells. 5-aza-dC induced significant anti-tumor effects in T-47D cells, including inhibition of cell viability, G1 phase arrest and apoptosis. This was associated with p73 promoter demethylation and a concomitant increase in TAp73 mRNA and protein expression. In contrast, the methylation status of promoter P2 was not associated with ${\Delta}Np73$ mRNA or protein levels. Furthermore, demethylation of P2 failed to inhibit the expression of ${\Delta}Np73$ with 5-aza-dC in the p53 knockdown cell model. Our study suggests that demethylation of the P1 and P2 promoters has opposite effects on the expression of p73 isoforms, namely up-regulation of TAp73 and down-regulation of ${\Delta}Np73$. We also demonstrate that p53 likely contributes to 5-aza-dC-induced ${\Delta}Np73$ transcriptional inactivation in breast cancer cells.

• Korean Journal of Food Science and Technology
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• v.36 no.6
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• pp.1001-1007
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• 2004

Chloroform layer from methanol extract of Corni fructus (Cornaceae) showed strong antiproliferation effect on human cancer cell lines by SRB assay. Anticarcinogenic-active compound was isolated and purified by silica gel column and thin layer chromatograpies, and identified as ursolic acid ($3{\beta}$-hydroxyrus-12-ene-28-oic acid, MW:456) by mass and IR spectrophotometries, and $^1H-and\;^{13}C-NMRs$. The compound inhibited proliferation of A549 (human lung cancer cell line) and MCF-7 (human breast cancer cell line) cells in dose-dependant manner when treated for 48 hr. Inhibition rates of both cells were over 40% and 90% compared with control cells at the $30\;{\mu}g/mL\;and\;100\;{\mu}g/mL$, respectively. Morphology of cells treated with the compound for 15 hr at $10\;{\mu}g/mL$ was distorted with shrinked cell mass, and cell number was lower than that of control cells. Cell cycle analysis showed sub-G1 phase arrest in both cell lines following 15 hr exposure to the compound; % of cell phase increased to 11.7 and 11.2% compared to the control of 4.0% and 2.1% in A549 and MCP-7 cells, respectively.

• Biomolecules & Therapeutics
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• v.20 no.6
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• pp.538-543
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• 2012

The Maillard Reaction Products (MRPs) are chemical compounds which have been known to be effective in chemoprevention. Death receptors (DR) play a central role in directing apoptosis in several cancer cells. In our previous study, we demonstrated that (E)-2,4-bis(p-hydroxyphenyl)-2-butenal, a MRP product, inhibited human colon cancer cell growth by inducing apoptosis via nuclear factor-${\kappa}B$ (NF-${\kappa}B$) inactivation and $G_2$/M phase cell cycle arrest. In this study, (E)-2,4-bis(p-hydroxyphenyl)-2-butenal diacetate, a new (E)-2,4-bis(p-hydroxyphenyl)-2-butenal derivative, was synthesized to improve their solubility and stability in water and then evaluated against NCI-H460 and A549 human lung cancer cells. (E)-2,4-bis(p-hydroxyphenyl)-2-butenal diacetate reduced the viability in both cell lines in a time and dose-dependent manner. We also found that (E)-2,4-bis(p-hydroxyphenyl)-2-butenal diacetate increased apoptotic cell death through the upregulation of the expression of death receptor (DR)-3 and DR6 in both lung cancer cell lines. In addition to this, the transfection of DR3 siRNA diminished the growth inhibitory and apoptosis inducing effect of (E)-2,4-bis(p-hydroxyphenyl)-2-butenal diacetate on lung cancer cells, however these effects of (E)-2,4-bis(p-hydroxyphenyl)-2-butenal diacetate was not changed by DR6 siRNA. These results indicated that (E)-2,4-bis(p-hydroxyphenyl)-2-butenal diacetate inhibits human lung cancer cell growth via increasing apoptotic cell death by upregulation of the expression of DR3.

• Journal of Chest Surgery
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• v.13 no.1
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• pp.60-65
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• 1980

We have experienced 2 cases of the hunshot wound sof the chest involving cardiac injuries at department of the thoracic surgery, Capital Armed Forces General Hospital during I year from April I 1979 to Jan. 1980. In one case of two patients , he was a 22 years old man who was transported to this emergency room 4 hour 10 minutes after having gunshot wound of the left chest by helicopter. Physical examination showed small inlet in left 3rd ICS and left parasternal border, large outlet in left 8th ICS and left scapular line, no breath sound on left side and distant heart sound. chest roentgenography demonstrated marked pleural effusion in left side and mediastinum shifted to right. As soon as chest X-ray was taken, the bleeding through penetrating wound became profuse and cardiac arrest ensued. Closed chest cardiac massage was started and vigorous transfusion continued, but no effective cardiac activity could not be obtained. The patient was pronounced dead due to exsanguinating hemorrhage from wuwpected cardiac wounds. In this critically injured patient with evidence of intrathoracic hemorrhage and suspected cardiac penetration, only emergency thoracic exploration and immediate surgical control of bleeding points might offer the maximum possibility of survival. The other case was a 23 years old man who was transferred to the emergency room 4 hours 50 minutes after having kmultiple communicated fractures of sternum and linear fracture of right mandible by a missile. Examination revealed about 30% skin loss of the anterior chest wall, weak pulse of 96 beats/min., distant heart sound and decreased breath sounds bilaterally. finding on the chest X-ray films showed multiple sternal fractures, marked pericardial effusion indicating hemopericardium. So, the patient was moved immediately to the operation room where, after endotracheal tube inserted, a median sternotomy was performced. A hemorrhagic congestion of the right upper lobe and marked bulging pericardium were disclosed. The pericardium was opened anterior to right phrenic nerve and exsanguinating hemorrhage ensued from the 0.5cm lacerated wound in the auricle of right atrium. The rupture site of right atrium was occluded with non-crushing vascular clamps and then was over sewn with interrupted sutures. It was thought to be highly possible that he was alive long enough to have cardiorrhaphy because of cardiac tamponade, which prevented exsanguinating hemorrhage. He was taken closed reduction for linear fracture of right mandible 2 weeks after repair of ruptured right auricle in dental clinic. This patient's post-operative course was not eventful.