• Molecules and Cells
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• v.42 no.3
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• pp.270-283
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• 2019

This study was aimed to explore if lncRNA MALAT1 would modify chemo-resistance of non-small cell lung cancer (NSCLC) cells by regulating miR-197-3p and p120 catenin (p120-ctn). Within this investigation, we totally recruited 326 lung cancer patients, and purchased 4 NSCLC cell lines of A549, H1299, SPC-A-1 and H460. Moreover, cisplatin, adriamycin, gefitinib and paclitaxel were arranged as chemotherapies, and half maximal inhibitory concentration (IC50) values were calculated to evaluate the chemo-resistance of the cells. Furthermore, mice models of NSCLC were also established to assess the impacts of MALAT1, miR-197-3p and p120-ctn on tumor growth. Our results indicated that MALAT1 and miR-197-3p were both over-expressed within NSCLC tissues and cells, when compared with normal tissues and cells (P < 0.05). The A549, H460, SPC-A-1 and SPC-A-1 displayed maximum resistances to cisplatin ($IC50=15.70{\mu}g/ml$), adriamycin ($IC50=5.58{\mu}g/ml$), gefitinib ($96.82{\mu}mol/L$) and paclitaxel (141.97 nmol/L). Over-expression of MALAT1 and miR-197-3p, or under-expression of p120-ctn were associated with promoted viability and growth of the cancer cells (P < 0.05), and they could significantly strengthen the chemo-resistance of cancer cells (P < 0.05). MALAT1 Wt or p120-ctn Wt co-transfected with miR-197-3p mimic was observed with significantly reduced luciferase activity within NSCLC cells (P < 0.05). Finally, the NSCLC mice models were observed with larger tumor size and weight under circumstances of over-expressed MALAT1 and miR-197-3p, or under-expressed p120-ctn (P < 0.05). In conclusion, MALAT1 could alter chemo-resistance of NSCLC cells by targeting miR-197-3p and regulating p120-ctn expression, which might assist in improvement of chemo-therapies for NSCLC.

• Journal of Chest Surgery
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• v.35 no.9
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• pp.664-667
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• 2002

Extracorporeal membrane oxygenation(ECMO) provides stable oxygenation to prevent elevation of pulmonary vascular resistance and bypasses a significant part of cardiac output to the pulmonary vascular bed to reduce pulmonary perfusion pressure. In addition, ECMO prevents right heart failure and low cardiac output by means of ventricular assist and reduction in volume load to right ventricle. As a result, ECMO can be used for the treatment of pulmonary hypertensive crisis after surgery for congenital heart disease, especially when it is refractory to conventional measures. We report a case of postoperative pulmonary hypertensive crisis, developed in a 37-year-old male with patent ductus arteriosus with secondary pulmonary hypertension, which was successfully managed including ECMO.

• Clinical and Experimental Pediatrics
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• v.48 no.2
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• pp.216-220
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• 2005

Pulmonary arteriovenous fistulas(PAVFs) is a rare disorder that occurs in two to three children per 100,000 population. It is presented as absence of intervening capillary beds between the pulmonary artery and vein with resultant persistent right to left shunt. Other causes include trauma, liver cirrhosis, malignancy and schistosomiasis. It is mostly asymptomatic, but it may present with respiratory difficulty, cyanosis, clubbed fingers induced by right to left shunt or hemoptysis, polycythemia and epistaxis. Major complications, such as brain abscess, brain embolism, paradoxical embolism and subacute infective endocarditis can be devastating, so therapeutic intervention is recommended in all patients. However, removal of low-resistance fistulas can aggrevate pulmonary hypertension, so detection of increased pulmonary pressure is important. We report two patients : One a 42 year-old male with PAVFs treated with coil embolization, and a 42 year-old female who was treated with anticoagulants due to pulmonary hypertension.

• Journal of Chest Surgery
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• v.10 no.1
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• pp.28-37
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• 1977

Authors had performed experimental study for ventilatory functions & pulmonary hemodynamics following reimplantation of lung. Preoperative & postoperative hemodynamic studies were obtained. A significant reduction in arterial $PO_2$ and $PCO_2$ was observed with the first few days. But these changes returned to near control levels from 1 week after operation in long-term survivors. Also abnormal pulmonary hemodynamic values returned toward control levels within 1 to 3 weeks, with the exception of a residual increase in pulmonary vascular resistance. Microscopically minimal focal pulmonary edema and limited alveolar infiltration developed in the reimplanted lung. But these changes never increased after the their postoperative day and were completely resolved by 1 to 3 weeks after autotransplantation.

• Journal of Chest Surgery
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• v.18 no.4
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• pp.569-573
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• 1985

A 18-year-old female underwent surgical correction of tricuspid atresia and complete transposition of great arteries combined with atrial 8 ventricular septal defect and pulmonary stenosis. After the transection of main pulmonary artery just above the pulmonic valve, proximal portion of main pulmonary artery was closed with running suture and distal portion of main pulmonary artery anastomosed with right atrial appendage without valve insertion. Atrial septal defect was closed with running suture. Postoperative course was uneventful and she discharged on 18th postoperative day. Her condition is in very good until present. Modified Fontan`s operation without valve placement [in the condition of low pulmonary vascular resistance and good left ventricular function] may has a good result.

• Journal of Chest Surgery
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• v.33 no.3
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• pp.221-229
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• 2000

Background: Thromboxane A2 and endothelin-1 are the potent vasoconstrictors affecting pulmonary pathophysiology in response to whole body inflammatin following CPB. Aprotinin, as an antiiflammatory agent, may decrease the release of such vasoactive substance from pulmonary tissues, preventing pulmonary hypertension after cardiopulmonary bypass. Material and Method: Ten mongrel dogs(Bwt. ac. 20kg) were subjected to cardioupulmonary bypass for 2 hours and postbypass pulmonary vascular resistance(0, 1, 2, 3 hours) were compared with prebypass level. The dogs were divided into 2 groups; control group(n-5) and aprotinin group(n=5). In the aprotinin group, aprotinin was administered as follows; 50,000 KIU/kg mixed in pump priming solution, 50,000 KIU/kg prebypass intravenous infusion over 30 minutes, 10,000 KIU/kg/hour postbypass continuous infusion. Prebypass and postbypass 0, 1, 2, 3 hour pulmonary vascular resistance were measured. At prebypass and postbypass 0, 90, 180 minutes, blood samples were obtained from pulmonary arterial and left atrial catherers for the assay of plasma thromboxane B2 a stable metabolite of thromboxane A2, and endothelin-1 concentrations. Result: The ratios of pustbypass over prebypass pulmonary vascular at postbypass 0, 1, 2, 3 hours were 1.28$\pm$0.20, 1.82$\pm$0.23, 1.90$\pm$0.19, 2.14$\pm$0.18 in control group, 1.58$\pm$0.18, 1.73$\pm$0.01, 1.66$\pm$0.10, 1.50$\pm$0.08 in aprotinin group ; the ratios gradually increased in control group while decreased or fluctuated after postbypass 1 hour in aprotinin group. There was statistically significant difference between control group and aprotinin group at postbypass 3 hours(P=0.014). Pulmonary arterial plasma concentration of thromboxane B2(pg/ml) at prebypass, postbypass 0, 90, 180 minutes were 346.4$\pm$61.9, 529.3$\pm$197.6, 578.3$\pm$255.8, 493.3$\pm$171.3 in control group, 323.8$\pm$118.0, 422.6$\pm$75.6, 412.3$\pm$59.9, 394.5$\pm$154.0 in aprotinin group. Left atrial concentrations were 339.3$\pm$89.2, 667.0$\pm$65.7, 731.2$\pm$192.7, 607.5$\pm$165.9 in control group, 330.0$\pm$111.2, 468.4$\pm$190.3, 425.4$\pm$193.6, 4.7.3$\pm$142.8 in aprotinin group. These results showed decrement of pulmonary thromboxane A2 generation in aprotinin group. Pulmonary arterial concentrations of endothelin-1(fmol/ml) at the same time sequence were 7.84$\pm$0.31, 13.2$\pm$0.51, 15.0$\pm$1.22, 16.3$\pm$1.73 in control group, 7.76$\pm$0.12, 15.3$\pm$0.71, 22.6$\pm$6.62, 14.9$\pm$1.11 in aprotinin group. Left atrial concentrations were 7.61$\pm$17.2, 57.1$\pm$28.4, 18.9$\pm$18.2, 31.5$\pm$20.5 in control group, 5.61$\pm$7.61, 37.0$\pm$26.2, 28.6$\pm$21.7, 37.8$\pm$30.6 in aprotinin group. These results showed that aprotinin had no effect on plasma endothelin-1 concentration after cardiopulmonary bypass. Conclusion: Administration of aprotinin during cardiopulmonary bypass could attenuate the increase in pulmonary vascular resistance after bypass. Inhibition of pulmonary thromboxane A2 generation was thought to be one of the mechanism of this effect. Aprotinin had no effect on postbypass endothelin-1 concentration.

• Tuberculosis and Respiratory Diseases
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• v.56 no.3
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• pp.248-260
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• 2004

Background : As an effective regimen for isoniazid (INH)-resistant pulmonary tuberculosis, several treatment regimens have been recommended by many experts. In Korea, a standard regimen has not been established for INH-resistant tuberculosis, and the treatment by individual physicians has been performed on an empirical bases. The purpose of the present study was to retrospectively describe the treatment characteristics and evaluate the treatment outcomes of patients with INH-resistant tuberculosis. Materials and Methods : Sixty of 69 patients reported to have INH-resistant tuberculosis from 1994 to 2001 were retrospectively analyzed. Exclusion criteria included: death from other causes, with the exceptions of tuberculosis and incomplete treatment, including a patient's transfer-out. Results : A previous tuberculosis history was found in 28 (46.7%) patients. The sputum smear for acid-fast bacilli was positive in 44 (73.3%) patients, and 30 (50.0%) had cavitary disease. Streptomycin resistance coexisted in 25.0% of isolates. INH was to be prescribed continuously, even after INH resistance was reported, in 86.0% of patients. The treatment regimens were diverse between the patients according to drug regimen composition and treatment duration. The most frequent prescribed regimen included rifampin, ethambutol and pyrazinamide, with and without INH, for the full 12-month term of treatment. Treatment failure occurred in 13 (21.7%) patients. Cavitary disease (p=0.005) and a treatment regimen with second-line drugs, excluding rifampin (p=0.015), were associated with treatment failure. One patient experienced a relapse. Conclusions : Standardized treatment guidelines will be needed in Korea to improve the treatment efficacy for INH-resistant tuberculosis.

• Tuberculosis and Respiratory Diseases
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• v.40 no.2
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• pp.135-146
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• 1993

Background: In acute pulmonary embolism it has been postulated that the constriction of bronchi and pulmonary artery secondary to neurohumoral response plays an important role in cardiopulmonary dysfunction in addition to the mechanical obstruction of pulmonary artery. Serotonin is considered as the most important mediator. Positive end expiratory pressure (PEEP) stimulates $PGI_2$ secretion from the vascular endothelium, but its role in acute pulmonary embolism is still in controversy. Methods: To study the cardiopulmonary effect and therapeutic role of Ketanserin, selective antagonist of 5-HT2 receptor, and PEEP in acute pulmonary embolism experimental acute pulmonary embolism was induced in dogs with autologous blood clot. The experimental animals were divided into 3 groups, that is control group, Ketanserin injection group and PEEP application group. Results: Thirty minutes after embolization, mean pulmonary arterial pressure and pulmonary vascular resistance increased and cardiac output decreased. $PaO_2,\;P\bar{v}O_2$ and oxygen transport decreased and physiological shunt and $PaCO_2$ increased. After injection of Ketanserin, comparing with control group, mean pulmonary arterial pressure, pulmonary vascular resistance and physiological shunt decreased, while cardiac output, $PaO_2$ and oxygen transport increased. All these changes sustained till 4 hours after embolization. After PEEP application pulmonary vascular resistance, $PaO_2$ and $PaCO_2$ increased, while physiological shunt, cardiac output and oxygen transport decreased. After discontinuation of PEEP, mean pulmonary arterial pressure and pulmonary vascular resistance decreased and were lower than control group, while $PaO_2$ and cardiac output increased and higher than control group. $PaCO_2$ decreased but showed no significant difference comparing with control group. Conclusion: It can be concluded that Ketanserin is effective for the treatment of acute pulmonary embolism. With PEEP hemodynamic status deteriorated, but improved better than control group after discontinuation of PEEP. Thus PEEP may be applied carefully for short period in acute pulmonary embolism if the hemodynamic status is tolerable.

• Journal of Chest Surgery
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• v.23 no.2
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• pp.213-221
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• 1990

We have experienced 62 cases of modified Fontan operations in Seoul Nat’l University Hospital from Apr. 1986 to Jul. 1989, They were 38 males and 24 females, and their age was ranged from 16 months to 15.5 years of age. [mean age : 5.73$\pm$2.99 years] There were 16 operative deaths and 2 late deaths, therefore 29% of overall mortality. Their diagnoses were as follows; 28 single ventricle, 11 tricuspid atresia, 6 DORV with LV hypoplasia, 3 pulmonary atresia with hypoplastic RV, 3 TGA with hypoplastic RV, 3 cor\ulcornerGA with hypoplastic LV and PA, 6 AV canal defects with PA, and 2 others. Low cardiac output and pleural effusion were developed frequently, so we divide 40 patients into some groups to analyze the physiologic and anatomic causes of them. By the degree of the LCO, group A was no LCO[mean amount of inotropics used: 0-5 \ulcornerg/kg/min] with 17 cases, B mild LCO [5-10] with 11, C moderate to severe LCO but alive[>10] with 8, D severe LCO to death with 4 cases. For the pleural effusion, group 1 was to be removed the chest tube within 1 week with 8 cases, group II within 3 weeks with 21 cases, group III beyond 3 weeks with 12 cases. We considered their age, diagnosis, pulmonary artery size[PA index], pulmonary artery abnormality, palliative shunt, systemic ventricular type, pulmonary artery wedge pressure, as preoperative factors, and operative methods, and as postoperative factors, CVP, LAP, arrhythmia, thrombosis, atrioventricular valvular insufficiency, etc. In the view of LCO, pulmonary artery size and PCWP were statistically significant [P<0.05], and arrhythmia, A-V valve insufficiency were inclined to the group C and D Pleural effusion was influenced by the pulmonary artery size, pulmonary artery resistance, PCWP, and CVP significantly. [P<0.05] And arrhythmia, residual shunt, and A-V valvular insufficiency were inclined to group II and III, too. As a results, the followings are to be reminded as the important factors at the care of post-Fontan LCO, and persistent pleural effusion [1] pulmonary artery size, [2] pulmonary artery resistance, [3] PCWP, [4] CVP, [5] arrhythmia, [6] residual shunt, [7]A-V valvular insufficiency.

• Journal of Chest Surgery
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• v.20 no.4
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• pp.695-705
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• 1987

This report provides follow - up data on 37 patients, aged 7 days to 25 years [median: 6.5 months], who underwent repair of total anomalous pulmonary venous connection at Seoul national University Hospital between May, 1978 and June, 1987. The patients were 22 males and 17 females and the sex ratio was 1.6 to 1, showing a male predominance. Sixteen patients had supracardiac, 13 cardiac, 3 infracardiac and 5 had a mixed type. The duration of follow up was from 1 month to 60 months [median: 14 months] There were eight early and one late deaths, and the overall mortality was 24%. The deaths during 1 year of life were eight [89%] and only one death [11%] occurred above 1 year of age. The mortality of cardiac type was unusually high, accounting for 56 percent of the total death, which was probably due to the preoperative poor clinical condition such as pulmonary edema and congestive heart failure. The major cause of death was the perioperative myocardial failure, and the survival was closely related to the preoperative clinical status, age and moderately elevated pulmonary arterial pressure, the sign of the elevated pulmonary vascular resistance and pulmonary venous obstruction. Early diagnosis and early application of surgical intervention is essential to the improved postoperative survival