• Journal of Chest Surgery
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• v.33 no.12
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• pp.941-947
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• 2000

Background: Central nervous system complication after coronary artery bypass grafting(CABG) is one of the major prognostic determinants and the use of the cardiopulmonary bypass(CPB) may increase the incidence of this devastating complication. In this study, the outcomes after off-pump CABG were studied and compared with those following the conventional CABG using CPB. Material and Method: Among the consecutive isolated CABG's performed in SNUH during Feb. 1995 and Jun. 1999, 338 coronary artery bypass grafting were divided into two groups. 223 patients underwent CABG using the CPB(Group I), and 115 patients underwent CABG without CPB(OPCAB)(Group II). All patients enrolled in this study received extensive preoperative examinations including thorough neurologic examination before and after surgery, transcranial doppler study, carotid duplex ultrasonography, and magnetic resonance angiography if necessary. Central nervous system(CNS) complications were defined as stroke, seizure, metabolic or hypoxic encephalopathy and transient delirium after surgery. Result: There were 61 cases(27.3%) who developed postoperative CNS complication in Group I, whereas 8 cases(7.0%) of CNS complications developed postoperatively in group II(p<0.05). Statistically significant predictors of postoperative CNS complications in group I were age and the use of cardiac assist devices perioperatively. Conclusion: This study suggested that omitting the use of CPB in CABG resulted in significant decrease of the postoperative CNS complications. OPCAB should be more widely applied especially to the elderly who have preexisting cerebrovascular disease.

• Neonatal Medicine
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• v.15 no.1
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• pp.32-37
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• 2008

Purpose : Perinatal asphyxia is an important cause of neonatal mortality and subsequent lifelong neurodevelopmental handicaps. Although many treatment strategies have been tested, there is currently no clinically effective treatment to prevent or reduce the harmful effects of hypoxia and ischemia in humans. In the clinical setting, maternal hyperthermia induces adverse effects on the neonatal brain, but recent studies have shown that hyperthermic pretreatment (PT) plays some role in hypoxic-ischemic (HI) injuries of the developing brain. The present study investigated the effect of hyperthermic PT on HI brain injuries in newborn rats. Methods : HI was produced in 7-day-old neonatal rats by unilateral common carotid artery ligation, followed by hypoxia with 8% oxygen at $38^{\circ}C$ for 2 hours. Twenty-four hours before HI, one-half of the pups were exposed to a $40^{\circ}C$ environment for 2 hours. The severity of the brain injury was assessed 7 days after the HI. Results : Hyperthermic PT reduced the gross and histopathologic findings of brain injury from 64.7 to 31.2% (P<0.05). There were no differences in location and severity of injury between the pretreated and control brains. Conclusion : These findings indicate that hyperthermic PT provides neuroprotective benefits on HI in the developing brain. Also, these findings suggest maternal hyperthermia may have protective effect on perinatal HI brain injuries.

• Clinical and Experimental Reproductive Medicine
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• v.36 no.3
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• pp.163-174
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• 2009

Objectives: Members of the immortalization-upregulated protein (IMUP) family are nuclear proteins implicated in SV40-mediated immortalization and cellular proliferation, but the mechanisms by which their expression is regulated are still unknown in placenta. To investigate to expression and functions of IMUPs in placenta, we conducted to compare IMUPs expression in normal and preeclamptic placenta tissues and analyzed the function of IMUP-2 in HTR-8/SVneo trophoblast cells after IMUP-2 gene transfection. Methods: The expression of IMUPs was analyzed in placental tissues from the following groups of patients (none underwent labor): 1) term normal placenta (n=15); 2) term with preeclamptic placeneta (n=15); and 3) pre-term with preeclamptic placenta (n=11) using semi-quantitative RT-PCR, RNA in situ hybiridization, immunohistochemistry, and Western blot. In order to evaluate the function of IMUP-2 in HTR-8/SVneo trophoblast cells, IMUP-2 plasmids were transfected into HTR-8/SVneo trophoblast cells for 24 hours. Results: We observed that IMUPs are mainly expressed in the syncytiotrophoblasts and syncytial knot of placental villi. The expression of IMUP-1 was not differences between normal and preeclamptic placenta tissues. However, IMUP-2 expression was significantly higher in preterm preeclamptic placenta tissues than in normal placenta tissues without labor (p<0.001). Furthermore, we confirmed overexpression of IMUP-2 induced apoptosis in HTR-8/SVneo trophoblast cells through up-regulation of pro-apoptotic proteins. Conclusions: These results suggest that the expression of IMUP-2 is involved in placental development as well as increased IMUP-2 expression is associated with preeclampsia through the inducing of trophoblast apoptosis.

• Journal of Chest Surgery
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• v.32 no.5
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• pp.471-479
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• 1999

Background: Patients with tetralogy of Fallot(TOF), pulmonary atresia(PA) and major aortopulmonary collateral arteries(MAPCAs) have been managed by heterogenous surgical strategies. We have taken 5 different surgical approaches to this lesion. In this study, relative advantages and disadvantages of each strategy were discussed by analyzing our surgical results. Material and Method: Between January 1986 and June 1998, 50 patients aged 1 to 177(39${\pm}$31) months at a various morphologic spectrum of this lesion were treated at our institution. The groups, which were classified according to the initial approaches, consisted of one-stage unifocalization(A-1, n=9), staged unifocalization(A-2, n=11), right ventricle to pulmonary artery connection(RV-PA)(B-1, n=11), one-stage RV-PA plus unifocalization (B-2, n=11), and one-stage definitive repair(C, n=8). Morphologic charateristics, operative mortalities, and probabilities of definitive repair were compared between the groups and the causes of death, complications and the follow-up results were described. Result: Mean ages at the first operation were 57${\pm}$18(A-1), 42${\pm}$48(A-2), 18${\pm}$14(B-1), 52${\pm}$55(B-2), and 32${\pm}$34(C) months (p<0.05). Mean numbers of MAPCAs were least in group C (A-1=4.3${\pm}$1.0, A-2=4.5${\pm}$1.3, B-1=4.1${\pm}$1.9, B-2=4.1${\pm}$1.6, C=3.4${\pm}$1.8 : p<0.05). The ratios of the direct and the indirect MAPCAs in each group were not different between the grousps (A-1=91%/9%, A-2=78%/22%, B-1=80%/20%, B-2=80%/20%, C=81%/19% : p>0.05). Nineteen patients had more than 1 dependent MAPCAs. True pulmonary arteries were not present 13 patients and they were confluent in 29. A total of 101 operations were performed. Operative mortalities of initial procedures were 33%(3/9, A-1), 18%(2/11, A-2), 0%(0/11, B-1), 36%(5/11, B-2) and 13%(1/8, C) (p<0.05). Percentages of the definitive repair among the patients of each group were 22%(2/9, A-1), 18%(2/11, A-2). 45%(5/11, B-1), 27%(4/11, B-2), and 100%(8/8, C)(p<0.05). Hypoxic respiratory and cardiac failure(6), hypoxic encephalopathy(2) and sepsis(4) were the major causes of death. Phrenic nerve palsy occured in 5 patients. Thirty-one patients among the survivals have been followed up for a mean duration of 74${\pm}$42(3-145) months. One and five year actuarial survival rates were 73% and 73 %. Conclusion: In conclusion, Right ventricle to pulmonary artery connection used in patients with TOF/PA/MAPCA as an inital procedure appeared to be highly successful in enhancing the chance of satisfactory definitive repair without the significant surgical risks. One-stage total repair at an ealier age group could be performed safely with the resonable outcomes. Unifocalization approach, whether it was performed in a single stage or in the multiple stages, resulted in the high operative mortality and the lowest chance of definitive repair, however more tailored selection of the patients and the long follow-up is mandatory to prove the usefulness of this approach.

• Tuberculosis and Respiratory Diseases
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• v.41 no.3
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• pp.231-238
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• 1994

Backgroud: Since the demonstration of the fact that vascular relaxation by acetylcholine(Ach) results from the release of relaxing factor from the endothelium, the identity and physiology of this endothelium-derived relaxing factor(EDRF) has been the target for many researches. EDRF has been identified as nitric oxide(NO). With the recent evidences that EDRF is an important mediator of vascular tone, there have been increasing interests in defining the role of the EDRF as a potential mediator of hypoxic pulmonary vasoconstriction. But the role of EDRF in modulating the pulmonary circulation is not compeletely clarified. To investigate the endothelium-dependent pulmonary vasodilation and the role of EDRF during hypoxic pulmonary vasoconstriction, we studied the effects of $N^G$-monomethyl-L-arginine(L-NMMA) and L-arginine on the precontracted pulmonary arterial rings of the rat in normoxia and hypoxia. Mothods: The pulmonary arteries of male Sprague Dawley(300~350g) were dissected free of surrounding tissue, and cut into rings. Rings were mounted over fine rigid wires, in organ chambers filled with 20ml of Krebs solution bubbled with 95 percent oxygen and 5 percent carbon dioxide and maintained at $37^{\circ}C$. Changes in isometric tension were recorded with a force transducer(FT.03 Grass, Quincy, USA) Results: 1) Precontraction of rat pulmonry artery with intact endothelium by phenylephrine(PE, $10^{-6}M$) was relaxed completely by acetylcholine(Ach, $10^{-9}-10^{-5}M$) and sodium nitroprusside(SN, $10^{-9}-10^{-5}M$), but relaxing response by Ach in rat pulmonary artery with denuded endothelium was significantly decreased. 2) L-NMMA($10^{-4}M$) pretreatment inhibited Ach($10^{-9}-10^{-5}M$)-induced relaxation, but L-NMMA ($10^{-4}M$) had no effect on relaxation induced by SN($10^{-9}-10^{-5}M$). 3) Pretreatment of the L-arginine($10^{-4}M$) significantly reversed the inhibition of the Ach ($10^{-9}-10^{-5}M$)-induced relaxation caused by L-NMMA($10^{-4}M$) 4) Pulmonary arterial contraction by PE($10^{-6}M$) was stronger in hypoxia than normoxia but relaxing response by Ach($10^{-9}-10^{-5}M$) was decreased, 5) With pretreatment of L-arginine($10^{-4}M$), pulmonary arterial relaxation by Ach($10^{-9}-10^{-5}M$) in hypoxia was reversed to the level of relaxation in normoxia. Conclusion: It is concluded that rat pulmonary arterial relaxation by Ach is dependent on the intact endothelium and is largely mediated by NO. Acute hypoxic pulmonary vasoconstriction is related to the suppression on NO formation in the vascular endothelium.