• Journal of Veterinary Clinics
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• v.29 no.1
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• pp.8-11
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• 2012

The results of surgical repair for pelvic factures in 31 dogs were reviewed. Lameness and weight bearing scores were used to evaluate functional recovery of the hind limbs. Simple fracture occurred in sacroiliac joint (n = 5) and ilium (n = 3). Pelvic fractures had acetabular (n = 7) and non-acetabular fractures (n = 23). Acetabular fracture cases were composed of additional surgical treatments with femoral head and neck ostectomy (FHNO) (n = 4) and only acetabular rim fixation (n = 3). Simple fractures had more rapid initial and complete recovery times than multiple fractures. Non-acetabular fracture cases (initial recovery time: 2.7 weeks, complete recovery time: 9.1 weeks) had more rapid initial and complete recovery times than acetabular fracture cases (8.4, 12.5 weeks) (p < 0.05). In addition, the cases of additional surgical treatment with FHNO (5.3, 7 weeks) had more rapid mean recovery times than surgical treatment without FHNO (11.1, 16.3 weeks). Surgical approach with FHNO in acetabular fracture was an alternative method to treat pelvic fractures in small breed dogs.

• Journal of Chest Surgery
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• v.31 no.9
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• pp.837-844
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• 1998

Background: Adenosine is secreted by myocardial cells during myocardial ischemia or hypoxia. It has many beneficial effects on arrhythmias, myocardial ischemia, and reperfusion ischemia. Although many investigators have demonstrated that cardioplegia that includes adenosine shows protective effects in myocardial ischemia or reperfusion injury, reports of the optimal dose of adenosine in cardioplegic solutions vary. We reported the results of beneficial effects of single dosage(0.75 mg/Kg/min) adenosine by use of self-made Langendorff system. But it is uncertain that dosage was optimal. The objective of this study is to determine the optimal dose of adenosine in cardioplegic solutions. Material and Method: We used a self-made Langendorff system to evaluate the myocardial protective effect. Isolated rat hearts were subjected to 90 minutes of deep hypothermic arrest(15$^{\circ}C$) with modified St. Thomas' Hospital cardioplegia including adenosine. Myocardial adenosine levels were augmented during ischemia by providing exogenous adenosine in the cardioplegia. Three groups of hearts were studied: (1) group 1 (n=10) : adenosine - 0.5 mg/Kg/min, (2) group 2(n=10): adenosine -0.75 mg/Kg/min, (3) group 3 (n=10) : adenosine -1 mg/Kg/min. Result: Group 3 resulted in a significantly rapid arrest time of the heart beat(p<0.05) but significantly slow recovery time of the heart beat after reperfusion(p<0.05) compared to groups 1 and 2. Group 2 showed a better percentage of recovery(p<0.05) in systolic aortic pressure, aortic overflow volume, coronary flow volume, and cardiac output compared to groups 1 and 3. Group 1 showed a a better percentage of recovery(p<0.05) in the heart rate compared to the others. In biochemical study of drained reperfusates, CPK and lactic acid levels did not show significant differences in all of the groups. Conclusion: We concluded that group 2 [adenosine(0.75 mg/Kg/min) added to cardioplegia] has better recovery effects after reperfusion in myocardial ischemia and is the most appropriate dosage compared to group 1 and 3.

• Journal of Chest Surgery
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• v.36 no.4
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• pp.242-254
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• 2003

Most of the studies conducted have investigated the beneficial effects of ischemic preconditioning on normothermic myocardial ischemia. However, the effect of preconditioning could be attenuated through the use of multidose cold cardioplegia as practiced in contemporary clinical heart surgical procedures. The purpose of this study was to investigate whether preconditioning improves postischemic cardiac function in a model of 25℃ moderate hypothermic ischemic heart induced by cold cardioplegia in isolated rat hearts. Material and Method: The isolated Sprague-Dawley rat hearts were randomly assigned to four groups. All hearts were perfused at 37℃ for 20 minutes with Krebs-Henseleit solution before the baseline hemodynamic data were obtained. Group 1 consisted of preconditioned hearts that received 3 minutes of global ischemic preconditioning at 37℃, followed by 5 minutes of reperfusion before 120 minutes of cardioplegic arrest (n=6). Cold (4℃) St. Thomas Hospital cardioplegia solution was infused to induce cardioplegic arrest. Maintaining the heart at 25℃, infusion of the cardioplegia solution was repeated every 20 minutes throughout the 120 minutes of ischemic period. Group 2 consisted of control hearts that underwent no manipulations between the periods of equilibrium and 120 minutes of cardioplegic arrest (n=6). After 2 hours of cardioplegic arrest, Krebs solution was infused and hemodynamic data were obtained for 30 minutes (group 1, 2: cold cardioplegia group). Group 3 received two episodes of ischemic preconditioning before 30 min of 37℃ normothermic ischemia and 30 minutes of reperfusion (n=6). Group 4 served as ischemic controls for group 3 (group 3, 4: warm ischemia group). Result: Preconditioning did not influence parameters such as left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), rate-pressure product (RPP) and left ventricular dp/dt (LV dp/dt) in the cold cardioplegia group. (p=NS) However, preconditioning before warm ischemia attenuated the ischemia induced cardiac dysfunction, improving the LVSP, LVEDP, RPP, and LVdp/dt. Less leakage of CPK and LDH were observed in the ischemic preconditioning group compared to the control group (p<0.05). Conclusion: Ischemic preconditioning improved postischemic cardiac function after warm ischemia, but did not protect cold cardioplegic hearts.

• Journal of Chest Surgery
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• v.36 no.5
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• pp.242-254
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• 2003

Background: Most of the studies conducted have investigated the beneficial effects of ischemic preconditioning on normothermic myocardial ischemia. However, the effect of preconditioning could be attenuated through the use of multidose cold cardioplegia as practiced in contemporary clinical heart surgical procedures. The purpose of this study was to investigate whether preconditioning improves postischemic cardiac function in a model of $25^{\circ}C$ moderate hypothermic ischemic heart induced by cold cardioplegia in isolated rat hearts. Material and Method: The isolated Sprague-Dawley rat hearts were randomly assigned to four groups All hearts were perfused at 37$^{\circ}C$ for 20 minutes with Krebs-Henseleit solution before the baseline hemodynamic data were obtained, Group 1 consisted of preconditioned hearts that received 3 minutes of global ischemic preconditioning at 37$^{\circ}C$, followed by 5 minutes of reperfusion before 120 minutes of cardioplegic arrest (n=6). Cold (4$^{\circ}C$) St. Thomas Hospital cardioplegia solution was infused to induce cardioplegic arrest. Maintaining the heart at $25^{\circ}C$, infusion of the cardioplegia solution was repeated every 20 minutes throughout the 120 minutes of ischemic period. Group 2 consisted of control hearts that underwent no manipulations between the periods of equilibrium and 120 minutes of cardioplegic arrest (n=6). After 2 hours of cardioplegic arrest, Krebs solution was infused and hemodynamic data were obtained for 30 minuts (group 1, 2: cold cardioplegia group). Group 3 received two episodes of ischemic preconditioning before 30 min of 37$^{\circ}C$ normothermic ischemia and 30 minutes of reperfusion (n=6) Group 4 soloed as ischemic controls for group 3 (group 3, 4: warm ischemia group). Result: Preconditioning did not influence parameters such as left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), rate-pressure product (RPP) and left ventricular dp/dt (LV dp/dt) in the cold cardioplegia group. (p=NS) However, preconditioning before warm ischemia attenuated the ischemia induced cardiac dysfunction, Improving the LVSP, LVEDP, RPP, and LV dp/dt. Less leakage of CPK and LDH were observed in the ischemic preconditioning group compared to the control group (p<0.05). Conclusion: Ischemic preconditioning improved postischemic cardiac function after warm ischemia, but did not protect cold cardioplegic hearts.

• Journal of Chest Surgery
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• v.32 no.9
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• pp.773-780
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• 1999

Background: It has been demonstrated that brief periods of calcium depletion and repletion (calcium-free preconditioning, CP) have cardioprotective effects as seen in ischemic preconditioning(IP) which enhances the recovery of post-ischemic contractile dysfunction and reduces the incidence of reperfusion-induced arrhythmia or infarct size after a prolonged ischemia. In the present study, we tested this paradoxical phenomenon in isolated rabbit hearts. Material and Method: Hearts isolated from New Zealand white rabbits(1.5∼2.0 Kg body weight) were perfused with Tyrode solution using the Langendorff technique. After stabilizing the baseline hemodynamics, the hearts were subjected to 45 minutes of global ischemia followed by 120 minutes of reperfusion with IP(IP group, n=7) or without IP (ischemic control group, n=7). IP was induced by a single episode of 5 minutes global ischemia and 10 minutes reperfusion. In the CP group(n=7), the hearts were subjected to perfusion with Tyrode solution with calcium depletion for 5 minutes and repletion for 10 minutes, and 45 minutes of ischemia and 120 minutes of reperfusion. Left ventricular function including developed pressure, dP/dt, heart rate, left ventricular end-diastolic pressure and coronary flow was measured. Infarct size was determined by staining with 1% triphenyltetrazolium chloride and planimetry. Data were analyzed by a one-way analysis of variance and Tukey's post-hoc test. Result: In comparison with the ischemic control group, IP significantly enhanced the recovery of the left ventricular function including the left ventricular developed pressure, contractility, and coronary flow; in contrast, these functional parameters of the CP group tended to be lower than those of the ischemic control group. However, the infarct size was significantly reduced by IP or CP(p<0.05). Conclusion: These results suggest that in isolated Langendorff-perfused rabbit heart model, CP(induced by single episode of 5 minutes calcium depletion and 10 minutes repletion) could not improve the post-ischemic contractile dysfunction(after a 45-minute global ischemia) but it has an infarct size-limiting effect.

• Applied Microscopy
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• v.19 no.1
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• pp.1-18
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• 1989

It has been debated whether postischemic reperfusion is necessarily beneficial to salvage the myocardium after ischemic insult or not. Therefore, this study was undertaken to compare the ultrastructural changes as well as the distribution of $Ca^{2+}$ in the ventricular myocardial cells after transient ischemia and after postischemic reperfusion, and to suspect to what extent the postischemic reperfusion is beneficial. After 10 minutes of ischemia, the heart developed wide I bands, glycogen depletion, intramyofibrillar edema, mitochondrial swelling, clumping and migration of chromatin, ghosts of lipid droplets, disintegration of cell junctions, sarcolemmal disruption, and loss of $Ca^{2+}$ binding capacity of the sarcolemma and the mitochondria. In spite of reperfusion, in a large number of cells, the ultrastructure was more severely damaged, however, $Ca^{2+}$ binding capacity of the sarcolemma and the mitochondria restored. These results suggest that postischemic reperfusion may help the myocardial cells to restore their function to control $Ca^{2+}$ to a certain extent, but that it could aggravate the ischemic insult.

• Journal of Chest Surgery
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• v.29 no.8
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• pp.807-815
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• 1996

The protective effect of'ischemic preconditioning'on ischemid-reperfusion injury of heart has been reported in various animal species. but without known mechAnism in detail, In An attempt to investigate the cardioprotective mechanism of ischemic preconditioning, we examined the effects of nitric oxide(UO) synthesis in preconditioned heart of rat The isolated hearts perfused by Langendorfr's method were ex- posed to 30min global ischemia followed by 30min reperfusion with oxygenated Krebs-Henseleit(K-H) sol- ution. Ischemic preconditioning was performed with three episodes of Sm n ischemia and Smin repeyfusion before the induction of prolong ischemia(30min)-reperfusion(30min). Ischemic preconditioning prevented the depression of cardiac function(left ventricular pressure .K heart rate) observed in the ischemia- reperfusion hearts and reduced the release of lactate dehydrogenase during the reperfusion period. On electromicroscopic pictures, myocardial ultrastructures wore relatively well preserved in isthemic preconditioned hearts. N6_nitro-L-arginine methyl ester(L-NAME) an inhibitor of L-arginine citric oxide pathway, was infused at a rate O.Smllmin In a dose of 10mg kg-1 before the initial ischemic preconditioning. neither the protection of cardiac function nor the reduction of LDH releAse in ischemic preconditioning hearts was altered in the presence of added L-NAME On ultrastructural finding, the preservation of morphology in ischemic preconditioning heart was not change by the pretreatment of L-UAME. The failure of the WO synthesis inhibitor to reduce t e effect of ischemic preconditioning may be related to be species specific in that NO may allot be the trigger for ischemic preconditioning in rats.

• Journal of the Korean Institute of Traditional Landscape Architecture
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• v.32 no.4
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• pp.105-119
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• 2014

With its growing awareness by public today, along with our heritage gaining higher standing - such as being listed as World Heritage - the needs for managing cultural heritage that meet global standard is required, and public's interest towards national heritage growing higher, Cultural Heritage Administration is actively pursuing related projects for scenic amenity that include systematic preserve/manage/restore the heritage including surrounding environment, also propose harmonious landscape. 1,834 cases of allowance limit for state-designated cultural heritage change are prepared as part of the plan, and the standards are being expanded actively towards designated cultural heritage across the country, contributing towards administrative efficiency and living conditions of the locals significantly. However, some definitions are unclear and possible complaints might arise when applied due to choice of the law, this research prepares the base material for efficient management of the establishment by diagnosing overall operational status and proposing alternatives towards the limit and improvements after reviewing the result. Through this, we expect to see establishment of policies for better management of cultural heritage and its scenic amenity via maximizing administrative efficiency, whilst positively enhance resident satisfaction around the heritage area as well as settling the regulations in short term.

• Journal of Dental Rehabilitation and Applied Science
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• v.30 no.2
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• pp.145-151
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• 2014

Purpose: The purpose of this study was to investigate the microleakage in class II cavity resin restorations used with resin-modified glass ionomer (RMGI) lining material depending on two different applying methods; classical delivery method using a dental explorer and a specially designed rotating bur. Materials and Methods: A total thirty-six extracted teeth were prepared with a class II proximal box, and randomly divided into three groups: 1) control group with no lining added and the proximal box restored (Group I), 2) the second group used RMGI as a lining material which was spread with an explorer (Group II), 3) the third group used a specially designed rotating bur to thin out RMGI (Group III). All teeth were restored with the same manner using incrementally placed resin composite. All 36 teeth were prepared and sectioned for the dye penetration test, and observed with a stereomicroscope for scoring the dye penetration. Results: When RMGI liners were used, both groups using an explorer and the special bur with the liner had significantly less microleakage than the control group with no liner (P < 0.05). The 50% of the group with RMGI liner using the bur showed no microleakage under a dye penetration test whereas all the teeth in control group showed microleakage of different degrees. However, there was no statistically significant difference between Group II and Group III. Conclusion: RMGI is an effective lining material to decrease microleakage in class II composite resin restorations regardless of applying methods.

• Journal of Life Science
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• v.15 no.4 s.71
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• pp.542-547
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• 2005

Hypersensitivity of cells lacking Brcal to DNA interstrand .ross-link (ICL) agents such as cisplatin and mitomycin C(MMC) implicates the important role of Brcal in cellular response following ICL treatment. Brca1 plays an essential role in DNA double-strand break (DSB) repair through homologous recombination (HR)-dependent and -independent process. Recently, our group has been reported that Brca1 involves in cellular ICL response through HR-dependent repair process (Yun J. et at., Oncogene 2005). In this report, the involvement of Brca1 protein in HR-independent repair process is examined using isogenic $p53^{-/-}\;and\;p53^{-/-}\;Brcal^{-/-}$ mouse embryonic fibroblast (MEF) and psoralen cross-linked reporter reactivation assay. Brcal-deficient MEFs showed significantly low HR-independent repair activity compare to Brca1-proficient MEFs. Hypersensitivity to MMC and ICL reporter repair activity were restored by the reconstitution of Brca1 expression. Interestingly, MEFs expressing exon 11-deleted isoform of Brca1 $(Brca1^{\Delta11/\Delta11})$ showed high resistance to MMC and ICL reporter repair activity comparable to Brca1-reconstituted MEFs. Taken together, these results suggest that Brca1 involves in ICL repair through not only HR-dependent process but also HR-independent process using N-terminal RINC finger domain or C-terminal BRCT domain rather than exon 11 region which mediate interaction with Rad50.