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백서에서 도서형 피판 작성시 덱사메타손 투여가 세포 자멸사에 미치는 영향
홍기웅,김한구,김승홍 중앙대학교 의과대학 의과학연구소 2003 中央醫大誌 Vol.28 No.1
In order to prevent the damages of the flap tissues due to ischemia following a flap surgery, numerous studies have been conducted for the physiochemical, hemodynamic, and metabolic changes in ischemic flap. There had also been many discussions on the use of different drugs to prevent such damages. Recently apoptosis has been regarded as an important tissue injury mechanism as well as tissue necrosis in flap surgery. In acute tissue injury that can be caused by different reasons, some cells die of tissue necrosis while others may go through a time period, which will determine whether die of apoptosis or not. So survival of certain tissues will depend on the degree of apoptosis. In the post flap surgery period, the degree of apoptosis may influence the survival of ischemic flap with tissue necrosis. The author studied the effects of steroids (dexamethasone) on apoptosis in ischemic skin flap after a flap surgery. Steroids are known to increase the survival of flap by increasing tissue tolerance against tissue necrosis of ischemic flap. For the control group (N=15), after elevating an island skin flap with inferior epigastric vessels as pedicle on the abdominal area of a rat, the pedicle is clamped to create an ischemic state. Microscopical observations confirmed apoptosis as well as tissue necrosis of the flap. For the experimental group (N=l5), dexamethasone, a steroid matter was administered before the the clamping of the pedicle. As a result of microscopic observations and comparison of the effects of dexamethasone on the apoptotic area of ischemic flap between the control and experimental group, apoptosis increased significantly in the experimental group. In this respect, steroids, that are known to increase the survival of flap by reducing tissue necrosis, seem to weaken the survival of a flap by increasing the number of dead cells from apoptosis since they stimulate apoptosis of ischemic flap. Results of this study call for related studies on other drugs that can influence apoptosis of ischemic flap.
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한국 신생아 황달에서 UDP-Glucuronosyltransferase 유전자(UGT1A1)의 다형성에 관한 연구
홍기웅,강훈,김일수,김지숙,김은령,이희제*,김성우*,정주호* 대한소아청소년과학회 2004 Clinical and Experimental Pediatrics (CEP) Vol.47 No.1
Purpose:The incidence of neonatal hyperbilirubinemia is twice as high in East Asians as in whites and its metabolic basis has not been clearly explained. Recently, UDP-glucuronosyltransferase gene (UGT1A1) mutation was found to be a risk factor of neonatal hyperbilirubinemia in Japanese and Taiwanese Chinese. We studied whether neonatal hyperbilirubinemia is associated with mutation of UGT1A1, which is a key enzyme of bilirubin catabolism, in Korean. Methods:The genomic DNA was isolated from 45 Korean full term neonates who had hyperbilirubinemia(serum bilirubin >12 mg/dL) with no obvious causes, and the 64 Korean neonates of the control population. We detected a missense mutation of Gly71Arg of UGT1A1 gene by using allele- specific polymerase chain reaction. Polymorphism was confirmed by direct sequencing. Results:Two of the 45 neonates with serum bilirubin above 12 mg/dL had homozygous mutation and 16 neonates had heterozygous mutation. Two of the 31 neonates with serum bilirubin above 15 mg/dL had homozygous mutation and 13 neonates had heterozygous mutation. Thirteen of the control group had heterozygous mutation and homozygous mutation was not found. Allele frequency of Gly71Arg mutation in hyperbilirubinemia group was 0.22, which was significantly higher than 0.11 in the control group(P<0.0144). Conclusion:The missense mutation causing Gly71Arg of UGT1A1 was detected in the Korean neonatal hyperbilirubinemia. The high frequency of this missense mutation may be attributed to the high prevalence of hyperbilirubinemia in the Korean. 목 적 : 신생아 황달은 백인에 비해 일본, 중국, 한국인등 동아시아인에서 두 배 이상 많이 발생한다고 한다. 이에 대한 대사적인 근거는 확실치 않지만, 최근 일본과 타이완 중국인에서 UDP-glucuronosyltransferase 유전자의 다형성이 위험요소로서 보고되었다. 저자들은 빌리루빈 대사의 핵심 효소인 UGT1A1 유전자의 다형성이 한국인 신생아 황달과 어떤 연관성이 있는지 알아보고자 본 연구를 시행하였다.방 법 : 혈중 빌리루빈 수치가 12 mg/dL 이상의 건강하고, 위험인자가 없는 만삭아 중 신생아 황달 환아 45명과 정상 환아 64명으로부터 혈액을 0.5 cc를 채취하여 DNA을 분리하였다. UGT1A1 유전자를 대립유전자 특이 중합효소반응(allele-specific polymerase chain reaction)방법으로 UGT1A1 유전자에서 exon 1의 Gly71Arg의 유전자 다형성을 확인하였으며, 염기서열 분석을 시행하였다.결 과 : UGT1A1 유전자의 Gly71Arg 돌연변이가 신생아 고빌리루빈군 중 총 혈청 빌리루빈이 12 mg/dL 이상인 45명 중 2명에서 변이형 동형접합으로 16명은 변이형 이종접합으로 나타났고, 총 혈청 빌리루빈이 15 mg/dL 이상인 31명중 2명이 변이형 동형접합, 13명이 변이형 이종접합으로 나타났다. 대조군 64명에서는 13명이 변이형 이종접합이고, 변이형 동형접합은 없었다. Gly71Arg의 대립유전자 빈도는 12 mg/dL 이상에서 0.22로 대조군 0.11보다 높았고(P<0.0144), 15 mg/dL 이상에서는 0.27로 대조군 0.11보다 더 높게 나타났다(P<0.0049).
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가토의 유경 TRAM 피판술시 하복벽 동맥의 결찰이 대측 임의형 피판 생존율의 증가에 미치는 영향
민대홍,김승홍,백무현,홍기웅 大韓成形外科學會 1995 Archives of Plastic Surgery Vol.22 No.5
The transverse rectus abdominis myocutaneous(TRAM) flap technique has been a widely accepted method of breast reconstruction after mastectomy, since the first introduction in 1982. Although free TRAM flap technique has been a superior method of breast reconstruction in comparison with the conventional pedicled TRAM flap with the development of microsurgery, it goes without saying that pedicled TRAM flap is the first choice of breast reconstruction, when free TRAM flap is impossible due to the inappropriate recipient vessels. Blood supply to the contralateral side of both the free & pedicled TRAM flap (especially in zone Ⅳ) is often precarious with previous midline abdominal scars or with significant rectus devarication. Various techniques have been described to improve the reliability of the blood supply to the contralateral portion in free & pedicled TRAM flap, including prior delay, double pedicled flap, supercharged & turbocharged flap. To improve flap vascularity of contralateral portion in pedicled TRAM flap, we ligated the superficial & deep inferior epigastric artery of the contralateral portion two weeks prior to raising the conventional TRAM flap. This TRAM flap was based on superior epigastric vascular pedicle attached to the ipsilateral underlying rectus abdominis muscle with a contralateral & ipsilateral random portion of skin. The effectiveness of preoperative ligation of the contralateral superficial & deep inf. epigastric artery in augmentation of skin viabliity was compared to the sham manipulated control group after raising the flap. The results were as follows : 1. Experimental (previous ligation) group; mean total flap area = 227.8cm², mean survival area = 218.46cm², mean survival rate = 96.2% 2. control group ; mean total flap area = 235cm², mean survival area = 205.74cm²mean survival rate = 87.54% From the above results, the increase in skin viability seemed to be accompanied by increased area of viable skin in the treated flap compared to the controls. We postulate that hypoxia resulting from the ligation of the superficial & deep inferior epigastric vessel of contralateral portion prior to the flap surgery may expand vascular territory by the remaining ipsilateral vessels over the contralateral portion.
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Phenobarbital 및 Halothane의 反復投與로 인한 肝損傷에 관한 形態學的 硏究
洪起雄,李圭植 한양대학교 의과대학 1982 한양의대 학술지 Vol.2 No.2
It is well known that halothane was introduced for clinical use as an anesthetic agent in 1956 and has since enjoyed enormous and ever increasing popularity because of its pharmacological properties and its safety as a non-explosive agent. Numerous investigators reported that varying degree of hepatic injury have been noted after halothane anesthesia in clinical experiences. Although myny investigators failed to demonstrate that no hepatic damage is caused by halothane in experimnetal animals, careful consideration has been given to the possibility that halothane, in common with many other halogenated hydrocarbon, might damage the liver, and potential hepatotoxicity caused by halothane has not been definitely extablished. It is important to note that the metabolism of volatile anesthetic agent occurs in microsomes where most of the drug metabolizing enzymes are known to be present. Halothane is metabolized, in part, by the microsomal drug metabolizing enzyme systems of the liver, and induction of drug metabolizing enzyme systems increases this metabolim. While pretreatment of phenobarbital, a well known enzyme inducer has already been shown to enhance the hepatotoxicity of another halogenated hydrocabons. since the metabolites of halothane may betyoxic, it has been suggested that hepatic drugmetabolizing enzyme induction might be expected to potentiate the hepatotoxicity. The present investigation, therefore, has demonstrated whether much drug metabolizing enzyme induction would affect the response of liver to halothane with phenobarbital pretreatment by repeat administration. A total of 105 healthy male albino mice divided into the control, thephenobarbital treated, the halothane treated, and the phenobarbital-halothane treated groups, and each group of the experimental animals were divided into the first, the second, and the third day groups according to repeat administration of phenobarbital or and halothane. The experimental animals were given 50 mg per kg of body weight of phenobarbital twice a day with an interval of 6 hours after having been depreived of food except drinking water ad libitum, and 0.5 ml per kg of body weight of halothane in olive oil are injected intraperitoneally with 6 hours interval after the administration of phenobarbital. the animals were killed at 12 hours after the last administration of halothane. The specimens, which were abtained from the left anterior lobe of the liver, were stained with methyl green-pyronin and oil red O methods and observed with light microscope, and the specimens were also stained with uranyl acetate and lead citrate double contrast methods and observed with Hitachi-H-300 model electron microscope. The liver of the phenobarbital-halothane treated mice showed as following significant changes; 1. the pyroninophilic granules were reduced markedly in the hepatic parenchymal cells of the centrilobular and intermediae zones by repeated adminitration of phenobarbital and halothane. 2. the fat deposits were observed markedly in the hepatic parenchymal cells of the centrilobular and intermediate zones by repeated administration of phenobarbital and halothane. 3. a prominent dilatation, sacculation of the cisternae of RER in companied with dissociation of membrane bounded-ribosomes, disaggregation of free polysomes, proliferation of SER associated with depletion of glycogen particles, atrophies of cisternae of Golgi complex, and production of numerous lipid droplets were recognized in the hepatic parenchymal cells by repeated administration of phenobarbital and halothane. consequently it is suggested that hepatic damage was induced with repeated administration of phenobarbital and halothane in mice.
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