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        Molecular and Cellular Studies of Seed Storage Proteins from Rice and Wheat

        김우택 한국농화학회 1989 Applied Biological Chemistry (Appl Biol Chem) Vol.32 No.1

        Near full length cDNA clones encoding the rice seed storage protein, prolamine, were isolated and divided into two homology classes based on cross-hybridization and DNA sequencing analysis. These cDNA clones contain a single open reading frame encoding a putative rice prolamine precursor(M.W.=17,200) possessing atypical 14 amino acid signal peptide. Clones of these two homology classes diverge mainly by insertions/deletions of short nucleotide stretches and point mutations. The deduced primary structures of both types of prolamine polypeptides are devoid of any major tandem repetitive sequences, a feature prevalent in other cereal prolamines. No significant homology teas detected between the rice prolamine and other cereal prolamines, indicating that the rice gene evolved from a different ancestor that gave rise to other cereal prolamine genes. Developing wheat and: rice endosperms were examined using ultrathin sections prepared from tissues harvested at various days after flowering. By immunocytochemical localization techniques, wheat prolamines are localized within vesicles from Golgi apparatus and in homogeneous regions of protein bodies. The involvement of the goli apparatus in the packaging of wheat prolamines into protein bodies indicates a pathway which differs from the mode of other cereal prolamines and resembles the mechanism employed for the storage of rice glutelin and legume globulins.

      • KCI등재
      • KCI등재
      • 주산기 저산소성 허혈성 뇌병증의 최신지견

        김우택 동국대학교 의학연구소 1998 東國醫學 Vol.5 No.-

        국문초록최근 관심이 고조되고 있는 주산기 저산소성 허혈성 뇌병증에 대한 최신 지견들을 살펴보아서 향후 주산기 가사로 인한 저산소성 허혈성 뇌병증을 조기 발견하고 조기 치료함으로서 영구적인 신경 정신학적 후유증을 막거나 최소화하는 데 도움이 되고자 한다.뇌세포 손상은 산소와 에너지의 결핍 때문에 세포막의 기능이 저하되고, 정상적인 이온 농도를 유지 못하고, 세포 부종이 생기며, 뇌세포의 괴사가 발생하는 일차적 뇌손상과 재관류나 재산소화 후에 산소와 에너지의 공급 때문에 세포막은 정상적으로 기능을 하나, 핵내효소가 활성화되어 DNA를 분해하고, 세포질을 농축시키는 고사가 생기는 이차적 뇌손상으로 나눌 수 있다. 그것은 흥분성 신경전달물질인 글루타민산염이 연접 부위에 과다 유리되어 글루타민산염 수용체를 활성화시켜 세포내로 칼슘이 급격히 유입되어 뇌손상을 입히고, 다른 기전들은 산소 유리기, 산화질소, 사이토카인, 면역반응, 대식세포, 성장인자 등이 관련되어 있다.임상증상은 신경원에 미토콘드리아의 부종으로 인한 세포질내 공포 때문에 선택적 신경원 괴사가 발생되고, 대뇌기저핵과 시상 부위에 비정상 수초 형태인 대리석 모양을 나타내고, 만삭아에서는 방시상 대뇌손상과 미숙아에서는 뇌실 주위의 백질연화증이 잘 생기며, 국소적 괴사에 의한 초점성 및 다초점성 허혈성 뇌 괴사 등이다.저혈당증, 저산소증, 산혈증, 암모니아 혈증등 대사산물을 측정한다. 뇌파검사법, 테크네튬 주사법, 단일 광자 방출 컴퓨터 단층촬영법, 뇌초음파 검사법, 컴퓨터 단층 촬영 주사법, 자기공명 영상법, 뇌간 유발전위법, 자기공명분광검사법, 근적외부 분광검사법, 양전자방출 단층촬영법, 두개내압 감시법 등을 이용하여 보다 조기에 진단하고 조기에 예후를 결정할 수 있다.지금까지 임상적으로 효과가 입증된 치료 약제는 아직 없으며, 보존적 치료로 적절한 관류나 환기를 유지하고, 체온, 혈당과 칼슘치, 그리고 산-염기 평형상태를 정상적으로 유지하며, 경련을 치료해야 하는 것이 중요하다. 그리고 잠재적 치료방법으로 산소유리기 억제제, 흥분성 신경절달 물질의 길항제, 칼슘이온 통로 차단제, 산화 질소 생산 억제제, 성장인자, 글루코콜티코이드, 페노바르비틀 등이 있고, 나트륨 통로 차단제, 아데노신 유사제, GABA 수용체 촉진제, k-opioid 수용체 길항제, 자유 지방산 축적 억제제, 유전자 표현 변화, 신경원조세포 및 간세포 이식 등도 현재 연구중이다.주산기 가사에 의한 저산소성 허혈성 뇌병증은 뇌성마비, 학습장애, 지능장애 및 간질 등과 같은 장기적인 신경학적 후유증을 남길 수 있으며, 산과력 및 분만력, 임상 증상 및 최신 진단 검사법을 사용하여 뇌손상의 심한 정도를 조기에 증명하고 예후를 판단해야한다. 그러기 위해서 뇌손상을 일으키는 기전에 대해 좀 더 명확히 밝히고, 주산기 가사의 위험성 인자를 가진 신생아를 조기에 진단하고, 앞으로 있을 수 있는 신경학적인 후유증을 조기에 예측할 수 있는 진단을 개발하며, 현재 연구중이거나 실험적으로 시도되고 있는 약물들을 하루 빨리 임상적으로 적용하여 영구적인 후유증이 생길 수 있는 주산기 저산소성 허혈성 뇌병증을 조기에 치료하여 뇌손상을 줄여야겠다. AbstractThis review reveals the new knowledge of perinatal hypoxic-ischemic encephalopathy and it is usefulness to inhibit or diminish permanent neuropsychotic sequeles through early diagnosis and early treatment.The following injuries to neonatal cell after hypoxic-ischemic encephalopathy are two-fold; Primary injuries are followed by sequential responses with depletion of oxygen and energy, loss of function in neuronal cell membranes, edema of neuronal cells, and necrosis of neuronal cells. Secondary injury are followed by sequential responses with lysis of DNA due to activation of endonuclease, and apoptosis of neuronal cells. The mechanisms of neuronal cell injuries are due to excitotoxicity of glutamate receptors, oxygen radicals, nitrogen oxides, cytokines, immune responses, macrophages, and growth factors.The main clinical manifestations are selective neuronal necrosis due to the vacoules in the cytoplasm, status marmoratus in basal ganglia and thalamus, parasagittal cerebral injury in full-term neonates, periventricular leukomalsia in preterm neonate, and focal ischemic brain necrosis.The clinical stages of Sarnet and Sarnet and measurements of metabolites after insult are helpful to diagnose. In addition, there are a lot of diagnostic tools such as electroencephalogram, technetium scan, single photon emission computed tomography, head ultrasound, computed tomography scan, magnetic resonance imaging, brain stem evoked potential, magnetic resonance spectroscopy, near-infrared spectroscopy, positron emission tomography, and intracranial pressure monitoring.Although numerous articles have been devoted to the descriptive events that occur in hypoxic ischemic encephalopathy, the mechanisms that control it have remained largely elusive. Therefore, the following conservative treatments have been used; prevention of perinatal asphyxia, maintenance of ventilation and perfusion, maintenance of normal level of glucose and body temperature, and control of convulsion and brain edema. Pharmacologic agents under experimental investigation are oxygen-free radical inhibitors, excitatory amino acid antagonists, calcium channel blockers, inhibitors of nitric oxide production, monosiaglogangliosides, growth factors, glucocorticoids, and phenobarbitals.In conclusion, we have to try to prevent the injuries of neuronal cell through early diagnosis with newly advanced techniques and early treatment with newly developed agents.

      • 에드워즈 증후군 2례

        김우택,김웅흠 동국대학교 경주대학 1993 東國論集 Vol.12 No.-

        We have seen two cases of Edwards syndrome, one is the female neonate who was born to a 22-year-old mother and a 30-year-old father at Dong-guk university Kyung-ju hospital and the other is the male neonate who was born beteeen a 38-year-old mother and a 40-year-old father at Dong-guk university Kyung-ju hospital and had a healthy 7-year-old sister. They had the multiple anomalies that were charaterized by intrauterine growth retardation, microcephalic skull with flat occiput, microphthalmia, low-set and malformed ears, micrognathia, shield chest & webbed neck, flexion deformity of fingers, simian crease, narrow pelvis, and rocker-bottom feet with short and big toes. Chromosomal analysis revealed 47,XX,+18 and 47,XX, + 18 respectively in these cases. A brief review of relevant literatures is made briefly.

      • 항-E 항체에 의한 신생아 동종면역성 용혈성 질환 1례

        김우택 東國大學校 1999 東國論叢 Vol.38 No.-

        The hemolytic disease of newborn caused by anti-E is characterized by the abnormal title of anti-E in the newborn infants and his or her mother's serum and neonatal progressive hyperbilirubinemia due to an IgG antiody transmitted from the mother to the fetus across the placenta. A 4-day old baby boy was admitted because of progressive jaundice. He was born to 31 year old mother. His blood type was A, Rh(+), his mother's was A, Rh(+), and his father's was AB, Rh(+). His serologic examination revealed a positive direct antiglobulin test and a weakly positive indirect antiglobulin test. His mother's serum revealed a negative direct antiglobulin test but a positive indirect antiglobulin test. The baby boy's and his mother's antibodies were identified as anti-E through an antibody screening and identification test. Phenotypes of baby, his mother, and his father were CcDEe, CcDe, and cDE, respectively. Jaundice was improved by only phototheraphy. Therefore, I report a case of hemolytic disease of newborn due to anti-E with a brief review of relevant literatures.

      • KCI등재

        브라질 경제 : 정부의 실패인가? 시장의 실패인가? Government Failure? Or Market Failure?

        김우택 서울大學校 스페인中南美硏究所 1991 이베로아메리카硏究 Vol.2 No.-

        This paper discusses the Brazilian economic policies during the last 20 years from the standpoint of what economic reasoning supported that kind of policies. And we investigate whether these policy-decisions are based on the belief in market mechanism or,on the contrary, on the idea that government can do better than market. If the underlying logic of policy making was the latter, we may conclude that the current Brazilian economic crisis is the outcome of government failure. The basic lines of economic policies in the 70s are: 1) promotion of deficit financed growth and 2) acceleration of government led import substitution. Motivated by the oil shock, the implementation of these policies were possible only through increasing borrowings of recycled petro-dollars. Inflation and consequent economic instability caused by the fiscal deficits and credit expansion became a burden to persistant growth, while gains from these were insignificant. The 1980s were marked by recurrent crises of debt and inflation. And economic policies of the 80s focused on these two issues. Bacuse of the requirement to meet the debt services, external economic policy turned to making of trade surpluses. And domestic economic policy was nothing but stabilization program to control the increasing inflationary pressure. Policies of the 80s, as those of the 70s, were inspired not by price mechanism of market, but were attempts to solve the problems by govermnent regulation and market control. We conclude that the current Brazilian economic crisis is government made. This government failure originated from the misjudgement of reality and the belief on wrong economic theory which promises prosperity without cost.

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