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Dichlorvos가 흰쥐 심근의 미세구조에 미치는 영향
백태경,이화모,정호삼,Baik, Tai-Kyoung,Lee, Wha-Mo,Chung, Ho-Sam 한국현미경학회 1994 Applied microscopy Vol.24 No.3
It is well known that dichlorvos (DDVP), an organophosphate insecticide in common use, is so easily and rapidly hydrolyzed and excreted that it has usually little toxic effect on human body. In these days, however, it is widely used as an industrial and domestic insecticide and as an anthelmintic agent for animals, so that the accident of chemical poisoning occurs frequently. DDVP acts as a powerful inhibitor of carboxylic esterase, which can cause accumulation of acetylcholine at the synapses so paralysis of muscle and the transmission failure in cholinergic synapses dueing to desensitization of acetylcholin receptor may occure. Moreover accumulation of the acetylcholine brings about the elevation of the cyclic-AMP, which alters the cellular metabolisms of nucleic acid, carbohydrate, protein and lipid. Present study has undertaken to investigate the cardiotoxic effect of DDVP by electron microscopic study. A total of 30 Sprague-Dawley strain rats, weighing about 250gm were used as experimental animals. 2mg/kg/day of DDVP is intraperitonealy injected 3 times with intervals of every other day. On 1 day, 3 days, 5 days, 7 days and 14 days after drug administration, the animals were sacrified by cervical dislocation. Left ventricular cardiac muscles were resected and sliced into $1mm^3$. The specimens were embedded with Epon 812 and prepared by routine methods for electron microscopical observation. All preparations were stained with lead citrate and uranyl acetate and then observed with Hitachi-600 transmission electron microscope. The results were as follows: 1. In the cardiac muscle of DDVP treated rats, mitochondria with disorganized double membrane and mitochondrial crista, and vacuole formation in mitochondrial matrix were observed. But structures of mitochondria were recovered to normal in 14 days group. 2. In the cardiac muscle of DDVP treated rats, cisternae of sarcoplasmic reticulum were dilated and sacculated. But these changes were recovered to normal in 14 days group. 3. In the cardiac muscle of DDVP treated rats, glycogen particles around damaged myofibrils were decreased. But amount of glycogen particles were restored in 14 days group. 4. In the cardiac muscle of DDVP treated rats, disruption and discontinuation of myofilaments and disorganization of Z-disc were observed. But the structures of myofibrils were recovered to normal in 14 days group. It is consequently suggested that DDVP would induce the reversible degenerative changes on the ultrastructures in cardiac muscle of rat.
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강지연,양필순,김형수,김옥영,이화모 대한소아청소년과학회 2000 Clinical and Experimental Pediatrics (CEP) Vol.43 No.6
Mauriac syndrome consists of a triad of poorly controlled diabetes, profound growth retardation and hepatomegaly. We experienced a case of Mauriac syndrome in an 18-year-old girl who had poorly controlled diabetes mellitus, short stature, hepatomegaly and central obesity. Also at the time of examination, she had complications of diabetic cataract and nephropathy. Fourteen years prior to admission, she was diagnosed as diabetes mellitus at a hospital. Thereafter, she had been managed with irregular insulin injection. On physical examination at admission, her height was 135cm(<3 percentile) and her weight was 39kg(<3 percetile). She was short and obese. The liver was 5 cm palpable below the right subcostal margin. Her sexual maturation was Tanner stage I. On ophthalmologic examination, the cataracts were observed on both eyes and diabetic retinopathy was absent. Diabetic nephropathy could not be confirmed by kidney biopsy due to her mother's refusal. We studied the hormonal, radiographic and histological abnormalities. The hormonal study was normal and the bone age was by delayed as much as 10 years. The liver biopsy revealed glycogen accumulation in hepatocyte. She was consistent with Mauriac syndrome. She was managed by strict diabetic control with insulin therapy, diabetic diet and intensive education. She was discharged with well controlled blood glucose. Five months later, growth acceleration and sexual maturation have not been observed, but hepatomegaly subsided. 저자들은 부적절한 치료로 장기간 동안 조절되지 않은 고혈당에 의한 당뇨병성 백내장과 신병증이 합병된 환아에서 저신장, 복부 비만과 간비대 소견을 보이며, 일차성 성장 장애 및 왜소증을 나타낼 만한 다른 내분비학적 요인은 발견되지 않는 전형적인 Mauriac 증후군 1례를 경험하였기에 문헌고찰과 함께 보고하는 바이다. 본 환아의 경우는 소아기부터 사춘기 이후까지 지속적으로 혈당 조절이 이루어지지 않아 극심한 왜소증과 성적 발달 미숙을 보였고, 이 후 혈당 조절이 잘 되었으나 더 이상의 성장이나 제 2차 성징 발현이 없었던 것을 보아 소아기와 사춘기의 혈당 조절이 성장과 성 성숙에 매우 중요하다는 것을 알 수 있었다.
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Apert 증후군에서 Fibroblast Growth Factor Receptor 2 EXON Ⅲa 돌연변이 1례
김형수,양필순,강지연,김옥영,구철회,이화모 대한소아청소년과학회 2000 Clinical and Experimental Pediatrics (CEP) Vol.43 No.7
저자들은 생후 1주일된 신생아(남아)에서 두부의 특징적인 기형, 손과 발의 합지증, 구개열, 비폐쇄를 동반한 Apert 증후군, acrocephalosyndactyly를 1례를 경험 하였기에 분자생물학적 연구결과 및 문헌 고찰과 함께 이에 보고하는 바이다.본 연구에서 저자들이 관찰한 환아는 Ser252Try 돌연변이를 갖고 있었으며 이러한 변이가 Apert 증후군의 임상적 특징을 야기하는 것으로 여겨지고 있다. 그러나 최근에는 이러한 돌연변이가 없는 Apert 증후군도 보고되고 있어23), FGFR2 유전자자체내의 아직 확인되지않은 이형성이 있을 가능성이 제시되고 있으며, 향후 많은 분자 생물학적 연구가 필요할것으로 사료된다. Apert syndrome is an uncommon congenital disorder characterized by malformation of the skull in association with symmetrical syndactyly of both hands and feet. This syndrome is autosomal dominant. The original description was presented by Apert in 1906. Since then more than 200 cases have been reported in the world. Recently, we experienced a case of newhorn male infant with congenital anomalies of the skull and extremities. Molecular biologically, he was found to have Ser252Try mutation in the FGFR2 exonⅢa. A brief review of literature was made.
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