No abstract available.
Endoscopy, Digestive System*

No abstract available.
Epilepsy*

We have tried this experiments about measure of Human Body Fat from transverse body scans with Magnetic Resonance Image (0.5, Tesla). Images were created with a spin echo sequence using a repetition time 500msec, echo time 20msec, and 1cm length between 10mm cross sectional slices, and gained through a whole body. In vivo quantification of body fat with MRI was measured by two healthy Females Volunteers, each cut obtained with MRI was analyzed, traced papers on the view finder, and then digitized, at last calculated for the areas of Human Body Fat. The results of this study can be summarized as follows : Through the analyses of the Ratio of Human Body % Fat with MRI and Densitiometry, in Sub.1, Sub.2, MRI is estimated higher than Densitiometry, that is, Keys & Brozek's Method (1960) has the most remarkable score gaps, 6.94% (Sub.1), 6.21%(Sub.2). Chinn & Alleys Method (1960) has showed the score getting closest to MRI, 1.67% (Sub.1), 1.36%(Sub.2). And Siri's (1956) Brozek et al's (1963), which have been used as the most popular methods, make the difference of 4% approximately. As a result of this study, such as preceding studies about it Ratio of Human Body Composition with MRI has considered to be validated and trusted. Therefore, if we estimate for Ratio of Human Body Fat with much more subjects than this experiments we can suggest that the method with MRI is possible to develope low data adaptable in every field.
Adipose Tissue ; Female* ; Human Body* ; Humans* ; Magnetic Resonance Imaging ; Methods ; Volunteers

BACKGROUND/AIMS: In order to determine the relationship between the HBV precore mutant and the severity of liver disease in Korea, we performed liver biopsies in patients with HBV related chronic liver disease and compared the types of mutations and histologic findings in the same liver tissue simultaneously. METHODS: HBV DNA in liver tissues was amplified by polymerase chain reaction (PCR). The precore mutants were detected by PCR-SSCP(single strand conformation polymorphism), cloning the amplified PCR products and direct sequencing for them. RESULTS: 1. HBV DNA was detected in liver tissues of 28 cases among 30 patients with PCR. And with SSCP, the most cases were mixed type infections. 2. The HBV precore mutants were found in 12 cases among the total number of 28 cases(42.9%) and all mutations were G to A change at nucleotide 1896, creating a stop codon at codon 28. However, 10 cases among 12 mutants were associated with simultaneous another mutation at different positions or regions;9 cases at core gene region, 2 cases at nucleotide 1856(C to T change at codon 15), one case at core promoter, and one case with double mutations at nucleotide 1837 and 1846 respectively. Also, all HBV precore mutants were combined with wild type HBV sequence. 3. The relationship between HBV precore mutants and HBeAg status revealed that 4 cases from 13 HBeAg positive(30.8%) and 8 from 15 HBeAg negative or Anti-Hbe positive(53.3 %) were mutants. 4. In analysis of the types of mutants and histopathological findings of liver diseases, 6 among 15 chronic active hepatitis(40.0%), all 3 cases with hepatocellular carcinoma(100,0 %), 2 among 4 asymptomatic carriers with minimal histopathologic changes(50.0%) and a case with chronic lobular heaptitis(100.0%) showed precore region mutation. CONCLUSION: The patterns of HBV precore mutants in Korea could be summarized as followings. Firstly, most of the mutations are composed of G to A change at nucleotide 1896. Secondly, the most of the mutants at nuclmtide 1896 have been associated with simultaneous mutations at core promoter, core gene, and rarely at other positions, and manifested usua'ly mixed type viremic conditions. Thirdly, although precore mutation could be occurred in asymptomatic carrier, this type of mutation might be closely related with chronic or severe liver disease. However, it needs further investigations hereafter.
Biopsy ; Clone Cells ; Cloning, Organism ; Codon ; Codon, Terminator ; DNA ; Hepatitis B e Antigens ; Hepatitis B, Chronic* ; Hepatitis, Chronic* ; Humans ; Korea ; Liver Diseases ; Liver* ; Polymerase Chain Reaction ; Polymorphism, Single-Stranded Conformational

PURPOSE: Short stature is the most constant finding in Turner syndrome. Short stature in Turner syndrome has lately received considerable attention, mostly because of recent attemp to improve growth by hormonal treatments; growth hormone, oxandrolone, estrogen. The aim of this study was to find out whether growth promoting treatment would improve final height in girls with Turner syndrome. METHODS:Seventy-one girls with the clinical chracteristics Turner syndrome verified by karyotype analysis were entered into this study. The following selection criteria for final adult height were used; Chronological age of more than 14years old, bone age of more than 15years old and growth velocity of less than 0.5cm per 6months. Analysis was performed by means of multiple regression analysis between descriptive data; modality of treatment with oxandrolone and/or estrigen, parental height, karyotype and final adult height. RESULTS: 1) The final adult height of untreated Turner syndrome was 138.9+/-3.9cm. 2)The final adult height in 29 GH treated Turner girls was 143.9+/-6.5cm, significant higher value than 42 GH untreated Turner girls height, 139.8+/-5.2cm(p<0.01). 3) The final height in GH only group and combined group were 141.2+/-6.0cm, 146.2+/-6.2cm, respectively. The combined therapy was more effective than GH therapy(p<0.01). 4) The final height in 32 patients with karyotype of 45,X was 141.6+/-5.6cm, and that of 31 structural aberration group was 140.3+/-6.2cm. There was no significant difference between two groups. But in mosaicism, only numeric abnormalities, the final height 145.9+/-6.1cm was much more higher than other two groups(p<0.05). 5) The final adult height in Turner syndrome was in good correlation with target height. Final adult height(cm)= 1.01*Target height(cm)- 4.97 r=0.51, p<0.05. 6) There was positive correlation between final adult height and height SDS at start GH treatment and negative correlation with age at start GH treatment. The delta height (final height - height at start treatment) correlate with GH treatment duration. CONCLUSIONS:The final adult height in Turner syndrome in a given ethinic or national population varies in the same way as adult height in normal women. Growth hormone therapy may increase final height in Turner syndrome irrespective of ethinic or national difference. Further growth was observed in GH combined with estrogen or oxandrolone.
Adult* ; Estrogens ; Female ; Growth Hormone ; Humans ; Karyotype ; Mosaicism ; Oxandrolone ; Parents ; Patient Selection ; Turner Syndrome*

Cytochemical demonstrations of lipase and nucleic acid in Trichomonas vaginalis were attempted. Modified Gomori tween method for lipase and acridine orange method for nucleic acid was applied. Trichomonas vaginalis incubated in the isolation mediurn (C.P.L.M.) were pooled and fixed using 0.1 N McIlvaine buffer saline and cold acetone for lipase and Walpole acetate buffer saline and acetic alcohol for nucleic acid. The results were obtained as follows: Activity of lipase and nucleic acid were recognized in the cytoplasm of T. vaginalis as scattered positive granules stained in blue yellow-green bright reddish color respectively. However these reactions were not shown in nucleus, nuclear membrane, undulating membrane etc. Present authos believe the negative finding of acridine orange staining in nucleus should be studied further.
parasitology-protozoa-Trichomonas vaginalis ; lipase ; nucleic acid ; histochemistry

To analyse the clinical characteristics of children with atrial flutter(AF1), we reviewed(the medical records of the children who had been admitted and diagnosed as AF1 or 12 leads surface ECG during the period between February, 1986 and Octobe, 1990. The onset age of 25 children was evenly distributed between gestational period and upto 14 years of age. The sex ratio between boys and girls was 11:14. The cardiac abnormalities were detected in 21 children(dilated cardiomyopathy in 3, congenital heart defect in 18). In 4 children, AF1 occured in apparently normal heart. In 9 children, AF1 developed without relation to cardiac surgery(4 in normal heart, 3 in dilated cardiomyopathy, 2 in preoperative CHD). AF1 developed in 9 children within 30 days postoperatively(group A) and in 7, after 30 days postoperatively(group B). In group A, various types of operation were done. In 2 of them, AF1 persisted beyond the immediate postoperative period and 1 died of cardiac decompensation 3 months postoperatively. In group B, operative procedures before AF1 were Senning operation in 2, Fontan operation in 2, operation for tetralogy of Fallot, ventricular septal defect with severe tricuspid regurgitation, endocardial cushion defect in 1 each. Five children in group B( except 1 Senning operation and 1 Fontan operation) had significant residual atrioventricular regurgitation. The associated rhythm disturbance besides AF1 could be determined in 23 children. The sinus node dysfunction was associated in 8 ; the supraventricular dysrhythmia in 10; the ventricular dysrhythmia in 6; the atrioventricular conduction disturbance in 3, and no other associated rhythm disturbance in 6. The efficacy of various methods in conversion of AF1 to sinus rhythm were 57.1%(4/7) with DC cardioversion, 38.5%(5/13) with digoxin and other antiarrhythmic drug(amiodarone, beta blocker, quinidine, verapamil, flecainide), 25%(5/20) with pacing in esophagus or endocardium. The follow-up evaluation was possible in 24 children. Eight children were dead : 5 due to chronic decompensation, 2 due to sudden cardiac arrest, and 1 due to sepsis. Of the 16 alive children, 14 had recovered the normal sinus rhythm and the other 2 had persistent AF1. Twelve children without AF1 and 1 with persistent AF1 were on medication, Although there were none cardiac death in children without persistent AF1, 7 out of 9 children with persistent AF1 were dead. Of the 7 children with significant atrioventricular regurgitation, corrective procedures were done in 4. There were no death in these 4 children, despite of 2 cardiac death out of 3 children on whom corrective procedure were not done. In conclusion, the atrioventricular regurgitation was a significant factor in relation to the occurrence and persistence of AF1 and the prognosis was bad in children with persistent AF1. It is recommended to trat the children with AF1 associated with atrioventricular regurgitation promptly and more aggressively.
Age of Onset ; Atrial Flutter* ; Cardiomyopathies ; Cardiomyopathy, Dilated ; Child* ; Death ; Death, Sudden, Cardiac ; Digoxin ; Electric Countershock ; Electrocardiography ; Endocardial Cushion Defects ; Endocardium ; Esophagus ; Female ; Follow-Up Studies ; Fontan Procedure ; Heart ; Heart Defects, Congenital ; Heart Septal Defects, Ventricular ; Humans ; Medical Records ; Postoperative Period ; Prognosis ; Quinidine ; Sepsis ; Sex Ratio ; Sick Sinus Syndrome ; Surgical Procedures, Operative ; Tetralogy of Fallot ; Tricuspid Valve Insufficiency ; Verapamil

No abstract available.
Aminolevulinic Acid*

No abstract available.
Child* ; Humans

No abstract available.
Qualitative Research