Three-dimensional finite element model was made from adult skull to find desirable direction of retraction force to treat skeletal class II malocclusion. The retraction force of 400g was applied to the first molar. The direction of the force application was 23degrees downward, parallel, 23degrees upward and 45` upward to the occlusal plane. The stress distribution and the displacement within the maxilla were analyzed by three-dimensional finite element method. The findings obtained were as follows: 1. Maxillary first molar was displaced posteriorly and inferiorly in 23degrees downward, parallel, 23degrees upward retraction but it was displaced posteriorly and superiorly in 45degrees upward retraction. 2. ANS, A point and prosthion were moved posteriorly and inferiorly and pterygornaxillary fissure was moved posteriorly and superiorly. Clockwise rotation of maxilla occurred when retraction force was applied. 3. The degree of clockwise rotation of maxilla was greatest when the force was applied 23degrees upward to the occlusal plane and was least when the force was applied 23degrees downward to the occlusal plane. 4. Large tensile stress appeared in maxillary first molar and alveolar bone and the infraorbital region of maxilla when the force was applied 23degrees downward to the occlusal plane. Tensile stress was smaller as the direction of force move upward. 5. Large compressive stress was appeared in maxillary first molar and infraorbital region in 45degrees upward case and large compressive stress occurred in the posterior part of maxilla as the retraction force was upward.
Adult ; Dental Occlusion ; Humans ; Malocclusion ; Maxilla* ; Molar ; Skull

PURPOSE:There were many controversies whether constitutional delay of growth and puberty(CDGP) is simple varient of normal growth pattern, or one of the cause of growth disturbance induced by the disturbance of growth hormone secrtion or its function. So we studied about the difference in serum peak growth hormone level after insulin, L-dopa provocation test, and serum IGF-I leve between constitutional delay of growth and puberty(CDGP) and familial short stature(FSS). METHODS:Measurement of serum peak growth hormone and insulin like growth factor-I(IGF-I) level after insulin, L-dopa provocation test were performed in 33 children with costitutional delay of growth and puberty (CDGP). Two groups of children with familial short stature (FSS) whose height were below 10 percentile for chronologic age of Korean national height standards were included as control groups. RESULTS: 1)There were no significant difference of serum peak growth hormone level between children with CDGP and children with FSS and these results were similar in both sex. 2)The mean serum IGF-I level of children with CDGP were 125.69+/-4.06 ng/ml(71.53-189.34ng/ml) in male, 157.7+/-3.17ng/ml(81.9-279.2ng/ml) in female. Both results were significantly lower to those of FSS children by chronologic age group because the mean serum IGF-I level of FSS children were 190.19+/-7.97ng/ml (87.64-297.6ng/ml) in male, 205.47+/-15.87ng/ml(61.7-433.1ng/ml) in female. But compared to FSS children by bone age of 72-96 months, there were no significant difference noted because the mean serum IGF-I level of children with FSSwere130.47+/-0.27ng/ml(63.24-198.2ng/ml)inmale,162.35+/-9.43ng/ml(54.9-217.53 ng/ml) in female. CONCLUSIONS:The results of this study showed that the serum peak growth hormone level after insulin, L-dopa provocation test with children of CDGP revealed no significant difference with those of FSS children in both sex. Serum IGF-I level of CDGP children was lower significantly to those of FSS children by chronologic age group, but no much difference with FSS children of bone age group.
Adolescent ; Child* ; Female ; Growth Hormone* ; Humans ; Insulin* ; Insulin-Like Growth Factor I ; Levodopa* ; Male ; Puberty*

PURPOSE: The aims of this study were to investigate the frequencies and role of hepatitis B virus(HBV) precore and core promotor mutations in children with chronic hepatitis B infection. METHODS: Sera from 46 children with chronic hepatitis B infection were analyzed by direct sequencing of polymerase chain reaction product of HBV DNA. In this study, the patients were divided into vertical and non-vertical groups according to the mode of HBV transmission. Statistical analysis was performed by using Fisher's exact test. RESULTS: Forty-six adr type of HBV DNA were analyzed. The mutations in HBV precore region were observed in 12(26.1Yo) of 46 cases. The GA mutation of nucletide(nt) 1896 was observed in 5 cases(10.9Yo). The frequency of mutations in HBV precore region of the non-vertical group (6/16; 37.5Fo) was higher than that of the vertical group(6/30; 20M), but there was no statistical significance. The mutation in HBV core promotor region was observed in 40(87.0%) of 46 cases. The A-->T mutation of nt 1762 or G-->A mutation of nt 1764 were observed in 24(52.2%) of 46 cases, and 23 cases revealed combined mutation at both positions 1762 and 1764. The frequency of mutations in HBV core promotor region of the vertical group(28/30; 93.3Yo) was higher than that of the non-vertical group(12/16; 75.0M), but there was no statistical significance. The frequencies of mutations in HBV precore and core promotor regions of the HBeAg negative patients was higher than that of HBeAg positive patients, but there was no statistical significance. Also there were no significant correlations between the frequencies of mutations in HBV precore and core promotor regions and AST, ALT level or the level of HBV DNA. CONCLUSION: These observations suggest that mutations in HBV precore and core promotor regions were frequently detected in children with chronic hepatitis B infection. There were no statistical significant differences in the frequencies of mutations in HBV precore and core promotor regions between vertical and non-vertical transmission groups. (J Korean Pediatr Soc 2000; 43:779-791)
Child* ; DNA ; Hepatitis B e Antigens ; Hepatitis B virus* ; Hepatitis B* ; Hepatitis B, Chronic* ; Hepatitis* ; Hepatitis, Chronic* ; Humans ; Polymerase Chain Reaction ; Promoter Regions, Genetic

No abstract available.

No abstract available.
Extracorporeal Circulation* ; Pulmonary Atresia* ; Ventricular Septum*

PURPOSE:This study was performed to investigate the status of cardiac structure and function and to assess their alterations after growth hormone(GH) treatment in children with growth hormone deficiency(GHD). METHODS:Interventricular septal thickness and left ventriclular posterior wall thickness, ejection fraction(EF), fractional shortening(FS), systolic time interval(STI) of left ventricle were measured by two-dimensional and M-mode echocardiography in sixteen children with GHD and age, sex matched sixteen children with GH normal short stature as control. The measure were done before GH treatment and at 6 and 12 months of GH treatment, respectively. RESULTS: 1)Left ventricular posterior wall thickness in GHD group was significantly thinner than that of control group(P<0.05). 2)Interventricular septal thickness and left ventricular posterior wall thickness were increased with GH treatment from 10.4+/-1.7mm, 8.1+/-1.8mm before GH treatment to 11.0+/-0.9mm, 8.7+/-0.7mm and 11.2+/-1.7mm, 9.7+/-1.8mm at 6 and 12 months of GH treatment, respectively. The increment of left ventricular posterior wall thickness after 12 months GH treatment revealed statistic significance(P<0.05). 3)There was no significant alterations of EF, FS, STI of left ventricle after GH treatment at 6 months and 12 months, respectively. CONCLUSION: Left ventricular posterior wall thickness in GHD group was significantly thin compared to that of control group(P<0.05). GH treatment in GHD children for 12 months, resulted statistically significant increase(P<0.05) in posterior wall thickness. There is no evidence of hypertrophic cardiomyopathy after GH treatment. But we could not exclude the possibility of these alterations were induced by an increased overall body size and body surface area after GH treatment. To clarify the exact alterations of cardiac structures and function in children with GHD after GH treatment, long term follow-up studies should be necessary.
Body Size ; Body Surface Area ; Cardiomyopathy, Hypertrophic ; Child* ; Echocardiography ; Follow-Up Studies ; Growth Hormone* ; Heart ; Heart Ventricles ; Humans

To investigate the correlation between urinary growth hormone(GH) level and peak serum GH level, urinary GH value measured by overnight collection of urine for 10 hours and serum GH value in response to GH provocation test using insulin and L-dopa were measured in 9 cases of GH complete deficiency(GCD), 19 cases of GH partial deficiency(GPD) and 40 cases of GH normal short stature(GHN). Urinary GH values were measured by the EIA method using PICOIA HGH plate(Joo Woo Pharmaceutical Co., Japan). Urinary GH was expressed in terms of nanograms per gm creatinine(ng/gCr). Serum GH was measured by immunoradiometric assay using "Daiichi kit"(Je Il Pharmaceutical Co., Japan). Wilcoxon ranked sum test and student's t-test were used to assess the significance of differences between the groups of the patients. The correlation between urinary GH level and peak serum GH level was assessed by the parametric Pearson correlation test. The correlation between peak serum GH level in GH provocation test using insulin and urinary GH level measured by overnight 10 hours collection method showed statistically significant results in all the patients(Y=0.464072X +9.208044, r=0.48987, p=0.0001) and in the GH deficiency groups(GCD+GPD) (Y=0.924659X +9.2385509, r=0.80437, p=0.0001). In case of L-dopa stimulation test, urinary GH values were also positively correlated with peak serum GH level when all the patients were participated(Y=0.572988X +8.312993, r=0.58212, p=0.0001). In contrast, no correlation was found when patients were confined to GH deficiency group(GCD+GPD)(Y=0.127712X +8.3129939, r=0.08044, p=0.6841).
Dihydroxyphenylalanine ; Growth Hormone ; Humans ; Immunoradiometric Assay ; Insulin ; Levodopa ; Methods

PURPOSE: The aims of this study were to investigate the frequencies and role of hepatitis B virus(HBV) precore and core promotor mutations in children with chronic hepatitis B infection. METHODS: Sera from 31 children with chronic HBV infection were analyzed by direct sequencing of polymerase chain reaction amplification of HBV DNA. RESULTS: Twenty-nine adr type were analyzed. The mutations in HBV precore region were observed in 8(27.6%) of 29 cases. The G->A mutation of nucleotide 1896(A1896; stop codon) were observed in 4 cases(13.8%). The mutations in HBV core promotor region were observed in 27 (93.1%) of 29 cases. The G(1764)->A mutation(A1764) was observed in 14 cases(48.3%), and among these 12 cases combined with a A to T change at nucleotide 1762(T1762). The mutations in HBV precore region were obsereved in 4(21%) of 19 cases of HBeAg positive group and 9(90%) of 10 cases of HBeAg negative group. A1896 mutation was observed in 2 cases in both HBeAg positive and negative group, respectively. The mutations in HBV core promotor region were observed in 18(94.7%) of 19 cases of HBeAg positive group and 9(90%) of 10 cases of HBeAg negative group. T1762 mutation were observed in 6(31.6%) of 19 cases of HBeAg positive group and 6(60%) of 10 cases of HBeAg negative group(P=0.14). A1764 mutation was obsereved in 7 (36.8%) of 19 cases of HBeAg positive group and 7(70%) of 10 cases of HBeAg negative group (P=0.089). A1896 mutation was observed in 2(18.2%) of 11 cases in increased AST/ALT group and 2(11.1%) of 18 cases in normal AST/ALT group. A1764 and T1762 mutations were higher (61.1%) in AST/ALT increased group than those(27.3%) in AST/ALT normal group, but there was no statistical significance(P=0.077). CONCLUSION: Mutations in the precore and core promotor regions can be frequently detected in children with chronic HBV infection. T1762 and A1764 mutations were observed more frequently in HBeAg negative group and in AST/ALT increased group but there was no statistical significance.
Child* ; DNA ; Hepatitis B e Antigens ; Hepatitis B virus* ; Hepatitis B* ; Hepatitis B, Chronic* ; Hepatitis* ; Hepatitis, Chronic* ; Humans ; Polymerase Chain Reaction ; Promoter Regions, Genetic

No abstract available.
Aortic Aneurysm*

No abstract available.
Humans ; T-Lymphocyte Subsets*