OBJECTIVES: The objective of this study was to compare the Korean Personality Rating Scale for Children (K-PRC) profile between children with attention-deficit hyperactivity disorder (ADHD) and typically developing children. We also aimed to investigate the association of K-PRC and ADHD symptoms. METHODS: Ninety-nine youth (age 8.3+/-2.4 years, 72 boys) with ADHD and 84 controls (age 9.2+/-2.5 years, 43 boys) were recruited from the Department of Pediatric Psychiatry of the Asan Medical Center Children's Hospital. Diagnoses of ADHD and comorbid psychiatric disorders were confirmed with the Kiddie-Schedule for Affective Disorders and Schizophrenia-Present and Lifetime Version (K-SADS-PL). The parents of the subjects completed the ADHD rating scale, and K-PRC. Independent t-tests, analysis of covariance, partial correlation analyses, and Mc Nemar test were used for analysis. RESULTS: Children and adolescents with ADHD showed higher K-PRC scores in verbal development, physical development, depression, delinquency, hyperactivity, family dysfunction and psychoticism. Delinquency and hyperactivity were significantly correlated with parent-rated ADHD rating scales and ADHD scores on K-SADS-PL. The hyperactive/impulsive and combined subtypes showed higher scores on hyperactivity and delinquency than the inattentive subtype, and the inattentive subtype showed higher scores on depression and social dysfunction of the K-PRC. CONCLUSION: Our results suggest that K-PRC could be used to comprehensively evaluate symptoms, combined psychopathologies, developmental delay and family dysfunction of children with ADHD.
Adolescent ; Child* ; Chungcheongnam-do ; Comorbidity ; Depression ; Diagnosis ; Humans ; Mood Disorders ; Parents ; Weights and Measures

BACKGROUND/AIMS: Epidermal growth factors (EGF) is known to activate mitogen activated protein kinase (MAP kinase) in hepatocytes by the route of both Raf-dependent and Raf-indefendent pathways. And this is likely to play important role in normal liver cell growth and regeneration. EGF is also reported as a potent mitogen and one of the angiogenic factors. To elucidate the dynamic changes of the serum concentration of epidermal growth factor in chronic liver disease and its correlation with role of EGF and mechanism of tumor development, this study is intended to employ an ELISA in 38 biopsy-proven cases. METHODS: Sera taken out of 5 patients with chronic persistent hepatitis. 4 patients with chronic active hepatitis, 19 patients with liver cirrhosis, 10 patients with hepato-cellular carcinoma that pathological diagnosis was proven later were tested for EGF employing Quantikine ELISA Kits (R & D Systems Inc. Minneapolis, MN). The statistical analysis was evaluated by student's t-test. RESULTS: EGF concentration was 253.33+ 69.5pg/ml(Mean+ SE) in hepatocellular carcinoma, 246.60+ 91.19pg/ml(Mean+ SE) in chronic active hepatitis, 222.71+ 115.97pg/ml (Mean+ SE) in chronic persistent hepatitis, 141.15+ 23.12pg/ml(Mean+ SE) in liver cirrhosis in orders. Serum EGF concentration in hepatocellular carcinoma was significantly higher than that in liver cirrhosis(p value=0.021695). However, comparing to the remaining other groups, no significant difference was found. CONCLUSION: These results support that the reconstruction of the capillary networks in liver cirrhosis resplts in down-regulation of the EGF in comparison to chronic hepatitis. But it is suggested that revaluation of EGF stimulates MAP kinase activity eventually playing in tumorigenesis of the liver with neoangiogenesis.
Angiogenesis Inducing Agents ; Capillaries ; Carcinogenesis ; Carcinoma, Hepatocellular* ; Diagnosis ; Down-Regulation ; Enzyme-Linked Immunosorbent Assay ; Epidermal Growth Factor* ; Fibrosis* ; Hepatitis, Chronic* ; Hepatocytes ; Humans ; Liver ; Liver Cirrhosis ; Liver Diseases ; Liver Regeneration ; Phosphotransferases ; Protein Kinases ; Regeneration

No abstract available.
Animals ; Autoradiography ; Carcinogenesis* ; Diethylnitrosamine ; gamma-Glutamyltransferase* ; Liver* ; Rats*

No abstract available.
Animals ; Autoradiography ; Carcinogenesis* ; Diethylnitrosamine ; gamma-Glutamyltransferase* ; Liver* ; Rats*

BACKGROUND: Liver fibrosis by the progression of the chronic processes of the liver diseases induces deforrned microcirculations of the hepatic lobules. And this eventually resolted in portal hypertension. On the other hands, angiogenic stimu4nt factors are physiologically activated in order to repair the tissue damage. Overexpression of angiogenic factors, however, can stimulate neovascularization as in a fonnation of the tumor that liberates uncontrolled overgrowing of the tumor cells. METHODS: To elucidate the dynamic changes of the serum concentration of angiogenin in chronic liver diseases, this study is intended to employ an ELISA in 44 pathologically proven patients. Quantikiae human angiogenin kit (R and D,systems Inc. Mmneapolis, MN) was used for this investigation. RESULTS: Mean value and standard error of angiogenin concentration (ng/ml) of the sera was 238.92+/-50.95 in 5 cases of chronic persistent hepatitis, 184.47+/-12.75 in 6 cases of chronic active hepatitis, 131.36+/-10.99 in 19 cases of liver cirrhosis, and 211.03+/-19.08 in 14 cases of hepatocellular carcinoma, respectively. Serum angiogenin level in the liver cirrhosis was significantly lower than in chronic persistent hepatitis(p=0.00336), and than in chronic active hepatitis(p=0.018673). Angiogenin concentration in hepatocellular carcinomas was significantly higher than the level of the liver cirrhosis investigated(p=0.00569). CONCLUSIONS: These data support that persistent inflammatory insults in the chronic hepatitis were compensated by the elevation of angiogenin but complete fibrosis as in liver cirrhosis showed the depressed level. And emerging of the hepatocellular carcinoma is accompanied by the elevated stimuli of angiogenin for the neovascularization.
Angiogenesis Inducing Agents ; Carcinoma, Hepatocellular ; Enzyme-Linked Immunosorbent Assay* ; Fibrosis ; Hand ; Hepatitis, Chronic ; Humans ; Hypertension, Portal ; Liver Cirrhosis ; Liver Diseases* ; Liver*