PURPOSE:Insulin induced hypoglycemia and L-dopa are potent for growth hormone(GH) secretion in children. We evaluated the effects of GH secretion with insulin and L-dopa in 22 children with height percentile below 3 and 11 children with height percentile between 10 to 25. METHODS:Thirty four children were performed GH secretion study after classified by height percentile and bone age according to their age and sex. Twenty two children are height percentile below 3 and bone age is delayed more than one years compare to chronologic age(group A). As a control group, twelve children took part in this study and their height percentile were between 10 to 25 but, bone age was not concerned(group B). Serum GH concentration and blood glucose level was detected on 0, 30, 60, and 90 minutes after insulin 0.1U/kg was injected intravenously. And then serum GH concentration was measured on 0, 30, 60, and 90 minutes after L-dopa 10mg/kg was administered orally. Serum GH was measured by radioimmunoassay. RESULTS:GH level in group A was below 7ng/mL in 13 children(59%) after insulin and L-dopa administration respectively but in 11 children(50%) GH level were all below 7ng/mL after insulin and L-dopa adminstration. GH deficiency(7ng/mL) was detected only one children in group B. In Group A and B, peak GH concentration was noted on 30 minutes after insulin administration, but on 60 minutes after L-dopa, peak GH concentration appeared in group B. GH concentration in zero time to 90 minutes after L-dopa was steady increased in group A. CONCLUSION: Anthropometric data such as height percentile and bone age are good for prediction of GH deficiency and if we use these data and GH secretory effects of insulin induced hypoglycemia and L-dopa, we can predict GH deficiency more accurately.
Blood Glucose ; Child* ; Growth Hormone* ; Humans ; Hypoglycemia* ; Insulin* ; Levodopa* ; Radioimmunoassay

The purpose of this study was to investigate the impact of leucine-rich repeats and immunoglobulin-like domains 3 (LRIG3) on the biological features of bladder cancer cell lines. The plasmids of over-expressed LRIG3 and the blank plasmid serving as control were transfected into the bladder cancer cell lines, T24, EJ and BIU-87, and the expression levels of LRIG3 mRNA and protein were detected by using real-time PCR and Western blotting. The changes in the cell cycle and apoptosis were examined by using flow cytometry. The invasive ability was measured by Transwell assay, and CCK-8 assays were used to measure the proliferation of cells. As compared with the control group, the LRIG3 mRNA and protein expression levels in LRIG3 cDNA-transfected group were raised significantly (P<0.05). The average number of cells with up-regulated LRIG3 passing through the inserted filter was decreased significantly as compared with the control group (P<0.05). Up-regulation of LRIG3 also could inhibit proliferation and induce apoptosis of T24, EJ and BIU-87 cells. Except BIU-87, the T24 and EJ cells transfected with LIRG3 cDNA were arrested in G(0)/G(1) phase compared to the control group (P<0.05). In conclusion, the over-expression of LRIG3 could influence the cell cycle and invasion, inhibit proliferation and induce apoptosis in the three bladder cancer cell lines.
Apoptosis ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Humans ; Membrane Proteins ; genetics ; metabolism ; Neoplasm Invasiveness ; Up-Regulation ; Urinary Bladder Neoplasms ; metabolism ; pathology