No abstract available.
Ultrasonography*

No abstract available.
Holoprosencephaly*

PURPOSE: We tried to find the relationships between the fetal beta-cell function and neonatal birth weight, anthropometric measures, and maternal characteristics, and to observe role of insulin as fetal growth factor in offsprings of mothers who have normal glucose metabolism. METHODS: We measured umbilical cord blood insulin and C-peptide concentrations in 236 neonates delivered at Cheil General Hospital from Jan. 1 to Jan. 31 1994. Their mothers had normal glucose metabolism during pregnancy. The birth weight and other anthropometric measures were performed within 24 hours after birth by same pediatrician. RESULTS: 1) The mean gestational age was 39.5+/--0.1 wk and mean birth weight was 3.3+/--0.2 Kg. According to birth weight percentile, the numbers of small for gestational age(SGA), adequete for gesational(AGA), and large for gestational age(LGA) infans were 3(1.3%), 178(75.4%), and 55(23.3%), respectively. There were no differences in gestational age, birth weight, length, head circumference, chest circumference, Ponderal index, and symmerty index between male and female infants. 2) The maternal weight gain during pregnancy was related to neonatal birth weight, length, and head circumference, but not to Ponderal index and symmetry index. 3) The mean cord blood insulin and C-peptide concentrations were 5.1+/--0.1uU/ml and 1.3+/--0.1 ng/ml. There was a significant positive correlation between insulin and C-peptide concentrations. 4) There were no significant differences in cord blood insulin and C-peptide concentrations among the SGA, AGA, and LGA group. 5) The cord blood insulin and C-peptide concentrations had weak positive correlations with neonatal birth weight, obesity, and gestational age, but nor with maternal weight gain during pregnancy. CONCLUSIONS: Although insulin has a significant role in fetal growth in diabetic pregnancy or intrauterine growth retardation(IUGR), our results suggest that it does not have a significant effect on fetal growth in offsprings of mothers who have normal glucose metabolism.
Birth Weight ; C-Peptide ; Female ; Fetal Blood* ; Fetal Development ; Gestational Age ; Glucose* ; Head ; Hospitals, General ; Humans ; Infant ; Infant, Newborn ; Insulin ; Male ; Metabolism* ; Mothers* ; Obesity ; Parturition ; Pregnancy ; Thorax ; Umbilical Cord* ; Weight Gain

We describe the use of a new urethral stent implanted in 6 patients with prostatic outflow obstruction. All patients were in a high risk group for surgery and treated successfully, for a follow-up of 6 to 13 (mean 8.5) months. The majority of patients were satisfied with the procedure, which provided a quick, safe and effective results, compared with conventional surgical treatment. The stent, woven from nitinol in the form of a tubular mesh, was inserted into the prostatic urethra via a delivery device using endoscopic control under local anesthesia. During follow-up period, the stent remained in situ and there were no urinary incontinence or other complications. The average maximum flow rate at postoperative 6 months was 19.5 ml/sec. This stent is a useful alternative to conventional surgical treatment in the high risk and large prostate patient.
Anesthesia, Local ; Follow-Up Studies ; Humans ; Prostate ; Stents* ; Urethra ; Urinary Incontinence

Glucokinase is expressed only in both liver and pancreatic beta cells and has a key role in the regulation of glucose metabolism in these tissues. A number of gene defects associated with glucokinase gene and the cause of non-insulin-dependent diabetes mellitus are known, and the defects along the -30bp promoter site in particular are thought to be related to diabetes and glucose intolerance. To research on gene study related to diabetes, we looked into the relationship between the variation at -30bp of pancreatic beta cell specific glucokinase gene promoter and gestational diabetes mellitus(GDM) in Korea. METHODS: Forty patients with GDM and 62 normal controls were studied. Genomic DNA was extracted from peripheral leukocyte of patients with GDM and normal controls. The nucleotide variation at -30 bp of pancreatic beta cell specific glucokinase gene promoter was analyzed by PCR-SSCP methods. The sequences of amplified DNA were confirmed with direct sequencing method. The clinical features and the response of insulin secretion to oral glucose were analyzed between patients with GDM according to genotypes. RESULTS: Allelic frequency of position -30 bp of pancreatic beta cell specific glucokinase gene promoter did not differ between patients with GDM and normal subjects. However the frequency of G/A and A/A genotypes seemed to show a higher tendency in patients with GDM compare to the normal subjects. Clinical features, insulin response to oral glucose did not differ according to the type of variation at -30bp of pancreatic beta cell specific glucokinase gene promoter. CONCLUSION: These data suggested that the variation at -30 bp of pancreatic beta cell specific glucokinase gene promoter in patients with GDM are unlikely to be one of the possibilities of the genetic factors in the development of GDM. Therefore more sophisticated studies will be needed to elucidate the role of variation at -30bp of pancreatic beta cell specific glucokinase gene promoter in the insulin secretion to oral glucose.
Diabetes Mellitus, Type 2 ; Diabetes, Gestational* ; DNA ; Female ; Genotype ; Glucokinase* ; Glucose ; Glucose Intolerance ; Humans ; Insulin ; Insulin-Secreting Cells ; Korea ; Leukocytes ; Liver ; Metabolism ; Pregnancy

Glucokinase is expressed only in both liver and pancreatic beta cells and has a key role in the regulation of glucose metabolism in these tissues. A number of gene defects associated with glucokinase gene and the cause of non-insulin-dependent diabetes mellitus are known, and the defects along the -30bp promoter site in particular are thought to be related to diabetes and glucose intolerance. To research on gene study related to diabetes, we looked into the relationship between the variation at -30bp of pancreatic beta cell specific glucokinase gene promoter and gestational diabetes mellitus(GDM) in Korea. METHODS: Forty patients with GDM and 62 normal controls were studied. Genomic DNA was extracted from peripheral leukocyte of patients with GDM and normal controls. The nucleotide variation at -30 bp of pancreatic beta cell specific glucokinase gene promoter was analyzed by PCR-SSCP methods. The sequences of amplified DNA were confirmed with direct sequencing method. The clinical features and the response of insulin secretion to oral glucose were analyzed between patients with GDM according to genotypes. RESULTS: Allelic frequency of position -30 bp of pancreatic beta cell specific glucokinase gene promoter did not differ between patients with GDM and normal subjects. However the frequency of G/A and A/A genotypes seemed to show a higher tendency in patients with GDM compare to the normal subjects. Clinical features, insulin response to oral glucose did not differ according to the type of variation at -30bp of pancreatic beta cell specific glucokinase gene promoter. CONCLUSION: These data suggested that the variation at -30 bp of pancreatic beta cell specific glucokinase gene promoter in patients with GDM are unlikely to be one of the possibilities of the genetic factors in the development of GDM. Therefore more sophisticated studies will be needed to elucidate the role of variation at -30bp of pancreatic beta cell specific glucokinase gene promoter in the insulin secretion to oral glucose.
Diabetes Mellitus, Type 2 ; Diabetes, Gestational* ; DNA ; Female ; Genotype ; Glucokinase* ; Glucose ; Glucose Intolerance ; Humans ; Insulin ; Insulin-Secreting Cells ; Korea ; Leukocytes ; Liver ; Metabolism ; Pregnancy