No abstract available.
Biopsy* ; Child* ; Humans

No abstract available.
Rupture* ; Thorax*

Background: The insulin-like growth factors, IGF-I and
Animals ; Calcimycin ; Calcium ; Egtazic Acid ; Extracellular Fluid ; Glucose ; Hepatocytes ; Insulin ; Insulin-Like Growth Factor Binding Protein 3 ; Insulin-Like Growth Factor Binding Proteins ; Insulin-Like Growth Factor I ; Liver ; Metabolism ; Parathyroid Hormone ; Perfusion ; Rats ; Somatomedins

BACKGROUND: Pregnancy in human and rodents is associated with dramatic matemal metabolic changes. Insulin-like growth factors (IGFs) are mitogenic peptides that are essential for fetal and maternal tissue growth during pregnancy. They circulate complexed primarily with a serum IGF-binding protein (IGFBP-3) which regulates the availability of the IGFs to their specific target tissues. METHODS: To examine the changes of IGFs and IGFB-3 during pregnancy, we measured serum total IGF-I, free IGF-I, IGF-II and IGFBP-3 by using specific radioimmunoassay, immunoradio-metric assay, western ligand blot and western immunoblot. Blood samples were obtained from 88 pregnant women between 6-40 weeks gestation. RESULTS: While serum IGF-I levels increased up to 50% in late pregnancy, serum IGF-II levels remained unchanged. However, serum free IGF-I levels were significantly higher during pregnancy than in nonpregnancy. Western ligand blot analysis revealed that IGFBP-3 in pregnancy serum was significantly decreased at 6 weeks of gestation, continued decreased level until term, and returned to a nonpregnant level by postpartum 10 day. Serum IGFBP-3 profiles in Western immunoblot analysis revealed that 30 kDa fragments of IGFBP-3 were detectable in pregnancy serum but not in nonpregnancy serum. In contrast, serum IGFBP-3 levels using radioimmunoassay was significantly increased in late pregnancy. CONCLUSIONS: 1) serum IGF-I was significantly elevated in late pregnancy 2) serum IGF-II was not significantly changed 3) free IGF-I significantly elevated throughout gestation 4) intact IGFBP-3 was markedly reduced after 6 weeks of gestation.
Blotting, Western ; Female ; Humans ; Insulin-Like Growth Factor Binding Protein 3 ; Insulin-Like Growth Factor I ; Insulin-Like Growth Factor II ; Peptides ; Postpartum Period ; Pregnancy* ; Pregnant Women ; Radioimmunoassay ; Rodentia ; Somatomedins

PURPOSE: Ataxia Telangiectasia (AT) is a hereditary multi-systemic disease resulting from mutations of AT gene and is characterized by progressive neurodegeneration, cancer, immune system defects, and hypersensitivity to ionizing radiation. AT gene has a homologue sequence of PI3-kinase. The activity and cellular function of PI3-kinase in AT gene remains unclear. This study was undertaken to evaluate the function of AT gene through the effect on cell survival and differentiation by the inhibition of AT gene expression. MATERIALS AND METHODS: NH2-terminal portion of AT gene was isolated from MCF-7 cells by RT-PCR. The isolated DNA fragment was ligated in reverse orientation in pcDNA3. This antisense ATM expression vector was transfected to PC-12 cells by calcium phosphate method, and the transformed cells were selected using G418 and immunohisto- chemistry. To analyze the cell survival and differentiation, cells were cultured in serum free medium supplemented with/without NGF. We performed the immunoprecipitation for the p53 induction of cells after ionizing radiation, and the FACS for the apoptosis of cells after the exposure of wortmanin. RESULTS: PC-12 cells which down-regulated AT gene (like ATM, AT mutated) showed decreased survival and ceased differentiation with NGF. Also, PC-12 (ATM) cells showed increased apoptosis with wortmanin and reduced or delayed p53 induction after ionizingradiation. CONCLUSION: Results obtained from these studies suggest that AT gene regulates survival and differentiation of PC-12 cells through PI3-kinase activity. It seems that apoptosis is induced by the inhibition of AT gene expression.
Apoptosis ; Ataxia Telangiectasia ; Calcium ; Cell Survival ; Chemistry ; DNA ; Gene Expression ; Hypersensitivity ; Immune System ; Immunoprecipitation ; MCF-7 Cells ; Nerve Growth Factor ; Phenotype* ; Phosphatidylinositol 3-Kinases ; Radiation, Ionizing

No abstract available.
Child* ; Humans ; Meningitis* ; Scrub Typhus*

No abstract available.
Pyelonephritis, Xanthogranulomatous*

No abstract available.
Pyelonephritis, Xanthogranulomatous*

Congenital myotonia is a benign familial disorder, main problem is muscle stiffness, delayed relaxation of skeletal muscles after voluntary contraction or following mechanical or electrical stimulation. Although weakness is always present with progression of myotonic dystrophy, many patients with myotonia congenita never develop weakness. In the autosomal dominantly inherited form of congenital myotonia (Thomsen's disease), symptoms revolve around myotonia but weakness is not present. However, in the autosomal recessive (Becker's) type congenital myotonia, mild weakness and marked muscle hypertrophy is common. We report two cases of sporadic developing Becker's type congenital myotonia with electrophysiologic and muscle biopsy findings and review of literatures.
Biopsy ; Electric Stimulation ; Humans ; Hypertrophy ; Muscle, Skeletal ; Myotonia ; Myotonia Congenita* ; Myotonic Dystrophy ; Relaxation

No abstract available.
Child* ; Hematuria* ; Humans ; Jeollabuk-do* ; Prevalence*