No abstract available.

Background: Goiter has been a common problem in the thyroid disease. The exact mechanism of goiter had not been clarified yet, but some goiters were increased with TSH(thyrotropin releasing hormone) dependent manner. TSH might be a major influencing factor for increasing size of goiter(goitrogen) and theres many cofactors those influenced to goiter size. One of the rnost prominent growth factor as a goitrogen is a IGF-I(insulin-like growth factor-I). IGF-I play a great role as a cofactor of goitrogen with TSH. This study, therefore, is aimed to investigate intracellular activation of IGF-I gene promoter in the surgical specimens of thyroid tumor. Methods: We used surgical specimen of various thyroid tissues from normal to malignant along its cell nature. Actually we used normal liver tissue as a IGF-I control tissue, normal thyroid, benign adenoma, and papillary thyroid cancer tissue with its malignat nature. We checked Mrna expression of whole IGF-I and IGF-I exon 6 by Northern blot method, and IGF-I, promoter 1 expression by RT-PCR-transcription method. Autoradiographied signals were analysed with densitometer. Results: We found whole IGF-I mRNAs were expressed with alternate splicing in exon 1, 2 and exon 4, 5 respectively. Striking events of IGF-I transcription were multiple tranascription initiatian in Pl and P2, and 3 sites for polyadenylation in exon 6. Four or more Mrna bands in Northern blot analysis of IGF-I(0.8, 1.4, 4.2, and 7.8kb) were noted. In low molecular weight IGF-I Mrna did not change their signal intensity with tissues, but exan 6(7.8kb) signals were significantly increased to its hepatic expression levels in malignant tissue. IGF-I, exon 1 expression by RT-PCR-T7 transcription was strikingly increased in thyroid cancer tissue, but exon 6 expression was not a great expession. Conclusion: One possible guess for this expression discrepancy of each exon may be originated from different Mrna degradation of each IGF-I signals. We need more preeise experiment for Mrna degradation speed of IGF-I.
Adenoma ; Alternative Splicing ; Blotting, Northern ; Exons ; Goiter ; Insulin-Like Growth Factor I ; Liver ; Methods ; Molecular Weight ; Polyadenylation ; RNA Stability ; RNA, Messenger ; Strikes, Employee ; Thyroid Diseases ; Thyroid Gland ; Thyroid Neoplasms

No abstract available.
Hyperglycemia

Background: Chronic use of glucocorticoid is known to result in osteoporosis. Deflazacort (DFZ), a synthetic glucocorticoid, has been reported to have bone sparing properties in vivo eompared to dexamethasone(DEX). Not only the direct effect of DFZ on human osteoblast but the mechanism by which the drug spares bone remains unclear. This study, therefore, is aimed to investigate the direct effect of DFZ on the proliferation and differentiation of human osteoblast as well as on the gene expression of osteocalcin and osteoblast as well as on the gene expression of osteocalcin and growth factor produced in osteoblast. Methods: Human osteoblast-like cells were cultured from a piece of the tibia removed during selective orthopedic surgery for patients without metabolic bone diseases. The morphological iden- tification of osteoblast-like cell was performed under the light microscope after alkaline phosphatase staining. Cell proliferation rate was determined by [3H] thymidine incorporation into DNA. Cell differentiation was determined by alkaline phophatase activity. mRNA expression was quanti- tatively measured by the competitive reverse transcription-polymerase ehain reaction(RT-PCR). Results: The cultured cells demonstrated 1,25-dihydroxyvitamin D3-induced increases in alkaline phophatase activity and osteocalcin mRNA expression which are the properties of osteoblast. Twenty six percent of the cultured cells were identified as osteoblast-like cells by alkaline phophatase staining. After 24hr incubation with DEX or DFZ, the [3H) thymidine incorporation was significantly inhibited by 100nM DEX or DFL Alkaine phophatase activity was significantly increased by 100nM DEX. Osteocalcin mRNA was significantly decreased by both glueocorticoids. While DEX significantly suppressed expression of asteocalcin mRNA at 10nM and 100nM, DFZ did so only at 100nM. IGF-I mRNA was significantly decreased by 100nM DEX. Conclusion: These results suggest that the inhibitory effect of DFZ on the cell proliferation and protein synthesis is less than that of DEX, which might be responsible for the bone sparing effect of DFZ in vivo.
Alkaline Phosphatase ; Bone Diseases, Metabolic ; Cell Differentiation ; Cell Proliferation ; Cells, Cultured ; Dexamethasone ; DNA ; Gene Expression ; Humans ; Insulin-Like Growth Factor I ; Orthopedics ; Osteoblasts ; Osteocalcin ; Osteoporosis ; RNA, Messenger ; Thymidine ; Tibia