Showing papers in "Okayama Igakkai Zasshi (journal of Okayama Medical Association) in 1992"

1, 25-Dihydroxyvitamin D3 stimulates the secretion of insulin-like growth factor binding protein 3 (IGFBP-3) by cultured human osteosarcoma cells

Abstract: Several types of specific insulin-like growth factor binding proteins have been reported. These binding proteins are produced by peripheral tissue-derived cells and they modulate the functions of insulin-like growth factors. In this study, we investigated both the secretion of insulin-like growth factor binding protein 3 (IGFBP-3) from a human osteosarcoma cell line MG63, and the effects of 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) on the production of this binding protein. The beta subunit of IGFBP-3 was detected in perinuclear cytoplasm of MG63 cells by immunocytochemical study. Immunoblotting and SDS-PAGE analysis revealed that both 150KD MW entire molecules and 40-60KD MW beta subunit molecules of IGFBP-3 were present in cell-conditioned media. 1,25-(OH)2D3 stimulated the production of the IGFBP-3 molecule by MG63 cells. The concentration of IGFBP-3 in conditioned media began to rise at 12 hours after the addition of 10(-8) M of 1,25-(OH)2D3 and reached peak level at 48 hours. Dose-dependent effects of 1,25-(OH)2D3 were demonstrated. The its maximum effect was observed at 10(-10) M. The concentration of IGFBP-3 in cytosol also increased at a 10(-10) M concentration of 1,25-(OH)2D3. We conclude from these results that human osteosarcoma cells MG63 produce the IGFBP-3 molecule and that 1,25-(OH)2D3 stimulates the production of this protein. These data suggests that the synergistic effects of 1,25-(OH)2D3 on the action of IGF-I on osteoblastic cells, which we reported previously, may be modulated by locally produced IGFBP-3.

Experimental Study on Cerebral Venous Circulatory Disturbance

Abstract: It is well known that the disturbance of cerebral venous circulation, such as resulting from dural sinus thrombosis or occlusion of large cerebral veins or dural sinus during surgery, often leads to brain swelling which causes neurological deficits. However, the pathophysiology of venous circulatory disturbance is poorly understood because of difficulties in making standardized experimental models. In this study, the authors have developed a new experimental model and studied the pathophysiology of cerebral venous circulatory disturbance using this model.