Transferrin receptor expression in oral tumors was examined by staining with monoclonal antibody against the human transferrin receptor. The cells with positive reaction were recognized in the basal and parabasal layers of the normal epithelium. The staining was found in all the malignant tumors but not in the benign tumors. These results suggest that the immunohistochemical analysis of the transferrin receptor is useful for the diagnosis of oral malignant tumor in addition to the clinical and pathological examinations.
The net cholesterol transfer activity from high density lipoprotein (HDL) to low density lipoprotein (LDL) was determined in the patients with coronary heart disease (CHD) to examine its effect on the pathogenesis of arteriosclerosis. Furthermore, in the CHD patients with high HDL cholesterolemia (more than 60 mg/dl), the HDL particle size was measured by high performance liquid chromatography. A significant cholesteryl ester transfer activity (P<0.02) was noted in the CHD patients with low HDL cholesterolemia (less than 60 mg/di). The rate of cholesteryl ester transfer activity (cholesteryl ester transfer activity/hour) inversely correlated with the serum HDL cholesterol value (r=-0.483, P=0.096) in the patients with CHD. These results suggest that an increase of CETA caused a low HDL cholesterol value in the CHD patients with low HDL cholesterolemia and it may have the risk of causing CHD. However, an increase of the CETA was not found in the CHD patients with high HDL cholesterolemia compared to the normal subjects, the HDL particle size beings significantly greater than that in the normal subjects. In the CHD patients with high HDL cholesterolemia, the large size of HDL may have the risk of causing CHD.
Calcium ionophore A23187-induced liver damage was studied in perfused rat liver and isolated hepatocytes. Two groups of calcium antagonists, dihydropyridine-type and nondihydropyridine-type, were examined for their protective effects on A23187-induced liver damage. The former calcium antagonist inhibited cell damage at pharmacological doses, whereas nondihydropyridine type calcium antagonists were unable to prevent A23187-induced cytotoxicity. Different inhibitors, such as cAMP phosphodiesterase inhibitor OPC3689, calmodulin inhibitor W-7, and C-kinase inhibitor H-7, were tested in isolated hepatocytes to determine whether intracellular signal transduction systems are involved in the liver cell injury produced by A23187. Calcium ionophore A23187-induced LDH activity of the medium was depressed by W-7 and H-7 to 55±4% and 63±4% of controls (p<0.01), respectively. However, OPC3689 did not show a protective effect. We conclude that A23187-induced liver cell injury was inhibited by dihydropyridine-type calcium antagonists which may interfere with activation of calmodulin and C-kinase.