[An autopsy case of mixed monoclonal cryoglobulinemia accompanied by hypertrophic cardiomyopathy].
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Biomedical subjects
Publications and source records attributed to I Sato.
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A study was carried out to investigate the influence of 3 kinds of hepatotoxic agents on the peripheral blood leucocyte population, the splenocyte population and the delayed type hypersensitivity (DTH) in mice. These parameters were not affected by the intraperitoneal injection of D-galactosamine (Gal). The intensity of picryl chloride induced DTH (PC-DTH) in mice was significantly lowered with the administration of carbon tetrachloride (CCl4) and 1-naphtylisothiocyanate (ANIT) in a dose-dependent manner after the mice were sensitized to picryl chloride (PC) from one to three days after the subcutaneous injection of CCl4 and ANIT. However the peripheral blood leucocyte population and splenocyte population were not affected by these chemicals. The lowering effect of CCl4 and ANIT on PC-DTH was somewhat weakened when PC sensitization was performed seven days after the injection of CCl4 and ANIT. No lowering effect was observed when PC sensitization was performed fourteen days after the injection of CCl4 and ANIT. The intensity of PPD induced DTH (PPD-DTH) was also lowered by the administration of CCl4 and ANIT when the sensitization to tubercle bacilli was performed three days after the injection of CCl4 and ANIT. Cianidanol (KB-53) prevented the decrease of PC-DTH and PPD-DTH in the mice injected with CCl4 and ANIT in a dose-dependent manner, but did not affect DTH in normal mice. So it seems that KB-53 has an immunostimulating effect on decreased cellular immunity.
Effects of cianidanol on chronic liver injury induced by prolonged administration of carbon tetrachloride (CCl4) and on liver regeneration after partial hepatectomy of normal liver and CCl4 chronically injured liver were investigated by the measurement of plasma and liver biochemical parameters. Cianidanol increased the total plasma protein and 14C-Leu incorporation into plasma protein, while it reduced the contents of liver cholesterol and triglycerides. In rats with chronically injured liver or regenerating liver after partial hepatectomy of chronically injured liver, cianidanol improved the retention rate of BSP and the content of liver sugar. In rats with chronically injured liver, plasma GPT and GOT activities were reduced with the administration of cianidanol. Cianidanol had no effect on the regeneration rate after partial hepatectomy of normal liver, but it increased the regeneration rate after partial hepatectomy of chronically injured liver. These results suggest that cianidanol has the effect of improving the function of liver cells damaged by CCl4 treatment and of promoting the recovery of cell function to a normal level.
The therapeutic effects of cianidanol on the rat liver cirrhosis induced by CCl4 were investigated by means of pathological examination. Rats were administered with CCl4 subcutaneously twice a week for a consecutive 10 weeks. From a macroscopical viewpoint, pailing grayish discoloration, granular hyperplastic nodules and the disappearance of luster on the surface of the liver, and the formation of pseudolobule on the cut surface were observed in the control group. In the histopathological findings, degenerative fatty change and ballooning degeneration of parenchymal liver cells, a formation of pseudolobule caused by septal fibrosis proliferation, an acinar arrangement caused by pericellular fibrosis, and a cholangiollar proliferation were observed. All these abnormalities were diminished by the oral administration of 200 and 400 mg/kg of cianidanol for 7 days. The therapeutic effects of cianidanol were dose-dependent on the liver cirrhosis rats. Consequently, it is suggested that cianidanol has therapeutic effects on liver cirrhosis induced by CCl4 by relieving hepatocytes disorder, improving regeneration of hepatocytes and the absorption of proliferated fibrotic tissues.
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A nation-wide sero-epidemiologic survey of adult T-cell leukemia virus (ATLV), detected es anti-ATLA (ATLV-associated antigen), was made in Japan. Sera from adult donors in 15 different locations were screened for anti-ATLA. High incidences (6 to 37%) of antibody-positive donors were found in seven regions, one in northern Japan, and the others in southwestern regions. These areas are ATLV-endemic areas corresponding to ATL-endemic areas. Examination of sera from healthy donors aged 6 to 80 years in ATL-endemic areas showed an age-dependent increase of seropositive donors with a maximum of about 30% at 40 years of age. Anti-ATLA was found in all but two of 142 patients with ATL. Anti-ATLA-positive patients with ATL were mainly found in ATLV-endemic areas, and only a few in ATL-nonendemic areas. Six patients with cutaneous T-cell lymphoma in ATLV-nonendemic areas gave a negative reaction for anti-ATLA. The geometric mean titer of anti-ATLA of patients with ATL was higher than that of healthy donors.
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