Japanese journal of medicine最新文献

IgA1(kappa)-transferrin complex was ascertained in a case of multiple myeloma with hypersiderinemia. On gel filtration, this complex disclosed an orange-colored protein with two peaks between the 19S and 7S fractions. On polyacrylamide gel electrophoresis and Western blotting analysis, the complex migrated at molecular weights of 430 and 700 kD in the non-reducing condition. A small amount of free transferrin was detected simultaneously. The complex was further separated into monoclonal IgA1(kappa) and transferrin at pH 4.5; these recombined at pH 7.2 after incubation (37 degrees C, 2 h). We also showed that the pepsin-digested F(ab')2 fragment of IgA1(kappa) combined with the transferrin. From these results it can be suggested that monoclonal IgA1(kappa) has an antibody activity for the transferrin. Clinically, this complex distributed the iron transport to erythroid cells in the bone marrow, resulting in hypersiderinemia, anemia, and iron deposits in the liver.

We tested for antibodies to hepatitis B virus (HBV), hepatitis C virus (HCV), and human T lymphotropic virus type-I (HTLV-I) in 629 normal inhabitants of an adult T cell leukemia (ATL) endemic area and in patients with ATL, HTLV-I associated myelopathy (HAM), and hepatocellular carcinoma (HCC) from the same district. The prevalence of serological positivity for each virus was 28.0, 6.4, and 32.6%, respectively, among the 629 inhabitants. There was a positive association between the presence of anti-HCV and serological HTLV-I positive or negative status of these subjects (9.3% vs 5.0%). Conversely, there was no correlation between HBV and HTLV-I serologic prevalence. Only inhabitants positive for anti-HCV showed significantly high serum aminotransferase levels. The levels were not affected by superimposed HTLV-I infection among anti-HCV positives. Fifty three percent of HCC patients were positive for anti-HCV; 35% of whom were simultaneously positive for antibody to HTLV-I. On the other hand, only 2 ATL patients (4.2%) and 2 HAM patients (7.7%) had anti-HCV. These findings suggest that high serum aminotransferase levels are mainly caused by HCV infection and persons with HCV and HTLV-I double infections are at a high risk for the development of HCC but not ATL or HAM.

We report a case of myasthenia gravis (MG) which became worse shortly after the administration of methimazole (MMI) for hyperthyroidism. The activation of immune responses was found during the worsening of MG. The findings suggests the possibility that the worsening of MG might be induced by MMI, presumably by its immunomodulatory property.

The pathogenic mechanism of diabetic nephropathy has been extensively investigated, and the significance of alteration in glomerular hemodynamics or mesangial cell metabolism has been recently clarified. It is expected that in the near future these pathologically important alterations can be corrected, and the development diabetic nephropathy can be halted.

Interactions of lipoproteins containing apolipoprotein (apo) A-I with or without apoA-II with human hepatoma cell line HepG2 were studied to investigate the ligand specificity for high density lipoprotein receptor on human hepatic cells and their metabolism. The two types of lipoproteins were isolated by immunoaffinity chromatography, in which apoE-containing lipoproteins were removed. Specific binding kinetics at 0 degrees C were observed for the apoA-I-containing lipoproteins with or without apoA-II (Kd = 18 or 20 micrograms protein/ml, Bmax = 110 or 120 ng/mg cell protein, respectively). The binding of these lipoproteins to HepG2 cells was competitively inhibited by excess unlabeled apoA-I-containing lipoproteins or apoA-I-phospholipid complexes, but not by apoA-II.phospholipid complexes. Interactions of these lipoproteins with HepG2 cells at 37 degrees C were further examined. These results suggested that HepG2 cells have a specific binding site for apoA-I-containing lipoproteins, and that apoA-I might be a crucial component in the binding of these lipoproteins to human hepatic cells.