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Lentinan inhibited the proliferation of MH-134 ascites hepatoma transplanted subcutaneously. The best result occurred when 1 mg-2 mg/kg of lentinan was administered for 10 consecutive days from the eighth day after tumor transplantation. Tumor proliferation was 33% inhibited as measured by the average tumor diameter. The average survival (days) when chemotherapy with mitomycin-C (MMC), 5-FU and Ara-C in combination with lentinan, was administered concurrently in the second week of the tumor transplantation was 29.2 days as compared to 20.5 days in the untreated group, 25.1 days in the group given lentinan alone, and 22.0 days in the group receiving chemotherapy alone. When lentinan was administered in combination with bacterial lipopolysaccharide (LPS), the group given lentinan for 5 consecutive days from the third day after tumor transplantation and 30 micrograms LPS i.p. on the thirteenth day, had 70% inhibition of tumor as measured by the average tumor weight. The antitumor activity of lentinan was studied by following changes in macrophage migration inhibition activity (MI). In the untreated group, MI activity disappeared on the 14th day after tumor transplantation. In the group treated with lentinan, spleen cells had positive activity suggesting a restorative action of lentinan on the immune suppression accompanying tumor growth.

Erythrocyte catalase in normal and Japanese type acatalasemia hemolysates was separated by chromatofocusing into several fractions in the pH range of 6.1 to 5.7. Normal hemolysate gave a major peak of catalase activity with a pH of 6.1 to 5.5, while acatalasemia hemolysate gave several small peaks in this pH range and a main peak with a pH of 6.6 to 6.2. The main protein band in catalase active fractions separated from normal erythrocytes had a molecular weight of 60,000 by SDS polyacrylamide gel electrophoresis. A similar faint protein band having a molecular weight of 60,000 was also found in acatalasemia hemolysate in addition to a fairly intense band with a molecular weight of about 30,000. Catalase active fractions from normal erythrocytes reacted with antihuman erythrocyte catalase rabbit serum by double immunodiffusion.

The patient was a 37-year-old female teacher with hyperemesis diabeticorum and juvenile Type-I diabetes. At the age of 29 years, nausea and vomiting developed and secured at nearly weekly intervals. She was started on clotiazepam (15 mg/day). The vomiting was cured and psychological improvement was evident; her anxiety about diabetes was markedly reduced. An X-ray examination after the administration of clotiazepam showed that she was entirely free from marked hypoperistalsis and the severe retention of gastric contents which had been present before this treatment. The present case is a clear example of stress closely related to the pathogenesis of hyperemesis diabeticorum.

Two factors from normal rat liver cytoplasm inhibited the proliferation of cultured L-929 fibroblasts. One was arginase, the other was a small molecular weight inhibitor stable to trypsin and heat treatment. The small molecular weight inhibitor inhibited the protein and DNA synthesis of L-cells. Inhibition of DNA synthesis was thought to be secondary to the inhibition of protein synthesis.

Response rates and survival times were studied in 47 patients who had multiple myeloma and who were being treated with Prednisolone and sequential Melphalan and Ifosfamide (MIP therapy). The clinical response was determined by objective parameters such as the reduction of M-protein level, tumor volume and healing of bone destruction. Twenty-eight of the patients (59.6%) responded to the MIP therapy. The 50% survival time as followed from the initiation of treatment to death was 19 months. Of the prognostic factors, the age (greater than or equal to 70 years), clinical stage III of Durie and Salmon, hypercalcemia, extensive bone lesions, and the patho-morphological type IV of Brucher were associated with a decreased life-span. Therefore, MIP therapy was more effective in poor risk (high tumor mass group) than in good risk (low or intermediate tumor mass group) patients, but the survival of patients on MIP therapy was shorter in the poor risk group than in the good risk one. In addition, the group which responded rapidly (i.e. within 2-5 weeks) had longer remission and longer survival than the group which improved slowly (i.e. after 6-16 weeks).