Adult male and female acatalasemic (C3H/AnLCsbCsb), hypocatalasemic (C3H/AnLCscCsc) and normal mice of C3H strain fed on regular laboratory chow for 15 months showed an increased incidence of spontaneous mammary tumor in the decreasing order of female acatalasemic, male acatalasemic, female hypocatalasemic and male hypocatalasemic mice. Normal mice did not develop mammary tumor. We conducted a prospective study with female acatalasemic mice, which showed the highest incidence of mammary tumor, to examine the preventive effect of vitamin E on mammary tumor. Female acatalasemic mice were fed on vitamin E‐deficient (28 animals) and vitamin E‐supplemented diet (25 animals) for 29 months. The incidence of mammary tumor in mice given the vitamin E‐supplemented diet was 47%, while that in mice given vitamin E‐deficient diet was 82% (P<0.002). Mammary tumors were apparent after 9 months of vitamin E deprivation and after 14 months of vitamin E supplementation. Female normal mice did not develop mammary tumor during a comparable period of time. The mean catalase activity of mammary gland in acatalasemic mice was 18.8% of that in normal mice. The results indicate that vitamin E protects acatalasemic mice against the development of mammary tumor.

A long-term follow-up study of Lennox-Gastaut syndrome (LGS) ( > 10 years) was conducted with 38 patients with severe motor and intellectual disabilities (SMID) to clarify the relationship between the rapid development of dysphagia and epileptic seizures, and to elucidate the long-term evolution of LGS in patients with SMID. Those who showed a relatively favourable seizure outcome were compared to those with a poor seizure outcome. Poor seizure outcome correlated strongly with: (a) an early appearance of dysphagia and additional deterioration of the already retarded mental function; (b) a predominance of atypical absence seizures; and (c) persistent frequent epileptiform discharges during electroencephalographic evaluations. Neither age at seizure onset nor intelligence level at the time of the last examination was correlated with seizure prognosis. Further, seizure prognosis was not related to the aetiology of LGS. Repeated seizures apparently caused development of progressive epileptic encephalopathy, in addition to the underlying severe brain damage. Since development of dysphagia burdens an already severely handicapped patient with intensive medical care, efforts to reduce the seizures and design a long-term care plan are of great importance.

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Newborn Sprague‐Dawley rats were inoculated intracranially with JC virus (Tokyo‐1), a human polyomavirus, which had been isolated by Nagashimaet al. from the autopsied brain of a patient with progressive multifocal leukoencephalopathy in Japan. Twenty‐one to 70 weeks later, 21 of 27 rats developed brain tumors in the cerebrum, but not in the cerebellum. Most of the tumor cells were of an undifferentiated neuroectodermal nature and showed nuclear palisades and pseudorosettes. In some tumor cells glial flbrillary acidic protein was positive immunohistochemically, and many glial filaments were demonstrated ultrastructurally. Neuronal differentiation was not proved. Two continuous lines of cultured tumor cells were established, and T antigen of JCV (Tokyo‐1) was present in both cell lines. Glial differentiation was confirmed also in the tumors produced by subcutaneous transplantation of cultured tumor cells.