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The laminar steady flow of non-Newtonian fluid (biviscosity fluid) through an axisymmetric stenosis is calculated using the finite element methods. The flow pattern, the separation and reattachment points, and the distributions of pressure and shear stress at the wall are obtained. Then, the axial force acting on the stenosis is evaluated. It is suggested by the authors that this force can become one of the causes of post-stenotic dilatation. Calculated results show that the non-Newtonian property of blood weakens the distortion of flow pattern, pressure and shear stress at the wall associated with the stenosis and that the non-Newtonian property of blood decreases the axial force acting on the stenosis.

Background. Patients with neurofibromatosis type 1 (NF1) are prone to develop malignancy, particularly malignant schwannoma and glioma in adults. Methods. To assess the risk for childhood malignancy in NF1, 26,084 patients with cancer younger than 15 years of age registered from 1969 to 1989 in the Japan Children's Cancer Registry were reviewed. The incidence of NF1 in each type of cancer was compared with that in the Japanese population. Results. Fifty‐six children with cancer had NF1 in the national registry. The incidence of NF1 (0.21%) was 6.45 times that of the expected estimated rate of 1 per 3000 in the Japanese population. These tumors tended to be type and site specific. The NF1 incidence was extremely high in optical nerve glioma (12.5%), other central nervous system gliomas (0.9%), and malignant schwannoma (31.4%). For nonneural tumors, NF1 incidence was increased in rhabdomyosarcoma (1.36%), particularly those in urogenital organs, and in myelogenous leukemia (0.27%). Epithelial carcinomas were not observed in the group of patients with NF1. Conclusion. The risk for glioma and malignant schwannoma increases in children and adults with NF1. Moreover, the risk for two childhood malignancies, myelogenous leukemia and rhabdomyosarcoma, increases in children with NF1. The NF1 gene seems to increase the risk not only for neural tumors but also for some non‐neural tumors in an age‐specific, organ‐dependent pattern of carcinogenesis.

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With the use of the more intensive induction regimen A plus blood stem cell transplantation for MYCN-amplified patients, survival curves for those with or without MYCN amplification now appear similar. Higher doses of chemotherapy may ameliorate the effect of MYCN amplification in patients with high-risk neuroblastoma.