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Phorbol 12-myristate 13-acetate (PMA) induces differentiation of human leukemic HL-60 cells into cells with macrophage-like characteristics and enhances the susceptibility of HL-60 cells to the Helicobacter pylori VacA toxin (de Bernard, M., Moschioni., M., Papini, E., Telford, J. L., Rappuoli, R., and Montecucco, C. (1998) FEBS Lett. 436, 218-222). We examined the mechanism by which HL-60 cells acquire sensitivity to VacA, in particular, looking for expression of RPTPbeta, a VacA-binding protein postulated to be the VacA receptor (Yahiro, K., Niidome, T., Kimura, M., Hatakeyama, T., Aoyagi, H., Kurazono, H., Imagawa, K., Wada, A., Moss, J., and Hirayama, T. (1999) J. Biol. Chem. 274, 36693-36699). PMA induced expression of RPTPbeta mRNA and protein as determined by RNase protection assay and indirect immunofluorescence studies, respectively. Vitamin D(3) and interferon-gamma, which stimulate differentiation of HL-60 cells into monocyte-like cells, also induced VacA sensitivity and expression of RPTPbeta mRNA, whereas 1. 2% Me(2)SO and retinoic acid, which stimulated the maturation of HL-60 into granulocyte-like cells, did not. RPTPbeta antisense oligonucleotide inhibited induction of VacA sensitivity and expression of RPTPbeta. Double immunostaining studies also indicated that newly expressed RPTPbeta colocalized with VacA in PMA-treated HL-60 cells. In agreement with these data, BHK-21 cells, which are insensitive to VacA, when transfected with the RPTPbeta cDNA, acquired VacA sensitivity. All data are consistent with the conclusion that acquisition of VacA sensitivity by PMA-treated HL-60 cells results from induction of RPTPbeta, a protein that functions as the VacA receptor.

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Primary renal angiosarcoma is very rare. To our knowledge, only 15 cases have been reported to date. A 77-year-old Japanese man with a unilateral kidney presented with massive hematuria followed by renal failure. A renal tumor was suspected and a left nephrectomy was performed. The histopathological diagnosis was angiosarcoma of the kidney. A hemorrhagic tumor measuring 10 x 5 cm and clotted blood was found in the medullary area. The atypical tumor cells had a sinusoidal and solid appearance, and showed immunohistochemically positive reactions for some of the endothelial markers. The patient died about 21 months after the nephrectomy and the autopsy revealed massive metastases to the liver and retroperitoneum. One of the differential diagnoses of the case was angiomyolipoma, because the tumor cells were relatively bland in their histological appearance with entrapped fat cells in the pelvic area. Fifteen case reports with titles that included the term 'hemangiosarcoma/angiosarcoma', 'hemangioendothelioma/endothelioma' or 'vascular sarcoma' of the kidney were reviewed and compared to the present case.

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Small mesenchymal nodules (SNs) are observed in some cases of renal angiomyolipoma (AML), with or without tuberous sclerosis. They are composed of blood vessels and/or nonvascular smooth muscle cells (SMCs) and/or fat cells. We examined 20 cases of AML, performed detailed histopathologic and immunohistochemical studies of SNs, verified the histologic relationship between SNs and AMLs, and compared the SNs of the tuberous/nontuberous sclerosis groups. Seventy-seven SNs were observed in five cases of AML. The SNs were 0.11 mm to 20.0 mm in diameter. The location of small-sized SNs in the kidney was variable; almost all of the SNs larger than 3.25 mm were in the renal capsule. The small-sized SNs contained mainly epithelioid-type nonvascular SMCs. Blood vessels and fat cells were not observed in the small-sized SNs but appeared gradually in the large-sized SNs. Almost all of the SNs were rounded lesions, and no fusion was observed between the SNs. Nonvascular SMCs of all of the SNs and AMLs were positive for vimentin, alpha-SM actin, and S-100 protein. The SNs less than 1.13 mm in diameter were negative for HMB-45; the nonvascular SMCs of AMLs and of SNs greater than 1.13 mm in diameter were positive for HMB-45. Nonvascular SMCs of SNs and AMLs showed a neurogenic phenotype. The SNs of the nontuberous sclerosis group contained only SMC components, whereas the same-size SNs of the tuberous sclerosis group contained SMCs, fat cells, and blood vessels. The SNs of the nontuberous sclerosis group may not increase in size or may grow slowly. Some of the SNs of patients with tuberous sclerosis grow to become AML. Although the SNs in patients with nontuberous sclerosis do not contain any blood vessels or fat cells, their SMCs show the histologic and immunohistochemical characteristics of AMLs; this indicates that SNs are the "buds" of AML.

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An 8-yr-old Japanese boy developed infantile digital fibromatosis in the right ring finger with recurrence and another lesion in the right middle finger. Histologic investigation of the tumor disclosed that the size and frequency of inclusion bodies were inversely proportional to the degree of fibrosis. Electron microscopic study revealed a variety of stages in the development of inclusion bodies, ranging from small, dense aggregates of filaments into bundles with dense bodies traversing the cytoplasm to typical inclusion bodies that also contained cytoplasmic organelles. In areas of dense fibrosis, the cytoplasm of the tumor cells showed areas of constriction and compression by adjacent bundles of collagen. The tendency for a decrease in the number of inclusion bodies in these areas necessitated a differential diagnosis from other fibrous or fibro-histiocytic lesions. Our findings suggest that the tumor may undergo a decrease in the numbers of inclusion bodies and spontaneously may become fibrotic with time. Thus, even as a form of fibromatosis featuring both recurrence and multiple lesions, it may not have a consistently aggressive nature. These findings support the concept that infantile digital fibromatosis should be managed by limited excision rather than by immediate aggressive surgical treatment.

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Perinuclear clear cytoplasm observed in the light microscopic specimens of the tumor cells of smooth muscle origin is in general, understood as the artefact caused by the formalin fixation. However, the precise mechanisms of the histogenesis of clear cytoplasm are still not clear. We observed the clear cytoplasm directly by mean of the electron microscopy of materials detached from light microscopic specimen. Furthermore, we observed the light microscopic specimens made by varying types of methods, examining whether the clear cytoplasm was present or not. The electron microscopy of materials detached from light microscopic specimens revealed the band-like defects of cytoplasm along the long axes of tumor cells. These defects were thought to result from the falling off of cytoplasm. The 1 mu section of the epon embedded block derived from the paraffin embedded block for light microscopic specimen presented no clear cytoplasm, suggesting that the cytoplasm falls off at the procedure of deparaffinization and staining. Although the specimen of conventional frozen section showed no clear cytoplasm, the specimen made by the frozen sectioning after formalin fixation revealed clear cytoplasm. Consequently, it is thought that the fixation of the tissue before the sectioning makes the cytoplasm fragile, thereafter, the cytoplasm falls off at the procedure of deparaffinization and staining.

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Histological localization of myosins of the smooth and skeletal muscles was investigated in comparison with that of myoglobin by immunoperoxidase technique using the antibody against each of them in surgical specimens from spindle cell tumors and tumor-like lesions of the soft tissue. Skeletal muscle myosin was demonstrated in all of the cases of rhabdomyosarcoma, whereas myoglobin was found in 75% of the examined cases. Smooth muscle myosin was widely distributed not only in the tumor cells of smooth muscle origin such as leiomyosarcoma and angioleiomyoma, but also in the tumor cells showing myofibroblastic differentiation such as malignant fibrous histiocytoma and in the epithelial components of synovial sarcoma. The results showed that skeletal muscle myosin can be regarded as an excellent marker in the diagnosis of rhabdomyosarcoma and that smooth muscle myosin is a useful marker of leiomyosarcoma and leiomyomas, and of tumors with myofibroblastic differentiation.

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Estudo prospectivo, comparativo da analgesia pos-operatoria em pacientes submetidas a cesareana e recebendo analgesico (dipirona) quando solicitado num grupo de analgesia espinhal com 0, 1,2 ou 4 mg de morfina peridural. Concluimos que a analgesia foi efetiva nos 4 grupos com uma incidencia maior de efeitos indesejaveis no grupo com 4 mg de morfina peridural

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