Acta pathologica japonica最新文献

An experimental model for induction of gliomas corresponding to human anaplastic astrocytomas and glioblastomas is reported. Eleven week old F344 and ACI rats were given 100 or 200 p.p.m. N-methyl-N-nitrosourea (MNU) solution as their drinking water for 42 weeks. Gliomas were induced at very high incidences (82.5-92.5%) in each group. Induced gliomas showed apparent evidence of morphologic malignancy by an analysis based on diagnostic criteria of human astrocytomas. All of the gliomas from the killed animals were classified histologically into subtypes according to the classification scheme used in the diagnosis of human gliomas. The majority of macrotumors more than 1 mm in diameter in both strains were diagnosed as anaplastic astrocytomas and glioblastomas. Immunohistochemically, tumor cells in these tumors were almost negative for glial fibrillary acidic protein, while ultrastructurally neoplastic astrocytes contained glial filaments. A strain difference was observed in the ratio of histological subtypes of macrotumors. In F344 rats, astrocytic tumors diagnosed as anaplastic astrocytomas and glioblastomas of an astrocytic type formed the majority, whereas glioblastomas of mixed oligo-astrocytic type predominated in ACI rats. The results indicate that MNU-administration to adult F344 rats may provide a suitable experimental model for gliomas which occur in adult humans.

The contrast medium Thorotrast, an agent well known to be carcinogenic, was injected into 400 congeneic Syrian hamsters. The resulting incidence of malignant hepatic tumors such as cholangiocarcinoma, hepatocellular carcinoma and hemangiosarcoma, was significantly higher in the male experimental group than in the control group, and the 50% survival period in the male group was shortened by about 100 days (P < 0.01). However administration of the antitumor drug PSK (Polysaccharide Kureha), a protein bound-polysaccharide extracted from basidiomycete fungi, prevented this carcinogenic effect. The incidence of malignant hepatic tumors in the experimental group was 22.5% compared with 2.8% in the control group (P < 0.01) and 10.5% in the PSK-treated group (P < 0.01). PSK also increased the 50% survival period by 61 days (P < 0.01).

Sclerosing hemangioma of the lung is a rare benign neoplasm of uncertain histogenesis. In this study, thirteen cases of sclerosing hemangiomas were analyzed by immunohistochemistry for various histochemical markers including surfactant apoprotein. The pale cells were shown to share several immunohistochemical markers with epithelial lining cells and were suggested to be immature cells differentiating toward epithelial lining cells. Electron microscopic study failed to characterize the exact nature of pale cells, but it disclosed the precise structure of large lamellar bodies, which are frequently present in the cystic spaces of sclerosing hemangioma. These large lamellar bodies had common morphological characteristics to lamellar inclusion bodies of type II pneumocytes or epithelial lining cells. Eight cases of sclerosing hemangioma obtained freshly at surgery had a quantitative analysis of estrogen and progesterone receptors performed by enzyme immunoassay. The value of estrogen receptors ranged from 0 to 7.8 fmol/mg protein. In addition to this quantitative analysis, the immunohistochemical study demonstrated estrogen receptors mainly in the pale cell nuclei of several sclerosing hemangiomas. Estrogen receptors may play an important role in growth, differentiation and surfactant production in the sclerosing hemangioma.

A patient is described with severe IgA nephropathy associated with psoriatic arthritis, idiopathic interstitial pneumonia and brain hemorrhage that developed serially over one and a half years. The histological findings of the renal biopsy showed severe endo- and extracapillary proliferative glomerulonephritis. Massive IgA deposits were observed by immunofluorescence not only in the mesangium but also along the capillary walls. Electron microscopy revealed abundant electron-dense deposits in the mesangial and subendothelial areas. The overlapping or coexistence of these conditions has rarely been reported.

Two cases of spindle cell hemangioendothelioma (SCH) are reported. One of the patients was a 16 year old Japanese female, who had been suffering from Ollier's disease (multiple enchondromatosis) since 3 years of age and had developed multiple SCH in the right leg at the age of 11 years. Spindle cell hemangioendothelioma lesions coincided with the site of enchondromatosis and increased in number thereafter. This is the first report of Ollier's disease complicated with multiple SCH. Another patient, a 33 year old Japanese female, who was a carrier of hepatitis B virus (HBV), developed solitary SCH in the lateral aspect of the right ankle where a lipoma was extirpated 10 years previously. Tumor cells of both cases were composed of four cell types: (i) spindle cells; (ii) epithelioid cells; (iii) vacuolated endothelial cells; and (iv) usual endothelial cells. Endothelia in the cavernous area and vacuolated cells reacted to Ulex europaeus agglutin 1 (UEA-I), factor VIII-related antigen and vimentin. Spindle cells and epithelioid cells reacted only to vimentin.

The chronic administration of cyclosporin A (CyA) could be associated with renal arteriolar damage. Endothelial cell injury is considered to be the first event in this pathological change. Bovine glomerular endothelial cells (GEN) were used to investigate whether CyA induces microvascular injury in vitro. The damage induced by CyA was demonstrated by cell detachment from the culture plate and cell lysis as characterized by the increase in lactate dehydrogenase (LDH) at the same time after CyA treatment. One mumol/L of CyA induced detachment of GEN within 3 h and lysis after 6 h. Cyclosporin A-induced GEN lysis appeared in a dose and time-dependent manner. These results indicate that GEN are vulnerable to CyA exposure, suggesting that GEN damage might be related to CyA-mediated glomerular injury.

Pulmonary disorders in infants are intimately related to the pulmonary development during the antenatal, neonatal and infantile period. In this review, normal pulmonary development is considered and several pulmonary disorders such as pulmonary hypoplasia, pulmonary sequestration, congenital cystic adenomatoid malformation, hyaline membrane disease, bronchopulmonary dysplasia, Wilson-Mikity syndrome and perinatal pneumonia are presented in light of the current literature.

Two cases of mixed medullary and follicular carcinoma of the thyroid (MFC) and two cases of thyroid carcinoma resembling MFC are reported with a description of their histological and immunohistochemical features. Two cases of MFC with lymph node metastasis were histologically distinguishable from each other because one had a follicular structure filled with a thyroglobulin (TG)-positive colloid-like substance and the other did not have it. Although one of the thyroid carcinomas resembling MFC was similar to the case of MFC with a follicular structure in its primary lesion, it showed no lymph node metastasis. The metastatic lesion of the thyroid carcinoma resembling MFC consisted of TG-positive cells and neighboring calcitonin (CT)-positive cells. However the primary lesion exhibited the typical features of papillary carcinoma except for the presence of a small lesion which stained negatively for both TG and CT. The two types of tumor were not intermingled in a single tumor. These cases of thyroid carcinoma resembling MFC have a possibility of being MFC. However they should not be classified as MFC because lymph node metastasis or the coexistence of medullary carcinoma and follicular carcinoma in their primary lesion was not proved.

In a 70 year old woman with a tumor in the head of the pancreas, the lesion was predominantly composed of papillary adenocarcinoma protruding into the main pancreatic duct, with periductal invasion. The major portion of the adenocarcinoma was intraductal and was composed of tall columnar epithelial cells with pseudostratified nuclei, had the appearance of primitive endodermal epithelium and was positive for carcino-embryonic antigen. In contrast, in the other portion of the adenocarcinoma which had the predominant component of periductal invasion, neoplastic cells had an irregular, eosinophilic cytoplasm, resembled ordinary pancreas adenocarcinoma of ductal origin and was positive for CA19-9. Neuro-endocrine and alpha-fetoprotein-positive cells with a primitive appearance were scattered among the neoplastic epithelial linings. In addition, a vimentin-positive sarcomatoid component intermingled with the adenocarcinoma. These findings suggest that the adenocarcinoma observed in this tumor with the primitive appearance also had a primitive phenotype. This was evidenced by immunohistochemistry and the divergent directions of differentiation. This particular case illustrates that pancreas adenocarcinoma of the ordinary histologic type can arise secondarily from the more primitive neoplastic cells during carcinogenesis within the pancreatic duct.

The phenotypes of B cells and dendritic cells in human thymus were examined immunohistochemically using various monoclonal antibodies. Normal thymus contained a few B lymphocytes recognized by CD19, CD20, CD22, L26 and LN-2, which were localized in the medulla. These B cells were negative for LN-1, L30 and CD11c (Leu M5). Activated B cells recognized by CD23 (B6) and L29 antibodies were not present in normal thymus. Dendritic cells stained by CD11c were weakly positive for L26 and CD20. There was no difference in the distribution of dendritic cells between normal thymus and thymus from the patients. In the thymus from patients with myasthenia gravis, numerous B cells were demonstrated in the medullary area and lymphoid follicles. Activated B cells were seen mainly in the germinal center of lymphoid follicles and were scarce in the medulla. Many B cells were also found in the medulla and lymphoid follicles of the thymus from patients with ulcerative colitis. However most of those B cells were not activated, even in the lymphoid follicles. These results suggest that thymic B cells may contribute to the induction of immune abnormalities in patients with myasthenia gravis and those with ulcerative colitis, however, the mechanisms by which thymic B cells participate in the pathogenesis of these two diseases would be different.