Yoshimi Yamashita

Malignant Cystosarcoma Phyllodes Of Prostate

A case of malignant cystosarcoma phyllodes of the prostate is reported in a 45‐year‐old male. This tumor was composed of benign columnar or squamous cystic folds and sarcomatous stroma including rhabdomyomatous elements. The prostatic origin of the tumor was clearly proved by the unlabeled immunoperoxidase method. ACTA PATHOL. JPN. 34: 663–668, 1984.

Amyloid Fibril Formation in the Rough Endoplasmic Reticulum of Plasma Cells from a Patient with Localized Aλ Amyloidosis

Evidence for amyloid fibril formation in rough endoplasmic reticulum (RER) of plasma cells from the duodenum of a 62-year-old man with localized A lambda amyloidosis is described. The inclusions in RER of plasma cells were composed of tightly packed, regular arrays of fibrils cut in both longitudinal and cross-sections. The fibrils within the inclusions, measuring 10 nm in width, were oriented parallel to the long axis of the inclusions. By immunoelectron microscopy with an antihuman A lambda antiserum, gold particles labeled the fibrils located both in the RER of plasma cells and in the extracellular space. In addition, electron-dense material in the dilated RER was occasionally labeled. These findings suggest that at least some amyloid fibrils are unequivocally created in the RER of plasma cells.

IMMUNOLOGICAL HOMOGENEITY OF LAFORA BODY, CORPORA AMYLACEA, BASOPHILIC DEGENERATION IN HEART, and INTRACYTOPLASMIC INCLUSIONS OF LIVER and HEART IN TYPE IV GLYCOGENOSIS

Antisera against Lafora bodies were made in rabbits by subcutaneous injection of the myocardium from a patient died of Lafora disease. Using this antisera, immunohistochemistry revealed that corpora amylacea, the basophilic degeneration of myocardium and deposits of type IV glycogenosis contained the materials which were antigenically common to Lafora bodies.

COMPARATIVE STUDY OF THE INTRACYTOPLASMIC INCLUSIONS IN LAFORA DISEASE AND TYPE IV GLYCOGENOSIS BY ELECTRON MICROSCOPY

We compared the ultrastructure of the intracytoplasmlc inclusion substance present in Lafora bodies and the myocardium of patients with Lafora disease, with that in the hepatocytes and myocardium of patients with type IV glycogenosis. Fibril‐like structures and associated electron‐dense clumps (crumpled plates) are the main components of the deposits in these two diseases. Ultrastructurally, the inclusions in both diseases appeared quite similar. In Lafora bodies, the electron‐dense materials formed their central cores, but were also scattered in their peripheral areas. In type IV glycogenosis, the materials tended to be localized in the centers of large storage masses. The fibril‐like structures in Lafora bodies were somewhat thicker and more electron‐dense than those in type IV glycogenosis. The fibril‐Hke structures and the crumpled plates in the intracytoplasmlc inclusions of both Lafora disease and type IV glycogenosis were intensely stained in sections subjected to Thiéry staining. Despite previous considerations to the contrary, the findings of the present study suggested that the fibril‐like structures are not true fibrils, but in fact plates.

Three Kinds of Foamy Cells in the Spleen: Comparative Histochemical and Ultrastructural Studies

By light and electron microscopy, we observed foamy cells in the spleens from a patient with hemolytic anemia due to red cell adenosine deaminase (ADA) overproduction, a patient with rheumatoid arthritis (RA) treated with gold, and patients with idiopathic thrombocytopenic purpura (ITP). The foamy cells associated with red cell ADA overproduction were essentially similar to Gaucher-like cells described in patients with thalassemia, and it was suggested that the accelerated destruction of red cells was one of the factors responsible for the development of foamy cells. Foamy cells in ITP and RA were closely associated with an increased destruction of platelets in the spleen. Morphologic transitions between phagocytosed platelets and myelin-like materials were traced in these disorders. In RA, however, foamy cells were heterogeneous from an ultrastructural standpoint, with different cytoplasmic inclusions. In addition to myelin-like materials, dense bodies, vacuoles with flocculent materials, and gold were noted in most of foamy cells. As gold compounds are known to inhibit lysosomal enzymes, we surmise that an acquired disturbance in lysosomal digestion is partially responsible for the accumulation of intermediate metabolites. In the pathogenesis of foamy cells associated with blood cell dyscrasia, the accelerated destruction of blood cells and/or acquired disorders in catabolic pathways within the macrophages are suggested to be the underlying mechanism of an intralysosomal accumulation of incompletely degraded cellular debris.

Morphologic study of three cases of insulinoma. Histochemical and ultrastructural studies

Ultrastructural and immunocytochemical features of three human insulinomas, one with metastases and the other two with psammoma bodies and amyloid, respectively, are described. Neoplastic cells of all patients reacted with antihuman insulin antibody using the peroxidase‐antiperoxidase (PAP) method. Ultrastructurally, neoplastic cells consisted of light cells and dark cells, both of which had a large number of secretory granules, microfilaments, ceroid bodies, and phagolysosomes. Psammoma bodies seemed to originate from neoplastic cell debris in one tumor. In another case, amyloid fibrils appeared to be produced by tumor cells, and there was a close association of amyloid with secretory granules.

An Ultrastructural and Histochemical Study of Alveolar Soft Part Sarcoma With Special Reference to The Nature of Crystals

We have presented a case of typical alveolar soft part sarcoma probably originating from the soft tissues of the retroperitoneum with metastasis to the brain. An ultrastructural study including histochemical observation of the metastatic lesion was performed to clarify the nature of the crystals characteristic to the tumor cells of this disease. The crystalline structures have acid‐phosphatase activtiy at a histological and ultrastructural level. Our results suggested that they might be derived from coalescence of primary lysosomes or by digestive disintegration of some protein.

Multihormone-producing islet cell tumor of the pancreas associated with somatostatin-immunoreactive amyloid: Immunohistochemical and immunoelectron microscopic studies

Pancreatic islet cell tumors, especially insulinomas, are often associated with amyloid deposition in the tumor tissue. Biochemical analysis has demonstrated that the amyloid protein from insulinoma is derived from islet amyloid polypeptide (or amylin) that is produced by tumor cells originating from beta cells of the islet of Langerhans. We examined a case of malignant pancreatic islet cell tumor with amyloid deposition in the tumor tissue using immunohistochemistry and double-labeling immunogold electron microscopy. The tumors were composed of cells producing multiple hormones, including somatostatin, gastrin, amylin, insulin, calcitonin gene-related polypeptide, and calcitonin. Amyloid deposits reacted with antisomatostatin antiserum but not with other antisera, including antiamylin. The present study demonstrated for the first time that amyloid associated with islet cell tumors is not always derived from amylin and can come from somatostatin.

Leiomyoblastoma and Leiomyomatosis of the Small Intestine in a Case of von Recklinghausen's Disease

A 70‐year‐old patient with von Recklinghausens neurofibromatosis 1 (NF1) developed a stomach ulcer and underwent a total gasterectomy. During the laparotomy, a leiomyoblastoma and multiple leiomyomas, which were histologically diagnosed as such later, were found in the small intestine and resected. It is quite possible that the association of gastrointestinal leiomyomas and NF1 is more than coincidental. It is thus important to take this complication into account in clinical treatment of patients with NF1.

AMYLOID ENHANCING FACTOR (AEF) : ISOLATION AND BIOCHEMICAL AND PATHOLOGICAL CHARACTERISTICS

Neutrophils and spleens were prepared from mice after treatment to induce amyloid deposition. The deposition of amyloid was accelerated in normal recipients by intravenous injection of more than 2x104 neutrophils, and intraperitoneal injection of supernatants obtained by homogenization and centrifugation of the neutrophils and spleens. The supernatants were subjected individually to DEAE ion–exchange chromatography. Amyloid enhancing factor (AEF) activity was present in peaks eluted at an NaCl concentration of 0.17 M. The fractions containing AEF were subjected to high‐performance liquid chromatography (HPLC), and AEF was eluted at a position corresponding to about 15 KDa. Purified AEF was analyzed by amino acid sequencing and gas chromatography. The N‐terminal amino acid was blocked, and AEF contained some saccharides including glucose, mannose, galactosamine and sialic acid, and an undefined substance (probably derived from certain proteins). Immunoelectron microscopy by the preembedding method using an anti‐AEF antiserum demonstrated that the cytosol, but not primary and specific granules in neutrophils from the spleen of amyloid‐laden mice, reacted with the antiserum. These findings suggest that AEF is a glycoprotein associated with neutrophils.