Biomedical subjects
Publications and source records attributed to M Kamata.
A case of malignant transformation to a squamous cell carcinoma in a long-standing lumbar dermoid cyst is described. Progress was slow during 6 years. This type of transformation in a dermoid cyst is extremely uncommon and has never been recorded at this site.
The localization of Trimetaphosphatase (TMPase) activity during the acrosomal formation in the mouse testis was enzyme cytochemically investigated by the cerium-salt method. In addition to the lysosomes of the Sertoli cells and the spermatogenic cells in the seminiferous tubules, positive TMPase activity was detected in the Golgi complex and in the acrosomal vesicles of the spermatids, as well as in the acrosomes of both spermatids and spermatozoa. In the Golgi complex of the spermatids, TMPase activity was observed in the first one or two lamellae of the trans-face and in the small vesicles in the vicinity of the Golgi complex. TMPase positive reaction was also detected in the acrosomes of the spermatozoa in the lumina of both the seminiferous tubules and the epididymal duct. The localization of this enzyme activity was compared with that of acid phosphatase (ACPase), as detected by the cerium-based method, using beta-glycerophosphate as substrate: ACPase activity was completely absent from the Golgi complex, small vesicles, acrosomal vesicle and acrosome throughout the entire process of acrosomal formation. TMPase is thought to become one of the acrosomal components, and may be involved in the acrosomal reaction during fertilization.
A 7-year-old boy with partial anomalous pulmonary venous drainage to the high superior vena cava (SVC) underwent surgical repair by Williams procedure. Right upper pulmonary vein was drained to the left atrium via the SVC and the surgically enlarged sinus venosus type ASD. SVC was ligated and divided. SVC was then anastomosed to RA appendage pedicle directly. Autologous pericardium was patched anteriorly to create a new SVC pathway. The postoperative course was uneventful without arrhythmia and cardiac catheterization 1 month postoperation revealed no stenosis of the SVC and right upper pulmonary venous return.
Production of HVJ (Sendai virus) virion is suppressed in the infected LLC-MK2 cells in the low Ca2+ condition. To clarify this phenomenon, the effect of Ca2+ on HVJ morphogenesis was examined under normal and low Ca2+ conditions. The HVJ production was observed in standard medium (containing 1.8 mM Ca2+) within 24 hr after infection and increased with the culture time. Indirect immunofluorescent staining with an anti-HVJ envelope antibody showed that the viral glycoproteins, HANA (HN) and F proteins, were synthesized within 10 hr after infection, diffused to the cell surface, and then many patches strongly stained with this antibody were formed on the cell surface. In contrast, when the infected cells were cultured in low Ca2+ medium, viral glycoproteins were synthesized as in the case of standard medium. However, the glycoproteins were almost all accumulated in the Golgi apparatus, suggesting that expression of viral glycoproteins at the cell surface was suppressed, and the patches were hardly seen on the cell surface. When the low Ca2+ medium was replaced by standard medium, the accumulated viral glycoproteins were rapidly diffused and expressed on the cell surface, HVJ production was restored and patches formed on the cell surface. By confocal laser scanning microscopy, the results were seen more clearly; Ca2+ is necessary for the expression of viral glycoproteins at the cell surface. By electron microscopy under normal conditions, groups of viral budding sites were seen collected in restricted areas, corresponding to the patches observed on immunofluorescent staining, but the budding sites were not seen on the cells cultured in low Ca2+ medium.(ABSTRACT TRUNCATED AT 250 WORDS)
Previously we have reported that Ca2+ concentration in culture medium affects the morphogenesis of HVJ from infected cells. We further investigated the effects of Ca2+ on HVJ morphogenesis in LLC-MK2 cells, focusing on M (matrix) protein which plays an important role in the assembly of viral components. On culture in standard medium (containing 1.8 mM Ca2+), most of the M protein accumulated on the apical surface in patches. On double immunofluorescent staining with anti-M protein monoclonal antibody and polyclonal antibody against HVJ glycoproteins, M protein and viral glycoproteins were observed in the same patches at the cell surface. By contrast, in low Ca2+ medium, M protein was evenly dispersed over the cell surface, especially in the regions of cell-cell contact, and was not seen in patches. Immunoblot analysis for M protein in the infected cells showed that the total amount of M protein was almost the same irrespective of Ca2+ concentration in the culture medium. But, there was a distinct difference in the forms of M protein found in the cells: most of the M protein in the cells cultured in standard medium was of the non-phosphorylated form, whereas the phosphorylated form of M protein was distinctly increased in the cells cultured in low Ca2+ medium. These results suggest that Ca(2+)-deficiency in the medium blocks dephosphorylation of phosphorylated M protein necessary for patch formation, resulting in disturbance of viral morphogenesis.
Although Rheumatoid Arthritis (RA) is categorized in the systemic autoimmune diseases, specific autoantibodies in RA have been reported to be rare. We have investigated autoantibodies found in sera from patients with RA and examined their clinical significance. Immunoprecipitation techniques using 32P-labeled or 35S-labeled HeLa cell extracts and immunoblotting were utilized to detect autoantibodies in sera from 42 patients with RA and 58 patients with other connective tissue diseases as controls. Certain autoantibodies were detected in 33 of 42 patients (79%) with RA by any of the assay systems mentioned above. Anti-SSA/Ro, anti-SSB/La, anti-7-2RNP, and anti-Sm antibodies were found in 13 (29%), 3 (7%), 4 (10%), and 1 (2%) patients with RA, respectively. All 3 patients with anti-SSB/La and 9 with anti-SSA/Ro revealed Sjögren's syndrome besides RA. However, all 4 patients with anti-7-2RNP and one patient with anti-Sm showed no evidence of scleroderma nor SLE. Besides of these known autoantibodies, we have also detected 4 new antibodies which reacted with a 60kD protein in 15 (36%), 45kD in 10 (24%), 75kD in 8 (19%), 180kD in 4 patients (10%) with RA. These autoantibodies were not found in other connective tissue diseases except one of SLE for anti-60kD and one of dermatomyositis for anti-75kD, and therefore appeared to be specific for RA patients. Anti-45kD antibodies were associated with low prevalence of anti-nuclear antibodies, and anti-180kD antibodies were associated with lymphadenopathy and Sjögren's syndrome. Thus, it was demonstrated that patients with RA develop a variety of autoantibodies as well as those with other connective tissue diseases.
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The objective of this study was to demonstrate the movement of type I and III collagens accompanying gingival inflammatory destruction. Experimental marginal periodontitis was induced by a calculogenic diet and a high-sucrose diet with feces in 3-week-old Wistar rats. We observed the changes in the interdental periodontium histopathologically by using the picrosirius-polarization method and an electron microscope. 1. After 5 weeks of eating the calculogenic diet, mild gingivitis was found. A small number of inflammatory cells consisting of neutrophils were seen. At the 2nd week, a variety of bone resorptions of alveolar crests began to appear. At the 10th week, an epithelial downgrowth was observed. At the 64th week, migration of epithelial attachment to half of the apex and a high degree of inflammatory cell infiltration of plasma cells could be seen. 2. Observations under the polarization microscope showed that interdantal horizontal fibers became coarse and type I collagen decreased but at the middle type III increased. However when the horizontal fasciculus were newly formed, type I was always dominant. Between interdental horizontal fibers and the alveolar crest, type III was increased. 3. Under the electron microscope microfibrils were found around adjacent degraded fibroblasts at the locations where collagen fibrils were destroyed and disappeared. In contrast, at the locations detached from inflammatory cell infiltration small bundles of microfibrils were seen. It is suggested that at the areas of destructive collagen structures the relative increase in type III and the appearance of microfibrils were caused by the reduction of type I. At the same time at the sites of detachment from the lesions, complete growth of type III and the appearance of microfibrils were found and were considered to be newly formed juvenile collagen structures. Moreover it is concluded that a balance proceeds with the qualitative changes in the types of collagen fibers involving breakdown and new formation.
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