[Sialography. 2. Sialolithiasis].
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Biomedical subjects
Publications and source records attributed to M Arisue.
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We have previously reported that malotilate (MT) inhibited the invasion and metastasis of rat mammary carcinoma cells through the modification of host endothelial cells. In this study, we examined the inhibitory effects of MT on invasion of human cancer, using five oral squamous cell carcinoma cells (SAS, Ca9-22 and HSC-2, -3 and -4). MT did not affect the growth of these tumor cells and the invasion of reconstituted basement membrane, Matrigel. In an in vitro invasion assay using rat lung endothelial (RLE) cells, invasion of tumor cells which had been treated with MT (10 ng/ml, 24 h) was not affected; however, when RLE cells had been treated with MT, invasion was significantly inhibited in three cell lines (SAS, Ca9-22 and HSC-4) and a tendency to inhibition was also observed in other cell lines. Electron-microscopical examination of the RLE monolayer treated with MT (MT-RLE) showed the development of gap and tight junction-like structures. Subsequently, junction-associated proteins, connexin 43, zonula occludin and desmoglein, were examined by Western blotting. Protein levels of connexin 43 and zonula occludin were elevated dose dependently, and connexin 43 was chronologically enhanced by MT whereas desmoglein was not. The enhanced gap junctional communication of MT-RLE cells was observed in the scrape-loading assay using lucifer yellow CH. These results suggest that MT promotes the development of cell-to-cell adhesion, e. g. gap junction and tight junction in endothelial cells, resulting in the inhibition of invasion by the tumor cells.
To investigate the effects of dietary alpha-linolenic acid (18:3, n-3; alpha-LNA) and linoleic acid (18:2, n-6; LA) on the development of hereditary hepatitis, we compared incidences and grades of acute hepatitis between the Long-Evans cinnamon (LEC) rats fed with safflower oil-supplemented diet and perilla oil-supplemented diet. Both safflower and perilla oil supplemented diets reduced the incidence of hepatitis and significantly prolonged its onset as compared to the non-supplemented conventional diet. No significant difference was observed between safflower and perilla oil diets in the rats of incidence of hepatitis. At the age of 16 weeks, just before the onset of hepatitis, serum levels of transaminase (AST, ALT) and concentration of copper in rats fed with both test diets were significantly reduced as compared with that of rats fed alpha-linolenate and linoleate have an inhibitory effect on the development of hepatitis in LEC rats due to the prevention of serum copper elevation.
We have previously reported that rat fibrosarcoma KMT-17 cells and their in vitro counterparts, cloned A3 cells, shed a tumor-associated antigen (TAA), termed CE7, from the cell surface on vesicular membranes, under growth-enhancing conditions. This study shows that irradiation (1 approximately Gy) from a 60Co source, inhibited A3 cell growth dose-dependently and correspondingly increased CE7 expression by A3 cells as determined by anti-CE7 monoclonal antibody using flow cytometry. CE7 expression gradually increased with increasing doses of irradiation and reached a peak level at 30Gy. After 30Gy irradiation, CE7 expressing A3 cells were fixed with 1% paraformaldehyde and were used to intradermally immunize syngenic rats. Immunized rats developed transplantation resistance to the parent KMT-17 cells as compared to rats immunized with unirradiated A3 cells. Rat MHC class 1 antigen expression was slightly decreased by irradiation and therefore, resistance to tumor transplantation appeared to arise solely due to the enhancing effects of irradiation on TAA expression which increases the antigenicity of the tumor cells coverting them to an effective stimulator of antitumor effector cells. This phenomenon may offer a possibility of the resistance to the re-emergence and metastasis of the tumor like a KMT-17 through the induction of antitumor memory cells.
Rat fibrosarcoma cells infected with Friend leukemia virus (FV-KMT-17) grow for a short time and then regress spontaneously in syngeneic hosts. This regression was caused by immunological mechanisms, because the tumor cells were renogenized. In this study, we have tried to find out whether tumor-associated antigen (TAA) expression in these xenogenized tumor cells can be modulated by xenogenization. FV-KMT-17 cells (1 x 10(7)), which were subcutaneously transplanted into ten rats, spontaneously regressed after temporary growth. All rats which rejected FV-KMT-17 cells showed strong resistance to rechallenge with KMT-17 (1 x 10(6)) cells. To reveal the chronological modulation of TAA and virus-associated antigen (VAA), a single-cell suspension was obtained from the subcutaneous tumors and expression of these antigens was chronologically measured. TAA, termed CE7 antigen, was examined by anti-CE7 monoclonal antibody (MoAb) and VAA was examined by anti-FK1 MoAb which recognizes the FV env gene product (gp 70). Expression of VAA was not modulated through either the progression or the regression phase, but expression of TAA was strongly enhanced in the regression phase. These results show that enhancement of TAA expression occurs during the regression phase of FV-KMT-17 growth in vivo and that TAA-expressing cells may stimulate anti-tumor immunity, resulting in acquisition of resistance against parental KMT-17 cells.
The LEC (Long-Evans Cinnamon) rat is well known as a useful animal model for hepatic disease. We noticed the green pigmentation in incisors 2-3 weeks after acute hepatitis accompanied by severe jaundice. This study was undertaken to elucidate the cause of this phenomenon. Half of the pigmented teeth were examined by histopathological analysis and microradiographic analysis. Pigmentation was observed as a green stripe that ran parallel to the incremental line in the dentine. The microradiographic analysis disclosed enhanced permeability of the pigmented area as compared with other areas. The rest of pigmented teeth were dried, powdered and bilirubin was extracted with chloroform /methanol/acetic acid, 30:10:0.5; v/v under sonication. After centrifugation, the supernatant was collected and evaporated. The residue was dissolved in chloroform and its absorption spectrum measured after diazo reaction to reveal the presence of bilirubin. The spectral characteristics indicated the presence of bilirubin in the pigmented teeth. Thus, the LEC rat may be useful animal model for bilirubin-induced tooth pigmentation.
We have previously reported that inhibition of anti-tumor immune responses and enhancement of metastatic tumor growth occurred in rats following cryosurgery of the transplantable 3-methlcholanthrene-induced rat fibrosarcoma KMT-17. In this study, to elucidate the immunological responses in rats following cryosurgery, we examined whether rat serum obtained from rats which underwent cryosurgery (c-serum) might affect the in vivo neutralizing activity of the Winn assay. In this assay, c-serum did not reduce the anti-tumor immunity, though spleen cells obtained from rats undergoing surgical excision indicated strong anti-tumor immunity as compared with cryosurgery. Thus, we examined the anti-tumor responses of spleen cells. Macrophages were obtained from the glass adherent fraction of rat spleen cells following cryosurgery and these macrophages were used for cytostatic activity against KMT-17 cells. Cytostatic activity was not reduced by cryosurgery. The spleen cells obtained from rats receiving cryosurgery were intravenously transferred into other rats that were previously immunized with 80 Gy-irradiated KMT-17 cells, and an alteration of tumor growth modulated by this adoptive cell transfusion was observed. The anti-tumor resistance of rats was diminished by the adoptive transfusion of spleen cells treated with cryosurgery, though this diminution disappeared following anti-T serum and immune complement treatment of spleen cells. These results suggest that immuno-suppression following cryosurgery may be mainly caused by suppressor T cells.
We have previously reported that inhibition of anti-tumor immune responses and a corresponding enhancement of metastatic tumor growth occurred in rats following cryosurgery of 3-methylcholanthrene-induced WKA rat fibrosarcoma (KMT-17). In this study, to evaluate the enhancement of metastasis arising from the inhibition of anti-tumor immune responses following cryosurgery, we examined how cryosurgery affected experimental pulmonary metastasis and the growth of subcutaneously transplanted tumor. To reveal the effect of cryosurgery on pulmonary metastasis, rats received a subcutaneous inoculation of KMT-17 tumor in the right flank (1 x 10(6)) and i.v. injection (1 x 10(5)) on the same day or 4 days later. The right flank tumors were treated with cryosurgery 5 days after subcutaneous transplantation. The pulmonary metastasis of the rats, which were injected i.v. one day before treatment, was enhanced by cryosurgery as compared with surgical excision, though the pulmonary metastasis of rats, which were injected i.v. 5 days before treatment, was un-affected by cryosurgery. These observations suggest that cryosurgery may enhance the pulmonary metastasis in its early steps but has no effects in its later stages. To reveal the effect of cryosurgery on the growth of distant tumors, rats received subcutaneous inoculations of KMT-17 tumor in the right (1 x 10(6)) and left (1 x 10(4) approximately 10(5)) flanks. Tumors in the right flank were treated with cryosurgery 5 days after inoculation and the growth of untreated left flank tumors was observed. In this double grafted tumor system, however, cryosurgery significantly inhibited the growth of the untreated left flank tumors. Spleen cells obtained from rats which had undergone cryosurgery 4 or 10 days previously (cryo-spleen cells) were used for in vivo neutralizing Winn assay. Antitumor activity of cryo-spleen cells was decreased as compared with that of rats after surgical excision in both spleen cells from 4 and 10 days after treatment. These findings suggest that effector cells in the spleen may not participate in subcutaneous tumor regression and that the evaluation of antitumor effect using the double grafted tumor system needs caution.