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Biomedical subjects

K Shinkai

Publications and source records attributed to K Shinkai.

At least 91 records · Page 5Linked to original sources
PubMed1989

[Results of abdominal surgery in patients over 90 years old].

During a year period (1978-1987), 105 cases of abdominal surgery were performed at Sasebo Chuo Hospital on patients over 80 years of age. This study discusses 4 patients who were over 90 years old at time of their surgery. Emergency surgery had been required for 2 patients (a 91-year-old male with a sigmoid colon ca., and a 91-year-old female with a descending colon ca.), and elective surgery had been performed on the other two patients (a 95-year-old male with a caecum ca., and a 97-year-old female with a leiomyosarcoma of stomach). The patients who underwent elective surgery had a uniformly smoother hospital course and an overall better prognosis then the patients who underwent emergency surgery, whose prognosis was poor. We have concluded that early diagnosis and elective surgery is the necessary procedure in the elderly patient.

Adenocarcinoma↗
PubMed1988

Factor from rat liver with antiinvasive potential on rat ascites hepatoma cells.

An acid/ethanol extract of normal rat liver, both in vitro and in vivo, inhibited the invasion by a highly invasive subpopulation of rat ascites hepatoma cells, AH 130 (LC-AH cells). The addition of 10-80 micrograms/ml extract inhibited the formation of penetrated colonies of LC-AH cells underneath the cultured mesothelial cell (M-cell) monolayer. The tumor cells pretreated with the extract showed the diminished colony formation. Preincubation of the extract with plasma membranes prepared from LC-AH cells abolished the effect of the extract, suggesting a binding of the inhibitory entity [tentatively termed as "invasion-inhibiting factor" (IIF)] to the tumor cell surface. The extract did not inhibit the growth of LC-AH cells, but suppressed their directed migration underneath the M-cell monolayer. A concomitant i.p. injection of the extract with LC-AH cells into rats prevented the invasion by tumor cells of the peritoneum and formation of tumor nodules in the peritoneum and mediastinum, indicating that IIF inhibited the tumor cell invasion and metastasis in vivo, as well. Upon ultrafiltration and gel fractionation, about 60% of IIF activity was recovered in the fraction corresponding to the molecular weight in the range of Mr 3000-4000. This activity was heat-stable at 100 degrees C at neutral pH but labile at acidic pH and was inactivated by the treatment with pronase. The rest of the activity of IIF was found in the fraction of more than Mr 25,000.

Animals↗
PubMed1987

Macrophage potentiation of invasive capacity of rat ascites hepatoma cells.

In vitro and in vivo invasive capacities of rat ascites hepatoma cells (AH 130) that had been cultured on the feeder layers of rat macrophages were examined. The in vitro invasive capacity of the tumor cells was measured by their ability to form tumor cell colonies underneath cultured mesothelial cell monolayers; in vivo invasive capacity was examined by the implantation of the tumor cells into the rat peritoneal cavity. When the tumor cells were precultured on a macrophage feeder layer, the in vitro invasive capacity of the tumor cells increased almost 10 times as much as that of uncocultred control cells. The cocultured tumor cells, when implanted in rat peritoneal cavity, infiltrated extensively in the peritoneum and formed many tumor nodules and enlarged metastatic lymph nodes. Implantation of the uncocultured tumor cells did not develop any macroscopically detectable nodules. The effect of macrophages was reversed by subculturing the cocultured tumor cells without macrophages. Treatment of the tumor cells with the medium conditioned by macrophage culture did not result in the increase in invasive capacity. Almost 50% of the macrophage-mediated enhancement of the in vitro invasive capacity was inhibited by the simultaneous addition of superoxide dismutase and catalase at the time of tumor cell-macrophage coculture.

Animals↗
PubMed1987

[Establishment of an experimental model for tumor cell invasion and potentiation and inhibition of the invasive capacity].

Seeding of rat ascites hepatoma cells (AH 130) on cultured mesothelial cell monolayers resulted in the penetration of single tumor cells and subsequent formation of tumor cell colonies underneath the monolayers. Determination of the number of colonies facilitated quantitative estimation of the in vitro invasive ability, which corresponded well with the in vivo invasive capability of the tumor cells. Preculture of AH 130 cells with macrophages greatly potentiated both the in vitro and in vivo invasive capacities of the tumor cells. This potentiation seems to be mediated by certain species of active oxygen radicals generated by macrophages. Acid/ethanol extract of normal rat liver inhibited both the in vitro and in vivo invasion by the tumor cells. The inhibiting entity in the extract was heat-stable and had a molecular weight in the range of 3.5-10 Kd. It did not suppress tumor cell attachment to mesothelial cell layers, or inhibit tumor cell growth, but selectively impaired the penetration step of the tumor cell invasion through its binding to the tumor cell surface.

Animals↗
PubMed1986

Superoxide radical potentiates invasive capacity of rat ascites hepatoma cells in vitro.

Effect of superoxide radical (O2-) produced extracellularly by hypoxanthine (HX) and xanthine oxidase (XO) on invasive capacity of rat ascites hepatoma cells was studied. Invasive capacity was estimated in vitro by counting the number of tumor cell colonies penetrated underneath cultured mesothelial cell monolayer. When the tumor cells had been treated with non-toxic doses of HX and XO, the formation of penetrated colonies increased with increasing concentrations of XO. This increment was completely inhibited by scavengers of active oxygen radicals, superoxide dismutase (SOD) in combination with catalase (CAT) added simultaneously at the time of HX-XO treatment.

Animals↗
PubMed1986

Interaction of rat ascites hepatoma cells with cultured mesothelial cell layers: a model for tumor invasion.

Interactions of rat ascites hepatoma cells with primary cultured layers of rat mesentery-derived cells were studied. The mesentery-derived cells were isolated from rat mesentery and cultured in Eagle's minimum essential medium with a 2-fold concentration of amino acids and vitamins supplemented with 10% calf serum. The primary cultured cells, consisting mainly of mesothelial cells in polygonal shape, forms a "paving stone" sheet. Upon seeding the tumor cells on the mesentery-derived cell layers, three different types of tumor cell growth were observed. Type 1 was the formation of piled-up tumor cell nests on mesothelial cell layers. Type 2 was the formation of flattened tumor cell islands underneath mesothelial cell layers. This island formation was clearly observed under a phase contrast microscope 2 days after the tumor cell seeding. Protrusion of cellular processes of the tumor cells beneath mesothelial cells was occasionally seen. Type 3 was the growth of tumor cells in suspension. These types of tumor cell growth closely resemble those in the peritoneal cavity observed after i.p. implantation of the tumor cells. When the tumor cells recovered from the blood of tumor-bearing rats were seeded, flattened tumor cell islands were formed 15 times more frequently than when the tumor cells isolated from host peritoneal cavity were seeded. Shortly after the appearance of small flattened tumor cell islands, a distinct morphological change of mesothelial cells from polygonal to spindle shape was seen preferentially at the marginal area of the cell layers (a partial retraction of cell edges). The retraction of mesothelial cells was induced not only by seeding the tumor cells but by adding the tumor ascites fluid or the medium conditioned by the tumor cell culture. The morphological change was reversed by changing the culture medium to remove the effectors. These results indicate that the system described in this study can provide a useful model to study tumor cell invasion.

Animals↗
PubMed1984

[Histopathological study on the vascular invasion in advanced gastric carcinomas].

Venous and lymphatic invasion and Ag-reactive cells were studied in 110 gastric carcinomas. Venous invasion was recognized in 28.2% by H.E. staining only; it was seen in 58.2% by E.V.G. staining. Argyrophil and argentaffin cells were recognizable in 27.3% and 14.5%, respectively. No venous invasion was observed in many carcinomas with Ag-reactive cells. It has been suggested that the incidence of carcinoma with Ag-reactive cells is in inverse proportion to cellular atypism. Our work suggests that venous invasion bears a relation to atypism; this tendency was not recognizable with respect to lymphatic invasion.

Adenocarcinoma↗
PubMed1982

Correlation of alkaline phosphatase activity with cell population density in tissue culture cells originated from rat liver.

Alkaline phosphatase (ALP) activity of cultured Li-10 cells obtained from rat liver was found to be a function of cell population density. After the cells grew to confluence, the enzyme activity per cell increased about 100 times that at a low population density. The increase of activity was inhibited by the addition of actinomycin D or cycloheximide to the culture medium. When the cells that had gained high ALP activity after confluency were subcultured, ALP activity decreased to a low basal level after about 48 h. Under cytochemical examination using an electron microscope, the induced ALP activity was seen exclusively at the apical surface region of the cells but scarcely at cell-cell and cell-substratum contact regions.

Alkaline Phosphatase↗
PubMed1982

[Effect of carboquone in complete regression of mouse mammary cancer MM-46].

Therapeutic effect of an alkylating agent, carboquone (CQ: Esquinon, 1mg/vial Sankyo Co., Tokyo) was investigated with a mouse mammary tumor MM-46 inherited the MM-antigen. MM-46 tumor cells (3 X 10(6)) were implanted subcutaneously into the axillary region of syngeneic C3H/He mice and CQ was administered intravenously at a dose of 2 mg/kg by a single injection on day 1, 4, 7 or 10. The experiment was carried out with 10 mice in each group. As a result, treatment of CQ elicited a complete regression effect on MM-46 tumor; the rate of complete regression in the group treated with CQ on day 4 or day 7 was 10/10, but that in control group was 0/10. Administration of CQ after the tumor inoculation brought about necrosis of the subcutaneous tumor, followed by complete regression and only a scar remained by day 25 at the site of tumor exclusion. In this experiment no recurrence or metastasis was observed after tumor regression. Since the mice which rejected the once developed tumor were resistant to them on rechallenge with the same amount of MM-46 tumor cells, it was suggested that an immunological response would play an important role in exclusion of the tumor. The complete regression effect described above has generally been reported on the antitumor pattern of the host-mediated agents such as polysaccharides of Basidiomycetes, while has hardly on that of the alkylating agents except cyclophosphamide. The mechanism of such the regression effect attributed to the activity of CQ is obscure, but these results suggest that this phenomenon may be dependent on the inherent antigenicity of MM-46 tumor.

Animals↗
PubMed1981

Antitumor activity of methyl (5-fluoro-1H-2-oxo-4-pyrimidinyl beta-D-glucopyranosid)uronate against various experimental tumors.

The antitumor activity of a glucuronide of 5-fluorouracil, methyl (5-fluoro-1H-2-oxo-4-pyrimidinyl beta-D-glucopyranosid) uronate (FU-O-G), which is a 5-fluorouracil (5-FU) derivative with remarkably low toxicity, was studied. The antitumor activity of this compound was superior to those of 5-FU and 1-(2-tetrahydrofuryl)-5-fluorouracil (Tegafur, Ftorafur) in the treatment of transplantable tumors, not only 5-FU-sensitive tumors such as adenocarcinoma 755, lymphosarcoma LS-1, and plasmacytoma X5563, but also 5-FU-resistant tumors such as Lewis lung carcinoma and Walker carcinosarcoma 256. Furthermore, in the treatment of Lewis lung carcinoma, which responds poorly to 5-FU and Ftorafur, daily administration of FU-O-G at a dose of 400 mg/kg for 30 days produced a 92% increase in life span without marked loss of body weight, though short-term administration (such as 5 days) was barely effective. Thus, it appears that FU-O-G is an antitumor agent suitable for long-term administration. These findings correspond with the results of an enzymological study which showed selective activation of FU-O-G by beta-glucosidase in tumor cells and indicated that the compound is a marked form of 5-FU.

Animals↗
PubMed1979

Quantitative structure-activity relationships in 2,5-bis(1-aziridinyl)-p-benzoquinone derivatives against leukemia L-1210.

Antileukemic activities of more than 30 2,5-bis(1-aziridinyl)-p-benzoquinones (4) were correlated against well-defined physicochemical constants. These compounds were evaluated against lymphoid leukemia L1210 in BDF1 mice. The best equations obtained exhibited a linear dependence on the hydrophobic constant, pi. Characteristic aspects of the equations are that the larger the relative hydrophilicity of the drugs the stronger the antileukemic activity will be and that the more hydrophilic compounds have a greater chemotherapeutic index. Steric and electronic effects were also determined to be important. Based on the correlations, three compounds (11, 15 and 19) were designed, synthesized, and biologically evaluated.

Animals↗
PubMed1977

Studies on the neutralization of herpes simplex virus. VIII. Significance of viral sensitization for inactivation by complement.

Early and late IgG of rabbits immunized with herpes virus showed, respectively, 8-fold and 2-fold enhancement of neutralization endpoint in the presence of complement (C). Kinetic curve experiments employing an appropriate amount of virus revealed that both neutralization and sensitization followed first-order reaction, and each IgG possessed a certain range of concentration where neutralization was negligible while sensitization was marked. Dose responses of neutralization and sensitization velocities demonstrated that the C enhancement of late IgG was about 7-fold and that of early IgG more than 20-fold. These facts suggested that the IgGs contained two different entities of complement-requiring (CRN) and non-requiring neutralizing (N) antibodies at different proportions, only the former being responsible for sensitization. The different CRN: N ratios obtained by the endpoint and kinetic methods may mean either that the two antibodies differ in avidity for the virus or that the number of critical sites per virion for CRN antibody is greater than that for N antibody. In this interpretation, sensitization by CRN antibody as well as neutralization by N antibody is thought to result from attachment of a single antibody molecule to the viral critical site. Alternative explanations, ascribing the mechanism of neutralization to steric hindrance of critical sites or to multiple hit of those sites by antibody, were denied by analyses of the present data.

Antibodies, Viral↗