[IVDSA while breathing--breathing technic].
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Angiography↗
Biomedical subjects
T Okayasu
Publications and source records attributed to T Okayasu.
[A case of breast carcinoma with lung metastasis].
A 37-year-old female, who had undergone a left standard mastectomy in May, 1983 for breast cancer, was treated with Tamoxifen and FT-207 postoperatively. The patient had no further evidence of disease until two and one-half years later, when a routine chest film showed a single, half-rounded density 6.5 cm in diameter in the hilus of her left lung. Bestrabucil, the benzoate of an estradiol-chlorambucil conjugate, was administered p.o. at a daily dose of 200 mg for four weeks. Thereafter, the tumor greatly decreased in size to 3.0 cm in diameter. When a left upper lobectomy was performed, the tumor was found to be necrotic tissue. Microscopically, a small cancer nest similar to the primary breast carcinoma was observed in the center of the necrosis. The necrotic tissue was surrounded with cellular infiltrate, markedly consisting of histiocytes.
Adenocarcinoma↗
[Clinical study of a synthetic calcitonin derivative (elcatonin) in patients with metastatic bone tumors].
Forty-three cases of metastatic bone tumor were treated with Elcatonin. The agent was injected intramuscularly to each patient at a dose of 40 units twice daily. Twelve patients (28%) experienced pain relief within 4 days after treatment and after 4 weeks, twenty-eight patients (65%) had palliation of pain. In patients with hypercalcemia (4 cases), a decrease of serum Ca was observed one week after administration of Elcatonin. Improved bone scintigram was observed in 37.5% of cases, and radiographic improvement in 20% of cases. These data indicate that Elcatonin is effective for achieving pain relief and in improving the state of invaded bones when administered in combination with conventional treatment modalities for patients with metastatic bone tumors.
Adult↗
Immune regulation of the L5178Y murine tumor-dormant state. I. In vivo and in vitro effects of prostaglandin E2 and indomethacin on tumor cell growth.
Immunization and intraperitoneal challenge of DBA/2 mice with L5178Y lymphoma cells results in the suppression and maintenance of the L5178Y cells in a tumor-dormant state in the peritoneal cavity for many months. Cell-mediated immune responses involving lymphocytes and macrophages are involved in maintenance of the tumor-dormant state. Macrophages that have increased immunosuppressive activity and that produce increased amounts of PGE2 appear in the peritoneal cavity of tumor-dormant mice before the breakdown of the tumor-dormant state and formation of ascitic tumors. We report here that the tumor-dormant state can be terminated with formation of ascitic tumors by treatment of tumor-dormant mice with PGE2. Treatment with indomethacin results in inhibition of tumor cell growth and elimination of all recoverable tumor cells. Cultures of peritoneal cells (PC) from mice harboring L5178Y cells in a tumor-dormant state were used to analyze the PGE2 and indomethacin effects. Tumor cells did not grow out in the high-cell density PC cultures prepared from many tumor-dormant mice, but addition of PGE2 to these cultures resulted in tumor cell growth. The tumor cell growth that did occur in the PC cultures from some tumor-dormant mice was associated with PGE2 production by the associated host cells, and the addition of indomethacin to these cultures inhibited both PGE2 synthesis and tumor cell growth. Removal of plastic-adherent cells from the PC cultures eliminated the restraint on tumor cell growth. These experiments suggest that L5178Y tumor cells are maintained in a tumor-dormant state by host peritoneal cells, which are under PGE2 regulation.
Animals↗
Metabolism of platelet-activating factor in primary cultured adult rat hepatocytes by a new pathway involving phospholipase C and alkyl monooxygenase.
The metabolic fate of 1-O-[3H]alkyl-2-acetyl-sn-glycero-3-phosphocholine (PAF-acether) upon interaction with primary cultured adult rat hepatocytes was investigated. [3H]PAF-acether was transformed time-dependently into [3H]lyso-PAF-acether, 1-O-[3H]alkylglycerol and finally converted to 3H-labeled fatty aldehyde. 1-O-[3H]Alkyl-2-acyl-sn-glycero-3-phosphocholine (alkylacyl-GPC) was formed after a long incubation time and with a smaller amount compared with that formed in platelets and neutrophils. When lipids from cells, cell surfaces and incubation medium were analyzed separately, most of the transformed products of [3H]PAF-acether remained in the cells. When 1-O-[3H]alkyl-2-lyso-sn-glycero-3-phosphocholine was incubated with hepatocytes, it was mainly converted into 1-O-[3H]alkylglycerol. 3H-labeled fatty aldehyde and [3H]alkylacyl-GPC were also found. Hepatocytes metabolized slowly from 1-O-[1-14C]hexadecylglycerol to 3H-labeled fatty aldehyde and 3H-labeled phospholipid. These findings suggest that cultured hepatocytes mainly catabolize exogeneous PAF-acether by removing the acetyl residue and the polar head group and, finally, by cleaving an ether bond. The deacetylation-reacylation step, which is important in platelets and neutrophils, was not shown to be a main metabolic pathway of PAF-acether in cultured hepatocytes.
Animals↗
The active immunotherapy of a 3-methylcholanthrene-induced rat tumor with Friend virus-infected (xenogenized) tumor cells.
We investigated the various conditions necessary for potentiating the immunogenicity of viable Friend virus (FV)-infected rat fibrosarcoma KMT-17 cells. The immunogenicity was most potent among cells passaged through three generations of FV-tolerant rats; a single subcutaneous immunization induced an increase in the transplantation resistance (LTD50) of 10,000 or more. It was also found that intradermal immunization of the tumor cells induced stable and potent resistance to the transplantation of non-xenogenized tumor cells soon after immunization, and that irradiated non-xenogenized tumor cells were effective in supplying booster immunization. Active immunotherapy against KMT-17 cells pre-transplanted subcutaneously was carried out on the basis of the above findings with the results that the active anti-tumor immunization alone caused a complete regression in 30% of the tumor-burdened rats. These findings indicate the possibility of achieving active immunotherapy with xenogenized tumor cells.
Animals↗
Rapidly reversible resistance to immune lysis of L5178Y lymphoma cells in a tumor-dormant state in DBA/2 mice.
L5178Y cells in a tumor-dormant state in DBA/2 mice escape lysis by cytolytic T-lymphocytes and activated macrophages. In the present report these tumor cells were found to be less susceptible to lysis by anti-H-2, anti-Thy 1.2, and anti-AKR antibodies plus complement than was the same tumor cell population removed from tumor-dormant mice and allowed to proliferate in a nonimmune environment in vivo or in vitro. This rapidly reversible resistance to immune lysis may be due to arrest of the tumor cells in the cell cycle during the tumor-dormant state.
Animals↗
Product identification and determination of optimal condition of 8, 11, 14-eicosatrienoic acid desaturation in rat liver microsomes.
delta 5-Desaturation of 8, 11, 14-eicosatrienoic acid in washed rat liver microsomes was studied in the presence of NADH, ATP, and coenzyme A. The product was identified as arachidonic (5, 8, 11, 14-eicosatetraenoic) acid by radiogaschromatography. Cytosol fraction stimulated delta 5-desaturation but did not participate in 8, 11, 14-eicosatrienoyl-CoA synthesis. The pH optimal to the desaturation was 6.8. The minimal concentrations of ATP and pyridine nucleotides which gave the maximal desaturation activity were 2 mM and 0.75 mM, respectively. Both NADH and NADPH were able to be electron donors for delta 5-desaturase, but cytochrome P-450 did not take part in the enzyme reaction because CO gas did not inhibit its activity. Apparent Km and Vmax for 8, 11, 14-eicosatrienoic acid were 18 microM and 154 pmol/min/mg, respectively.
8,11,14-Eicosatrienoic Acid↗
Structural alterations of the inner mitochondrial membrane in ischemic liver cell injury.
Mitoplasts were prepared from 3-h ischemic livers in an attempt to define the structural alterations in the inner membrane that may account for the functional deficiencies of ischemic mitochondria. Mitoplasts from both control and ischemic livers had similar specific activities of cytochrome oxidase and succinate-cytochrome c reductase. With both preparations, the specific activity of rotenone-insensitive NADH-cytochrome c reductase was 10-fold lower than in the mitochondria from which they were prepared. Ischemic mitoplasts had no respiratory control with ADP, and had a slightly reduced phospholipid to protein ratio and an increased cholesterol to protein ratio. As a result, the cholesterol to phospholipid molar ratio was increased from the control of 0.04 to 0.08. There were also differences in the content of individual phospholipid species. Phosphatidylcholine increased by 15%, while cardiolipin decreased by 60%. There were increases in sphingomyelin and in the lysophospholipids of phosphatidylcholine, ethanolamine, and cardiolipin. Pretreatment with chlorpromazine did not prevent these changes. Linoleic acid was decreased by 35% in ischemic phospholipids, and the content of free fatty acids was increased 4-fold. Electron spin resonance spectroscopy of mitoplasts spin labeled with either 5- or 12-doxyl stearic acid revealed an increased molecular order (decreased fluidity) of ischemic inner mitochondrial membranes consistent with the increased cholesterol to phospholipid ratio. The data indicate activation of a phospholipase A in ischemic mitochondria with the resulting accumulation of products of lipid hydrolysis. This conclusion further emphasizes the close similarity between the structural and functional consequences of ischemia in the intact animal and the effect on isolated mitochondria of the activation of the endogenous phospholipase A. In both cases the major functional alterations are attributable to changes in the permeability of the inner mitochondrial membrane induced by the accumulation of lysophospholipids.
Animals↗
Inhibitory effect of chloroquine on concanavalin A internalization into cell monolayer culture.
When cultured rat hepatoma cells (R-Y121B) were incubated with insulin in the presence of chloroquine at 25 degrees C, chloroquine increased both insulin binding to the cell surface and its internalization into cells. In addition, in order to elucidate whether or not the effect of chloroquine on insulin receptors is specific, concanavalin A binding to the cells was examined in the presence or absence of chloroquine, since insulin receptors have concanavalin A binding sites. When the cells were incubated with concanavalin A in the presence of chloroquine, this drug decreased concanavalin A internalization in a dose-dependent manner: The inhibitory effect of chloroquine on concanavalin A internalization was evident at a concentration as low as 0.05 mM, and increased up to 0.5 mM. The effect of chloroquine was not related to the degradation of concanavalin A incubated with cells. When the cells were incubated with concanavalin A at 4 degrees C in the presence of chloroquine even at 0.5 mM, the inhibitory effect of chloroquine was not observed. It is concluded that the behavior of insulin receptors in the presence of chloroquine is different from that of concanavalin A receptors, although insulin receptors have concanavalin A binding sites. Chloroquine apparently increases insulin binding to cells in vitro, and this is due to the effect of chloroquine on insulin-receptor recyclization to which lysosome contributes [16, 31, 32]; this drug inhibits the function of lysosome which digests insulin-receptor complexes and eventually insulin bound to its receptors is accumulated in intracellular compartments.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Cytochalasin delays but does not prevent cell death from anoxia.
The role of alterations in the cytoskeleton in the anoxic death of cultured hepatocytes was evaluated with the use of cytochalasin B and colchicine. The addition of 50 microM Cytochalasin did, however, reduce the rate of accumulation of dead cells but was without effect on the number of cells that died. After 6 hours of anoxia in the presence of cytochalasin, 80% of the cells were dead. The same number of cells were dead after 4 hours in the absence of cytochalasin. Colchicine was without effect on the cell killing by anoxia. Cytochalasin also did not prevent the increase in the molecular order of the membranes of the anoxic hepatocytes as determined by electron spin resonance spectroscopy. In the presence or absence of cytochalasin, anoxia increased the order parameter, S, of hepatocytes spin-labeled with 12-doxyl stearic acid. These data indicate that changes in the organization of microfilaments that can be prevented by cytochalasin may aggravate the mechanisms mediating the anoxic death of the hepatocytes, but such mechanisms are essentially independent of these alterations in the cytoskeleton. The data do not exclude from a role in anoxic cell death other cytoskeletal changes that may not be affected by either cytochalasin or colchicine.
Adenosine Triphosphate↗
Possible involvement of NADPH-cytochrome P450 reductase and cytochrome b5 on beta-ketostearoyl-CoA reduction in microsomal fatty acid chain elongation supported by NADPH.
The chain elongation products from [2-14C]malonyl-CoA and palmitoytl-CoA by rat liver microsomes initiated by NADPH were found mainly to be 18:1 and 18:0. When anti-NADPH-cytochrome P450 reductase or anti-cytochrome b5 immunoglobulin G were included in this system, not only was the overall chain elongation significantly suppressed, but also a new radioactive product, which was identified as 2-heptadecanone derived from an intermediate beta-ketostearate, is accumulated depending upon the amounts of IgG added. These results suggest that NADPH-cytochrome P450 reductase and cytochrome b5 participate in the conversion from beta-ketostearoyl-CoA to beta-hydroxystearoyl-CoA, which is the first reductive step of the microsomal chain elongating system.
Acyl Coenzyme A↗
Immunochemical evidence for the enzymatic difference of delta 6-desaturase from delta 9- and delta 5-desaturase in rat liver microsomes.
The enzymatic properties of the three types of microsomal acyl-CoA desaturases, delta 6-, delta 9- and delta 5-desaturases, were immunologically compared using a monospecific antibody raised against the purified linoleoyl-CoA desaturase (delta 6-desaturase). By the double immunodiffusion technique, the anti-delta 6-desaturase antibody showed a single precipitin line to the purified delta 6-desaturase and microsomes treated with Triton X-100, but no line was observed with the partially purified delta 9-desaturase. The antibody even inhibited definitely delta 6-desaturase activity in microsomes, but neither stearoyl-CoA (delta 9-) nor eicosatrienoic acid (delta 5-) desaturations were inhibited. By these immunological investigations it was confirmed that terminal delta 6-desaturase is different enzyme from desaturases delta 9- and delta 5.
Animals↗
Up-regulation of insulin receptors with dexamethasone in cultured human urinary bladder carcinoma cells.
Cultured human urinary bladder carcinoma cells ( JTC -32) were used to investigate the regulation of insulin receptors by dexamethasone. When the cells were preincubated with dexamethasone at 37 degrees C, insulin binding sites increased up to 24 h. A large increase in insulin binding sites took place for 14 h of preincubation with dexamethasone. At lower concentrations of dexamethasone (less than 1 nM), no significant increase in insulin binding sites was observed, but the maximal increase was observed at more than 10 nM. Scatchard plots showed that dexamethasone increased the number of high affinity insulin binding sites (2.8 fold) without any change in the apparent equilibrium constant in JTC -32 cells. In addition, this steroid hormone also increased the number of low affinity insulin binding sites (1.6 fold) with a small change in the apparent equilibrium constant. Although insulin and dexamethasone did not affect the number of cells or the amount of cellular proteins per dish, dexamethasone plus insulin slightly increased them.
Cells, Cultured↗
Enhanced suppressor macrophage activity associated with termination of the L5178Y cell tumor-dormant state in DBA/2 mice.
Both cytolytic T-lymphocytes and cytolytic macrophages have been implicated in the long-term maintenance of L5178Y cells in a tumor-dormant state in DBA/2 mice. Eventually, however, the tumor-dormant state terminates, and all mice develop ascitic tumors. In an evaluation of the mechanisms involved in termination of the tumor-dormant state, we detected in the peritoneal cavity of many tumor-dormant mice macrophages with increased capacity to suppress the in vitro generation of a secondary anti-L5178Y cell cytolytic T-lymphocyte response. The incidence of macrophage-mediated immunosuppressive activity in individual tumor-dormant mice was related directly to the number of tumor cells in the peritoneal cavity of those mice. Furthermore, in tumor-dormant mice harboring fewer than 5 X 10(4) L5178Y cells, the detection of macrophage-mediated immunosuppressive activity was a prognostic indicator of termination of the tumor-dormant state and development of an ascitic tumor. These data suggest that peritoneal macrophage-mediated immunosuppressive activity, through inhibition of cytolytic T-lymphocyte generation in vivo, contributes to the termination of the tumor-dormant state and development of ascitic tumors.
Animals↗
[Case of arteriovenous malformation of the cecum].
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Aged↗
Alteration of immunogenicity of xenogenized tumor cells in syngeneic rats by the immune responses to virus-associated antigens produced on immunizing cells.
A strong transplantation resistance to a fibrosarcoma (KMT-17) is induced in syngeneic Wistar King Aptekman/Hok rats after a single s.c. immunization with Friend virus-infected (xenogenized) viable KMT-17 cells. The resistance induced by the repeated immunizations with irradiated Friend virus-infected KMT-17 cells, however, was unexpectedly weaker when compared with that induced by irradiated KMT-17 cells. The immunogenicity of tumor-associated antigen on xenogenized Friend virus-infected KMT-17 cells was correlated with their shortened survival time in the peritoneal cavity after i.p. inoculation, especially in rats preimmunized with xenogenized tumor cells. Furthermore, xenogenized tumor cells producing a medium amount of virus-associated antigen (VAA) but not those producing a large amont of VAA showed an augmented immunogenicity even in normal rats. On the other hand, the tumor-associated antigen immunogenicity was augmented by immunization with xenogenized tumor cells which expressed a relatively small amount of VAA in rats presensitized with VAA. These findings indicate that the immunogenicity of xenogenized tumor cells is augmented by the middle-grade immune responses to VAA produced on xenogenized tumor cells.
Animals↗
[Immunochemotherapy of resectable lung cancer--a preliminary study on a comparison of the control, levamisole, and OK-432].
We conducted a prospectively controlled study of adjuvant immunochemotherapy for resectable lung cancer in 37 cases of the control group, in 34 cases of levamisole group and in 40 cases of OK-432 group. No significant difference was noted in patient characteristics of age, sex, histological type, stage, cure rate, etc. The survival rates were calculated by Kaplan and Meier method. Survival curves were measured by generalized Wilcoxon test and Cox-Mantel test. When the levamisole group and the control group were compared in terms of survival rate, a significant increase of survival curves of patients treated with levamisole was observed in surgicopathological stage III + IV and relative curative operation groups (p less than 0.05). The survival rate of levamisole group was higher than that of OK-432 group in patients of surgicopathological stage III and III + IV (p less than 0.05). There was no statistically significant difference between OK-432 group and the control group, when in survival rates.
Adult↗