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Biomedical subjects

F Okada

Publications and source records attributed to F Okada.

At least 91 records · Page 5Linked to original sources
PubMed1992

Malignant progression of a mouse fibrosarcoma by host cells reactive to a foreign body (gelatin sponge).

The QR regressor tumour (QR-32), a fibrosarcoma which is unable to grow progressively in normal syngeneic C57BL/6 mice, was able to grow progressively in 13 out of 22 mice (59%) when it was subcutaneously coimplanted with gelatin sponge. We established four culture tumour lines from the resultant tumours (QRsP tumour lines). These QRsP tumour lines were able to grow progressively in mice even in the absence of gelatin sponge. The ability of QRsP tumour cells to colonise the lungs after intravenous injection and to produce high amounts of prostaglandin E2 (PGE2) during in vitro cell culture was much greater than that of parent QR-32 cells. These biological characteristics of QR-32 cells and QRsP tumour cells were found to be stable for at least 6 months when they were maintained in culture. We also observed that QR-32 cells were able to grow progressively in five out of 12 (42%) mice after coimplantation with plastic non-adherent peritoneal cells obtained from mice which had been intraperitoneally implanted with gelatin sponge. These host cells reactive to gelatin sponge increased the production of high amounts of PGE2 by QR-32 cells during 48 h coculture. Preliminary in vitro studies implicated the involvement of hydrogen peroxide and hydroxyl radical as some of the factors necessary to induce QR-32 cells to produce high amounts of PGE2 and to accelerate tumour progression.

Animals↗
PubMed1992

Species dependency of in vitro macrophage activation by bacterial peptidoglycans.

The effect of various bacterial cell wall components on in vitro biological function of murine peritoneal exudate macrophages was evaluated. We examined four different parameters of metabolic activity and monokine secretion. Peritoneal exudate macrophages from rats and guinea pigs, all of the strains tested, were stimulated by whole bacterial cell wall preparations, purified bacterial cell wall peptidoglucans, its water-soluble peptidolglycan fragments, muramyl dipeptides and amphipathic substances. Murine peritoneal exudate macrophages were activated by amphipathic substances of gram-positive bacteria. However, macrophages from mice, irrespective of strains, were not stimulated in the in vitro assay systems by purified bacterial cell wall peptidoglycan, water-soluble bacterial peptidoglycan fragments or muramyl dipeptides. These results suggest that macrophage activation by bacterial peptidoglycan in vitro is animal species specific.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1992

Progression of weakly malignant clone cells derived from rat mammary carcinoma by host cells reactive to plastic plates.

Tumor progression is the process by which tumor cells acquire more malignant properties, such as invasiveness and metastasis, during tumor development. To elucidate mechanisms of tumor progression, we examined the role of interactions between the tumor and its host by using a cloned cell line, ER-1, which was derived from a rat mammary carcinoma. ER-1 is weakly tumorigenic and non-metastatic when s.c. injected into syngeneic hosts in single cell suspension. However, ER-1 cells show a high incidence of lethal growth when s.c. implanted (5 x 10(2) cells), being attached to a 10 x 5 x 1 mm polystyrene plate. Tumor cell lines (PLT) obtained from tumors which had arisen from the plate-attached ER-1 cells no longer required plates for their growth in normal hosts, and had acquired metastatic ability to the lungs. The malignant phenotypes of PLT were stable under a usual culture condition for at least 6 months. Furthermore, the incidence of tumor development increased when small numbers of ER-1 cells were injected onto plates (or at their periphery) which had previously been implanted s.c. without tumor cells. The tumorigenicity of ER-1 cells increased after they were cocultivated for more than 30 days with host reactive cells obtained from the tissues surrounding the plates. These results suggest that host cells reactive to the foreign body (plastic plate) may not only promote the local growth of ER-1 cells but also convert them into much more malignant tumors.

Animals↗
PubMed1992

Differentiation between parasystole and reentry in concealed bigeminy.

There are two different theories to explain the mechanism of concealed bigeminy: one is '2:1 concealed reentry'; the other is 'irregular parasystole.' Two exemplary cases of the even-number variant of concealed bigeminy are presented. In case 1, the mechanism can be explained by an irregular parasystole due to a modulated parasystole; however, findings during temporary sinus arrest caused by vagal stimulation indicate that this case is not governed by a parasystole, but by a 2:1 concealed reentry. In case 2, the mechanism can be explained by a 2:1 concealed reentry without parasystole; however, findings during temporary sinus arrest indicate that this case is governed by an irregular parasystole due to a type-I second-degree entrance block. Thus, in cases of concealed bigeminy without pure ectopic cycles, it does not seem easy to explain the mechanism of concealed bigeminy on the theory of a modulated parasystole.

Adult↗
PubMed1992

Mechanism of bradycardia-dependent appearance of manifest extrasystoles in concealed bigeminy. A theoretical model derived from the concepts of longitudinal dissociation and multilevel block in the reentrant pathway of extrasystoles.

A case of bradycardia-dependent appearance of manifest extrasystoles in concealed bigeminy is presented. To explain the mechanism of such bradycardia-dependent appearance, a theoretical model is derived from the concepts of "longitudinal dissociation" and "multilevel block" in the reentrant pathway of extrasystoles. In the theoretical model, functional longitudinal dissociation divides the reentrant pathway into dual pathways F and S. When manifest extrasystoles are not found for a long time, alternate sinus impulses pass through both pathways F and S, but become concealed extrasystoles because of insufficient conduction delay in the pathways. The other alternate sinus impulses are blocked in the pathways; in pathway F, the impulses are blocked at the entrance, while in pathway S, the impulses are blocked at a more distal level. When sinus cycles gradually lengthen, one of such alternate sinus impulses passes through the entrance of pathway F and, traveling very slowly, is blocked at a more distal level. The next sinus impulse is blocked at the entrance of pathway F; namely, 3:2 Wenckebach block occurs at the entrance of pathway F. Thus this sinus impulse enters only pathway S and passes through pathway S with enough conduction delay to become a manifest reentrant extrasystole.

Bradycardia↗
PubMed1991

Changes in expressions of proteasome and ubiquitin genes in human renal cancer cells.

Proteasomes and ubiquitin (Ub) are essential components of the energy-dependent, nonlysosomal proteolytic pathway. To clarify the physiological role of this proteasome/Ub-dependent pathway, we meaured the levels of expressions of proteasomes and Ub in human renal cancers by Northern blot and immunochemical analyses. The mRNAs for two of the multiple subunits of proteasomes, C2 and C9, were expressed at abnormally high levels in most neoplastic lesions of patients with various primary renal cell carcinomas and in all renal cancer cell lines examined. However, no significant difference was found by enzyme immunoassay in the proteasomal contents of cancerous and normal parts of the kidney. The levels of mRNAs for the subunits of proteasomes were high in rapidly proliferating renal cells and appeared to be correlated with the activities of these cells for proteasome synthesis, but the cellular contents of proteasomes in these cells were normal, suggesting rapid turnover of proteasomes in rapidly proliferating cancer cells. Consistent with the increased expressions of proteasomal mRNAs, the expressions of three Ub genes, mono-UbA80, mono-UbA52, and poly-UbC, were found to be greatly increased in these renal cancer cells. Immunohistochemical staining of normal kidney showed that the levels of both proteasomes and Ub were high in cells of renal tubules and collecting ducts, but low in the glomerulus. The levels of both proteins appeared to be considerably increased in the nuclei of granular and clear carcinoma cells of the kidney. Moreover, the profiles of cellular proteins conjugated with Ub in normal kidney tissues were different from those in cancerous parts of the kidney and in established renal cancer cells. These results suggest that the proteasome- and ubiquitin-mediated system is functionally involved in the cancerous state in human kidney.

Adult↗
PubMed1991

G proteins (Gi, Go) in the medial temporal lobe in schizophrenia: preliminary report of a neurochemical correlate of structural change.

We have measured the amount of Gi (the inhibitory G-protein) or Go (a similar G-protein of unknown function) in 5 areas of the medial temporal lobe of control and schizophrenic brains utilizing pertussis toxin-catalyzed ADP ribosylation. The material used has previously been shown to have asymmetrical structural abnormalities of the ventricular system. The amount of Gi or Go was reduced on the left side in the hippocampus, amygdala and parahippocampal gyrus, the difference reaching significance in the hippocampus. This data is the first report of a neurochemical correlate of the structural change in the brains of patients with schizophrenia. Decreased Gi or Go in hippocampus may relate to other reported neurochemical deficits or other transmembrane signalling abnormalities. Further investigations of these indices of secondary messenger function in relation to structural changes are indicated.

Adenosine Diphosphate Ribose↗
PubMed1991

The improved effects of specific active immunotherapy on a rat fibrosarcoma by antitumor drugs.

We have tried to find out if the combination of a xenogenized tumor cell vaccine and antitumor drugs is able to induce a synergistic increase in the antitumor therapeutic effect. The degree of increase in the LTD50 (50% lethal tumor dose) is expressed numerically, as a quantitative index designed to compare degrees of transplantation resistance to tumor cell challenge. A LTD50 was achieved by an intradermal (i.d.) immunization with xenogenized tumor cells when challenged with tumor cells implanted intraperitoneally 2 weeks after the immunization: this LTD50 value was 527,000 times higher than that of the non-immunized group. When we combined this type of immunization with appropriate doses of bleomycin (BLM) or cyclophosphamide (CY), which are able to augment antitumor immunity, the LTD50 was 723,000-1,190,000 times higher than that of the non-immunized group. This increase in the LTD50 is definitely higher than that achieved by a single immunization with irradiated tumor cells (x 33,000) and combined with either BLM (x 93,000) or CY (x 140,000). We also studied the therapeutic effect of a tumor cell vaccine combined with antitumor drugs BLM or CY in tumor-bearing rats. We observed a synergistic effect caused by BLM or CY after i.d. immunization with xenogenized tumor cells: this showed a significant increase when compared with the therapeutic effects obtained by chemotherapy alone (P less than 0.01). Nevertheless, there was no evidence that the above antitumor effects is superior to the effect achieved by irradiated tumor cells.

Animals↗
PubMed1991

Association of increased tumor cell responsiveness to prostaglandin E2 with more aggressive tumor behavior.

Secretion of prostaglandin E2 (PGE2) by cloned variants of QR fibrosarcoma or of Lewis lung carcinoma (LLC) did not correspond with their in vivo aggressive behavior. However, aggressiveness may be influenced by tumor responsiveness to PGE2. Each of the metastatic LLC or progressor QRpP variants was more motile in an in vitro migration model than were either the nonmetastatic LLC or regressor QR variants. One of the two tested progressor QR variants and all of the metastatic LLC variants were also more responsive to PGE2 in their in vitro migration through a membrane than were either regressor QR or nonmetastatic LLC variants. Thus, responsiveness to PGE2 by tumors may regulate the degree of tumor aggressiveness in vivo.

Animals↗
PubMed1990

Methylcholanthrene-induced murine fibrosarcoma cell line BMT-11 secretes granulocyte colony-stimulating factor.

Murine fibrosarcoma cell line BMT-11 was induced with 3-methylcholanthrene and maintained in culture. Transplantation of BMT-11 into syngeneic C57BL/6 mice produced leukocytosis consisting of marked increments of neutrophils and monocytes associated with massive splenomegaly. In order to elucidate the mechanisms of this leukemoid reaction, we studied the changes occurring in hematopoietic progenitor cells in BMT-11-transplanted mice. The numbers of granulocyte-macrophage colony-forming units (CFU-GM), erythroid colony-forming units (CFU-E), erythroid burst-forming units (BFU-E), and mixed colony-forming units (CFU-Mix) in the spleen showed dramatic 216-fold, 18-fold, 64-fold, and 80-fold increases, respectively, relative to the value in the control mice 5 weeks after the BMT-11 implantation. In contrast, the levels of progenitor cells in the bone marrow remained within normal limits. The nature of the colony-stimulating factor (CSF) secreted from BMT-11 tumor cells was also studied. BMT-11-conditioned medium (BMT-11-CM), BMT-11 tumor extract, and sera from the mice bearing transplanted BMT-11 tumor contained CSF that stimulated mainly granulocyte and macrophage lineages. Furthermore, the expression of the granulocyte colony-stimulating factor (G-CSF) gene in BMT-11 cells were detected by Northern blot analysis.

Animals↗
PubMed1990

G-proteins (Gi, Go) in the basal ganglia of control and schizophrenic brain.

We detected the existence of Gi (the inhibitory G-protein) or Go (a similar G-protein of unknown function) in the striatum of control and schizophrenic brains utilizing pertussis toxin-catalyzed ADP ribosylation. The level of Gi/Go was significantly decreased by 42% in the putamen of the left hemisphere in schizophrenics; caudate head and globus pallidus levels were unchanged. Decreased Gi or Go may underlie enhanced dopamine function in the schizophrenic brain.

Aged↗