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Biomedical subjects

T Odaka

Publications and source records attributed to T Odaka.

At least 55 records · Page 3Linked to original sources
PubMed1987

[Tissue reaction of the bone marrow to glass ceramic powder in the femurs of rats fed on a low-calcium diet].

Glass ceramic powder was injected into the bone marrow of 36 rats which were fed a low calcium (21 rats) or normal (15 rats) diet. They were sacrificed 7 or 8, 32 and 60 days after treatment. Histomorphometrical measurement revealed that the ratio of length of bone tissue which was in contact with glass ceramic mass to the circumference of each mass was larger in 32-day and 60-day groups than in the 7 or 8-day groups. Osteocyte-like cells were observed in the narrow space between ceramics and bone tissue in all specimens. Giant cells were seen in 1-2% of the glass ceramic surfaces in low calcium diet group and in 0.3% in normal diet group. No inflammatory reaction such as aggregation of lymphocytes nor leukocyte infiltration was observed in any specimens. Eighty-two percent of the surface of glass ceramic mass was covered with bone tissue 60 days after treatment in normal diet group.

Animals↗
PubMed1986

Relationship between the cellular resistance to Friend murine leukemia virus infection and the expression of murine leukemia virus-gp70-related glycoprotein on cell surface of BALB/c-Fv-4wr mice.

Fv-4r is a dominant resistance gene which controls resistance of mice to exogenous infection with ecotropic murine leukemia viruses. Cell lines with various degrees of resistance to ecotropic Friend murine leukemia virus infection were established from BALB/c-Fv-4wr mice which are partially congenic with BALB/c. The degree of resistance of these cell lines correlated well to the amount of glycoprotein with mol wt 80 K on cell surface. The resistance of cells was reduced by the treatment of glycosylation inhibitors, tunicamycin and 2-deoxy-D-glucose. The results indicate that the Fv-4 resistance is ascribed to the unique glycoprotein on cell surface.

Animals↗
PubMed1986

A culture technique for chromosome analysis in human myeloid leukemias.

A simple culture technique for the study of cells from myeloid leukemias and other blood disorders of myeloid series is described. The procedure is the same with that of the ordinary cultures, except for the addition of colony stimulating factor. A large number of mitotic cells can be obtained, and they are quite suitable for banding treatments. Clear banding patterns are consistently obtained.

Cells, Cultured↗
PubMed1986

Detection of an antigen (AN6520), possibly related to non-A, non-B hepatitis, by monoclonal antibodies. I.

The antibody to AN6520 antigen, which was isolated from the liver of a patient with non-A, non-B hepatitis (NANBH), has been detected frequently in convalescent sera from patients with NANBH by the passive hemagglutination (PHA) test. In a further study, we established hybridoma cells secreting antibodies against AN6520 antigen and obtained ascitic fluids with PHA titers ranging from 1:10(5) to 1:10(7). In immunodiffusion with AN6520 antigen, all monoclonal antibodies were found to form an identical precipitin line. These lines were also identical to those formed by rabbit antiserum against AN6520 antigen and by convalescent sera from patients with NANBH. With one of the monoclonal antibodies, 1-F12, solid-phase radioimmunoassay (SP-RIA) for detecting AN6520 antigen was developed as well as blocking RIA for anti-AN6520 antibody detection. The antigen assay was 50 times more sensitive than the reverse passive hemagglutination (R-PHA) test, with a sensitivity threshold of the 1 ng/ml of antigen solution; the antibody assay was 10 times more sensitive than PHA. The results with this blocking RIA were mostly in agreement with the data obtained by PHA. Furthermore, the antigen in human sera, which had never been detected by R-PHA test, could be detected by SP-RIA.

Aged↗
PubMed1986

Non-A, non-B hepatitis related AN6520 Ag is a normal cellular protein mainly expressed in liver. II.

Detection of AN6520 Ag/Ab in human sera had indicated a close association with non-A, non-B hepatitis (NANBH). In this study, we investigated the immunochemical nature of AN6520 Ag and measured the amounts in various human and chimpanzee organs in order to clarify the association with NANBH. AN6520 Ag was found to be composed of polypeptide(s) with an apparent molecular weight of 45,000 daltons (45 kD), which are noncovalently linked together. Human antibodies in convalescent sera from NANBH patients as well as monoclonal antibodies were found to recognize only the high-order structure of the antigen, whereas rabbit antibody recognized both the high-order structure and the reduced form of 45 kD polypeptide(s). AN6520 Ag could be detected in most of the livers tested including those without any liver damage and fetal livers; their amounts varied considerably from each other. The antigen could be detected also in organs other than liver, but in contrast to liver, the amounts were small and did not vary as much between individuals. From the data of immunoblotting using rabbit antibody, our observed variation of antigen content in liver was considered to be due to the difference in expression of 45 kD polypeptide(s). Although no specific relationship was found between the amount of the antigen in liver and NANBH, the antigen was found to increase several times in livers of chimpanzees after the inoculation of NANBH virus. These data suggest that AN6520 Ag is a normal cellular protein existing mainly in liver and that its quantity may vary under some conditions such as NANBH.

Adult↗
PubMed1985

Murine leukemia virus maturation: protease region required for conversion from "immature" to "mature" core form and for virus infectivity.

Murine leukemia virus (MuLV) genome encodes a protease (Y. Yoshinaka, I. Katoh, T.D. Copeland, and S. Oroszlan (1985), Proc. Natl. Acad. Sci. USA 82, 1618-1622), which has been shown to cause maturation, specified as morphological conversion from "immature" to "mature" form of virus cores. To examine whether "immature" particles have infectivity or not, we constructed mutant DNAs with deletions in the protease region. The NIH/3T3 cells transfected with mutant DNAs produced "immature" particles, having immature morphology and containing Pr65gag, a polyprotein precursor of core proteins. The specific infectivity of the extracellularly released and purified particles was shown to be greatly reduced based on reverse transcriptase activity and protein content as compared with the "mature" particles obtained from wild-type DNA-transfected cells. The mutant genomes encoded functionally normal surface glycoprotein, gp70. These results strongly suggest that maturation of MuLV from "immature" to "mature" form of virus particles is indispensable to virus infectivity. The importance of processing of gag and pol, as well as transmembrane protein precursors by the viral protease is discussed.

Amino Acid Sequence↗
PubMed1985

Transmission of human T-cell leukemia virus type I to an S+L- cat kidney cell line.

The S+L- cat kidney cell line CCC was cocultivated with lethally irradiated human lymphoid cell lines that were producing human T-cell leukemia virus type I (HTLV-I). Eight of nine S+L- CCC sublines that had been cocultivated with nine different HTLV-producing T-cell lines gave positive reactions for HTLV antigens by indirect immunofluorescence assay. One subline CCC/2M was cloned. The percentages of fluorescent cells differed markedly in different sublines and clones. Southern blot hybridization with HTLV probes and electrophoresis of immunoprecipitates indicated that defective HTLVs were often transmitted into S+L- cat cells. S+L- CCC cells were permissive for HTLV and the properties of HTLV-infected cat cells were heterogeneous.

Animals↗
PubMed1984

A cell membrane "gp70" associated with Fv-4 gene: immunological characterization, and tissue and strain distribution.

Fv-4r is a dominant resistance gene which controls susceptibility of mice to exogenous infection with ecotropic murine leukemia virus (MuLV). A MuLV env-gene product related to gp70 on cells from uninfected Fv-4r mice has been found. Expression of this molecule is closely linked to the resistance allele. Antigenic determinants on the Fv-4r gp70 are similar to many ecotropic and some dualtropic MuLV gp70s but different from xenotropic and amphotropic MuLV gp70s. The Fv-4r gp70 molecule also has unique antigenic determinants since it is recognized by Fv-4 specific antisera which do not recognize other cell membrane gp70s or viral gp70s. The Fv-4-specific cell membrane gp70 is detectable on cells from thymus, spleen, lymph node, bone marrow, and embryo fibroblasts from Fv-4r mice, but not from Fv-4s mice. Slight differences in electrophoretic mobility of Fv-4r gp70 are found on different tissues. This unique cell membrane gp70 may be causally related to Fv-4 resistance.

Animals↗
PubMed1983

Cellular expression of murine leukemia virus gp70-related antigen on thymocytes of uninfected mice correlates with Fv-4 gene-controlled resistance to Friend leukemia virus infection.

Alleles at the Fv-4 locus have been shown to determine susceptibility (Fv-4s) and resistance (Fv-4r) to infection with ecotropic murine leukemia viruses (MuLV). The resistance is dominant in heterozygous mice. BALB/c mice are Fv-4ss and a semicongenic line BALB/c-Fv-4wr, homozygous for Fv-4r allele and called C4W, is being developed. Extracts of 125I-labeled thymocytes from BALB/c and C4W mice were precipitated by a series of antisera against MuLV and the precipitates examined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). Thymocytes from C4W mice expressed 80K and 73K glycoproteins related to the gp70 of MuLV, while only the 73K glycoprotein was occasionally detectable on BALB/c thymocytes. Genetic studies showed that a locus controlling expression of the 80K protein was dominant and associated with the resistant allele at Fv-4. This membrane gp70 may be important in the Fv-4-mediated resistance to exogenous virus infection.

Animals↗
PubMed1983

Strain difference in immune response of the rat to NRK cells infected with spleen focus-forming virus of the Friend leukaemia virus complex.

Five rat strains were studied for immune responsiveness to SFFV-NRK, a normal rat kidney cell line non-productively infected with spleen focus-forming virus (SFFV) of the Friend leukaemia virus (FLV) complex. Antisera from ACI, JAR, Fischer and SD strains precipitated SFFV-specific gene product, gp55, whereas those from LEW did not. In the cross of Fischer X LEW, immune responsiveness to gp55 was controlled by a single or a few dominant genes. The immune responsiveness was neither related to the susceptibility to FLV infection, nor to the amount of SFFV-related RNA in spleen cells. Unresponsiveness of LEW rats to gp55 was not absolute; when LEW rats were immunized with FLV preparations from infected mice or xenotropic virus-infected NRK cells, they produced antibody that could precipitate gp55.

Animals↗
PubMed1982

Characterization of N-type and dually permissive cells segregated from mouse fibroblasts whose Fv-1 phenotype could be modified by another independently segregating gene(s).

Though the inbred DDD mouse strain is essentially of the N type, the primary culture of this strain was about 100-fold more sensitive to B-tropic WN1802B virus than were the typical N-type strains (C3H/He, C57L, etc.). After cloning, DDD mouse cells segregated two types of cells, typical N-type cells and cells lacking in Fv-1 restriction. As both types of cells so far tested retained glucose-6-phosphatase-1 coded by a locus closely linked to Fv-1 and genetic cross experiments indicated the presence of a gene(s) modifying the Fv-1 phenotype, variation in Fv-1 restriction could presumably be brought about by genetic changes in a gene(s) other than Fv-1 itself. N-type and dually permissive cell clones were similarly established from the inbred G mouse. Compositions of polypeptides labeled with [35S]methionine in the N-type and dually permissive cells of DDD and G mouse origins were compared by two-dimensional gel electrophoresis. The polypeptide maps of these cells were similar except for a few spots. Among these dissimilar spots, a spot of about 20,000 daltons with a pI of about 5.5 was always present in N-type cells, whereas it was absent in dually permissive cells. In DDD mouse-derived clones, a proportional relation was observed between the intensity of the spot and the restriction to the B-tropic virus.

Animals↗
PubMed1982

Surface antigen expressed in hematopoietic cells derived from Fv-4r mouse strains.

Fv-4 locus controls the susceptibility of mice to ecotropic murine leukemia virus (MuLV). Antiserum against Fv-4r/s mice with BALB/c background was raised in inbred BALB/c mice. In the complement-dependent cytotoxicity test, the antiserum killed the hematopoietic cells derived from Fv-4r/- mice but not these from Fv-4s/s mice, and the genetic cross experiments located the locus controlling the expression of the target molecule of the antibody in the close vicinity of Fv-4. In addition, the antigenic expression of the exogenously infecting MuLV suppressed the expression of the target molecule of the antiserum. The expressions of these two antigens appear to compete with each other on the cell surface.

Animals↗
PubMed1981

Mapping of the Fv-4 mouse gene controlling resistance to murine leukemia viruses.

Fv-4, a gene controlling susceptibility to ecotropic murine leukemia viruses, was linked to both Pre-I (prealbumin) and Igh-I (immunoglobulin heavy-chain constant region) loci on chromosome 12 in mice. The gene order was Fv-4 - Pre-I - Igh-I, and the estimated frequency of recombination between Fv-4 and Pre-I was about 20%.

Animals↗
PubMed1981

Inheritance of susceptibility to the myeloproliferative sarcoma virus: effect of the Fv-2 locus and evidence for a myeloproliferative sarcoma virus resistance locus.

Myeloproliferative sarcoma virus (MPSV) causes a generalized stem cell leukemia with erythroid and myeloid hyperplasia in adult mice. MPSV also transforms fibroblasts. Mice congenic for the Fv-2 locus showed marked differences in susceptibility to MPSV according to the Fv-2 genotype. MPSV was injected into C57BL/6 Fvs and C57BL/6 Fv-2r mice congenic except for the Fv-2 locus. C57BL/6 mice with the Fvs genotype were much more susceptible to MPSV than were those with the Fvr genotype. Both DDD Fv-2r mice congenic with DDD Fv-2s mice except for the Fv-2 locus and DDD Fv-2s mice, however, were sensitive to spleen focus formation by MPSV. These data indicate that at least one additional resistance locus to MPSV is present in C57BL/6 mice but not in DDD mice. Both the Fv-2 locus and the putative MSPV resistance locus (loci) Mpsvr appear to be epistatic to either of the sensitivity loci. Fibroblast focus formation by MPSV was obtained well in C57BL/6 Fv-2r and C57BL/6 Fvs fibroblasts, indicating that the genes for MPSV resistance (Fv-2r and Mpsvr) were not operating in fibroblast cells. A model is proposed which may account for the differences in response of genetically different mice to MPSV and Friend spleen focus-forming virus.

Alleles↗
PubMed1981

Fv-4: gene controlling resistance to NB-tropic Friend murine leukemia virus. Distribution in wild mice, introduction into genetic background of BALB/c mice, and mapping of chromosomes.

A gene controlling resistance to NB-tropic Friend murine leukemia virus (F-MuLV) was studied in wild mice. Mice of various subspecies were crossed with inbred BALB/c mice, and their F1 hybrids were tested for resistance to F-MuLV. Some mice of Mus musculus molossinus (Japan), M. musculus castaneus (Taiwan and the Philippines), and M. musculus urbanus (Sri Lanka) appeared to have a dominant resistance gene. A partially congenic strain, BALB/c-Fv-4wr (C4W), was established by the introduction of the gene Fv-4wr from a M. musculus molossinus into the genetic background of BALB/c mice. [(C4W X DBA/2) X C57BL/6-Fvs] crosses revealed that Fv-4wr is located on chromosome 12 with the gene order of Fv-4w-Pre-1-lgh-1, apparently at the same site as the Fv-4. The resistance of C4W mice was indistinguishable from the Fv-4-controlled resistance of FRG mice.

Animals↗
PubMed1980

Restricted expression of endogenous N-tropic XC-positive leukemia virus in hybrids between G and AKR mice: an effect of the Fv-4r gene.

G mice carrying the Fv-4r gene are resistant to exogenous infections of various strains of ecotropic MuLVs (Suzuki, 1975). The expression of endogenous N-tropic XC-positive virus was studied in the progency of a cross between G and AKR mice. In the F1 mice, the virus expression was almost completely supressed, and no leukemia developed during 1 year of observation. Results of successive backcrossings with AKR mice indicated that a single dominant gene, the Fv-4r suffices for supression. It can be concluded that the extensive growth of N-tropic XC-positive virus is a prerequisite for leukemia development in AKR mice.

Animals↗
PubMed1979

Expression of Fv-4r allele in hematopoietic cells from G mice resistant to Friend leukemia virus.

G mice carrying the Fv-4r resistant allele supported virus growth neither at an early nor a later (Kai et al., 1976) stage of infection with NB-tropic FLV. This resistance could not be abolished by treatment of G mice with cyclophosphamide or cortisone acetate. By bone-marrow or spleen-cell transplantation into irradiated mice, the resistan-e of G mice could be transferred to Fv-4-susceptible mice. Conversely, transfer of bone-marrow or spleen cells of Fv-4-susceptible mice rendered G mice susceptible. It could be concluded that, as assessed by the virus content in the spleen, helper LLV grows mainly in radiosensitive, bone-marrow-derived cells, and the Fv-4 gene is expressed in these cells.

Alleles↗