PubMed Health⌕ Search

Biomedical subjects

T Shinomiya

Publications and source records attributed to T Shinomiya.

At least 73 records · Page 4Linked to original sources
PubMed1988

Three Japanese families with members carrying C7 silent allele (C7*Q0). Possibility for an association between C7*Q0 and C6*B.

Three Japanese families with members carrying C7 silent allele(s) (C7*Q0) are presented. C6 types in the family members were also examined, and it was found that C7*Q0 was transmitted from a parent to offsprings as a haplotype, C7*Q0-C6*B. In another study of C6 types in sera from 3 volunteer blood donors with homozygous C7 deficiencies, the C6 phenotypes were found to be C6 B (homozygote). It seems remarkable that C7*Q0 can be associated with C6*B.

Alleles↗
PubMed1987

Immunosuppressive activity of serum from liver-grafted rats: in vitro specific inhibition of mixed lymphocyte reactivity by antibodies against class II RT1 alloantigens.

The immunosuppressive activity of serum from PVG rats following orthotopic transplantation of DA liver has been examined in vitro. Liver grafts in this combination are never rejected, but induce a state of specific transplantation tolerance in the recipient. Serum from such tolerant animals was able to inhibit proliferation of normal PVG lymph node cells in response to DA stimulators in the mixed lymphocyte reaction (MLR); inhibition was specific for donor (DA) antigens. Interleukin-2 (IL-2) production during the MLR was also reduced. The production of anti-DA cytotoxic T cells developing in the MLR was not affected, but the total yield of such cells was reduced. Evidence was obtained that part of the inhibitory serum activity was due to IgG antibody against class II RT1a alloantigens. Thus, a purified IgG fraction retained much of the inhibitory activity which could be removed by an anti-IgG absorbent. Studies of MLR inhibition in different rat strains indicated the anti-class II specificity of the inhibitory IgG. Lymph node cells from DA-liver-grafted PVG rats responded normally against DA stimulators in vitro, and this MLR was also blocked by the inhibitory IgG. Our results suggest that anti-class II allo-antibody may play a role in immunosuppression and long-term graft survival following liver transplantation in this combination.

Animals↗
PubMed1986

Serology of liver transplantation in the rat. I. Alloantibody responses and evidence for tolerance in a nonrejector combination.

The antibody response against class I and class II RT1 antigens has been studied in PVG rats grafted with DA liver. In this nonrejector combination, liver grafts survive permanently in all normal recipients and in about 50% of recipients presensitized by a DA skin graft, with concurrent induction of transplant tolerance for other DA organs and skin. Using a two-stage radioimmunoassay, the anti-class I (RT1Aa) levels in sera of normal PVG recipients of DA liver grafts were found to be low (maximal titer 1:50 serum dilution or less); after peaking at 2 weeks posttransplantation, they diminished to background levels by 6 weeks. The anti-RT1Aa response showed a close parallel to cell-mediated rejection events in the liver graft recipients. In contrast, anti-class II (RT1Ba/Da) responses reached much higher titers (over 1:1000), which were maintained for several weeks before declining after 4 months. Similar observations were made in presensitized recipients. The induction of tolerance in the alloantibody response was indicated by the inability of DA skin grafts to restimulate anti-RT1 antibody in liver recipients. The observations support the picture of "split tolerance" indicated by previous cellular studies in this combination.

Animals↗
PubMed1986

Immunosuppressive activity of serum from liver-grafted rats. Passive enhancement of fully allogeneic heart grafts and induction of systemic tolerance.

Immunological enhancement of allogeneic heart graft survival by serum from rats tolerized by liver grafting has been studied. Serum taken from long-term-surviving PVG rats carrying orthotopic DA liver transplants (OLT serum) was able to increase the survival time of PVG.RT1a heterotopic heart grafts in PVG recipients. Administration of 1 ml of OLT serum at the time of heart grafting led to permanent survival of the grafts in all animals. The recipients became systemically tolerant of RT1a and several weeks later were able to accept permanently skin grafts from the same donor strain, while rejecting third-party grafts. Enhancement appeared to be mediated initially by IgG antibodies in the OLT serum against class II donor RT1a antigens; significant enhancement was produced by as little as 100 micrograms of antibody. Recipient alloantibody responses following enhancement were studied and showed selective suppression of the anti-class-I (RT1Aa) antibody levels, while the anti-class-II antibody response was apparently unaffected. The implications of these results for mechanisms of unresponsiveness following enhancement and liver transplantation are discussed.

Animals↗
PubMed1985

Clonal deletion as the mechanism of abrogation of immunological memory following liver grafting in rats.

In the rat strain combination of DA into PVG, an orthotopic liver graft has the ability to abrogate an existing state of sensitization against donor (DA) antigens. Fifty-four percent of PVG rats sensitized against DA by skin grafting accepted a DA liver graft permanently, and about half of these became systemically tolerant of DA MHC antigens, as demonstrated by permanent acceptance of a subsequent (second-set) DA skin or heart graft. The cellular basis of this tolerant state was studied in vivo. An adoptive transfer assay provided evidence for functional deletion of DA-reactive cells responsible for graft rejection from the recirculating lymphocyte pool. There was no evidence of a role for suppressor T cells in maintaining tolerance. However, a graft-versus-host assay showed normal reactivity in thoracic duct lymphocytes from tolerant animals. Hence, specific clonal deletion is apparently responsible for the abolition of immunological memory by liver grafting, but is selective in respect of the sets of alloreactive lymphocytes affected.

Animals↗
PubMed1984

Identification of sperm antigenic determinants with phylogenetically diverse and limited distribution using monoclonal antibodies.

Mouse monoclonal antibodies capable of recognizing mouse sperm antigens were produced and the inter-species cross-reactivity of the antigenic determinants was examined. Of the seven clones independently established, it was found by indirect immunofluorescence staining that one was bound to the tail, one could recognize the head and five other antibodies reacted with the crescent-shaped anterior acrosome. Ultrastructural studies showed that the anti-head antibody recognized the sperm surface, and the anti-tail antibody reacted with the fibrous sheath. Five acrosomal antigenic determinants were found in the acrosome. These antibodies reacted with sperm from the male reproductive tract (testis, cauda epididymis, vas deferens), but not with somatic tissues. The anti-tail antibody reacted with sperm from four other mammalian species (musk shrew, rat, boar and human). The anti-head antibody and one of the anti-acrosome antibodies were bound only to mouse sperm. The other four acrosomal antigenic determinants showed various degrees of inter-species cross-reactivity. None of these antibodies reacted with chicken sperm.

Animals↗
PubMed1984

Isolation and characterization of the rat tyrosine aminotransferase gene.

Tyrosine aminotransferase (TAT; L-tyrosine:2-oxoglutarate aminotransferase, EC 2.6.1.5) from rat liver is subject to glucocorticoid, cAMP, and developmental control. To study the underlying regulatory mechanisms, the TAT structural gene was isolated from a lambda bacteriophage rat DNA library. Heteroduplex analysis revealed that the 2.4-kilobase-long TAT mRNA is encoded by a gene that extends over 11 kilobases and is interrupted by 11 introns. To characterize the presumptive control region, the DNA sequence around the 5' end of the gene was determined and the start site of transcription was identified by nuclease S1 protection experiments. A short sequence homology in an equivalent position relative to the cap site was detected between TAT and tryptophan oxygenase, another glucocorticoid-controlled gene from rat liver. This sequence is related to the sequence 5' T-G-T-T-C-T 3' found in regions of the long terminal repeat of mouse mammary tumor virus, which has been shown to interact with the glucocorticoid receptor [Scheidereit, C., Geisse, J., Westphal, H. M. & Beato, M. (1983) Nature (London) 304, 749-752].

Animals↗
PubMed1984

Phenotypic mixing of pyocin R2 and bacteriophage PS17 in Pseudomonas aeruginosa PAO.

Previous results indicate that a group of bacteriocins in Pseudomonas aeruginosa, named R-type pyocins, have a structure resembling bacteriophage tails and share some serological homology with certain bacteriophages. This paper presents genetic evidence which strongly suggests that components of pyocin R2, an R-type pyocin of P. aeruginosa PAO, and tail components of bacteriophage PS17 are interchangeable. Complementation tests with pyocin R2-deficient mutants of PAO and ts mutants of PS17 revealed that various phenotypic interactions occur between the pyocin and bacteriophage in PAO cells lysogenized or infected with PS17. (i) Certain pyocin R2-deficient mutations were phenotypically suppressed in cells carrying PS17 prophage. (ii) A temperature-sensitive mutant of PS17, tsQ31, was phenotypically suppressed in PAO cells treated with mitomycin C. (iii) Phenotypically mixed phages with receptor and serological specificities of pyocin R2 were formed in PS17 lysogens of certain pyocin R2-deficient mutants.

Bacteriocins↗
PubMed1983

Genetic determinant of pyocin R2 in Pseudomonas aeruginosa PAO. I. Localization of the pyocin R2 gene cluster between the trpCD and trpE genes.

Thirty-seven mutants defective in pyocin R2 production in the P. aeruginosa PAO strain were subjected to fine mapping of pyocin R2 genes by transduction with phage F116L. Sixteen complementation groups (designated prtA through prtP) involved in pyocin R2 production were tentatively identified by complementation tests using phage F116L. Their linkages to trpC and trpE markers and fine mapping by three point crosses demonstrated that most of the mutations (prtA through prtN) were located in between trpC and trpE, and that the prtP mutation was localized outside this major prt cluster but in the proximity of the rifA and strA region.

Bacteriocins↗
PubMed1983

Genetic determinant of pyocin R2 in Pseudomonas aeruginosa PAO. II. Physical characterization of pyocin R2 genes using R-prime plasmids constructed from R68.45.

The chromosome segment which contains the genes responsible for production of pyocin R2 in P. aeruginosa PAO was defined physically using R-prime plasmids constructed in vivo from R68.45. The previous conclusion from genetic mapping that the cluster of pyocin R2 genes is located in between trpC and trpE genes was confirmed by deletion mapping of various R prime plasmids bearing the trpC gene. The pyocin R2 gene cluster was further localized on two contiguous HindIII fragments of 16 kb and 8.0 kb. PML14 strain, in which R-type pyocin genes were completely deleted, had only one 11 kb HindIII fragment instead. Heteroduplexes between this 11 kb fragment with the two HindIII fragments of PAO revealed that the cluster of pyocin R2 genes was an insertion 13 kb long.

Bacteriocins↗
PubMed1983

The typing of group-specific component (Gc protein) in human blood stains.

It is known that the typing of group-specific component (Gc protein) in human blood stains is difficult since Gc protein of the extracts of blood stains migrates more anodally to the alpha 1-globulin region in agar-gel immunoelectrophoresis, while Gc protein in liquid blood normally migrates to the alpha 2-globulin region. We have reported that the Gc protein found in the alpha 1-region is the result of binding of actin to Gc protein (Shinomiya, K., Kimura, H., Yoshida, K., and Shinomiya, T., J. Biochem., 92 (1982) 1163-1171, which renders it difficult to determine the Gc-phenotypes in the blood stains. On the basis of the above findings, we developed the method of phenotyping the Gc protein of human blood stains by agar-gel immunoelectrophoresis. Since the binding activity of actin to Gc protein is lost after treatment with a high concentration of guanidine HCl, the extracts of blood stains were treated with 4 M guanidine HCl to dissociate Gc protein and actin and then dialyzed to remove guanidine HCl. By this method we are able to determine the phenotypes of Gc protein in blood stains. The method we have developed is a useful tool in the forensic laboratory.

Alpha-Globulins↗