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D Sawamura

Publications and source records attributed to D Sawamura.

85 records · Page 5Linked to original sources
PubMed1988

[Rapid diagnosis of experimental tumor by FITC-Con A lectin--a comparative study of smear and section specimens].

FITC-Con A staining as a rapid diagnostic method for tumor cells was applied to the tumors smeared on glass slide and section specimens to evaluate the reactivity with FITC-Con A. Good staining results were obtained in smear specimens with clear fluorescence on the membrane of tumor cells. Con A and LCH lectins bound well with tumor cells to produce strong fluorescence in comparison with PEA and DBA. It indicates that tumor cells expressed dominantly the receptors of alpha-D-glucose and alpha-D-mannose sugar chain on the membrane of tumor cells. From these results it was concluded that FITC-Con A staining method applied to smear specimens is more advantageous in the rapidity and the simplicity for tumor cell diagnosis than section specimen method.

Animals↗
PubMed1985

[Shared antigens between BCG and tumor cells--immunotherapy with BCG for mouse tumor].

Cytotoxic activity of anti-BCG rabbit serum (A-BCG) and the antigenic relationship between BCG and tumor cells were studies. A-BCG showed high cytotoxic activity against line 10 tumor cells of guinea pig Strain 2 and Colon 26 tumor cells of BALB/c mouse but not to cells of human bladder cancer (HT 1197, HT 1376). Cell-killing activity of A-BCG against line 10 and Colon 26 was dependent on complement participation. It was also found that Colon 26 cells were heterogenous in their susceptibility to the killing activity of A-BCG. Antigenic studies between BCG and tumor cells were undertaken using on indirect immunofluorescence method and it was found that all tumor cells used in the experiment shared common antigens with BCG. In immunotherapy with BCG for Colon 26 tumors, BCG worked effectively for suppressing tumor growth. However, enhancement of tumor growth in some of the BCG-treated mice was observed.

Animals↗
PubMed1985

[Antitumor activity of BCG--inhibition and enhancement of tumor growth by anti-BCG rabbit serum].

Administration of heat-killed BCG into BALB/c mice with colon 26 tumors which have common antigens to those of BCG has been shown to enhance tumor growth. The present experiments were undertaken to clarify this phenomenon. It was found that anti-BCG rabbit serum played a role in augmenting tumor growth when injected intraperitoneally into tumor-bearing mice. Interestingly, bi-phasic activity of anti-BCG rabbit serum (inhibition and enhancement of tumor growth) was observed, which was dependent on the concentration of BCG antibodies present. By contrast, immune-complex prepared with BCG antigen-antibody was not considered to be an agent for directly enhancing tumor growth. It was therefore concluded that anti-BCG rabbit serum was a specific agent for augmenting tumor growth.

Animals↗
PubMedDate not supplied

In vivo introduction of the interleukin 6 gene into human keratinocytes: induction of epidermal proliferation by the fully spliced form of interleukin 6, but not by the alternatively spliced form.

The achievement of keratinocyte gene therapy in clinical practice requires fundamental experiments using human keratinocytes or skin. We have recently demonstrated that the in vivo introduction of the interleukin 6 (IL-6) gene into rat keratinocytes induces epidermal proliferation and lymphocyte infiltration into the skin. In this study, we first amplified the human IL-6 cDNA from oligo-dT-primed keratinocyte cDNA and then detected the fully spliced (FS) form and the alternatively spliced (AS) form of IL-6 cDNA. Sequence analysis showed that the AS form, which was composed of the IL-6 coding region with all of exon II deleted except for the first guanine, was identical to that reported to be present in lymphocytes. We constructed the expression vectors phIL6 of the FS form and phIL6S of the AS form. We transplanted human skin onto nude rats and introduced phIL6 and phIL6S into the human keratinocytes using the naked DNA method. Keratinocytes prepared 24 h after introduction from the areas treated with them were examined by reverse transcriptase (RT)-PCR and enzyme linked immunosorbent assay (ELISA). RT-PCR showed that the amounts of FS IL-6 mRNA and AS IL-6 mRNA were similar, whereas the ELISA showed that the amount of FS IL-6 peptide was four times that of the AS IL-6 peptide. Histological examination 48 h after introduction showed that the FS form had induced epidermal proliferation, whereas the AS form had not. The epidermal thickening without lymphocyte infiltration induce by the FS form indicates that keratinocyte proliferation is caused by a direct effect of overexpressed IL-6, and not by a secondary effect of infiltrating lymphocytes. This is the first report of the introduction of a human gene into human keratinocytes to produce a biologically active transgenic gene product in human skin using the naked DNA method.

Alternative Splicing↗
PubMedDate not supplied

In vivo gene transfer method in keratinocyte gene therapy: intradermal injection of DNA complexed with high mobility group-1 protein in rats.

In order to develop a more efficient method of introducing genes into keratinocytes in vivo, we intradermally injected DNA bound to high mobility group 1 protein, thereby taking advantages of the naked DNA and hemagglutinating virus of the Japan-liposome method reported previously. First we performed a gel mobility shift assay, which confirmed DNA binding to high mobility group 1. Then we injected beta-galactosidase expression vector complexed with high mobility group 1 into the rat skin and the activity of sample with the protein was 2-3 times higher than that without the protein as control. Semiquantification of transferred-DNA content using polymerase chain reaction and a time course of transgene expression in keratinocytes suggested that high mobility group 1 protein increased transfer of the DNA from the cytoplasm to the nucleus. Direct injection of the DNA-high-mobility-group-1 complex is a highly efficient method for introducing genes into keratinocytes in connection with gene therapy.

Animals↗