100 results match your criteria: "Japanese Red Cross Central Blood Center.[Affiliation]"

A new HLA-B18 allele (B*1802) derived from a Thai individual was sequenced. Comparison of this B18 nucleotide sequence with the published B*1801 sequence indicated that this Asian B18 allele has a nucleotide sequence different from that of B*1801. Three nucleotide changes were observed in exon 3, in which two substitutions at codon 97, AGG in B*1801 to AAT in the B*1802, result in an amino acid change from arginine to asparagine.

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Nucleotide sequences of alleles encoding four serologically defined splits of the HLA-A10 group, A26.1, A26.3, A26.

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HLA-A11 has two serologically-defined splits, A11.1 and A11.2, and two alleles coding for HLA-A11, A*1101 and A*1102, have been published so far.

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In human platelets stimulated with thrombin (40 mU/ml), Na+/H+ exchange activity [the ethylisopropylamiloride (EIPA)-sensitive increase of cytoplasmic pH (pHc)] and protein kinase C (PKC) activity [phosphorylation of 47 kDa protein (P47), a substrate for PKC] were determined in the presence of protein kinase inhibitors, staurosporine (0.05-1 microM), K-252a (0.5-10 microM), H-7 (100 microM) and sphingosine (20-40 microM).

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The presence of an antibody which reacts strongly at lower temperatures to C100-3 antigen derived from the hepatitis C virus (HCV) was demonstrated in blood donors' sera. These sera reacted with the antigen most strongly at 4 C and most weakly at 37 C and are termed 'cold antibody group'. The cold antibody group reaction was specifically inhibited with soluble C100-3 antigen.

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In November 1989, Japanese Red Cross Blood Centres started screening for hepatitis C virus (HCV) with enzyme-linked immunosorbent assay (Elisa) for the C100-3 viral peptide as the first such nationwide programme in the world. Thereafter post-transfusion non-A non-B hepatitis (PTNANBH) was reduced by 61-80%, but this was not as complete a success as our programme to prevent post-transfusion hepatitis B by screening for high titer hepatitis B core antibody, which we began in the same period. In order to acquire more effective control of PTNANBH, the HCV core-related antigen (GOR, N14) and second-generation Elisa (Ortho2, Abbott2) and second-generation antigen agglutination (PA, PHA) tests have been employed.

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An extensive family study on HLA-DPB1 was performed in 105 families living in northeastern Japan. In a linkage study between HLA-DPB1 and other HLA loci, five apparent recombinations between DPB1 and DR/DQ loci were observed. The recombination frequency (theta) with maximum probability was estimated to be 0.

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Serum samples with lower temperature-dependent antibody with low avidity to C100-3 (HCV) antigen were found in 0.19% of 23,197 voluntary blood donors at this blood center. They showed positive C100-3 antibody activity at 24 C but not at 37 C.

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Arachidonic acid (AA)- or thromboxane A2/prostaglandin H2 (TXA2/PGH2) analog (STA2 and U-46619)-induced aggregations yielded a bell-shaped dose-response curve. The inhibitory mechanism by high concentrations of the agonists was examined. STA2 elevated cAMP level of platelet in a dose-dependent manner.

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Because of the high incidence of non-A non-B post transfusion hepatitis and its relation to hepatocellular carcinoma, HCV antibody screening for blood transfusion was begun in November 1989. Seroepidemiological studies revealed the great magnitude of HCV infection in acute hepatitis, chronic hepatitis, liver cirrhosis and hepatocellular carcinoma in Japan. Approximately 1.

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In a 6-month follow-up study of acute hepatitis in Japan, 31 out of 41 (75.6%) cases of post-transfusion non-A and non-B hepatitis (NANB-PTH) and 14 out of 40 (35.0%) cases of sporadic non-A non-B hepatitis (NANB-SPO) were found to be positive for antibody to the hepatitis C virus (HCVAb).

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Since demonstration of causative relationship of hepatocellular carcinoma (HCC) and persistent hepatitis B virus (HBV) infection, nation-wide preventive measures have made remarkable progress in Japan. This will contribute to minimizing the probability to create new sources for HBV infection resulting in reduction of the incidence with liver cirrhosis and HCC due to HBV infection in the next generation. Currently, however, HCC not due to HBV increased twice in the pastdecade up to three quarters of total HCC cases and 30-40% of them had previous history of blood transfusion.

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Effects of extracellular Na+ on platelet responses were examined. Cytoplasmic pH decreased by stimulation with thrombin, TPA and AA in Na(+)-containing buffer as well as in Na(+)-free buffer. Thrombin-induced aggregation and serotonin release were higher in Na(+)-containing buffer, but TPA- and A23187-induced responses exhibited lower values.

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In Japan, hepatocellular carcinoma (HCC) is one of the most prevalent cancers, with a reported fatality rate showing a consistent and significant increase in the last decade. At most, only 25% of HCC cases are positive for the hepatitis B surface antigen (HBsAg). To investigate a potential role for hepatitis C virus (HCV) in the development of HCC, sera from 105 HBsAg-negative HCC patients were collected from five districts of Japan and assayed for antibody to HCV antigen (HCVAb).

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Human T-cell leukemia virus type I (HTLV-I) provirus DNA from the cultured cell line HUT 102 and from peripheral mononuclear cells (PBMC) of anti-HTLV-I antibody-positive Japanese blood donors was detected by the nested double polymerase chain reaction (PCR) method. This procedure consists of a first amplification and a second amplification with the products of the first amplification and primers interior to the first primers. Using this method, we demonstrated that it is possible to detect single-template DNA.

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Prospective studies of posttransfusion hepatitis carried out in the past decade showed that 18.1% of the blood transfusions resulted in non-A non-B hepatitis in Japan. As an approach to the prevention of posttransfusion non-A non-B hepatitis (PTNANB), anti-hepatitis C virus (HCV) positivity was measured in 2,970 blood donations in the Tokyo area, and in 200 children aged between 6 and 15 years.

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The cytoplasmic pH (pHc) of human platelets was lowered to 6.8-7.2 by treatment with various doses of nigericin (K+/H+ ionophore), then these platelets were stimulated with thrombin, arachidonic acid (AA), A23187 or 12-o-tetradecanoylphorbol-13-acetate (TPA), to monitor the pHc changes using a pH-sensitive fluorescent dye, BCECF.

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The effects of cytoplasmic acidification by nigericin, monovalent cation ionophore, on platelet activation induced by arachidonic acid (AA) were examined. AA-induced aggregation and TXB2 formation were inhibited with decreasing cytoplasmic pH (pHc). Although TXA2 receptor agonists (STA2, U-46619)-induced aggregation of some platelet samples were suppressed by nigericin, the suppression did not correspond to the acidification of pHc.

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The intracellular pH of platelets was measured by the fluorescent dye technique using 9-aminoacridine and BCECF-AM. Although platelet cytoplasmic pH determined by BCECF remained constant, the intracellular pH, determined by 9-aminoacridine, decreased during storage then increased when the stored platelets were incubated with fresh plasma, which led to the restoration of platelet functions. Since the average pH of cytoplasm and cell organelles is detected by 9-aminoacridine and only the cytoplasmic pH is detected by BCECF, the results suggested that changes of the organelle pH affected the platelet functions.

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Relationships among intracellular Ca2+ level, membrane potential in resting state and platelet functions were examined. Membrane potential of platelets was increased (hyperpolarized) during storage and decreased (depolarized) by 37 degrees C incubation with plasma after storage. The degree of depolarization was greater in fresh plasma than in stored plasma.

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