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H Ida

Publications and source records attributed to H Ida.

At least 91 records · Page 5Linked to original sources
PubMed1997

CD94 ligation induces apoptosis in a subset of IL-2-stimulated NK cells.

CD94 (Kp43) is a member of the human C-type lectin superfamily encoding type II membrane glycoproteins expressed on NK cells and a subset of T cells. Ligation of CD94 has been shown to either potentiate or inhibit NK cell proliferation and cytolytic effector function. Here we show that CD94 ligation triggers apoptosis in IL-2-primed NK cells. Evidence for CD94-induced apoptosis includes: 1) chromatin condensation as measured by increased fluorescence of Hoechst dye, 2) induction of DNA fragmentation, and 3) characteristic morphology by transmission electron microscopy. IL-2 priming (at least 12 h) is required for activation-induced NK cell death triggered by CD94. Activation-induced NK cell death triggered by CD94 ligation is extremely rapid (DNA fragmentation is first observed at 120 min). Unlike activation-induced T cell death, it is not inhibited by neutralizing Abs reactive with TNF-alpha or Fas ligand. Our results suggest that CD94 may play a role in the elimination of activated NK cells during the transition from the innate to the Ag-specific immune response.

Antibodies, Monoclonal↗
PubMed1997

Mutation prevalence among 47 unrelated Japanese patients with Gaucher disease: identification of four novel mutations.

Utilizing PCR and PCR-SSCP analysis we investigated the prevalence of glucocerebrosidase gene mutations in 47 unrelated Japanese patients with Gaucher disease. Sixty alleles (63.8%) and 20 alleles (21.3%) were identified by analysis for common mutations and PCR-SSCP analysis, respectively. The L444P and F213I mutations were common, accounting for 41 alleles (43.6%) and 14 alleles (14.9%). R496C, D409H, S366G and 1447-1466 del ins TG mutations were identified in 5, 3, 3 and 3 alleles, respectively. The other mutations were unique. In spite of vigorous screening, 14 alleles (14.9%) could not be identified. Four novel mutations were identified by PCR-SSCP analysis: G189V, S366G, K413Q and R433G. These data indicate that besides the L444P mutation no other frequent mutation is present and there is broad heterogeneity of the glucocerebrosidase gene mutations in Japanese patients with Gaucher disease.

Alleles↗
PubMed1997

Differences in origin of the 1448C mutation in patients with Gaucher disease.

Gaucher disease (GD) can be caused by any of over 50 mutations of the gene of glucocerebrosidase (D-glucosyl acylsphingosine glucohydrolase; EC 3.2.1.45). The 1448T to C mutation is found among all ethnic groups. In Ashkenazi Jews, the patients who are homozygous for the 1448C mutation are associated with the neuropathic form of the disease, but this is not the case in Japanese patients. This present study was the analysis of the two haplotypes, the Pv1.1 and the liver/erythrocytes pyruvate kinase (PKLR), in Japanese GD patients who were homo- or heterozygous for the 1448C mutation, and comparison of the results with other ethnic patients with the same genotypes in order to show ethnic differences. Of 28 patients, 20 had type I disease (7 were homozygous for the 1448C), five had type II (1 was homozygous) and 3 had type III (all were heterozygous). In Japanese GD patients with the 1448C mutation, the two haplotypes showed complete matching in (+) or (-). The Pv1.1/PKLR(+) alleles accounted for 84.0% and this frequency was opposite to that reported in Ashkenazi Jews and other Caucasians. The 1448C homozygous state showed no obvious linkage with either of the haplotypes. From this haplotype analysis, it is postulated that the origin of the 1448C mutation in Japanese GD patients is different from that reported in other ethnic groups.

DNA Mutational Analysis↗
PubMed1996

Mutation screening of 17 Japanese patients with neuropathic Gaucher disease.

Using PCR and PCR-single strand conformation polymorphism (SSCP) we have identified gene mutations in 17 Japanese patients with neuropathic Gaucher disease (type 2, 9 cases; type 3, 8 cases). The L444P, F213I, D409H, and 1447 del 20 and 1447 ins TG mutations accounted for eight (type 2, 6; type 3, 2), seven (type 2, 2; type 3, 5), three (type 3), and three (type 2) alleles, respectively. Three alleles were unique. Ten alleles (type 2, 5; type 3, 5) could not be identified. The genotypes, D409H/?, L444P/?, L444P/F213I, and F213I/?, were identified in three, three, two, and two patients, respectively. Six patients had a unique genotype and none of the mutant alleles could be identified in one patient. The data indicate that the genotypes in Japanese patients with neuropathic Gaucher disease are found to be heterogeneous and the genotype prevalence and mutated alleles are unique.

Alleles↗
PubMed1996

Clinical and genetic studies of five fatal cases of Japanese Gaucher disease type 1.

Five fatal cases of Japanese patients with type 1 Gaucher disease were studied. The causes of death included hemorrhage secondary to esophageal varices (two cases), respiratory distress (one case), hepatic failure (one case) and postoperative sepsis (one case). All of the patients had previous splenectomies, four patients had bone involvement and hepatic cirrhosis. The identified Gaucher genotypes were 1448C/1213G, 1603T/1603T, 1448C/1390G, and 1213G/1213G. The prognosis of type 1 Gaucher disease is generally good. We propose that patients with a similar clinical course and genotype to those presented in the present study should receive prompt comprehensive treatment. Patients with the 1213G mutation, pulmonary and liver involvement and a previous splenectomy should be considered as candidates for early vigorous treatment.

Adolescent↗
PubMed1996

Effect of deaerated water on serum biochemical values and on the cecum concentration of short-chain fatty acids in the rat.

The effects of drinking deaerated water on serum biochemical values, and on the concentrations of short-chain fatty acids (SCFAs) derived from bacterial fermentation in the colon were examined in rats. Drinking deaerated water decreased the levels of serum alkaline phosphatase (SAP) and serum urea nitrogen (SUN), and increased the serum potassium (SK) and serum phosphorus (SP) levels. Although the concentration of propionic acid in the cecum was decreased by drinking deaerated water, the concentrations of isobutyric, valeric, and isovaleric acid in the cecum were increased.

Alkaline Phosphatase↗
PubMed1996

Antitumor activity of zinostatin stimalamer (YM881) in human hepatoma cell lines and VX2 liver tumor-bearing rabbits.

Antitumor activities of zinostatin stimalamer (YM881) were examined in human hepatoma cell lines (SK-Hep1 and HuH2) and VX2 liver tumor-bearing rabbits. YM881 inhibited the growth of human hepatoma cells in a dose-dependent manner. The IC50 values of YM881 causing a 50% inhibition of growth of SK-Hep1 and HuH2 cells were 6.7 and 27 nM, respectively. In VX2 tumor-bearing rabbits, administration of YM881 suspended in Lipiodol, an iodinated fatty acid ethylester of poppyseed oil, (YM881/Lipiodol suspension, 0.2 mg/0.2 ml/body) into the hepatic artery showed significant (p < 0.01, vs. sham-operated and Lipiodol-treated groups) inhibitory effects on tumor growth and histopathological changes at 1 and 2 weeks after administration. In contrast, Lipiodol (0.2 ml/body) tended to inhibit the growth of VX2 tumor (p < 0.1, vs. sham-operated group) at 1 week after administration, but showed only moderate effects at 2 weeks after administration. Minimal necrosis was observed at 1 and 2 weeks after administration of Lipiodol, and histopathological findings were similar to those in the sham-operated group. From the present study, it is suggested that YM881/Lipiodol suspension showed antitumor activity in VX2 tumor-bearing rabbits presumably due to the inhibition of the growth of hepatoma cells by YM881 itself. Lipiodol, on the other hand, is considered to augment the antitumor activity of YM881 by maintaining high YM881 concentrations in tumor tissue.

Animals↗
PubMed1996

[Molecular studies of Gaucher disease].

Gaucher disease is characterized by a deficiency of glucocerebrosidase and hence the accumulation of glucocerebroside in visceral organs such as liver and spleen. Clinically, this disorder can be classified into three types according to clinical phenotype; types I, II and III. More than 50 different gene mutations have been reported previously in the world. Gene mutations in the Japanese showed that the most common mutations are LEU444Pro and Phe313Ileu mutations, accounting for about 40% and 10% of the total alleles, respectively. In the Japanese, there were no mutations in N370S and 84GG among the Japanese. Gaucher disease is recently treated by the administration of purified placental glucocerebrosidase. Aided by the Japanese Ministry of Welfare, six patients with Gaucher disease have been under treatment for almost two years. All cases responded to this treatment as seen in Hb value, platelet count, plasma acid phosphatase value, ACE value, and size of liver and spleen. Gene therapy for Gaucher disease is also currently under consideration.

Asian People↗
PubMed1996

Increased population of high fluorescence 1F7 (CD26) antigen on T cells in synovial fluid of patients with rheumatoid arthritis.

OBJECTIVE: To investigate the activation of T cells in peripheral blood (PB) and synovial fluid (SF) of patients with rheumatoid arthritis (RA). METHODS: The expression of CD26 (Ta1 and 1F7) antigen on T cells was analyzed in 7 women with RA and 7 healthy control subjects by immunofluorescence. RESULTS: The percentage of CD3+ CD26+ cells was significantly higher in PB of patients with RA compared with healthy subjects. The IF7+ cell population was divided into high (1F7+high cells) and low fluorescence populations (1F7+low cells), based on 1F7 antigen density. The percentage of 1F7+high cells in SF of RA was markedly increased compared with PB of patients and healthy subjects. However, RA SF contained lower percentages of whole 1F7+ cells compared with PB. CONCLUSION: Our results indicate that SF of patients with RA contains activated T cells, and suggest that T cells with high levels of CD26 antigen may preferentially migrate into the rheumatoid synovium to induce inflammation and tissue destruction.

Adult↗
PubMed1995

Characteristics of gene mutations among 32 unrelated Japanese Gaucher disease patients: absence of the common Jewish 84GG and 1226G mutations.

The prevalence of seven different mutations (84GG, IVS2 + 1, 754A, 1226G, 1342C, 1448C, and 1504T) was investigated in 32 unrelated Japanese Gaucher patients of which 20 were type I, 6 were type II, and 6 were type III). These mutations constitute 95% of the mutations observed in Jewish patients with Gaucher disease and 75% of the mutations in non-Jews (European). The most frequent mutation, 1448C (L444P), accounted for 26 alleles (40.6%); the second most prevalent mutation was 754A (F213I), accounting for 7 alleles (10.9%); 27 alleles (42.2%) were unidentified. To data, neither the 1226G (N370S) nor 84GG mutations have been identified in the Japanese population though these alleles account for approximately 70% and 10% of mutations in the Jewish population. These data suggest that mutant alleles identified from the Japanese population are distinct from those observed in Jewish and non-Jewish (European) patients with Gaucher disease.

Alleles↗
PubMed1995

Synovial cells are potent antigen-presenting cells for superantigen, staphylococcal enterotoxin B (SEB).

There is ample evidence suggesting that superantigens may act as a triggering factor in the pathogenesis of rheumatoid arthritis (RA). We investigated whether superantigen could activate T cells in the presence of synovial cells. T cells were cultured with SEB in the presence of interferon-gamma (IFN-gamma)-treated synovial cells. T cell proliferation and activation were assessed by 3H-thymidine incorporation and IL-2 production. The expression of HLA class II antigens and adhesion molecules on synovial cells was detected by flow cytometer. In the presence of IFN-gamma-treated synovial cells, T cells proliferated vigorously and produced IL-2 in response to SEB. A low SEB-induced T cell response was noticed in the presence of untreated synovial cells. Allogeneic as well as autologous IFN-gamma-treated synovial cells markedly enhanced SEB-induced T cell proliferation. IFN-gamma-treated synovial cells had increased expression of HLA class II antigens and intercellular adhesion molecule-1 (ICAM-1) adhesion molecules. MoAbs towards these antigens markedly inhibited the SEB-induced T cell response. These results indicate that activated synovial cells are potent antigen-presenting cells for SEB to T cells, and that superantigens may play a critical role in the pathogenesis of RA through activated synovial cells.

Antibodies, Monoclonal↗
PubMed1995

Increased levels of serum IgM antibody to staphylococcal enterotoxin B in patients with rheumatoid arthritis.

OBJECTIVE: To investigate the role of superantigen in rheumatoid arthritis (RA) by assaying the serum levels of staphylococcal enterotoxin B (SEB) antibodies. METHODS: Serum IgG and IgM SEB antibodies were measured using an enzyme linked immunosorbent assay (ELISA), and confirmed by Western blot analysis. The T cell receptor V beta (TCR V beta) repertoire was analysed using the reverse transcriptase polymerase chain reaction. RESULTS: RA patients had increased levels of serum IgM SEB antibody compared with normal subjects, patients with systemic lupus erythematosus, Sjögren's syndrome, and Behçet's disease. The titres of rheumatoid factor (RF) showed no correlation with the levels of IgM SEB antibodies, and the levels of SEB antibodies were not inhibited by the addition of human immunoglobulin, or after absorption of RF. RA patients whose disease duration was less than 10 years had greater levels of serum IgM SEB antibodies than those with disease duration more than 10 years. The levels of IgM and IgG SEB antibodies in synovial fluid from RA patients were correlated with those in their sera. Western blot analysis detected IgM and IgG SEB antibodies as a band of approximately 30 kDa molecular size. The percentage of TCR V beta 2, V beta 5.2, and V beta 12 in phytohaemagglutinin stimulated peripheral T cells correlated significantly with the levels of serum IgM SEB antibody in RA patients. CONCLUSION: These results suggest that SEB, one of the superantigens, may have a critical role in the pathogenesis of RA.

Adult↗
PubMed1994

Single exon mutation in arylsulfatase A gene has two effects: loss of enzyme activity and aberrant splicing.

The arylsulfatase A gene of a Japanese patient who has the juvenile form of metachromatic leukodystrophy, and who has been previously reported as a heterozygote of the 1070A mutation, was investigated. Nucleotide sequence analysis revealed the presence of a previously unreported C-to-T substitution (designated 2330T), 22 nucleotides downstream from the exon 8 splice acceptor site. Although the 2330T mutation itself results in a single amino acid substitution of Thr409 by Ile, the analysis of the patient's cDNA fragments amplified by the reverse transcription-polymerase chain reaction revealed that transcripts of the 2330T allele were spliced both normally and aberrantly. The aberrant splicing produced a 27-nucleotide deletion from the usual exon 8 splice acceptor site. These results indicate that the new mutation is a rare case of an exon mutation affecting splice site selection. The mechanism of this aberrant pre-mRNA splicing is discussed.

Adolescent↗
PubMed1994

Expression of adhesion molecule ICAM-1 (CD54) in thyroid papillary adenocarcinoma.

The expression of adhesion molecules in thyroid specimens from 10 cases of papillary adenocarcinoma, 5 cases of follicular adenoma and 3 normal thyroid specimens was examined by an immunohistochemical method. Thyroid epithelial cells from all cases of papillary adenocarcinoma expressed the intercellular adhesion molecule 1 (ICAM-1, CD54). The ICAM-1-positive staining in these was detected predominantly on the apical site of malignant thyroid epithelial cells. However, no ICAM-1 expression was detected on thyrocytes of adenoma, and normal thyroid tissues. Furthermore, thyroid epithelial cells in patients with thyroid tumor and normal thyroid tissue did not react with anti-LFA-1, anti-VLA-4, anti-VCAM-1 and anti-ELAM-1 monoclonal antibodies. It is speculated that ICAM-1 expression in thyroid papillary adenocarcinoma may have a functional significance.

Adenocarcinoma, Follicular↗