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Fujio Takeuchi

Publications and source records attributed to Fujio Takeuchi.

11 recordsLinked to original sources
PubMed2006

Telomere shortening with aging in the human pancreas.

We have conducted systematic studies to measure telomere length in human tissues of all types. Progressive telomere shortening with aging was studied in specimens of normal pancreas obtained at autopsy from 69 subjects aged 0 to 100 yr, and age-related shortening of telomere length at a rate of 36 base pairs (bp) per year was detected. Mean telomere length (+/-SD) was 13.9+/-1.4 kilobase pairs (kbp) in 16 neonates, as opposed to 8.4 kbp in 2 centenarians. Mean telomere length (+/-SD) in four age groups, 0-24, 25-49, 50-74, and 75-100 yr, was 13.5+/-1.5, 12.3+/-0.7, 11.3+/-2.5, and 10.7+/-1.8, respectively.

Adolescent↗
PubMed2005

Association of TAP1 and TAP2 gene polymorphisms with systemic sclerosis in Korean patients.

We sought to determine whether transporter associated with antigen processing (TAP) gene polymorphism is associated with susceptibility to systemic sclerosis (SSc). TAP1 and TAP2 gene polymorphisms were analyzed in 61 Korean patients with SSc and 100 ethnically matched healthy Koreans by polymerase chain reaction-restriction fragment length polymorphism. Human leukocyte antigen (HLA)-DRB1 genotyping data of the patients from our previous study was used for the assessment of independent role of TAP genes to SSc susceptibility. Patients were stratified according to anti-topoisomerase I (anti-topo I) antibody status and clinical subsets of diffuse and limited cutaneous SSc (dcSSc and lcSSc). TAP1 and TAP2 gene polymorphisms were associated with different subsets of SSc: TAP1*A/A genotype with anti-topo I-positive dcSSc (p = 0.01, p corrected = 0.04), TAP2*A1/C genotype with anti-topo I-positive lcSSc (p < 0.05), TAP2*Bky2 and *C alleles with anti-topo I-negative dcSSc (both p < 0.05), and TAP2*B/E genotype with anti-topo I-negative lcSSc (p = 0.004). Although TAP gene associations were generally weak, some associations (TAP2*A1/C, TAP2*C, and TAP2*B/E) with different subsets of SSc were independent of HLA-DR associations, revealing even stronger associations (TAP2*A1/C and TAP2*C) among individuals not possessing the risk HLA-DR alleles. These results suggest the possible role of TAP gene polymorphisms in the genetic susceptibility to SSc.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2005

Enhanced expression of CD69 and CD25 antigen on human peripheral blood mononuclear cells by prolactin.

Several clinical reports have suggested that prolactin (PRL) plays an important role in the pathogenesis of autoimmune diseases such as rheumatoid arthritis (RA) or systemic lupus erythematosus (SLE). We have investigated the influence of PRL on immune system, by evaluating the effects of PRL on the expression of CD69 and CD25 on human peripheral blood mononuclear cells (PBMCs). Human PBMCs obtained from healthy female volunteers were incubated with phytohemagglutinin (PHA) in the presence or absence of various concentrations of PRL. The expression of CD69 and CD25 was monitored using immunofluorescence staining and flow cytometry. PRL significantly enhanced the expression of CD69 and CD25 on activated PBMCs compared with that in the absence of PRL (p<0.05, paired t-test). Increasing doses of PRL enhanced the expression of CD69 up to 2 microg/ml and CD25 up to 1 microg/ml. The enhanced expression of CD69 was observed on CD8+ T lymphocytes but not on CD4+ T lymphocytes. Our data suggest that PRL can significantly enhance the expression of CD69 and CD25 molecule on human PBMCs when induced by PHA. However, PRL would have to be at optimal concentration in order to enhance their expression.

Adult↗
PubMed2003

The mitochondrial DNA A3243G mutation in Werner's syndrome.

OBJECTIVE: The contribution of the A3243G mutation in mitochondria DNA (mtDNA) to diabetes mellitus (DM) in Werner's syndrome (WS) was studied. PATIENTS AND METHOD: DNA samples from peripheral white blood cells (WBCs) originating from 24 Japanese WS patients aged 30-56 were used. For control, 239 subjects aged 15-95 were also used. The mtDNA was amplified using specific primers. After HaeIII digestion, the ratio of the A3243G mutation was compared. RESULTS: The ratio of the A3243G mutation is 0.45+/-0.13% in WS, which is statistically insignificant from those in the control groups at various age. The mutation types of WRN in genomic DNA did not affect the ratio of the A3243G mtDNA mutation. No significant difference was observed concerning to the ratios among the WS patients with and without DM, and also controls. Furthermore, no significant difference was observed in the ratios of A3243G mutation among controls from various age groups. CONCLUSION: The A3243G mutation in mtDNA does not accumulated in WBCs from WS. Mitochondria A3243G mutation may not contribute to the pathogenesis of DM observed in WS.

Adult↗
PubMed2002

Comparison of the level of mitochondrial DNA A3243G mutation in esophageal epithelium and myocardium from individuals of very advanced age.

The A3243G mutation, one of the changes of human mitochondrial DNA (mtDNA) that accumulates in cells during aging, is a useful marker for investigating the aging of cells. We measured the mutation level of the mtDNA A3243G mutation using DNAs from two different tissues (esophageal epithelium and myocardium) from advanced elderly individuals. The mean level of the A3243G mutation for the esophageal epithelium was 0.0063+/-0.0019, and that for the myocardium was 0.0098+/-0.0031. The mutation level in the myocardium was significantly higher than that in the esophageal epithelium, indicating that more mtDNA A3243G mutations accumulated in the myocardium than in the esophageal epithelium. Since the myocardium is static with respect to cell turnover, but in the esophageal epithelium renewal is very rapid, it is possible that the mtDNA A3243G mutation in the myocardium accumulates more rapidly than in the esophageal epithelium. This phenomenon may reflect the difference in the longevity of cells in each of these tissues and their different levels of oxidative stress.

Aged↗
PubMed2002

Structural studies on IgG oligosaccharides of patients with primary Sjögren's syndrome.

Sjögren's syndrome (SS) is an autoimmune disease, and some patients have been found to have SS complicated with rheumatoid arthritis (RA), in which IgG is known to carry abnormal N-linked oligosaccharides. In order to investigate the relationship between SS and RA, the structures of N-linked oligosaccharides of IgG from 12 primary SS patients without RA, 9 RA patients, and 8 healthy individuals were analyzed using reversed-phase high-performance liquid chromatography, in combination with sequential exoglycosidase treatment and matrix-assisted laser desorption ionization time-of-flight mass spectrometry. All of the IgG samples obtained from primary SS patients, RA patients, and healthy individuals contained the same series of biantennary complex-type oligosaccharides, but the ratio of each oligosaccharide differed among these 3 groups. The incidence of galactose-lacking N-linked oligosaccharides obtained from the IgG of RA patients was significantly higher than that from healthy individuals, but that from the serum IgG of primary SS patients varied among individuals. The patients with primary SS were classified into two groups based on the galactosylation levels of IgG oligosaccharides; one group exhibits galactosylation levels as low as those of RA patients and another exhibits levels similar to those of healthy individuals. Measurement of levels of rheumatoid factor (RF) revealed that primary SS patients with a high incidence of RF belonged to the low galactosylation group, as did RA patients. These results suggest that appearance of IgG carrying abnormal N-linked oligosaccharides in primary SS may be related to future complication with RA.

Adult↗