Biomedical subjects

Yoshio Ban

Publications and source records attributed to Yoshio Ban.

9 recordsLinked to original sources

PubMed2006

Impact of increased plasma serotonin levels and carotid atherosclerosis on vascular dementia.

Serotonin (5-HT), a potent vasoconstrictor in the large cerebral arteries, is considered to play a key role in atherothrombosis and to be implicated in ischemic cerebrovascular events followed by delayed neuronal death. The present study aims at evaluating the relationship between plasma levels of 5-HT and vascular dementia (VaD) caused by stroke or atherosclerotic small vessel disease. Carotid artery intima-media thickness (IMT), plaques, plasma 5-HT levels and atherosclerotic parameters were determined in 20 patients with VaD and 40 age-matched controls. Age, gender, body mass index, systolic and diastolic blood pressure, fasting plasma glucose levels and serum levels of insulin, triglycerides, high-density lipoprotein cholesterol, leptin, adiponectin and interleukin-6 and plasma levels of plasminogen activator inhibitor-1 were not significantly different between the two groups. Serum levels of insulin-like growth factor-1 (IGF-1) were significantly lower in VaD patients than in controls. Plasma 5-HT levels, serum levels of hepatocyte growth factor (HGF), low-density lipoprotein (LDL) cholesterol and high-sensitive C-reactive protein (hs-CRP), max IMT and plaque frequency were significantly greater in VaD patients than in controls. There was a significant positive correlation of max IMT with 5-HT or HGF levels. Multiple logistic regression analysis revealed that increased plasma levels of 5-HT and carotid plaque prevalence had significantly independent association with VaD as compared with serum levels of IGF-1, HGF, LDL cholesterol and hs-CRP. These results suggest that increased plasma levels of 5-HT and carotid atherosclerotic plaques may be involved in the pathogenesis and progression of VaD.

Aged↗

PubMed2006

[Thyroid cyst].

Explore the source record for details and available documents.

Biopsy, Fine-Needle↗

PubMed2006

Association of a C/T single-nucleotide polymorphism in the 5' untranslated region of the CD40 gene with Graves' disease in Japanese.

CONTEXT: Graves' disease (GD) is caused by an interplay of genetic factors and environmental triggers. Recently, a susceptibility locus for GD was mapped to chromosome 20q11 (GD-2). Furthermore, a novel single nucleotide polymorphism (SNP) in the CD40 gene, which is located in 20q11, was found to be associated and linked with GD in Caucasians and in Koreans. OBJECTIVES: To examine a C/T SNP in the 5' untranslated region of the CD40 gene (CD40-E1SNP) for association with autoimmune thyroid diseases (AITDs) in a Japanese dataset. DESIGN, SETTING, AND PATIENTS: Case-control association studies were performed using the CD40-E1SNP. We studied 485 Japanese patients with AITD (301 with GD, 184 with Hashimoto's thyroiditis [HT]) and 177 matched Japanese control subjects in association studies. MAIN OUTCOME: Frequencies of genotypes and alleles of the CD40- E1SNP. RESULTS: The distribution of genotype frequencies differed significantly between patients with GD and controls in a dominant manner (p = 0.039). The CC+CT genotypes of the CD40-E1SNP were associated with the increased risk for GD (p = 0.015, odds ratio [OR] = 1.9). In contrast, no differences in genotype frequencies were observed between HT patients and controls for the CD40-E1SNP. CONCLUSION: These results suggested that the CD40 gene is involved in susceptibility for GD in the Japanese.

5' Untranslated Regions↗

PubMed2005

Subtle 17alpha-hydroxylase/17,20-lyase deficiency with homozygous Y201N mutation in an infertile woman.

Steroid 17alpha-hydroxylase deficiency is characterized by failed sexual development and mineralocorticoid hypertension. Female patients usually exhibit primary amenorrhea. Some patients with partial deficiency are reported to have menses, yet they have hypertension and hypokalemia. We describe here a normotensive, infertile female patient with menses and minimal defects in secondary sex characteristics. The patient experienced menarche at age 13, and her menstrual cycles were regular until age 18 and irregular thereafter. Pubic hair was present (Tanner stage 3), and breast maturation was within normal range (Tanner stage 5). The patient's resting blood pressure was normal, and hypokalemia was not observed despite high blood corticosterone levels and reduced plasma renin activity. Analysis of the CYP17 gene revealed that the patient was homozygous for the Y201N mutation. In vitro expression of the mutated Y201N enzyme revealed reduced activities of both 17alpha-hydroxylase and 17,20-lyase; however, these reductions were less than those of the F53/54DEL mutation, which also shows mild clinical deficiency of 17alpha-hydroxylase/17,20-lyase. Thus, the 17alpha-hydroxylase/17,20-lyase deficiency in the present case is very mild both clinically and enzymatically. This case raises the possibility that there are infertile, menstruating women with undiagnosed 17alpha-hydroxylase deficiency.

Adult↗

PubMed2005

Association of a CTLA-4 3' untranslated region (CT60) single nucleotide polymorphism with autoimmune thyroid disease in the Japanese population.

The etiology of the autoimmune thyroid diseases (AITDs), Graves' disease (GD) and Hashimoto's thyroiditis is largely unknown. However, genetic susceptibility is believed to play a major role. The cytotoxic T-lymphocyte antigen-4 (CTLA-4) gene, encoding a negative regulator of the T-lymphocyte immune response, had been reported to be associated and/or linked to AITD. Recently, AITD susceptibility in the Caucasians was mapped to the 6.1-kb 3'UTR of the CTLA-4 gene, in which the single-nucleotide polymorphism (SNP), CT60, was most strongly associated with AITD. In order to determine the association of the CTLA-4 gene with AITD in the Japanese, case-control association analysis for the CT60 of the CTLA-4 gene using 264 AITD patients and 179 healthy controls was done. The frequency of the disease-susceptible G allele of the CT60 of the Japanese control was higher than that of the Caucasians (72.6 vs. 52.3%). However, the G allele of the CT60 was associated with GD (84.0 vs. 72.6%, P=0.0008) and AITD (80.1 vs. 72.6%, P=0.009) in the Japanese. Furthermore, the G allele of the CT60 was associated with the increased risk for GD [P=0.004, odds ratio (OR)=2.0] and AITD (P=0.03,OR=1.6) in a recessive model. These results suggested that the CTLA-4 gene is involved in the susceptibility for GD and AITD in the Japanese.

3' Untranslated Regions↗

PubMed2005

The codon 620 single nucleotide polymorphism of the protein tyrosine phosphatase-22 gene does not contribute to autoimmune thyroid disease susceptibility in the Japanese.

The etiology of the autoimmune thyroid diseases (AITDs), Graves' disease (GD), and Hashimoto's thyroiditis (HT) is largely unknown. However, genetic susceptibility is believed to play a major role. The lymphoid tyrosine phosphatase (LYP), encoded by the protein tyrosine phosphatase-22 (PTPN22) gene, is a powerful inhibitor of T cell activation. Recently, a single-nucleotide polymorphism (SNP), encoding a functional arginine to tryptophan residue change at PTPN22 codon 620 in Caucasians has been shown to be associated with GD and other autoimmune diseases. We have used a polymerase chain reaction (PCR)-restriction fragment (XcmI) assay to examine genotypes at the codon 620 polymorphism in 334 unrelated patients with AITD and 179 controls. None of the patients with AITD and controls had the tryptophan allele. These data suggest that the codon 620 polymorphism of the PTPN22 gene does not have a causal role for AITD in the Japanese. However, we cannot exclude the PTPN22 region as harboring another susceptibility locus for AITD in linkage disequilibrium with the Trp/Arg SNP.

Asian People↗

PubMed2004

Association of a thyroglobulin gene polymorphism with Hashimoto's thyroiditis in the Japanese population.

OBJECTIVE: The aetiology of the autoimmune thyroid diseases (AITDs), Graves' disease (GD) and Hashimoto's thyroiditis is largely unknown. However, genetic susceptibility is believed to play a major role. Two whole genome scans from Japan and from the USA identified a locus on chromosome 8q24 which showed evidence for linkage with AITD and HT. Recent studies have demonstrated an association between a Tg polymorphisms and AITD, suggesting that Tg is the susceptibility gene on 8q24. PATIENTS: We studied 308 Japanese AITD patients (194 GD and 114 HT patients) and 417 Japanese control subjects in association studies. DESIGN: Case-control association studies were performed using D8S284 and D8S272, microsatellite markers located in the 8q24 region, Tgms1 and Tgms2, microsatellite markers in introns 10 and 27, respectively, of Tg, and a SNP in exon 33 of Tg. RESULTS: No differences in allele frequencies were observed between AITD patients and controls for D8S284, D8S272 and Tgms1. Similarly, for Tgms2 and the exon 33 SNP no significant differences in allele frequency distribution were observed for all AITD patients. However, when analysing the HT patients alone we found a significant association between the 330 bp/352 bp genotype of Tgms2 and HT (HT = 16.7%, controls = 7.1%; corrected P-value = 0.01, OR = 2.6). CONCLUSION: Our results confirm the previous reports of an association between the Tg gene and AITD and suggest that Tg is an AITD susceptibility gene.

Alleles↗

PubMed2002

Accelerated production of nucleosome in cultured human mononuclear cells in untreated Graves' disease.

The apoptosis of lymphocytes, which occurs in autoimmune diseases, is usually induced by the Fas/Fas ligand system. As the assay of nucleosomes produced by apoptotic cells can be used to quantitate apoptosis, we evaluated nucleosome and soluble Fas ligand (sFasL) levels of cultured mononuclear cells to clarify the apoptosis of mononuclear cells in patients with autoimmune thyroid diseases by enzyme-linked immunosorbent assay. Nucleosome levels of cultured mononuclear cells in patients with untreated Graves' disease were significantly higher (3.27+/-2.90 U/ml) than those of control subjects (1.39+/-0.24 U/ml) and euthyroid patients with treated Graves' disease (1.53+/-0.33 U/ml). Nucleosome levels of cultured mononuclear cells were positively correlated with sFasL levels (r=0.544, p<0.01). It is therefore likely that increased sFasL levels elicit apoptosis of these cells in untreated Graves' disease.

Adult↗

PubMed2002

Circulating nuclear matrix protein in Graves' disease.

The Fas/Fas ligand system induces apoptosis, while soluble Fas (sFas) blocks the system and soluble Fas ligand (sFasL) functions to induce apoptosis. The assay of nuclear matrix protein (NMP) released from dead or dying cells can be used to quantitate cell death. Therefore, we evaluated the relationship among serum levels of NMP, sFas, and sFasL in patients with Graves' disease. We measured serum levels of sFas, sFasL, NMP, thyroid hormones and TSH receptor antibody in 20 normal control subjects (5 men, 15 women; mean age, 44.3 years), 32 patients with untreated Graves' disease (4 men, 28 women; mean age, 44.1 years), and 10 patients with Graves' disease treated by methimazole (3 men, 7 women; mean age 39.2 years). Serum NMP was significantly lower (10.4 +/- 4.3 IU/ml, p < 0.02) in patients with untreated Graves' disease than in patients with treated Graves' disease (16.4 +/- 7.3 IU/ml) and control subjects (15.3 +/- 8.9 IU/ml). Serum sFas and sFasL were significantly higher in patients with untreated Graves' disease than in patients with treated Graves' disease and in control subjects. In the patient groups with Graves' disease, serum NMP was negatively correlated with sFas (r = -0.612, p < 0.001) and serum sFas was positively correlated with FT4 (r = 0.360, p < 0.05) and TRAb (r = 0.384, p < 0.05). Serum NMP was correlated with sFas. These results suggest that serum NMP is decreased in patients with untreated Graves' disease, and that cell death or apoptosis in patients with Graves' disease is affected by soluble Fas under the influence of thyroid function.

Adult↗