Biomedical subjects

Shih-Chang Lin

Publications and source records attributed to Shih-Chang Lin.

7 recordsLinked to original sources

PubMed2006

Association of a BTLA gene polymorphism with the risk of rheumatoid arthritis.

B and T lymphocyte attenuator (BTLA) is an immuno-inhibitory receptor with the ability to deliver inhibitory signal for suppressing lymphocyte activation. To test the potential association of the human BTLA gene with the development of rheumatoid arthritis (RA), a genetic case-control association study was conducted, by using a single nucleotide polymorphism (SNP), C+800T SNP, in the exon 5 of the human BTLA gene for genotyping 93 RA patients and 294 normal control individuals. The results showed that there is statistically significant difference in the genotype distributions between RA and control groups (p = 0.022). When compared with the heterozygous genotype (C/T genotype), the homozygous genotype (C/C or T/T genotype) appears to confer the increased risk of the RA susceptibility with the odds ratio of 1.88 (p = 0.015). These data indicate the significant association between the C+800T SNP in the BTLA gene with the RA susceptibility.

Amino Acid Sequence↗

PubMed2005

Identification of an NF-Y/HMG-I(Y)-binding site in the human IL-10 promoter.

The cis-acting elements and transcriptional factors that control interleukin 10 (IL-10) promoter activity remain to be clarified. In this report, by performing electrophoresis mobility shift assay (EMSA) with nuclear extracts from the Raji B cell line, the nuclear factor Y (NF-Y) was found to be capable of binding to a CCAAT box-containing region between the -215 and -192bps (the -215/-192 region), relative to the transcription initiation site, in the human IL-10 promoter. The binding of NF-Y to the promoter appears to be enhanced by the presence of HMG-I(Y), since anti-HMG-I(Y) antibody diminished the NF-Y-binding activity in EMSA. Two T nucleotides at -192 and -193bps were found to be critical for the binding of NF-Y and HMG-I(Y) to the -215/-192 promoter region, suggesting the possibility that HMG-I(Y) binds to the AT-rich promoter region downstream of the CCAAT box at the -210/-199 region. These findings suggest that NF-Y and HMG-I(Y) may play an important role in regulating the IL-10 promoter activity in B cells.

B-Lymphocytes↗

PubMed2005

High prevalence of immunoglobulin A antibody against Epstein-Barr virus capsid antigen in adult patients with lupus with disease flare: case control studies.

OBJECTIVE: Systemic lupus erythematosus (SLE) is a severe autoimmune disease with rare remission and recurrent flare. Epstein-Barr virus (EBV) infection has been reported to be strongly associated with SLE in the United States, but with an inconclusive role in Asia. We investigated the role of EBV infection in patients with SLE in Taiwan, with one of the highest population densities in Asia. METHODS: We conducted case-control studies to test whether EBV infection was associated with adult SLE in Taiwan. In the first study, 36 adults with SLE and 36 sex and age matched controls were enrolled for examination of serum IgG, IgM, and IgA antibody against EBV-virus capsid antigen (EBV-VCA). In the second study, another 36 adult lupus cases and 36 matched controls were enrolled to confirm the high prevalence of IgA antibody against EBV-VCA found in the first study. Further, both groups of SLE patients were combined to analyze the association between the existence of IgA antibody against EBV-VCA and disease activity (determined by SLEDAI score) and disease flare in patients with SLE. RESULTS: In the first study, IgA antibody against EBV-VCA was the only marker with significantly higher prevalence in adults with SLE compared to healthy adults (36.1% vs 5.6%; p < 0.005). In the second study, we confirmed that the prevalence of IgA antibody against EBV-VCA was indeed higher in adults with SLE (38.9% vs 2.8%; p < 0.001). With further analysis (pooling analysis), adult SLE patients with IgA antibody against EBV-VCA had higher disease activity compared to SLE patients without IgA antibody against EBV-VCA (SLEDAI 7.8 +/- 6.6 vs 3.3 +/- 2.1; p < 0.001). SLE patients with flare showed much higher prevalence of IgA antibody against EBV-VCA compared to those without flare (81.3% vs 25.0%; p < 0.001). CONCLUSION: This is the first evidence that IgA antibody against EBV-VCA is strongly associated with disease flare in SLE patients. It suggests that EBV reactivation may contribute toward the disease flare of SLE.

Adult↗

PubMed2004

Association of a programmed death 1 gene polymorphism with the development of rheumatoid arthritis, but not systemic lupus erythematosus.

OBJECTIVE: The expression of autoimmunity in mice deficient in programmed death 1 (PD-1) suggests that PD-1 is a candidate gene involved in the development of human autoimmune diseases such as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). We therefore tested the potential association between PD-1 and the development of SLE and RA by conducting case-control genetic-association studies. METHODS: Ninety-eight SLE patients, 84 RA patients, and sex-matched control subjects for each disease group were recruited and genotyped for a single-nucleotide polymorphism, C+872T, in the human PD-1 gene. The significance of the association of the PD-1 gene with SLE or with RA was analyzed by statistical tests for the difference in genotype distribution between disease and control groups. RESULTS: The human PD-1 gene was found to be significantly associated with disease development in RA patients, but not SLE patients. The risk of RA development appeared to be significantly increased by carriage of the T allele (odds ratio 3.32, P < 0.0001) or the C/T genotype (odds ratio 3.52, P < 0.00005). CONCLUSION: The PD-1 gene is significantly associated with RA susceptibility, suggesting the possibility that PD-1 may contribute to the pathogenesis of RA.

Alleles↗

PubMed2003

Clubbed fingers and hypertrophic osteoarthropathy in a patient with squamous cell carcinoma of the lung.

Hypertrophic osteoarthropathy (HOA) is characterized by clubbed fingers and periosteal new bone formation. Etiologically, it can be divided into primary and secondary HOA, but its pathogenesis is uncertain. We report a 42-year-old male patient who suffered from painful clubbing fingers and toes. Serial examinations revealed periosteal new bone formation in the four limb long bones and a solid mass lesion in the right upper lung field. Pathologic examination of the resected mass lesion showed squamous cell carcinoma. After surgery and chemotherapy, the severity of clubbed fingers decreased and joint pain improved. Follow-up bone scan also suggested regression of the uptake of radioactivity in the four limb bones. We concluded that the HOA in this case was probably caused by lung cancer.

Adult↗

PubMed2002

Tumor necrosis factor microsatellite alleles in patients with rheumatoid arthritis in Taiwan.

OBJECTIVE: To investigate the association of tumor necrosis factor (TNF) microsatellite alleles with the pathogenesis of rheumatoid arthritis (RA) in Taiwan. METHODS: The TNF a, b, c, d, and e microsatellites were determined in 112 patients with RA and 99 healthy controls by using polymerase chain reaction (PCR) and electrophoresis with sequencing gel. All of these patients and controls had known HLA-DR genotypes and TNF-308 polymorphisms. RESULTS: The phenotypic frequency of TNFa9 was significantly higher in DR4(-) RA patients than in DR4(-) controls. However, the phenotypic frequency of TNFb6 was significantly higher in RA patients than in controls in the presence of HLA-DR4. The phenotypic frequency of TNFa3-e1 was significantly lower in DR4(+) RA patients than in DR4(+) controls, while a negative linkage disequilibrium was noted between TNFa3-e1 and HLA-DR4. TNF microsatellite alleles were not related to the prevalences of bone erosion, rheumatoid nodule, sicca syndrome, pulmonary fibrosis, and seropositivity of rheumatoid factor (RF) in patients with RA. CONCLUSION: The associations of TNF microsatellites with the susceptibility to RA in Taiwan are not completely independent of the HLA-DR associations. The association of TNFb6 with the susceptibility to RA depends on the presence of HLA-DR4, and the correlation of TNFa9 to RA depends on the absence of HLA-DR4. The negative association of TNFa3-e1 with RA may be secondary to the negative linkage disequilibrium between TNFa3-e1 and HLA-DR4. Moreover, TNFb6 and HLA-DR4 have a synergistic effect on the susceptibility to RA. TNFa3-e1 and TNF-308A have a synergistic effect on preventing from RA. The TNF microsatellite alleles are not related to the clinical manifestations and severity of RA patients in Taiwan.

Alleles↗

PubMed2002

Numerical simulation of protein stamping process driven by capillary force.

Numerical simulations based on first-principle conservation laws of mass and momentum are performed to observe flow characteristics during the stamping process. The protein solution is transferred by a new design of microstamps with microchannels and printed on a bottom substrate. Furthermore, key physics of the stamping process and the control factors achieving uniform spot size can be identified and optimized after these simulations.

Adsorption↗