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Sökning: WFRF:(Sun Chengjun)

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1.
  • Wang, Fang, et al. (författare)
  • Emerging contaminants: A One Health perspective
  • 2024
  • Ingår i: Innovation. - 2666-6758. ; 5
  • Forskningsöversikt (refereegranskat)abstract
    • Environmental pollution is escalating due to rapid global development that often prioritizes human needs over planetary health. Despite global efforts to mitigate legacy pollutants, the continuous introduction of new substances remains a major threat to both people and the planet. In response, global initiatives are focusing on risk assessment and regulation of emerging contaminants, as demonstrated by the ongoing efforts to establish the UN's Intergovernmental Science-Policy Panel on Chemicals, Waste, and Pollution Prevention. This review identifies the sources and impacts of emerging contaminants on planetary health, emphasizing the importance of adopting a One Health approach. Strategies for monitoring and addressing these pollutants are discussed, underscoring the need for robust and socially equitable environmental policies at both regional and international levels. Urgent actions are needed to transition toward sustainable pollution management practices to safeguard our planet for future generations.
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2.
  • Sun, Chengjun (författare)
  • A study of biomarker analysis in association with type 1 diabetes and their shared features in rheumatoid arthritis
  • 2014
  • Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
    • Type 1 diabetes (T1D) is mediated by abnormal immune system (autoimmunity) that targeting specifically to self insulin-producing cells (β-cells). People with T1D require treatments based on life-long insulin substitution. In addition to the damages in health caused by T1D complications, the complexity of insulin treatment and the fear of glucose dysregulation often place extra burden to the affected family. There is a current need for better understanding of the disease etiology therefore guide the construction of successful prediction and prevention strategies for the disease. There are many immune-related genes playing important roles in T1D etiology. In addition, there is a trend of autoimmune diseases segregating within individuals and families where those genes are critically involved. Exploration of these genes can provide knowledge related to the disease pathogenesis. In my studies, we select two genes functioning in the immune system and explored their potential roles in T1D. In addition, we analyzed the association between HLA alleles and T1D autoimmune markers (autoantibodies) in rheumatoid arthritis patients. Killer cell immunoglobulin like receptors (KIRs) is a group of receptors expressed on the surface of natural killer cells and subgroups of T cells. KIRs could accelerate autoimmune diabetes in rodent models. However their roles in human T1D are not clear. In Study I, we studied the T1D association of KIR genes and their combination with HLA-C ligand genes in Chinese Han population. Our results indicated that KIR modifies the T1D association of HLA-C ligand genes. Recent studies indicated that KIRs exert their function in a collective fashion and their effects can initiate as early as life in uterus by maternal-fetal interaction. Therefore in Study II, we studied the T1D association with the collection of maternal KIR genes and their combination with fetal HLA-C ligand genes in the Chinese Han population. Results from study II indicated that the accumulation of maternal activating KIRs along with fetal HLA-C2 genes predispose T1D in the fetus. Alpha-B crystallin (encoded by CRYAB) is a major autoimmune target in multiple sclerosis (an autoimmune disease occurred in central nervous system). In Study III, we tested the association between CRYAB gene and islet autoantibodies in T1D using two well-established Swedish cohorts. Our results suggested that genetic variant in the promoter region of CRYAB is associated with increased T1D risk and islet autoantibodies in T1D patients. In Study IV, we aimed to identify genetic factors that cause the aggregation of the two autoimmune disorders, T1D and rheumatoid arthritis (RA). We measured islet autoantibodies among RA patients and analyzed the association between HLA and islet autoantibodies in RA patients and in subgroups of RA positive for anti-citrullinated protein antibodies. We identified that HLA DR4 alleles were associated with increased islet autoantibodies in RA patients, however HLA DR3 alleles were the major genetic contributors toward elevated islet autoantibodies among RA patients positive for both anti-CCP and anti-CEP-1. In conclusion, our studies indicated that KIR, CRYAB are among the genetic factors predisposing T1D. In addition, HLA alleles are the major contributors to the presence of islet autoantibodies among RA patients.
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3.
  • Sun, Chengjun, et al. (författare)
  • CRYAB-650 C>G (rs2234702) affects susceptibility to type 1 diabetes and IAA-positivity in Swedish population
  • 2012
  • Ingår i: Human Immunology. - : Elsevier. - 0198-8859 .- 1879-1166. ; 73:7, s. 759-766
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Single nucleotide polymorphisms (SNPs) in the promoter region of CRYAB gene have been associated with in multiple sclerosis. CRYAB gene, which encodes alpha B-crystallin (a member of small heat shock protein), was reported as a potential autoimmune target. In this study we investigated whether SNPs in the promoter region of CRYAB gene were also important in the etiology of Type 1 diabetes (T1D).METHODS: Genotyping of SNPs in the promoter region of CRYAB gene was performed in a Swedish cohort containing 444 T1D patients and 350 healthy controls. Three SNPs were included in this study: CRYAB-652 A>G (rs762550), -650 C>G (rs2234702) and -249 C > G (rs14133). Two SNPs (CRYAB-652 and -650) were not included in previous genome wide association studies.RESULTS: CRYAB-650 (rs2234702)*C allele was significantly more frequent in patients than in controls (OR = 1.48, Pc = 0.03). CRYAB-650*C allele was associated with IAA positivity (OR = 8.17, Pc < 0.0001) and IA-2A positivity (OR = 2.14, Pc = 0.005) in T1D patients. This association with IAA was amplified by high-risk HLA carrier state (OR = 10.6, P < 0.0001). No association was found between CRYAB-650 and other autoantibody positivity (GADA and ICA). CRYAB haplotypes were also associated with IAA and IA-2A positivity (highest OR = 2.07 and 2.11, respectively), these associations remain in high HLA-risk T1D patients.CONCLUSIONS: CRYAB-650 was associated with T1D in the Swedish cohort we studied. CRYAB-650*C allele might confers susceptibility to the development of T1D. CRYAB-650 was also associated with the development of IAA-positivity in T1D patients, especially in those carrying T1D high-risk HLA haplotypes.
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