{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,7,1]],"date-time":"2025-07-01T15:44:22Z","timestamp":1751384662239},"reference-count":46,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2013,7,12]],"date-time":"2013-07-12T00:00:00Z","timestamp":1373587200000},"content-version":"vor","delay-in-days":11,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clinical Laboratory Analysis"],"published-print":{"date-parts":[[2013,7]]},"abstract":"<jats:sec><jats:title>Background<\/jats:title><jats:p>Genetic, environmental, immunological, and hormonal factors contribute to the etiology of Tourette syndrome (TS). From the genetic standpoint, TS is a heterogeneous disorder. In our previous study, we found that a single nucleotide polymorphism (SNP) of x\u2010ray repair cross\u2010complementing group 1 (<jats:italic>XRCC1<\/jats:italic>), a DNA repair gene, was associated with TS. Previous studies also showed that tyrosyl\u2010DNA phosphodiesterase 1 (TDP1) interacts with XRCC1 to repair damaged DNA. However, the relationship between TS and SNPs of <jats:italic>TDP1<\/jats:italic> gene is unknown. Therefore, the aim of this study was to test the hypothesis that if the <jats:italic>TDP1<\/jats:italic> SNP, rs28365054 (c.400G&gt;A, Ala134Thr), was associated with TS or not.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>A case\u2010control study was designed to test the hypothesis. A total of 122 TS children and 106 normal children participated in the study. We used polymerase chain reaction to identify the SNP, rs28365054, of the <jats:italic>TDP1<\/jats:italic> gene in the TS patients and the normal children.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>A polymorphism at position rs28365054 in the <jats:italic>TDP1<\/jats:italic> gene had a significant difference (<jats:italic>P<\/jats:italic> &lt; 0.05) in the genotype distributions between the TS patients and the control group. The AG genotype was a risk factor for TS with an odds ratio of 2.26 for the AG versus AA genotype (95% CI 1.08\u20134.72).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>The findings of this study suggested that variants in the <jats:italic>TDP1<\/jats:italic> gene might play a role in TS susceptibility.<\/jats:p><\/jats:sec>","DOI":"10.1002\/jcla.21606","type":"journal-article","created":{"date-parts":[[2013,7,12]],"date-time":"2013-07-12T15:55:11Z","timestamp":1373644511000},"page":"323-327","source":"Crossref","is-referenced-by-count":3,"title":["Association of Tyrosyl\u2010DNA Phosphodiesterase 1 Polymorphism With Tourette Syndrome in Taiwanese Patients"],"prefix":"10.1002","volume":"27","author":[{"given":"Bor\u2010Tsang","family":"Wu","sequence":"first","affiliation":[{"name":"Department of Physical Therapy Graduate Institute of Rehabilitation Science, China Medical University Taichung 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