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Linfa Chen,1,2,* Xinglan Chen,1,3,* Yajun Wang,4,* Shengnan Li,1,5 Shaoting Huang,1,5 Zhaochun Wu,1,5 Jiawen He,1,5 Shaofeng Chen,1,5 Fu Deng,1,5 Peiyi Zhu,1,5 Wangtao Zhong,1,3 Bin Zhao,1,5 Guoda Ma,1,4 You Li1,5 1Guangdong Key Laboratory of Age-Related Cardiac and Cerebral Diseases, Affiliated Hospital of Guangdong Medical University, Zhanjiang, People’s Republic of China; 2Department of Neurology, Huizhou Third People’s Hospital, Guangzhou Medical University, Huizhou, People’s Republic of China; 3Department of Neurology, Affiliated Hospital of Guangdong Medical University, Zhanjiang, People’s Republic of China; 4Maternal and Children’s Health Research Institute, Shunde Maternal and Children’s Hospital, Guangdong Medical University, Shunde, People’s Republic of China; 5Institute of Neurology, Affiliated Hospital of Guangdong Medical University, Zhanjiang, People’s Republic of China*These authors contributed equally to this workCorrespondence: You Li, Guangdong Key Laboratory of Age-Related Cardiac and Cerebral Diseases, Affiliated Hospital of Guangdong Medical University, Zhanjiang, 524001, People’s Republic of China, Email youli805@163.com Guoda Ma, Maternal and Children’s Health Research Institute, Shunde Maternal and Children’s Hospital, Guangdong Medical University, Shunde, 528300, People’s Republic of China, Email sihan1107@126.comBackground: The S100/calgranulin gene appears to modulate neuroinflammation following cerebral ischemia and could be a valuable biomarker for stroke prognosis, according to growing research. This study aimed at evaluating the correlation between calgranulin gene variants and susceptibility to ischemic stroke (IS) in the Southern Chinese population.Methods: Using an enhanced multi-temperature ligase detection reaction genotyping, 310 IS patients and 324 age-matched healthy controls were genotyped to identify five calgranulin gene variants.Results: According to the obtained resul

Xiaoyao Xiang,1 Linfa Chen,2 Jiawen He,3 Guoda Ma,3,4 You Li3 1Department of Urology, The Second Affiliated Hospital of Guangdong Medical University, Zhanjiang, 524001, People’s Republic of China; 2Department of NeUrology, Huizhou Third People’s Hospital, Guangzhou Medical University, Huizhou, 516000, People’s Republic of China; 3Guangdong Key Laboratory of Age-Related Cardiac and Cerebral Diseases, Affiliated Hospital of Guangdong Medical University, Zhanjiang, 524001, People’s Republic of China; 4Maternal and Children’s Health Research Institute, Shunde Maternal and Children’s Hospital, Guangdong Medical University, Shunde, 528300, People’s Republic of ChinaCorrespondence: Guoda Ma, Maternal and Children’s Health Research Institute, Shunde Maternal and Children’s Hospital, Guangdong Medical University, Shunde, 528300, People’s Republic of China, Email sihan1107@126.com You Li, Guangdong Key Laboratory of Age-Related Cardiac and Cerebral Diseases, Affiliated Hospital of Guangdong Medical University, Zhanjiang, 524001, People’s Republic of China, Email youli805@163.comObjective: Recent studies have demonstrated that the long non-coding RNA (lncRNA) GAS5 is closely associated with the onset and progression of several tumor types, including renal cell carcinoma (RCC). This study sought to evaluate the relationship between two functional GAS5 polymorphisms (rs145204276 and rs55829688) and the risk for RCC in the Han Chinese population.Methods: The rs145204276 and rs55829688 polymorphisms in the GAS5 promoter region were genotyped in 624 RCC patients and 655 age/sex-matched healthy participants. The association between these polymorphisms and RCC risk was then evaluated using odds ratios (ORs) and corresponding 95% confidence intervals (CIs). Additionally, quantitative RT-PCR was used to determine whether these polymorphisms were associated with changes in the levels of expression of GAS5 in 58 RCC patients.Results: There were significant differenc

Linfa Chen,1,2,* Ying Wang,1,3,* Yajun Wang,4,* Shaoting Huang,1,3 Zhaochun Wu,1,3 Jiawen He,1,3 Wangtao Zhong,3 Bin Zhao,1,3 Guoda Ma,1,4 You Li1,5 1Guangdong Key Laboratory of Age-Related Cardiac and Cerebral Diseases, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, 524001, People’s Republic of China; 2Department of Neurology, Huizhou Third People’s Hospital, Guangzhou Medical University, Huizhou, Guangdong, 516002, People’s Republic of China; 3Department of Neurology, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, 524001, People’s Republic of China; 4Maternal and Children’s Health Research Institute, Shunde Maternal and Children’s Hospital, Guangdong Medical University, Shunde, Guangdong, 528300, People’s Republic of China; 5Institute of Neurology, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, 524001, People’s Republic of China*These authors contributed equally to this workCorrespondence: You Li, Guangdong Key Laboratory of Age-Related Cardiac and Cerebral Diseases, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, 524001, People’s Republic of China, Email youli805@163.com Guoda Ma, Maternal and Children’s Health Research Institute, Shunde Maternal and Children’s Hospital, Guangdong Medical University, Shunde, Guangdong, 528300, People’s Republic of China, Email sihan1107@126.comBackground: Emerging evidences suggest that the angiotensin receptor type 1 (AT1R) contributes heavily to the pathogenesis of atherosclerotic cerebral infarction (ACI). Herein, we examined a potential link between AT1R gene polymorphisms and ACI risk among a Southern Han Chinese population.Methods: The rs3772616, rs275645, and rs377262 AT1R polymorphisms were genotyped in 689 ACI patients and 712 healthy controls, using the iMLDR-TM assay.Results: The genotypic and allelic frequencies of AT1R rs3772616 differed tremendously be

Striated muscle signaling protein and transcriptional regulator ANKRD2 participates in myogenesis, myogenic differentiation, muscle adaptation and stress response. It is preferentially expressed in slow, oxidative fibers of mammalian skeletal muscle. In this study, we report on characterization of chicken ANKRD2. The chicken ANKRD2 coding region contains 1002 bp and encodes a 334-amino acid protein which shares approximately 58% identity with human and mouse orthologs, mostly in the conserved region of ankyrin repeats. Comprehensive analysis of the ANKRD2 gene and protein expression in adult chicken demonstrated its predominant expression in red muscles of thigh and drumstick, compared to white muscle. It was not detected in heart and white pectoral muscle. Uneven expression of ANKRD2 in chicken skeletal muscles, observed by immunohistochemistry, was attributed to its selective expression in slow, oxidative, type I and fast, oxidative–glycolytic, type IIA myofibers. Association of chicken ANKRD2 with phenotypic differences between red and white muscles points to its potential role in the process of myofiber-type specification. In addition to expression in slow oxidative myofibers, as demonstrated for mammalian protein, chicken ANKRD2 was also detected in fast fibers with mixed oxidative and glycolytic metabolism. This finding suggests that ANKRD2 is responsive to metabolic differences between types of avian myofibers and orientates future studies towards investigation of its role in molecular mechanisms of myofiber-type-specific gene expression.

Striated muscle signaling protein and transcriptional regulator ANKRD2 participates in myogenesis, myogenic differentiation, muscle adaptation and stress response. It is preferentially expressed in slow, oxidative fibers of mammalian skeletal muscle. In this study, we report on characterization of chicken ANKRD2. The chicken ANKRD2 coding region contains 1002 bp and encodes a 334-amino acid protein which shares approximately 58% identity with human and mouse orthologs, mostly in the conserved region of ankyrin repeats. Comprehensive analysis of the ANKRD2 gene and protein expression in adult chicken demonstrated its predominant expression in red muscles of thigh and drumstick, compared to white muscle. It was not detected in heart and white pectoral muscle. Uneven expression of ANKRD2 in chicken skeletal muscles, observed by immunohistochemistry, was attributed to its selective expression in slow, oxidative, type I and fast, oxidative–glycolytic, type IIA myofibers. Association of chicken ANKRD2 with phenotypic differences between red and white muscles points to its potential role in the process of myofiber-type specification. In addition to expression in slow oxidative myofibers, as demonstrated for mammalian protein, chicken ANKRD2 was also detected in fast fibers with mixed oxidative and glycolytic metabolism. This finding suggests that ANKRD2 is responsive to metabolic differences between types of avian myofibers and orientates future studies towards investigation of its role in molecular mechanisms of myofiber-type-specific gene expression.

Jiawu Fu,1,* Guoda Ma,1,* Hui Mai,1,* Xudong Luo,2 Jingwen Yin,2 Qing Chen,2 Zhixiong Lin,2 Hua Tao,1 You Li,1 Lili Cui,1 Zheng Li,3 Juda Lin,2 Bin Zhao,1 Keshen Li1 1Institute of Neurology, Affiliated Hospital of Guangdong Medical University, 2Department of Psychiatry, Affiliated Hospital of Guangdong Medical University, Zhanjiang, People’s Republic of China; 3Unit on Synapse Development and Plasticity, National Institute of Mental Health, National Institutes of Health, Bethesda, MD, USA *These authors contributed equally to this work Abstract: Sepiapterin reductase participates in the biosynthesis of tetrahydrobiopterin, which plays very important roles in the pathogenesis of schizophrenia via dysregulation of ­neurotransmitter systems. Here, two single nucleotide polymorphisms (rs1876487 and rs2421095) in the promoter region of SPR were genotyped in 941 schizophrenic patients and 944 controls in a Han Chinese population using the SNaPshot technique. No significant differences were found in the distribution of alleles or genotypes of the two single nucleotide polymorphisms (SNPs) between schizophrenic patients and controls (all P>0.05). Likewise, no haplotype was found to be associated with schizophrenia. However, sex-stratified analysis revealed that the frequencies of the A allele of rs1876487 and the A–A (rs2421095–rs1876487) haplotype were all significantly different between schizophrenia and controls in females (P=0.040 and P=0.033, respectively), but not in males. Additionally, luciferase reporter gene assays revealed that the A–A haplotype had significantly higher SPR transcriptional activity compared with the A–C haplotype in SH-SY5Y cells. Our data indicate that the two SNPs do not influence the risk of schizophrenia when using the total sample, but the A allele of rs1876487 and the A–A haplotype may contribute to protective roles for schizophrenia in females. Keywords: sc