Substitution for / 中国医学科学杂志(英文版)

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The Alpha-2A Adrenergic Receptor Gene -1291C/G Single Nucleotide Polymorphism is Associated with the Efficacy of Methylphenidate in Treating Taiwanese Children and Adolescents with Attention-Deficit Hyperactivity Disorder

OBJECTIVE: The therapeutic effect of methylphenidate (MPH) in treating attention-deficit/hyperactivity disorder (ADHD) has been related to the alpha-2A adrenergic receptor (ADRA2A) gene -1291C/G single nucleotide polymorphism (SNP). We investigated the effect of MPH in treating Taiwanese children and adolescent with ADHD and its relation to the ADRA2A gene -1291C/G SNP. METHODS: The subjects with DSM-IV ADHD diagnosis underwent a titration period to find out the dose of MPH for maintenance treatment. After 4 weeks maintenance treatment, the effect of MPH was evaluated by the Swanson, Nolan and Pelham version IV total scores. The subjects with more than 25% score reduction were referred to responders and those with ≥50% improvement were considered as better responders. The -1291C/G variant of the ADRA2A gene was identified by DNA sequencing and what relevance it has to the MPH response was examined by binary logistic regression analysis. RESULTS: Of the 59 subjects, 44 (74.6%) were responsive to MPH treatment and the responsiveness was not shown to be associated with the ADRA2A gene -1291C/G SNP. As the responsive subjects were categorized as moderate responders and better responders and subjected to statistical analysis, the GG homozygotes showed a greater chance to have a better response to MPH treatment than CC homozygotes (p=0.02), with an odds ratio of 32.14 (95% CI=1.64–627.80). CONCLUSION: The ADRA2A gene -1291C/G SNP is associated with the efficacy of MPH for the treatment of ADHD in Taiwanese children and adolescents. The responsive subjects bearing homozygous -1291G allele are more likely to have a better response to MPH treatment.

SDF-1/CXCR4 axis induces apoptosis of human degenerative nucleus pulposus cells via NF-κB pathway / 基础医学与临床

Objective To investigate the role of SDF-1/CXCR4 axis on the apoptosis of human degenerative nucleus pulposus cells (NPCs) and its potential molecular mechanism .Methods The intervertebral disces tissues from clinical discectomy were divided into normal group and intervertebral disc degeneration ( IVD) group according to Pfirrmann classification.The different expression of SDF 1 and CXCR4 in human IVDs was tested by immunohistochemistry, quantify polymerase chain reaction (q-PCR) and Western blot.The primary degenerative NPCs were primary cultured.The generation Ⅲ~Ⅴ NPCs was treated with 10 ng/mL SDF-1, in the presence of or in the absence of CXCR4 siRNA transfection and 20 μmol/L NF-κB inhibitor (pyrrolidine dithiocar bamate,PDTC).The transfection efficiency and target protein of signal pathway were verified by Western blot , the apoptosis of NPCs were tested by Annexin V /PI, the nucleus transferlocation of P65 from NF-κB were tested by immunofluorescent method.Results SDF-1and CXCR4 were both expressed in all donor tissues, however, there was a significantly increased in the degenerative IVDs .The apoptosis of degenerative NPCs was expedited by SDF -1 stimulation,which was significantly suppressed by CXCR 4 silencing by siRNA (P<0.05).Furthermore, with SDF-1 stimulation,the expressions of phosphorylated P 65 was significantly increased and the P65 perssad transferred to the nucleuses,which could be suppressed by the NF-κB inhibitor, PDTC(P<0.05).Conclusions The expression levels of SDF-1 and CXCR4 are increased in degenerative NP tissue.The SDF-1/CXCR4 axis is considered to induce apoptotic of human degenerative NPCs via the NF-κB signaling pathway.