采用PCR-RFLP方法对蒙古绵羊和哈萨克绵羊MHC-DRB3基因第2外显子285bp的扩增产物进行多态性分析，共检测到,17种基因型，由A、B、C、D、E、F和H共7个复等位基因控制。通过酶切图谱分析表明，蒙古绵羊和哈萨克绵羊的MHC-DRB3基因第2外显子的第154、168和220位的碱基表现出多态性。统计分析表明，MHC-DRB3基因的部分基因型频率和等位基因频率在两个群体之间差异显著或极显著（P<0.10、P<0.05或P<0.01）。X2适合性检验结果表明，蒙古绵羊和哈萨克绵羊的MHC-DRB3基因第2外显子的HaeIII酶切位点均未达到Hardy-Weinberg平衡状态（P<0.01）。

采用限制性内切核酸酶HaeIII对蒙古山羊和哈萨克山羊GOLA-DRB3基因外显子2的285bp扩增产物进行了PCR-RFLP多态性分析，共检测到17种基因型，由A、B、C、D、E、F和H等7个复等位基因控制；通过酶切图谱分析发现蒙古山羊和哈萨克山羊的GOLA-DRB3基因外显子2的154、168和220位碱基表现出多态性。并对基因型频率和等位基因频率进行了统计分析，结果表明，GOLA-DRB3基因的部分基因型频率和等位基因频率在两个群体之间差异显著(P<0.10或P<0.05)或极显著(P<0.01)；X2适合性检验结果表明，蒙古山羊和哈萨克山羊的GOLA-DRB3基因外显子2的HaeIII酶切位点均未达到Hardy-Weiberg平衡状态(P<0.01)。

利用mRNA 差异显示技术，对白洛克肉鸡、中国丝羽乌骨鸡及其正反交组合8周龄肝脏组织的基因表达进行了分析。发现了3个杂种鸡特异表达的基因和1个杂种鸡表达增强的基因，进一步克隆、测序和比对分析初步表明：杂种特异表达的cDNA片断分别为鸡细胞质异柠檬酸脱氢酶基因和2个未知功能的新基因；杂种表达增强的cDNA片断为鸡蛋白酶体亚基p112基因。功能基因和调控基因在杂种鸡的特异表达和增强表达可能与部分屠体性状杂种优势形成有关。

以2个品种鸡亲本及其F1代基因组为实验材料，使用荧光标记替代甲基敏感扩增片段多态性（methylation sensitive amplified polymorphism, MSAP）方法中的同位素杨，优化了实验条件，建立了荧光标记的甲基敏感扩增片段多态性方法（fluorescent labeled methylation sensitive amplified polymorphism, F-MASP）。结果显示，鸡个体基因组的甲基化模式分为3种，甲基化片段约占40%；F1代与亲本比较，F1代甲基化多态模式约有95%来自亲本，变异的甲基化位点约5%，虽然变异的甲基化点数量少但种类多，共发现14种甲基化程度减弱型，12种甲基化程度增强型，结果表明，F-MSAP是一种有效地检测鸡基因组甲基化的方法，可以用于其他真核生物尤其是基因组复杂、甲基化多态性丰富的高等动物植物基因组甲基化研究。

Our previous genetic studies demonstrated that variants of the g-Aminobutyric acid B receptor subunit 2 (GPR51) and neurotrophic tyrosine kinase receptor type 2 (NTRK2) genes are significantly associated with nicotine dependence (ND) in smokers. However, whether such genetic associations lead to changes in the expression of the two genes in response to nicotine remains undetermined. In this study, we investigated the regulatory effect of nicotine on the expression of Gpr51 and Ntrk2 in seven rat brain regions during the administration of nicotine in a daily dose of 3.15 mg/kg for 7 days. With quantitative real-time RT-PCR, we found that nicotine increased the mRNA of Gpr51 by 70, 78, and 32% in the amygdala, striatum, and prefrontal cortex (PFC), respectively, but decreased by 54% in the nucleus accumbens (NA). The Gpr51 protein was upregulated by nicotine in the amygdala (26%), striatum (73%), PFC (28%), and medial basal hypothalamus (MBH; 19%) but downregulated in the NA (72%). Similarly, the mRNA level of Ntrk2 was enhanced by nicotine in the striatum (86%) and PFC (38%), but decreased in the NA (46%) and ventral tegmental area (VTA; 49%). A significant change in protein expression was also obtained for Ntrk2 in the PFC (24%), MBH (33%), NA (33%), and VTA (70%). Interestingly, these two genes showed a closely coordinated expression pattern in response to nicotine in most of the brain regions examined. In summary, our results demonstrate that the expression of Gpr51 and Ntrk2 is significantly regulated by nicotine at both the mRNA and protein levels in various brain regions, which provides further evidence that these two genes are involved in the etiology of ND, as reported in our previous genetic association studies in humans.