目的探讨磁共振成像(magnetic resonance imaging,MRI)联合血清γ-氨基丁酸受体相关蛋白2(GABA receptorassociated protein like 2,GABARAPL2)、锌指蛋白706(zinc finger protein 706,ZNF706)与BGCN同族体(within BGCNhomolog,WIBG)对...目的探讨磁共振成像(magnetic resonance imaging,MRI)联合血清γ-氨基丁酸受体相关蛋白2(GABA receptorassociated protein like 2,GABARAPL2)、锌指蛋白706(zinc finger protein 706,ZNF706)与BGCN同族体(within BGCNhomolog,WIBG)对早期类风湿关节炎(rheumatoid arthritis,RA)的诊断价值。方法选取2014年9月至2017年9月于本院就诊的260例RA患者为研究对象,根据病程将入选患者分为早期组(167例)和晚期组(93例),随机选取同期于本院体检的100例健康成人纳入对照组。分析RA患者的MRI征象,比较三组研究对象的血清GABARAPL2、ZNF706和WIBG水平,并采用受试者操作特征曲线的曲线下面积(receiver operating characteristic,AUC)评价其诊断价值。结果早期组和晚期组患者的骨质侵蚀、骨髓水肿和滑膜炎的发生率比较差异均无统计学意义(均P >0.05)。早期组患者血清GABARAPL2、WIBG和ZNF706水平均显著高于晚期组和对照组(均P <0.05);晚期组患者血清GABARAPL2、WIBG和ZNF706水平均显著高于对照组(均P <0.05)。在3个MRI征象中,骨髓水肿对早期RA的诊断价值最高,其次是滑膜炎与骨质侵蚀,三者的灵敏度较高,特异度较低,且三征象联合诊断的价值更高(Youden指数= 0.408)。血清WIBG水平对早期RA的诊断价值最高(AUC=0.708),其次是GABARAPL2(AUC=0.683)与ZNF706(AUC=0.662),三者的灵敏度较低,特异度较高,且三因子联合诊断的价值更高(Youden指数=0.495)。MRI联合血清GABARAPL2、ZNF706与WIBG对早期RA的诊断灵敏度、特异度分别为88.0%、68.9%,诊断价值最高(Youden指数=0.569)。结论 MRI联合血清GABARAPL2、ZNF706与WIBG能显著提高RA的早期诊断水平,值得临床推广应用。展开更多
GABA transporter 1(GAT1) takes important roles in multiple physiological processes through the uptake and release of GABA, but the regulation of GAT1 gene expression in different tissues is rarely known. To address th...GABA transporter 1(GAT1) takes important roles in multiple physiological processes through the uptake and release of GABA, but the regulation of GAT1 gene expression in different tissues is rarely known. To address the question, first, 5’ Rapid amplification of cDNA end (RACE) was used to determine GAT1 transcriptional starting sites in neonatal mouse cerebral cortex and intestine, adult mouse brain and adult rat testis. The products of 5’RACE were confirmed by DNA sequencing. We found that the transcript of GAT1 in neonatal mouse cerebral cortex and adult mouse brain starts at the same site (inside of exon 1), while in mouse intestine, GAT1 starts transcription in intron 1, and in rat testis, the transcript of GAT1 has an additional untranslation exon to the 5’ direction.展开更多
目的:观察电针对1-甲基-4-苯基-1,2,3,6-四氢吡啶(1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine,MPTP)诱导的帕金森病(Parkinson's disease,PD)模型小鼠纹状体抑制性突触前标志物囊泡γ-氨基丁酸转运蛋白(vesicular GABA transpor...目的:观察电针对1-甲基-4-苯基-1,2,3,6-四氢吡啶(1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine,MPTP)诱导的帕金森病(Parkinson's disease,PD)模型小鼠纹状体抑制性突触前标志物囊泡γ-氨基丁酸转运蛋白(vesicular GABA transporter,vGAT)、突触后标志物桥尾蛋白(Gephyrin)以及树突棘密度和无翅型MMTV整合位点家族成员5a(wingless-type MMTV integration site family member 5a,Wnt5a)表达的影响,探讨电针改善PD运动功能的部分作用机制。方法:将雄性C57BL/6小鼠随机分为空白组、模型组、电针组、左旋多巴组,每组10只;除空白组外,MPTP腹腔注射复刻PD小鼠模型。造模成功后第一天对电针组小鼠开始针刺“合谷”“太冲”穴,同日左旋多巴组小鼠腹腔注射左旋多巴注射液,各组小鼠干预2个疗程后采用爬杆及悬挂实验评估各组小鼠运动功能;苏木素伊红染色观察纹状体神经元细胞形态;免疫荧光标记纹状体抑制性突触前标志物vGAT和突触后标志物Gephyrin表达;Western Blot检测纹状体Wnt5a蛋白的表达。结果:与模型组相比,电针组及左旋多巴组小鼠爬杆耗时缩短(P<0.05),悬挂评分升高(P<0.05)。模型组小鼠神经元细胞稀疏,残留的多巴胺神经元萎缩,胞核皱缩偏移,水肿空泡变性增多;而电针组及左旋多巴组小鼠神经元细胞形态圆润,水肿变性细胞减少,形态清晰。各组小鼠纹状体抑制性突触前标志物vGAT表达无明显差异(P>0.05)。与模型组相比,纹状体神经元树突棘密度增加(P<0.05),电针组及左旋多巴组小鼠纹状体突触后标志物Gephyrin的阳性表达升高(P<0.05),Wnt5a蛋白表达水平升高(P<0.05)。结论:早期对帕金森病模型小鼠进行电针干预可改善其运动功能障碍,其治疗机制可能是电针激活Wnt5a信号进而调控抑制性突触,改善纹状体GABA能神经元功能。展开更多
基金foundations from Chinese Academy of Sciences and Special Funds for Major State Basic reseaxch of China (G1999053903).
文摘GABA transporter 1(GAT1) takes important roles in multiple physiological processes through the uptake and release of GABA, but the regulation of GAT1 gene expression in different tissues is rarely known. To address the question, first, 5’ Rapid amplification of cDNA end (RACE) was used to determine GAT1 transcriptional starting sites in neonatal mouse cerebral cortex and intestine, adult mouse brain and adult rat testis. The products of 5’RACE were confirmed by DNA sequencing. We found that the transcript of GAT1 in neonatal mouse cerebral cortex and adult mouse brain starts at the same site (inside of exon 1), while in mouse intestine, GAT1 starts transcription in intron 1, and in rat testis, the transcript of GAT1 has an additional untranslation exon to the 5’ direction.
文摘目的:观察电针对1-甲基-4-苯基-1,2,3,6-四氢吡啶(1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine,MPTP)诱导的帕金森病(Parkinson's disease,PD)模型小鼠纹状体抑制性突触前标志物囊泡γ-氨基丁酸转运蛋白(vesicular GABA transporter,vGAT)、突触后标志物桥尾蛋白(Gephyrin)以及树突棘密度和无翅型MMTV整合位点家族成员5a(wingless-type MMTV integration site family member 5a,Wnt5a)表达的影响,探讨电针改善PD运动功能的部分作用机制。方法:将雄性C57BL/6小鼠随机分为空白组、模型组、电针组、左旋多巴组,每组10只;除空白组外,MPTP腹腔注射复刻PD小鼠模型。造模成功后第一天对电针组小鼠开始针刺“合谷”“太冲”穴,同日左旋多巴组小鼠腹腔注射左旋多巴注射液,各组小鼠干预2个疗程后采用爬杆及悬挂实验评估各组小鼠运动功能;苏木素伊红染色观察纹状体神经元细胞形态;免疫荧光标记纹状体抑制性突触前标志物vGAT和突触后标志物Gephyrin表达;Western Blot检测纹状体Wnt5a蛋白的表达。结果:与模型组相比,电针组及左旋多巴组小鼠爬杆耗时缩短(P<0.05),悬挂评分升高(P<0.05)。模型组小鼠神经元细胞稀疏,残留的多巴胺神经元萎缩,胞核皱缩偏移,水肿空泡变性增多;而电针组及左旋多巴组小鼠神经元细胞形态圆润,水肿变性细胞减少,形态清晰。各组小鼠纹状体抑制性突触前标志物vGAT表达无明显差异(P>0.05)。与模型组相比,纹状体神经元树突棘密度增加(P<0.05),电针组及左旋多巴组小鼠纹状体突触后标志物Gephyrin的阳性表达升高(P<0.05),Wnt5a蛋白表达水平升高(P<0.05)。结论:早期对帕金森病模型小鼠进行电针干预可改善其运动功能障碍,其治疗机制可能是电针激活Wnt5a信号进而调控抑制性突触,改善纹状体GABA能神经元功能。