高血压合并肾动脉狭窄46例临床分析

高血压可以导致弥漫性动脉粥样硬化,肾动脉粥样硬化是全身动脉粥样硬化的一部分,肾动脉粥样硬化可进展至肾动脉狭窄(RAS),甚至完全闭塞,最后发展为肾功能衰竭。研究发现在高血压患者中,RAS的发生率为3%～5%[1]。早期做出诊断并进行有效及时的治疗,对改善患者的生活质量及预后有     

基层医院铜绿假单胞菌耐药基因检测北大核心CSCD

目的对聊城市二级医院临床分离的铜绿假单胞菌耐药机制进行研究,为指导基层临床用药提供参考依据。方法收集医院2015年4-12月分离出的铜绿假单胞菌30株,其中22株为亚胺培南耐药株,8株为亚胺培南敏感株;所有菌株均经手工鉴定和K-B法药敏试验。结果 OprD2基因缺失21株,OprM阳性22株,mexB阳性24株,VIM阳性24株,OXA-10阳性1株,intⅠ-1阳性8株,qacE△1-sul1阳性8株,mucB阳性24株,IMP、OXA-23、MucA三个耐药基因未检出。结论铜绿假单胞菌耐药机制主要与细菌产VIM型金属β-内酰胺酶、细胞主动外排机制以及膜微孔蛋白基因OprD2缺失、生物膜形成有关,Ⅰ类整合子标志物也是铜绿假单胞菌流行的原因之一。     

大鼠TRESK基因重组腺病毒载体的构建

目的 构建大鼠TRESK基因重组腺病毒载体.方法 从大鼠背根神经节细胞中克隆TRESK全长cDNA,进行PCR鉴定及DNA测序验证,构建以CMV启动子转录调控的pAd/CMV/V5DEST-TRESK.转化DH5α大肠杆菌,挑选阳性重组克隆行PCR鉴定并行DNA测序.将测序正确的质粒经PacⅠ酶切线性化,转染包装293T细胞,包装产生腺病毒,逐孔稀释滴度法测定病毒滴度.结果 从大鼠背根神经节细胞中克隆的TRESK全长cDNA为781 bp,DNA测序验证DNA序列与GeneBank 中收录的大鼠TRESK序列完全一致.以pAD-GFP空载体为对照,pAD/CMV/V5-DEST-TRESK gDNA为模板的PCR扩增,目的 片段781 bp,鉴定结果 与预期相符.腺病毒滴度为1.31×109 TU/ml.结论 本研究成功地构建了大鼠TRESK基因重组腺病毒载体:pAD/CMV/V5-DEST-TRESK.

Abstract：

Objective To construct rat TRESK gene recombinant adenovirus expression vector.Methods TRESK full-length cDNA was cloned from rat dorsal root ganglion cells and confirmed by RT-PCR and sequencing. pAd/CMV/V5-DEST-TRESK was then constructed under the control of CMV-promotor. DH5α colibacillus was translated and the positive recombinants were subsequently identified by PCR and DNA sequencing. 293T cells were cotransfected and packed to produce adenovirus. Results The titer of virus was tested using Hole-by-dilution titer method. The full length of TRESK from rat dorsal root ganglion cells is 781 bp. It was demonstrated that the DNA sequencing was completely consistent with TRESK sequencing of rat recorded in GeneBank. The PCR amplification of the pAd/CMV/V5-DEST-TRESK gDNA was matched with pAD-GFP blank vector as anticipated. The titer of the concentrated virus was 1.31×109 TU/ml. Conclusion Rat TRESK gene recombinant adenovirus vector is constructed successfully.