缬沙坦、苯那普利、非洛地平治疗高血压左室肥厚

目的研究缬沙坦、苯那普利、非洛地平的降压效果,对高血压左室肥厚(LVH)的逆转作用并观察治疗中的醛固酮(Ald)逃逸现象与LVH关系。方法入选高血压左室肥厚患者111例随机分成服用缬沙坦组(36例)或苯那普利组(39例)或非洛地平组(36例),监测治疗过程中的血压变化及服药10～14周、20～26周时血浆血管紧张素Ⅱ(AngⅡ)、醛固酮(Ald)变化,治疗前后超声心动图检查及检测血尿常规、血糖、血脂、肝肾功能检查,记录药物不良反应。结果3组均能有效降压,效果相当(组内治疗前后比较,P<0.01,组间比较,P>0.05)。缬沙坦组、苯那普利组均能逆转LVH。左室质量(LVM)、左室质量指数(LVMI)下降(组内治疗前后比较P<0.01;组间P>0.05),舒张功能改善,二尖瓣血流舒张早期与晚期最大流速比值(E/A)升高(组内治疗前后比较,P<0.01;组间比较,P>0.05);非洛地平组虽有LVM下降(P<0.05),但LVMI、E/A无明显变化(P>0.05)。缬沙坦组治疗后AngⅡ显著上升(P<0.01);苯那普利组治疗10～14周AngⅡ明显下降(P<0.01),20～26周Ald升高,接近治疗前水平(P>0.05),与10～14周比较明显升高(P<0.01);非洛地平组AngⅡ较治疗前显著上升(P<0.01)。缬沙坦组治疗后Ald浓度明显下降(P<0.01)。苯那普利组Ald逃逸发生率36%,有逃逸者LVH逆转较差。结论缬沙坦、苯那普利、非洛地平降压效果相当。3组对LVH均有逆转作用。缬沙坦、苯那普利作用优于非洛地平。缬沙坦长期应用无Ald逃逸。非洛地平治疗期间对血浆Ald无明显影响。     

缬沙坦对自发性高血压大鼠血压和肾素-血管紧张素水平的对照研究

目的:动物实验观察缬沙坦的降压效果及其对血浆肾素活性和血管紧张素Ⅱ的影响.方法:24只雄性14周龄的SHR分为生理盐水组、苯那普利组、小剂量缬沙坦和大剂量缬沙坦组,另用6 只同龄雄性WKY大鼠对照.观察用药4周前后的血压、肾素活性和血管紧张素Ⅱ水平.结果:与生理盐水组、苯那普利组比较,缬沙坦的降压效果明确;大剂量缬沙坦平均下降41.7±4.93 mmHg,明显大于小剂量组的降压幅度27.7±4.46 mmHg,(P <0.01).SHR与WKY大鼠比较,血浆肾素活性仅在大剂量缬沙坦组明显升高;血管紧张素Ⅱ水平,大剂量缬沙坦组更为明显升高,而苯那普利组有所下降.结论:缬沙坦的降压效果优于苯那普利,苯那普利使血浆AngⅡ水平减低,而缬沙坦使血浆AngⅡ水平升高.在长期用药过程中,较高的血浆AngⅡ水平对人体的影响或对器官的影响如何,尚待进一步研究.     

缬沙坦及其与培哚普利合用对慢性心力衰竭患者醛固酮代谢的影响

目的观察慢性心力衰竭(心衰)患者长期应用缬沙坦及缬沙坦与培哚普利联合治疗是否存在醛固酮逃逸。方法120例慢性心衰患者随机分为缬沙坦组、培哚普利组及联合治疗组,每组40例,疗程24周。测定治疗前、治疗后12周及24周血浆血管紧张素Ⅱ(AngⅡ)及醛固酮变化。对照组40例为健康查体者。结果120例慢性心衰患者血浆AngⅡ、醛固酮水平较对照组健康查体者升高(P<0.01)。缬沙坦组治疗后12周及24周醛固酮水平较治疗前降低(P<0.01),AngⅡ水平治疗后12周升高(P<0.05);24周与12周比较醛固酮及AngⅡ水平均无显著差异(P>0.05)。培哚普利组治疗后12周及24周醛固酮、AngⅡ水平均较治疗前降低(P<0.01),治疗后24周较12周时又明显升高(P<0.05)。联合治疗组治疗后12周及24周醛固酮水平下降(P<0.01),而AngⅡ水平无显著性改变(P>0.05);治疗后24周与12周比较差异均无显著性(P>0.05)。结论缬沙坦及培哚普利与缬沙坦联合长期治疗慢性心衰患者不产生明显的醛固酮逃逸。     

肾性高血压大鼠心肌组织和血浆醛固酮变化对左室肥厚和心功能的影响及缬沙坦的干预作用

目的:探讨肾性高血压大鼠心肌组织和血浆血管紧张素Ⅱ(AngⅡ)和醛固酮(Ald)的变化对心肌肥厚和心功能的影响,并观察AngⅡ受体拮抗剂缬沙坦对心肌肥厚和心功能的治疗作用。方法:34只SD大鼠分为缬沙坦治疗组(13只,V组),非缬沙坦治疗组(11只,NV组)和假手术组(10只,S组)。V组和NV组在左肾动脉置入内径为0·3mm的银夹(2K1C)。术后2周,V组每天给予缬沙坦30mg/kg,一次性灌胃治疗;S组和NV组每天给予相同容量的饮用水灌胃,共10周。观察各组大鼠的血压、心脏结构、心肌收缩功能、血浆和心肌中AngⅡ、Ald的变化。结果:①各组间治疗前体重、尾动脉收缩压、左室质量(LVM)、相对室壁厚度(RWT)、左室射血分数(LVEF)、短轴缩短率(FS)、中层短轴缩短率(mFS)、室壁应力(MESS)均差异无统计学意义(均P>0·05);②NV组术后第10周尾动脉收缩压、RWT、LVM、LVM指数(LVMI)较S组和V组均明显增加,而左室舒张末期内径(LVDd)明显减小,差异有统计学意义(均P<0·01)。V组高于S组,但差异无统计学意义(均P>0·05);③NV组的LVEF、MESS、mFS、实测mFS/预测mFS明显小于S组和V组(均P<0·05),V组和S组比较差异无统计学意义(P>0·05);④V组和NV组大鼠血浆AngⅡ明显高于S组(均P<0·01),V组和NV组比较差异无统计学意义(P>0·05);⑤血浆Ald各组比较差异无统计学意义(P>0·05),心肌组织Ald NV组与V组比较差异差异有统计学意义(P<0·05),但与S组比较无统计学意义。结论:①2K1C大鼠可产生明确的肾素增高所致的高血压左室肥厚和心功能不全;②Ald与高血压左室肥厚和几何构型及其心力衰竭发展密切相关;③缬沙坦可抑制左室肥厚和收缩功能不全的发生发展。     

培哚普利、非洛地平缓释片对老年原发性高血压患者血小板活化及纤溶活性的影响

目的:探讨培哚普利及非洛地平缓释片对老年原发性高血压(EH)患者血小板活化及纤溶活性的影响.方法:采用放射免疫法及发色底物法测定55例老年Ⅰ、Ⅱ期EH患者分别应用培哚普利(Ⅰ组28例)及非洛地平缓释片(Ⅱ组27例)治疗前后活化血小板α颗粒膜蛋白(GMP-140)、组织型纤溶酶原激活剂(t-PA)及其抑制物(PAI-1)、血管紧张素Ⅱ(AngⅡ)及醛固酮(Ald)水平.结果:治疗后,两组患者GMP-140含量及PAI-1活性均显著下降(P分别＜0.01,0.05),t-PA活性显著升高(P＜0.05);Ⅰ组患者AngⅡ及Ald显著下降(P＜0.01),Ⅱ组患者AngⅡ及Ald未见明显变化(P＞0.05).治疗前,55例EH患者GMP-140含量与PAI-1水平呈显著正相关(r=0.407 6,P＜0.01),二者与AngⅡ水平均呈显著正相关(r=0.416 2,0.4237,P＜0.01).结论:以上结果提示,培哚普利降低体内AngⅡ水平是其抑制老年EH患者血小板活化、改善纤溶活性的机制之一,而非洛地平缓释片抑制血小板活化、改善纤溶活性的作用与肾素-血管紧张素系统无关.     

缬沙坦和苯那普利联合治疗慢性心力衰竭患者的神经内分泌激活及其临床作用

目的研究苯那普利和缬沙坦联合治疗慢性心力衰竭后神经激素的变化及其临床效果.方法本研究选择39例慢性心衰患者(心功能NYHAⅡ～Ⅲ级),于口服利尿剂的基础上加服苯那普利和缬沙坦,治疗6个月比较心功能及血浆肾素活性(PRA)、血管紧张素Ⅱ(AngⅡ)、醛固酮(ALD)浓度的变化;以21例口服苯那普利的慢性心衰患者为对照组.结果两组ALD均下降,苯那普利+缬沙坦组＞苯那普利组,且有统计学意义(P＜0.01).两组在用药后心功能均得到改善,但元统计学差异(P＞0.05).结论缬沙坦与苯那普利合用可更完全抑制慢性心衰患者过度激活的RAS,且心功能与治疗前相比得到进一步改善,以及有良好的耐受性.     

咪达普利和缬沙坦联合治疗对原发性高血压患者左心室肥厚的逆转

目的:探讨咪达普利和缬沙坦联合治疗对原发性高血压(EH)患者左心室肥厚(LVH)的逆转。方法:将137例伴LVH的EH患者随机分成咪达普利组、缬沙坦组和联合治疗组。设定血压达标值为收缩压(SBP)<140mmHg(1mmHg=0.133kPa)和舒张压(DBP)<90mmHg。3组患者分别口服起始剂量咪达普利10mg/d、缬沙坦80mg/d和咪达普利10mg/d加缬沙坦80mg/d。随访周期为2周,若血压未能达标,则增加剂量直至联合治疗,最大剂量为咪达普利20mg/d加缬沙坦160mg/d。3组患者均口服氢氯噻嗪12.5mg/d。总疗程24周。检测治疗前后24h动态血压、左室质量指数(LVMI)和心率(HR)。结果:①3组治疗后24hSBP、24hDBP均分别较治疗前显著降低(均P<0.01),而3组治疗前后24hSBP、DBP的降低幅度差异均无统计学意义(均P>0.05)。②3组治疗后LVMI和HR均分别较治疗前显著性降低(均P<0.01)。联合治疗组治疗前后LVMI和HR的降低幅度均分别大于咪达普利组和缬沙坦组,差别均具有统计学意义(均P<0.05)。结论:咪达普利和缬沙坦联合治疗在逆转LVH和抑制心脏交感活性方面较咪达普利或缬沙坦单药治疗具有更加显著的作用,且这些作用独立于降压疗效之外。     

苯那普利、缬沙坦对自发性高血压大鼠肾脏血管紧张素转换酶2表达的影响

目的观察苯那普利与缬沙坦对自发性高血压大鼠(SHR)血浆血管紧张素Ⅱ(Ang Ⅱ)和肾脏血管紧张素转换酶2(ACE2)表达水平的影响,探讨ACE2在高血压发病机制和药物治疗中的意义.方法12周龄雄性SHR 28只,分为空白对照组(Sc)、苯那普利组(10 mg/kg·d)(Sb)、小剂量缬沙坦组(10 mg/kg·d)(Sl)、大剂量缬沙坦组(30 mg/kg·d)(Sh),每组7只,7只雄性WKY大鼠为正常对照.药物治疗3月后,用放射免疫法测定血浆Ang Ⅱ含量,RT-PCR法测定肾脏中ACE和ACE2 mRNA的表达水平,免疫组化法比较肾脏中ACE2蛋白的表达.结果与WKY大鼠相比,SHR肾脏中ACE2 mRNA及其蛋白的表达均明显降低,而ACE mRNA的表达和血浆Ang Ⅱ水平则明显升高(P<0.05).缬沙坦治疗后SHR血压显著下降而血浆Ang Ⅱ水平则进一步升高,肾脏中ACE2的表达水平明显升高,且呈剂量依赖性(P<0.05).苯那普利治疗对SHR血浆Ang Ⅱ水平及肾脏ACE2的表达则无明显影响.结论SHR体内ACE和ACE2的表达失衡可能在高血压的发病机制中有重要意义.血管紧张素受体拮抗剂(ARB)可能通过升高SHR血浆Ang Ⅱ的水平而增加肾脏中ACE2的表达,ACE2表达的增加可能是ARB抗高血压治疗的一个新药理机制.     

原发性高血压患者肝细胞生长因子、血管紧张素Ⅱ、内皮素的变化及苯那普利的干预作用

目的:探讨原发性高血压(EH)患者血清肝细胞生长因子(HGF)及血管紧张素Ⅱ(AngⅡ)、内皮素(ET)的浓度与原发性高血压进展的关系及苯那普利对其生成的影响.方法:以20例健康人做对照(正常对照组),另选择1、2级原发性高血压患者40例(为1级原发性高血压组18例,2级原发性高血压组22例),分别采用酶联免疫吸附法和放射免疫法测定苯那普利治疗前及治疗6周后血清中HGF、AngⅡ和ET浓度.结果:1、2级原发性高血压组治疗前血清HGF、ET和AngⅡ水平明显高于正常对照组(P＜0.05～0.01);并与平均动脉压呈正相关(r分别为0.568、0.460、0.623);血清HGF与ET、AngⅡ亦有良好相关性(r分别为0.512、0.563).治疗后血压下降,同时血清HGF、ET和AngⅡ水平较治疗前明显下降(P＜0.05).结论:HGF、AngⅡ及ET水平与高血压有关.苯那普利在降压的同时能降低HGF及AngⅡ、ET水平.     

美多洛尔、苯那普利和非洛地平对高血压血管活性肽的影响

目的:探讨原发性高血压(EH)患者的血清血管紧张素I、Ⅱ(Ang I、Ⅱ)、心钠素(ANF)和醛固酮 (ALD)水平,及美多洛尔、苯那普利和非洛地平干预治疗后的变化和意义。方法:放射免疫法测定356例EH组和 68例非高血压组血清Ang I、Ⅱ,ANF和ALD水平,对EH患者分组给予美多洛尔、苯那普利和非洛地平干预治疗, 比较其治疗前、后的变化。结果:EH患者血清Ang I、Ⅱ和ALD水平显著高于对照组(P均<0．01),ANF则否 (P>0．05);高血压I、Ⅱ、Ⅲ期组间血清4种活性肽水平的差异无显著性(P均>0．05)。Ang I与AngⅡ(r=0．511, P<0．01),ALD与Ang Ⅱ间(r=0．431,P<0．05)呈显著正相关,Ang I与ANF、ALD,AngⅡ与ANF,ANF与 ALD间无显著相关性(P均>0．05);Ang I、Ⅱ,ALD水平均与平均动脉压呈显著正相关(r=0．451,0．432,0．512, P均<0．01),ANF则否(P>0．05)。EH患者中,美多洛尔干预组(66例)治疗后血清Ang I、Ⅱ、ALD水平分别显著下降(P均<0．01);苯那普利干预治疗组(68例)后血清AngⅡ水平显著下降、ALD水平却显著升高(P均 <0．01);非洛地平干预组(80例)治疗后血清Ang I水平显著升高(P<0．05)。结论:EH患者血清Ang I、Ⅱ和 ALD水平显著升高,美多洛尔可使三者水平均显著下降,苯那普利仅使AngⅡ水平显著下降,ALD水平却显著升高, 而非洛地平却使血清Ang I水平显著升高。     

妊娠时间与肺结核复发的相关性研究及诊治对策

目的 分析肺结核史患者妊娠时间和肺结核复发间相关性.方法 选取我院收治的有肺结核史的妊娠妇女576例作为研究对象,对其妊娠前肺结核治疗、治愈后妊娠时间、妊娠后复发肺结核等进行分析,总结有肺结核史育龄女性的妊娠时间和肺结核复发之间的关系.结果 肺结核治愈后不同时间段妊娠者的结核复发率比较,差异具有显著性（P＜0.05）,停药后间隔时间越久妊娠,肺结核复发的几率越小.结论 加强孕期痰菌检查,及早发现复发肺结核,提高母婴安全.     

我国骨关节结核诊治的回顾与展望

骨关节结核是危害人们健康的严重感染性疾病,近95％由他处结核病继发而来.罹患骨关节结核疾病后几乎均将致残,严重影响人们的健康、工作和生活.建国以来在党和国家的关心和支持下,骨关节结核的诊治水平取得了长足进步.时至今日,由于多种原因,学科发展和被重视程度受到一定的制约,同整个医疗行业的发展不相适应.回顾过去,展望未来,我们需要重新审视骨关节结核的诊治方法,努力推进骨关节结核诊疗技术的科学发展.     

Effect of phosphorylation of MAPK and Stat3 and expression of c-fos and c-jun proteins on hepatocarcinogenesis and their clinical significance

AIM To study the effect of phosphorylation ofMAPK and Stat3 and the expression of c-fos andc-jun proteins on hepatocellular carcinogenesisand their clinical significance.METHODS SP immunohistochemistry was usedto detect the expression of p42/44~(MAPK), p-Stat3,c-fos and c-jun proteins in 55 hepatocellularcarcinomas (HCC) and their surrounding livertissues.RESULTS The positive rates and expressionlevels of p42/44~(MAPK), p-Stat3, c-fos and c-junproteins in HCCs were significantly higher thanthose in pericarcinomatous liver tissues (PCLT).A positive correlation was observed between theexpression of p42/44~(MAPK) and c-fos proteins, andbetween p-Stat3 and c-jun, but there was nosignificant correlation between P42/44~(MAPK) and p-Stat3 in HCCs and their surrounding livertissues.CONCLUSION The abnormalities of Ras/Raf/MAPK and JAKs/ Stat3 cascade reaction maycontribute to malignant transformation ofhepatocytes. Hepatocytes which are positive forp42/ 44~(MAPK), c-fos or c-jun proteins may bepotential malignant pre-cancerous cells.Activation of MAPK and Stat3 proteins may be anearly event in hepatocellular carcinogenesis.     

Overweight and Obesity and Progression of ADPKD

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Replication and Inhibitors of Enteroviruses and Parechoviruses

The Enterovirus (EV) and Parechovirus genera of the picornavirus family include many important human pathogens, including poliovirus, rhinovirus, EV-A71, EV-D68, and human parechoviruses (HPeV). They cause a wide variety of diseases, ranging from a simple common cold to life-threatening diseases such as encephalitis and myocarditis. At the moment, no antiviral therapy is available against these viruses and it is not feasible to develop vaccines against all EVs and HPeVs due to the great number of serotypes. Therefore, a lot of effort is being invested in the development of antiviral drugs. Both viral proteins and host proteins essential for virus replication can be used as targets for virus inhibitors. As such, a good understanding of the complex process of virus replication is pivotal in the design of antiviral strategies goes hand in hand with a good understanding of the complex process of virus replication. In this review, we will give an overview of the current state of knowledge of EV and HPeV replication and how this can be inhibited by small-molecule inhibitors.     

Effect of phosphorylation of MAPK and Stat3 and expression of c-fas and c-jun proteins on hepatocarcinogenesis and their clinical significance

AIM To study the effect of phosphorylation ofMAPK and Stat3 and the expression of c-fos andc-jun proteins on hepatocellular carcinogenesisand their clinical significance.METHODS SP immunohistochemistry was usedto detect the expression of p42/44MAPK, p-Stat3,c-fos and c-jun proteins in 55 hepatocellularcarcinomas (HCC) and their surrounding livertissues.RESULTS The positive rates and expressionlevels of p42/44MAPK, p-Stat3, c-fos and c-junproteins in HCCs were significantly higher thanthose in pericarcinomatous liver tissues (PCLT).A positive correlation was observed between theexpression of p42/44MAPK and c-fos proteins, andbetween p-Stat3 and c-jun, but there was nosignificant correlation between p42/44MAPK and p-Stat3 in HCCs and their surrounding livertissues.CONCLUSION The abnormalities of Ras/Rat/MAPK and JAKs/ Stat3 cascade reaction maycontribute to malignant transformation ofhepatocytes. Hepatocytes which are positive forp42/ 44MAPK, c-fos or c-jun proteins may bepotential malignant pre-cancerous cells.Activation of MAPK and Stat3 proteins may be anearly event in hepatocellular carcinogenesis.     

心电图、心电向量图与冠状动脉造影结果对比分析

目的:通过分析心电图(Electrocardiogram,ECG)和心电向量图(Vectorcardiogram,VCG)的改变与冠脉造影（CAG）结果进行对比,探讨ECG、VCG在冠状动脉病变中的诊断价值。方法: 选择2008年1月~2009年12月临床拟诊断为冠心病患者108例,行常规ECG、VCG检查,并于1周内进行CAG,对检查结果依据各自的诊断标准进行判定,以CAG为标准诊断法,利用四格表法,计算相关评价真实性的指标并进行比较。结果: ①VCG检测的灵敏度、特异度、准确度显著高于ECG(P<0.05,P<0．01)。②ECG、VCG阳性率与冠脉病变支数组间比较:在单支病变、双支病变中,VCG阳性率明显高于ECG(P<0.05),左主干或三支病变无统计学意义;组内比较:ECG组左主干或三支病变组较单支病变、双支病变阳性率高(P<0.05,P<0.01);VCG组左主干或三支病变组较单支病变阳性率高(P<0.05);与双支病变阳性率比较无统计学意义;③ECG、VCG阳性率与冠脉病变程度组间比较:冠脉病变狭窄50%～69%的VCG阳性率明显高于ECG (P<0.05),其他两组阳性率比较无统计学意义;组内比较:ECG组冠脉病变狭窄≥90%较50%～69%、70%～89%的阳性率高(P<0.05,P<0.01); VCG组狭窄≥90%较50%～69%阳性率高（P<0.01),其他无统计学意义。结论: VCG对冠心病检测价值显著高于ECG。     

Detection and characterization of the product of hydroethidine and intracellular superoxide by HPLC and limitations of fluorescence

Here we report the structural characterization of the product formed from the reaction between hydroethidine (HE) and superoxide (O(2)(.-)). By using mass spectral and NMR techniques, the chemical structure of this product was determined as 2-hydroxyethidium (2-OH-E(+)). By using an authentic standard, we developed an HPLC approach to detect and quantitate the reaction product of HE and O(2)(.-) formed in bovine aortic endothelial cells after treatment with menadione or antimycin A to induce intracellular reactive oxygen species. Concomitantly, we used a spin trap, 5-tert-butoxycarbonyl-5-methyl-1-pyrroline N-oxide (BMPO), to detect and identify the structure of reactive oxygen species formed. BMPO trapped the O(2)(.-) that formed extracellularly and was detected as the BMPO-OH adduct during use of the EPR technique. BMPO, being cell-permeable, inhibited the intracellular formation of 2-OH-E(+). However, the intracellular BMPO spin adduct was not detected. The definitive characterization of the reaction product of O(2)(.-) with HE described here forms the basis of an unambiguous assay for intracellular detection and quantitation of O(2)(.-). Analysis of the fluorescence characteristics of ethidium (E(+)) and 2-OH-E(+) strongly suggests that the currently available fluorescence methodology is not suitable for quantitating intracellular O(2)(.-). We conclude that the HPLC/fluorescence assay using HE as a probe is more suitable [corrected] for detecting intracellular O(2)(.-).     

Effects of sex and time of day on metabolism and excretion of corticosterone in urine and feces of mice

Non-invasive techniques to monitor stress hormones in small animals like mice offer several advantages and are highly demanded in laboratory as well as in field research. Since knowledge about the species-specific metabolism and excretion of glucocorticoids is essential to develop such a technique, we conducted radiometabolism studies in mice (Mus musculus f. domesticus, strain C57BL/6J). Each mouse was injected intraperitoneally with 740 kBq of 3H-labelled corticosterone and all voided urine and fecal samples were collected for five days. In a first experiment 16 animals (eight of each sex) received the injection at 9 a.m., while eight mice (four of each sex) were injected at 9 p.m. in a second experiment. In both experiments radioactive metabolites were recovered predominantly in the feces, although males excreted significantly higher proportions via the feces (about 73%) than females (about 53%). Peak radioactivity in the urine was detected within about 2h after injection, while in the feces peak concentrations were observed later (depending on the time of injection: about 10h postinjection in experiment 1 and about 4h postinjection in experiment 2, thus proving an effect of the time of day). The number and relative abundance of fecal [3H]corticosterone metabolites was determined by high performance liquid chromatography (HPLC). The HPLC separations revealed that corticosterone was extensively metabolized mainly to more polar substances. Regarding the types of metabolites formed, significant differences were found between males and females, but not between the experiments. Additionally, the immunoreactivity of these metabolites was assessed by screening the HPLC fractions with four enzyme immunoassays (EIA). However, only a newly established EIA for 5alpha-pregnane-3beta,11beta,21-triol-20-one (measuring corticosterone metabolites with a 5alpha-3beta,11beta-diol structure) detected several peaks of radioactive metabolites with high intensity in both sexes, while the other EIAs showed only minor immunoreactivity. Thus, our study for the first time provides substantial information about metabolism and excretion of corticosterone in urine and feces of mice and is the first demonstrating a significant impact of the animals' sex and the time of day. Based on these data it should be possible to monitor adrenocortical activity non-invasively in this species by measuring fecal corticosterone metabolites with the newly developed EIA. Since mice are extensively used in research world-wide, this could open new perspectives in various fields from ecology to behavioral endocrinology.     

大鼠骨髓间充质干细胞的分离培养和外源基因的导入

目的探讨绿色荧光蛋白基因转染骨髓间质干细胞的可行性。方法采用F icoll-PaqueTMP lus淋巴细胞分离液,根据细胞密度梯度原理,分离大鼠骨髓间充质干细胞(rM SC s)并进行体外原代培养和传代扩增,倒置相差显微镜观察细胞生长情况,免疫细胞化学法对其初步鉴定。流式细胞仪分析转染效率。结果原代和传代培养的细胞呈现梭形外观,具有较强的生长增殖能力;细胞均一表达CD44、CD54、CD106、CD29抗原。电穿孔法转染rM SC s转染率为32.8%±3%。结论采用比重为1.077 g/L的F icoll-PaqueTMP lus能分离获得大鼠骨髓间充质干细胞,经原代培养和传代培养能够迅速扩增。电穿孔法具有较高的介导外源基因表达于rM SC s的效率。