Ovid医学信息平台在医学科研中的应用

详细介绍了Ovid 医学信息平台的特点及功能,并对其数据库所涉及学科作了介绍,指出Ovid 医学信息平台以其超大容量、完美服务及快捷查阅等特点优于同类软件,可以为医学科研人员提供高质量、深层次、全方位的服务.     

荧光分光光度法检测半乳糖化白蛋白磁性阿霉素纳米粒在大鼠体内分布的研究

目的观察由半乳糖化白蛋白磁性纳米粒运载的阿霉素经舌静脉给药后在大鼠体内的的分布状况.方法全部大鼠随机分为四组,经舌静脉,按分组分别注射相应药物,剂量均为阿霉素2.5 mg/kg体重.取全血、心、肺、肝、脾、肾.全血制成血浆,器官组织制成匀浆,盐酸乙醇法提取阿霉素,用荧光光度计测量.结果静脉注射同等剂量、不同剂型的阿霉素药物后,阿霉素在器官中的蓄积程度从高到低:肝:D靶肝＞D非靶肝、C＞B＞A;心脏、肾、血浆:A＞B＞D、C;脾:B＞A、C、D;肺:B＞A＞C、D.磁性阿霉素白蛋白纳米粒注入体内后,在心、肺、肝、脾、肾中的药物浓度在15～30min达峰值,而半乳糖化后,阿霉素的药物峰值提前到5 min或之前.外加磁场和未加磁场的半乳糖化白蛋白磁性阿霉素纳米粒组的药物靶向指数和药物选择指数是均高于磁性白蛋白纳米粒.结论磁性阿霉素白蛋白纳米粒经半乳糖化后,可显著增强阿霉素对肝脏的靶向性,并显著降低心、肺、脾、肾、血浆肝外器官的组织阿霉素浓度.利用外加磁场,可提高阿霉素在肝脏特定部位蓄积的能力.因此,静脉注射半乳糖化白蛋白磁性阿霉素纳米粒是可行的.     

外加磁场对半乳糖化白蛋白磁性阿霉素纳米粒在大鼠体内分布影响的研究

目的观察半乳糖化白蛋白磁性阿霉素纳米粒(ADR-GHMN)在正常肝脏中的靶向性,并观察ADR-GHMN在全身各脏器的分布特征及外加磁场对其分布的影响.方法大鼠正中开腹,肝动脉插管并固定,肝动脉注射125I-ADR-GHMN(相当于阿霉素0.5 mg/kg),左外叶加磁场,磁场应用30 min,移去磁场后,动物立即处死;对照组:肝动脉注射ADR-GHMN,左外叶不加磁场,30min后,移去磁场后,动物立即处死,立即取靶区肝、非靶区肝、肾、心、肺、小肠、脾及周围血作γ计数.肝组织作病理切片.结果注入的纳米粒75～85%分布于肝脏,其它脏器极少.病理切片显示磁区小动脉见大量纳米粒存在,对照组及非磁区肝中纳米粒很少见.结论ADR-GHMN在正常肝组织中有明显的磁靶向性;在磁场作用下,ADR-GHMN主要分布于肝脏,其它脏器含量很少;试验组肾、心、肺、小肠、脾及外周血于对照组的放射活性比较明显降低,表明磁性物质的存在使这些脏器的相对药物暴露明显减少.     

MR显微成像检测活体阿尔茨海默病转基因小鼠老年斑沉积的效果

目的利用MR显微成像技术研究阿尔茨海默病转基因小鼠老年斑的沉积情况。方法2只17个月龄阿尔茨海默病转基因[V717I]小鼠和2只野生型小鼠，行活体T2WI，然后对照影像定位结果进行组织学切片及免疫组织化学染色。观察T2WI中老年斑的沉积情况以及其与免疫组织化学染色结果的对应关系。结果转基因小鼠T2WI上显示大脑皮层和海马区可见点状低信号，且部分低信号可以和组织学切片所显示的老年斑相对应；野生型小鼠T2WI未见明显的低信号，免疫组织化学染色也未见到染色阳性的斑块。结论MR显微成像技术检测老年斑的沉积是可行的，且可用来特异性地诊断阿尔茨海默病。     

双J管临床应用及美蓝在置管术中的作用

目的探讨双J管(双J输尿管支架管)在泌尿系疾病治疗中的应用效果以及美蓝在置放术中的作用。方法对215例患者采用放置双J管作内支架和内引流治疗,近期48例术中以美蓝协助定位。结果术后留置尿管5~7d,无切口感染、尿瘘等并发症。术后1~3个月拔除双J管,随访3~6个月,肾功能、肾积水明显好转,吻合口通畅。以美蓝协助定位者无双J管上移致拔管困难。结论双J管具有内支架和内引流作用,操作简单,引流效果好,并发症少,缩短住院时间。以美蓝协助定位,值得推广应用。     

Effect of nuclear factor-κB p65 ASOND on I typ collagen expression and rat hepatic stellate cells proliferation

Objective Sstudy effect of nuclear factor-κB ASOND on I type collagen expression and rat hepatic stellate cells(HSC)proliferation.Methods Rat HSCs were separated by affusing and digestingof Ⅳ type collagenenzyme and density acentric method.Lipid-mediated NF-κB p65 ASOND(0.001,0.01,0.1,1μmol/L)Was transferred into rat HSCs.Toxicity of HSCs caused by NF-κB p65 ASOND and activity of LDH were determined by trypan blue staining.Proliferation affection of transferring NF-κB p65 ASOND into HSCs was determined by MTT.In different concentration NF-κB p65 ASOND.expression of Ⅰ type collagen stimulated by 1mg/L TNF-αwas determined by RT-PCR and ELISA.Results After transfection of NF-κB p65 ASODN,expression of NF-κB protein in HSCs was decreasing.Toxicity experiment indicated that NF-κB p65 ASOND of different concentration(0.001,0.01,0.1 and 1.0 μmol/L)had no effect on HSCs livability and LDH activity(P<0.05).Four different concentration NF-κ B p65 ASOND could restrain HSCs proliferation stimulated by 1 mg/L TNF-α.The expression of I type collagen and mRNA stimulated by 1mg/LTNF-αwas increased,and had a positive correlation with concentration(P>0.05).Conclusion NF-κB p65 ASOND may depress NF-κB activity to restrain HSCs proliferation and Ⅰ type collagen expression,and reduce extracellular matrix.     

光敏剂ATX-S10.Na(Ⅱ)在大鼠脑胶质瘤模型不同组织中分布的实验研究

目的探讨新型光敏剂ATX-S10.Na(Ⅱ)在大鼠脑胶质瘤模型不同组织中的分布和代谢。方法在已经建立的SD大鼠C6胶质瘤模型中,经尾静脉注射ATX-S10.Na(Ⅱ)(20mg/kg)。分别于1h、2h、4h、8h、12h和24h后处死并取出大鼠的血液、皮肤、肿瘤组织、瘤周组织以及对侧正常脑组织,应用荧光分光光度计连续测定ATX-S10.Na(Ⅱ)在大鼠C6胶质瘤模型各种组织中的分布和代谢。结果ATX-S10.Na(Ⅱ)的药物浓度于静脉注射2h后在肿瘤组织中达到峰值,以后8h维持在一个持续较高的水平,显著高于对侧正常脑组织及瘤周组织。而正常皮肤和脑组织中也吸收少量的药物,但是它们峰值很低,并且几乎均在4h内完全代谢消失。结论新型光敏剂ATX-S10.Na(Ⅱ)具有优良的胶质瘤组织与正常脑组织的对比度,并且能快速从体内清除。     

延迟一期修复外周神经损伤38例报告

目的 探讨应用显微外科技术延迟一期修复四肢外周神经损伤的治疗体会。方法 应用显微外科技术延迟一期修复各种原因所致的四肢外周神经损伤38例41条，手术方法包括神经瘢痕松解、神经直接缝合术等。结果 术后随访6个月～7年，平均33个月，优良率为81．6％。结论 对失去一期修复手术治疗机会的周围神经损伤患者应尽早行延迟一期手术，可取得较好疗效。     

应用门控SPECT测量左心室功能的方法学研究

目的：试用门控心肌显像测定左室功能并与心血池显像结果比较。材料和方法：61例受检者进行了Tc-99m—MIBI门控心肌显像及心血池显像．结果：门控断层心肌显像的短轴中间部左室功能结果与平衡法心血池显像有良好的相关性(r=0．82）。结论：门控心肌断层显像测定的左室功能结果方法简便可靠．能同时反映心肌直流及左室功能。     

Brain natriuretic peptide enhances the endothelium-independent cAMP and vasorelaxant responses of calcitonin gene-related peptide in rat aorta

Calcitonin gene-related peptide (CGRP) causes vasorelaxation in rat aorta involving endothelium/nitric oxide (NO)-dependent elevations of both cAMP and cGMP levels. When endothelium is removed, preincubation with exogenous NO uncovers and potentiates direct (endothelium-independent) cAMP elevations and vasorelaxations caused by CGRP. This enhancing effect of NO potentially involves elevation of cGMP and inhibition of Type III (cGMPinhibitable) phosphodiesterase, causing accumulation of cAMP. However, NO may have other actions. The aim of the present study was to determine if brain natriuretic peptide (BNP), which elevates cGMP levels independent of NO, could enhance cAMP accumulations and vasorelaxations induced by CGRP in rat aortic rings denuded of endothelium. When added separately, neither CGRP (100 nM) nor BNP (10 nM) altered cAMP levels. When added in combination, CGRP (100 nM) and BNP (10 nM) significantly elevated cAMP levels (from control of 0.95 ± 0.08 to 1.53 ± 0.09 pmol/mg protein) at 2 min. BNP (10 nM) elevated cGMP levels 10-fold at 2 min and this response was not altered by co-administration of CGRP (100 nM).Pretreatment with BNP at concentrations as low as 1 nM in endothelium-denuded aortic rings greatly enhanced the direct vasorelaxant effects of CGRP (100 nM) (from control of 0% to 57.6 ± 6.8% relaxation of phenylephrineprecontractions). Our findings indicate that BNP enhances direct (endothelium-independent) cAMP elevations and vasorelaxations caused by CGRP in rat aorta, thus supporting the concept that cGMP inhibits cAMP metabolism and enhances CGRP-induced responses in aortic smooth muscle cells.