应用VTK技术建立唇腭裂可视化模型

目的:寻求一种高效率、高精度建立唇腭裂患者颌面部可视化模型的方法.方法:利用薄层CT获取原始数据,运用k-均值聚类算法进行图像分割,结合VTK(Visualization Toolkit)技术进行可视化模型的建立.结果:建立了更为精确的唇腭裂患者颌面部的可视化模型,总结出了一种更为方便高效的通用可视化建模方法.结论:应用VTK方法建立可视化模型,软件开发周期更短,精度更高,应用更广泛.     

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.     

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。     

Rapid Immunofluorescence Microscopy for Diagnosis of Melioidosis

An immunofluorescent (IF) method that detects Burkholderia pseudomallei in clinical specimens within 10 min was devised. The results of this rapid method and those of an existing IF method were prospectively compared with the culture results for 776 specimens from patients with suspected melioidosis. The sensitivities of both IF tests were 66%, and the specificities were 99.5 and 99.4%, respectively.     

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.     

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。     

Extracellular matrix remodeling in oral submucous fibrosis: its stage-specific modes revealed by immunohistochemistry and in situ hybridization

BACKGROUND: Oral submucous fibrosis (OSF) is a chewing habit-related pre-cancerous condition of the oral mucosa affecting predominantly south Asians. It is histopathologically characterized by epithelial atrophy and fibrosis of the subepithelial connective tissue. Fibrosis extends all the way into the muscle layer, leading to difficulty in mouth opening. However, the dynamics of extracellular matrix (ECM) remodeling with OSF progression is largely unknown. METHODS: Forty biopsy specimens of OSF and 10 of normal buccal mucosa were examined for expression/deposition modes of eight ECM molecules by histochemistry, immunohistochemistry, and in situ hybridization. RESULTS: In the early stage of OSF, tenascin, perlecan, fibronectin, collagen type III were characteristically enhanced in the lamina propria and the submucosal layer. In the intermediate stage, the ECM molecules mentioned above and elastin were extensively and irregularly deposited around muscle fibers. In the advanced stage, such ECM depositions decreased and were entirely replaced with collagen type I only. Their gene expression levels varied with progression of fibrosis, but the mRNA signals were confirmed in fibroblasts in the submucosal fibrotic areas. CONCLUSIONS: The results indicate that the ECM remodeling steps in OSF are similar to each phase of usual granulation tissue formation. Restricted mouth opening may be a result of loss of variety of ECM molecules including elastin into the homogeneity of collagen type I replacing muscle fibers.