Temporal effects of a COX-2-selective NSAID on bone ingrowth

The effects of a short course of a COX-2 inhibitor on bone healing when the drug is discontinued are unknown. We examined the effects of rofecoxib on bone ingrowth over a 6-week period using a well-defined animal model. The Bone Harvest Chamber was implanted bilaterally in mature rabbits. After osseointegration of the chamber, the following treatments were given for 6 weeks each, followed by a harvest in each case: control-no drug; oral rofecoxib (12.5 mg/day) for the first 2 of 6 weeks; washout period-no drug; oral rofecoxib for the last 2 of 6 weeks; washout period-no drug; rofecoxib given continuously for all 6 weeks. Harvested specimens were snap-frozen, cut into serial 6-microm sections, and stained with hematoxylin and eosin and alkaline phosphatase (osteoblast marker), and processed using immunohistochemistry to identify the vitronectin receptor (osteoclast-like cells). Rofecoxib given continuously for 6 weeks yielded statistically less bone ingrowth compared to the control treatment. Rofecoxib given during the initial or final 2 weeks of a 6-week treatment did not appear to interfere with bone ingrowth. This suggests that the effects of COX-2 inhibitors on bone are less profound when the drug is administered for a short period of time.     

含人基质金属蛋白酶组织抑制因子-1重组腺病毒的构建与体外表达

从人肝癌组织中提取总RNA，RT—PCR合成hTIMP-1的全长cDNA，克隆到腺病毒载体AdEasy系统的穿梭质粒pAdTraek—CMV上，与骨架质粒pAdEasy-1在BJ5183受体菌中进行同源重组，成功构建含hTIMP-1全长eDNA的重组腺病毒载体，经293细胞的包装、扩增，生成含hTIMP-1基因的重组腺病毒AdhTIMP-1并实现体外表达，为进一步研究肝癌浸润和转移机理以及肝癌的基因治疗提供实验基础。     

血管紧张素Ⅱ对心房颤动患者外向钾电流的作用

目的：研究血管紧张素Ⅱ(AngⅡ)对心房颤动(AF)患者心房肌外向钾电流的作用及其受体机制。方法: 采用急性酶解法获取游离心房肌细胞，应用膜片钳全细胞技术记录外向钾电流。结果: (1) 在钳制电位-10 mV~+50 mV时, AF组瞬时外向钾电流(I_to1)密度明显低于窦性心律(SR)组（P<0.01），而持续性外向钾电流（I_sus）密度与SR组无明显差异。(2) 以0.1 μmol/L AngⅡ灌流后，在钳制电位0 mV~+50 mV时，SR患者的Ito1密度明显低于灌流前（P<0.01），其动力学特性没有改变，AngⅡ对AF组I_to1的抑制作用明显低于SR组 (P<0.01)。0.1 μmol/L AngⅡ对两组I_sus没有影响。(3) AngⅡ对Ito1的抑制作用可逆，10 μmol/L缬沙坦（valsartan）以及1 μmol/L沙拉新(saralasin)均能完全消除0.1 μmol/L AngⅡ对Ito1的抑制，以10 μmol/L valsartan灌流后，膜电位+50 mV时I_to1的电流密度增加（22.46±4.30）%。结论: AngⅡ通过Ⅰ型受体（AT₁R）介导，明显抑制心房肌细胞膜I_to1，是AF患者心房肌瞬时外向钾通道电重构的机制之一。     

基于LEADTOOLS的DICOM标准医学图像通讯的研究

支持DICOM协议是PACS系统的基本特征,而DICOM存储和查询获取则是DICOM通讯中的关键环节。本文利用LEADTOOLS14.5是LEADTOOLS公司最新开发的医学软件开发包,它提供了完成DICOM通信的各种类库,在此基础上本文对SCU和SCP之间的DICOM协商、存储、查询与获取等通讯过程进行了探讨。为各种医学信号与图像设备、服务器、及诊断工作站,提供了符合DICOM 3.0标准的通信功能。     

IFN-γ对体外培养系统中IL-18诱导的肿瘤特异性CTL杀伤效应的影响

目的应用rhIL-18在体外培养系统(Coculture system in vitro,CCs)中诱导肿瘤特异性细胞毒性T淋巴细胞(Cytotoxic T Lymphocyte,CTL),探讨IFN-γ在rhIL-18诱导的肿瘤特异性CTL产生过程及杀伤效应中的作用.方法采用Stem SepTM免疫磁性细胞分离法分离人外周血NK细胞、T细胞及DCs细胞,流式细胞仪分析细胞表型,125Ⅰ-UdR标记的细胞毒实验检测杀伤活性,ELISA方法检测IFN-γ蛋白产生量,RT-PCR检测IFN-γ mRNA表达含量.结果在肿瘤抗原存在的条件下,IL-18在CCs中能够诱导并促进CTL介导的肿瘤特异性杀伤效应;IL-18能够在肿瘤抗原刺激的CCs中诱导IFN-γ mRNA的表达及IFN-γ蛋白的产生,并与IL-18的含量呈剂量依赖关系,在rhIL-18含量为100 ng时,培养上清中IFN-γ为4 410±210 pg/ml.但加入抗IFN-γ抗体对rhIL-18诱导的肿瘤特异性CTL产生过程无明显影响,不能抑制IL-18诱导的这种肿瘤特异性CTL的杀伤效应.结论IL-18能够在肿瘤抗原刺激的CCs中有效地诱导CTL介导的肿瘤特异性杀伤效应,并诱导IFN-γ的产生,但其诱导肿瘤特异性CTL的产生过程及杀伤效应与IFN-γ无关.     

重组人β2糖蛋白1第一结构域对抗磷脂抗体综合征患者血清诱导人脐静脉内皮细胞产生ICAM-1、MCP-1的影响

目的：探讨重组人β2糖蛋白1第一结构域（hrβ2GPⅠDⅠ）对抗磷脂抗体综合征（APS）患者血清诱导人脐静脉内皮细胞产生细胞间黏附分子-1（ICAM-1）、单核细胞趋化蛋白-1（MCP-1）的影响。方法：应用hrβ2GPⅠDⅠ二聚体处理前后的APS患者血清分别与人脐静脉内皮细胞（HUVEC）共孵育，细胞EL／SA和RT-PCR方法分析处理前后HUVEC表达ICAM-1、MCP-1的变化。结果：hrβ2GPⅠDⅠ二聚体处理后的APS患者血清较处理前相比，与其孵育的HUVEC表达ICAM-1、MCP-1在蛋白和mRNA水平均明显降低。结论：邮：GPⅠDⅠ可中和APS患者血清中的大部分致病性抗β2GPⅠ抗体（anti-β2 GPⅠ）。     

基于LEADTOOLS V14.5的医学数字图像与通讯图像阅读软件的设计

医学数字图像与通讯(DICOM)图像阅读软件是一个相对独立的软件,它既可以嵌入到医疗影像管理系统(PACS)的影像工作站中,用于DICOM图像的读写、显示和基本的图像处理,也可以单独安装于个人电脑上,方便医生随时随地浏览DICOM图像.LEADTOOLS V14.5是Leadtools公司最新开发的医学软件开发包,在它的基础上开发DICOM图像阅读软件,可以大大缩短开发时间,降低开发成本.我们将从设计原理、编程思路、具体实现等几个方面详细介绍如何应用VC++.NET和LEADTOOLS V14.5,设计DICOM 3.0标准下的DICOM图像阅读软件.     

Evaluation and Validation of an Enzyme-Linked Immunosorbent Assay and an Immunochromatographic Test for Serological Diagnosis of Severe Acute Respiratory Syndrome

A newly developed severe acute respiratory syndrome (SARS)-specific enzyme-linked immunosorbent assay (ELISA) was further validated to confirm cutoff values and evaluate its diagnostic performance with clinical samples. In parallel, an immunochromatographic test was also evaluated. A total of 227 clinical serum specimens collected from SARS patients were used in the study, together with 385 samples from healthy donors. By use of an immunofluorescent (IF) test as the “gold standard, ” both the ELISA and the immunochromatographic test were able to detect immunoglobulin G antibodies to SARS not only from late-convalescent-stage samples (>21 days from the onset of clinical symptoms), as previously established, but also from early-acute-phase samples (1 to 10 days from onset). The ELISA, using an optical density (OD) of 0.25 as its cutoff value, produced the best sensitivity while maintaining high specificity. It detected SARS-specific antibodies in 58, 70, 75, and 95%, respectively, of the four groups of samples collected from patients 1 to 10 days, 11 to 20 days, 21 to 30 days, and more than 30 days after the onset of clinical symptoms. Similarly, the immunochromatographic test detected SARS-specific antibodies in 55, 68, 81, and 79% of the four groups, respectively. The overall specificities for the ELISA and the rapid test were 99.5 and 97.7%, respectively. Although the positive correlation observed between the ELISA OD values and the IF titers was moderate (r = 0.6915; P < 0.001), the detection rates of both the ELISA and the rapid test were found well in agreement with the IF titers.     

52 例病毒性肝炎患者肝组织中丙型肝炎病毒 RNA 和 HCAg-NS3 的测定

应用地高辛标记探针原位杂交法和单克隆抗ＨＣＶ－ＮＳ３－ＨＲＰ建立直接酶标免疫组化法分别测定５２例肝炎患者肝组织ＨＣＶＲＮＡ和ＨＣＡｇ－ＮＳ３。结果抗ＨＣＶ阳性组ＨＣＶＲＮＡ检出率５７．１％（１６／２８），ＨＣＡｇ－ＮＳ３检出率５３．６％（１５／２８）；抗ＨＣＶ阴性组其两项检出率均为１２．５％（３／２４）。肝组织中ＨＣＶＲＮＡ阳性物呈蓝紫色细小颗粒存在于肝细胞核或胞浆内，其在肝小叶中的分布可分为３型，即弥漫型、局灶型、散在型。肝组织中ＨＣＡｇ－ＮＳ３阳性物呈棕黄色细小颗粒分布于肝细胞核或胞浆内，以单个或数个阳性细胞散布于肝小叶中。２３例ＨＣＶＲＮＡ或／和ＨＣＡｇ－ＮＳ３阳性病例以肝炎后肝硬化（ＬＣ）病例占多数（１４／２３），其次为慢性重型肝炎（ＣＳＨ）和中度慢性肝炎（ＣＡＨ）。此两种检测方法具有较高符合率（９０．４％，４７／５２），表明病毒核酸及其表达产物均存在于肝细胞内，与ＨＣＶ感染密切相关。这为ＨＣＶ感染诊断提供了直接依据，有利于研究ＨＣＶ感染中病毒复制、慢性化进程、抗病毒治疗监测及重叠感染时病毒相互关系。     

表皮生长因子和甲硫氨酸脑啡肽诱导人白细胞c—fos基因表达的研究

由健康人外周血分离淋巴细胞及溶血处理后的全白细胞，以外源性表皮生长因子和甲硫氨酸脑啡肽培育后取细胞液帛晟滴片和滴膜，用生物素标记的ｃ－ｆｏｓｃＤＮＡ探针进行原位杂交和斑点印迹杂交。结果显示表皮生升因子和甲硫氨酸脑啡肽两组ｃ－ｆｏｓ原癌基因的表达对照组增。