抗戊型肝炎病毒重组蛋白单克隆抗体的制备和初步应用

目的:制备抗-戊型肝炎病毒的单克隆抗体,并将其用于分析戊型肝炎病毒不同毒株结构蛋白的抗原表位。方法:采用来自墨西哥株(Mexicanstrain)的戊型肝炎病毒重组蛋白(p166Mex)免疫Balb/c小鼠,取其脾细胞与SP2/0骨髓瘤细胞进行融合,经酶联免疫吸附试验(ELISA)法筛选阳性克隆,并将获得的单克隆抗体与戊型肝炎病毒缅甸株(Burmastrain)和美国株(USAstrain)的重组蛋白(p166Bur、p166US)进行交叉反应测定。结果:最终获得4株能稳定分泌抗-p166Mex的杂交瘤细胞株,即D8G10、E5E12、D4A3、B7E6。其中D8G10,E5E12和B7E6细胞株的培养上清液,还能分别与p166Bur和p166US重组蛋白发生阳性反应。结论:利用已获得的抗-p166Mex单克隆抗体,初步确定3种不同的戊型肝炎病毒重组蛋白(p166Bur、p166US、p166Mex)含有一种共同的抗原表位。     

基层医院护理科研论文的现状和护士长工作指导

护理作为一门独立的专业，其发展应以科学研究为基础。护理科研、论文的数量和水平是评价一个地区或单位的护理整体水平的重要指标之一。笔者通过我院10年间医院工作人员科研立项、科研论文发表交流情况及护理人员论文写作的调查，对护理科研滞后的应用进行了综合分析，认为缺乏科研意识、科研潜力不足，观行制度制约，客观条件制约是重要因素。提出改变这种状态应从学科带头人入手，详细阐述了护士长对护理科研、论文工作的指导。     

免疫吸附治疗在肾移植致敏受者中的应用

目的：探讨蛋白A免疫吸附（immunoads Orption，IA）治疗对清除肾移植致敏受者体内特异性抗HLA抗体的疗效和安全性。方法：10例肾移植致敏（PRA〉50％）受者用彤新蛋白A免疫吸附柱行IA治疗，测定治疗前后血免疫球蛋白及PRA水平。结果：10例患者IA治疗次数为4～15次（中位数9）。所有患者IA治疗后血清总IgG水平都明显下降（P〈0．001），IgA和IgM也较治疗前显著降低（P〈0．01）。PRA8例转阴，1例〈30％，1例仍为100％。结论：对于肾移植致敏受者，IA是一种特异性高、安全有效的治疗措施。     

散发型Creutzfeldt-Jakob病的MRI表现

目的探讨散发型Creutzfeldt-Jakob病（sCJD）的MR特点。方法回顾性分析3例临床诊断为sCJD的患者资料，MR采用SE T1 WI、快速自旋回波（FSE）T2 WI、扩散加权成像（DWI）扫描，观察其MR表现特征。结果3例SE TI WI和FSE T2 WI序列对基底节区和皮质的病变显示不佳，DWI则可清晰地显示病变，额、顶、枕叶皮质最常受累，表现为高信号，病变可对称，也可不对称，皮层下区脑白质信号未见异常。双侧尾状核、丘脑也可受累，DWI上呈高信号。晚期脑实质广泛萎缩，以皮质为著。结论sCJD采用DWI序列结合其特征性的临床表现可作出较为准确的诊断。     

影响原发性肝癌肝移植治疗的预后因素分析

目的分析影响肝癌肝移植术后生存率和无瘤生存率的危险因素,探讨国内肝移植治疗肝癌的选择标准。方法对67例接受同种异位原位肝移植治疗的原发性肝癌病人的基本资料和肿瘤相关资料包括术前病情分级、血清AFP水平、术前辅助治疗以及肝癌大小、数目、pTNM分期、肿瘤恶性程度分级等因素进行单因素和多因素分析。结果术后1年、2年累积生存率为77%、67%,6个月和12个月无瘤生存率为66%和58%。单因素分析显示对肝癌肝移植术后累积生存率影响有统计学意义的因素为CHILD分级(MELD积分)和肝外大血管侵犯;多因素分析影响肝癌肝移植术后无瘤生存率有统计学义的因素是肿瘤大小、大血管侵犯和肿瘤分化程度。结论影响肝癌肝移植术后生存率的因素仍是术前患者肝功能状态。对存在大血管侵犯的肝癌患者需严格控制肝移植术适应证,而无血管侵犯的患者在选择肝移植治疗时肿瘤大小指标可较米兰标准适当放宽。     

松质骨螺钉骨水泥强化的生物力学和组织学研究

目的通过动物实验观察不同骨水泥强化松质骨螺钉的生物力学和组织学变化动态,为骨质疏松骨折患者内固定提供理论基础。方法在10只杂种犬胫骨近端制作松质骨螺钉植入的动物模型,分别采用碳酸化羟基磷灰石水泥(CHC)和聚甲基丙烯酸甲酯(PMMA)强化,分别于术后5d、4、8、12和16周处死动物,观察螺钉拔出的生物力学和组织学变化。结果CHC强化的螺钉拔出力随手术后时间的延长而逐渐升高,16周时达到(512.5 14.5)N,而PMMA强化组螺钉拔出力则随手术后时间的延长而逐渐降低。CHC-骨界面结合紧密,并且随时间延长出现CHC降解和骨长入,而PMMA-骨界面形成一层纤维组织。结论CHC强化能够提高松质骨螺钉植入体内的稳定性,并且随植入时间延长而逐渐升高。     

Arthroscopic Double-Row Suture Anchor Fixation of Minimally Displaced Greater Tuberosity Fractures

In cases of displaced greater tuberosity fractures, treatments by arthroscopic-assisted reduction and percutaneous screw fixation have been reported. However, in cases in which there is a comminuted fracture or a minimally displaced fracture combined with concomitant lesions such as rotator cuff tear or labral pathology, it is difficult to reduce the fracture and to treat other pathologies by use of a percutaneous screw. Recently, many surgeons have used the double-row repair method in rotator cuff repair, which provides a tendon-bone interface better suited for biologic healing and restoring normal anatomy. In accordance with this method, we used the arthroscopic technique of double-row suture anchor fixation for a minimally displaced greater tuberosity fracture without additional incision. Initially, debridement was performed on the fracture surface by use of a shaver, and the medial-row anchor was inserted through the anterior portal or the intact cuff. Two lateral-row anchors were inserted just anterior and posterior to the lower margin of the fractured fragment under C-arm guidance. The medial-row sutures and lateral-row sutures were then placed. Arthroscopic double-row suture anchor fixation of a displaced greater tuberosity fracture restores the original footprint of the rotator cuff and normal tendon-bone interface of the displaced greater tuberosity fracture.     

Fidgetin-like 1 gene inhibited by basic fibroblast growth factor regulates the proliferation and differentiation of osteoblasts.

The FIGNL1 gene was proven to be a new subfamily member of ATPases associated with diverse cellular activities (AAA proteins). In this in vitro study, the AAA proteins inhibited osteoblast proliferation and stimulated osteoblast differentiation. We showed that FIGNL1 may play some regulatory role in osteoblastogenesis. INTRODUCTION: The fidgetin-like 1 (FIGNL1) gene encodes a new subfamily member of ATPases associated with diverse cellular activities (AAA proteins). Although the FIGNL1 protein localizes to both the nucleus and cytoplasm, the function of FIGNL1 remains unknown. In a previous study, we identified several genes that mediate the anabolic effects of basic fibroblast growth factor (bFGF) on bone by using microarray data. FIGNL1 was one of the genes that downregulated >2-fold in MC3T3-E1 cells after treatment with bFGF. Therefore, this study was aimed to identify and confirm the function of FIGNL1 on osteoblastogenesis. MATERIALS AND METHODS: We examined the effect of the FIGNL1 gene on proliferation, differentiation, and apoptosis in mouse osteoblast cells (MC3T3-E1 and mouse primary calvarial cells) using flow cytometry, RT-PCR, cell proliferation assay, and cell death assay. MC3T3-E1 cells and mouse calvarial cells were transfected with small interfering RNA (siRNA) directed against the FIGNL1 or nontargeting control siRNA and examined by cell proliferation and cell death assays. Also, FIGNL1 was fused to enhance green fluorescent protein (EGFP), and the EGFP-fused protein was transiently expressed in MC3T3-E1 cells. RESULTS: Reduced expression of FIGNL1 by bFGF and TGF-beta1 treatment was verified by RT-PCR analysis. Overexpression of FIGNL1 reduced the proliferation of MC3T3-E1 and calvarial cells, more than the mock transfected control cells did. In contrast, siFIGNL1 transfection significantly increased the proliferation of osteoblasts, whereas overexpression of FIGNL1 did not seem to alter apoptosis in osteoblasts. Meanwhile, overexpression of FIGNL1 enhanced the mRNA expression of alkaline phosphatase (ALP) and osteocalcin (OCN) in osteoblasts. In contrast, siFIGNL1 decreased the expression of ALP and OCN. A pEGFP-FIGNL1 transfected into MCT3-E1 cells had an initially ubiquitous distribution and rapidly translocated to the nucleus 1 h after bFGF treatment. CONCLUSIONS: From these results, we proposed that FIGNL1, a subfamily member of the AAA family of proteins, might play some regulatory role in osteoblast proliferation and differentiation. Further analyses of FIGNL1 will be needed to better delineate the mechanisms contributing to the inhibition of proliferation and stimulation of osteoblast differentiation.