老年人微小病变性肾病综合征的临床特征和长期随访

探讨老年人微小病变性(MC)特发性肾病综合征(PNS)的临床特征及预后。方法 观察成人MC性PNS118例,其中老年患者18例,占15.2％。结果 发现老年患者NS的临床表现与成年组相似;但血尿发病率较低,22％比38％;高血压和肾功能不全的发病率明显增高,38.9％比16％和33.3％比19％(P<0.01)。老年组对激素治疗的敏感性略差;但NS复发率明显减少,11.1％比43％。结论 尽管NS的复发和对激素依赖使治疗有一定困难,但激素、细胞毒性药物和环孢素A对于消除蛋白尿,延缓肾功能不全是有助的。     

腰椎峡部裂的CT诊断

目的：回顾性分析腰椎峡部裂的ＣＴ表现并讨论其诊断与鉴别诊断，材料与方法，２３例患先行腰椎侧位扫描定位图像，采用与椎间盘平行的角度，自病变脊椎的上一椎体下缘边续发描至于下椎体上缘，层厚４或５ｍｍ必要时在峡部行２ｍｍ，层厚扫描，结果；２３例中，累及双侧２１例，单侧２例，发生在Ｌ５１６例，Ｌ４７例，ＣＴ表现为同一脊椎关节突间的低密度裂隙，出瑞椎弓根下缘平面，走行不规则，裂隙可宽可窄，表面不光滑。     

4125例哈萨克族儿童斜视及弱视调查

本文对本地区五个县九所哈萨克族小学学生共计4125人进行了斜视、弱视的调查。调查对象全部为4—14岁哈萨克儿童。在受检儿童中发现斜视者48例,患病率为1.1％。外斜视32例占66.67％,内斜视16例占33.33％,斜视并有弱视者15例占31.25％。斜视而视力正常者33例占68.75％。在4125例受检儿童中发现弱视139例(209只眼),其患病率为3.37％,双眼弱视70例,单眼弱视69例,二者无显著差异。139例弱视中男性患者73例,女性患者66例,二者亦无差异。209例只弱视眼中轻度弱视84只眼占40.19％,中度弱视104只眼占49.76％,重度弱视21只眼共占10.05％。调查中笔者发现哈萨克族儿童弱视眼尤以屈光不正为多,209例眼中有106只为单纯性远视眼,因此笔者提出如何早期发现屈光不正并予以纠正将有可能防止许多弱视的发生。     

99mTc标记结肠癌单克隆抗体片段CEA．Fab的研制方法

目的　探讨一种高效便捷的99mTc CEA Fab标记化合物的研制方法。方法　采用 2 亚氨噻酚盐酸盐修饰CEA Fab ,通过GH转换 ,将99mTc标记在结肠癌单克隆抗体CEA Fab上。结果　已修饰抗体的标记率为 93.5 %,99mTc胶体含量为 2 .5 %,标记化合物有良好的稳定性和免疫活性。结论　成功地建立了结肠癌单抗片断CEA Fab的99mTc标记方法 ,该技术可以应用于其他抗体片段标记领域。     

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。     

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。     

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.