Increasing bending strength and pullout strength in conical pedicle screws: biomechanical tests and finite element analyses

STUDY DESIGN: Comparative in vitro biomechanical study and finite element analysis. OBJECTIVES: To investigate the bending strength and pullout strength of conical pedicle screws, as compared with conventional cylindrical screws. SUMMARY OF BACKGROUND DATA: Transpedicle screw fixation, the gold standard of spinal fixation, is threatened by screw failure. Conical screws can resist screw breakage and loosening. However, biomechanical studies of bending strength have been lacking, and the results of pullout studies have varied widely. METHODS: Ten types of pedicle screws with different patterns of core tapering and core diameter were specially manufactured with good control of all other design factors. The stiffness, yielding strength, and fatigue life of the pedicle screws were assessed by cantilever bending tests using high-molecular-weight polyethylene. The pullout strength was assessed by pullout tests using polyurethane foam. Concurrently, 3-dimensional finite element models simulating these mechanical tests were created, and the results were correlated to those of the mechanical tests. RESULTS: In bending tests, conical screws had substantially higher stiffness, yielding strength, and fatigue life than cylindrical screws (P<0.01), especially when there was no step at the thread-shank junction. In pullout tests, pullout strength was higher in screws with a conical core and smaller core diameter and also in situations with higher foam density (P<0.01). In finite element analysis, the maximal deflection and maximal tensile stress were closely related to yielding strength (r=-0.91) and fatigue life (r=-0.95), respectively, in the bending analyses. The total reaction force was closely related to the pullout strength in pullout analyses (r=0.84 and 0.91 for different foam densities). CONCLUSIONS: Conical screws effectively increased the bending strength and pullout strength simultaneously. The finite element analyses reliably predicted the results of the mechanical tests.     

Analysis of genes encoding laminin β2 and related proteins in patients with Galloway–Mowat syndrome

Galloway-Mowat syndrome (GMS) is a rare autosomal recessive disorder characterized by early onset nephrotic syndrome and microcephaly with various anomalies of the central nervous system. GMS likely represents a heterogeneous group of disorders with hitherto unknown genetic etiology. The clinical phenotype to some extent overlaps that of Pierson syndrome (PS), which comprises congenital nephrotic syndrome and distinct ocular abnormalities but which may also include neurodevelopmental deficits and microcephaly. PS is caused by mutations of LAMB2, the gene encoding laminin beta2. We hypothesized that GMS might be allelic to PS or be caused by defects in proteins that interact with laminin beta2. In a cohort of 18 patients with GMS or a GMS-like phenotype we therefore analyzed the genes encoding laminin beta2 (LAMB2), laminin alpha5 (LAMA5), alpha3-integrin (ITGA3), beta1-integrin (ITGB1) and alpha-actinin-4 (ACTN4), but we failed to find causative mutations in these genes. We inferred that LAMA5, ITGA3, ITGB1, and ACTN4 are not directly involved in the pathogenesis of GMS. We excluded LAMB2 as a candidate gene for GMS. Further studies are required, including linkage analysis in families with GMS to identify genes underlying this disease.     

Inhibition of 11beta-hydroxysteroid dehydrogenase enzymatic activities by glycyrrhetinic acid in vivo supports direct glucocorticoid-mediated suppression of steroidogenesis in Leydig cells

Previous studies have suggested that glucocorticoid (GC) can directly affect testicular testosterone (T) biosynthesis by Leydig cells through a receptor-mediated mechanism. Interconversion of corticosterone (CORT), the active form in rodents, and 11-dehydroCORT, the biologically inert 11-keto form, is catalyzed by 11betaHSD1. This enzyme thus controls the intracellular concentration of active GC. We have postulated that elevated CORT levels resulting from stress exceed the Leydig cell's capacity for metabolic inactivation of CORT, resulting in suppressed T production. The present study tested whether inhibition of 11betaHSD1 in vivo, by the administration of glycyrrhetinic acid (GA), increases intracellular active GC concentration and thereby affects serum T concentration and Leydig cell T production. Adult Sprague-Dawley rats were treated with vehicle (corn oil), CORT, GA, or GA + CORT. Serum luteinizing hormone (LH), CORT, and T levels were measured, as were the steroidogenic capacities of purified Leydig cells. Twofold elevations of CORT were achieved by the administration of either CORT or GA alone, but in both cases there was no effect on serum T levels. However, when CORT and GA were administered in combination, serum CORT levels increased 3.5-fold (to 420 +/- 34 ng/mL) and serum T levels were reduced significantly (to 0.72 +/- 0.07 ng/mL; control, 2.12 +/- 0.23 ng/mL). Serum levels of LH were not affected by CORT, GA, or GA + CORT. Consistent with the reduced serum T levels following GA + CORT, steroidogenic enzyme expression and capacities were significantly reduced compared to control. These data support a role for 11betaHSD1 in modulating intracellular CORT concentrations and, in turn, for a direct effect of GC on Leydig cells in response to stress.     

Characterization of EGFP-labeled mesenchymal stem cells and redistribution of allogeneic cells after subcutaneous implantation

INTRODUCTION: Bone marrow mesenchymal stem cells (MSCs) are ideal target cells for cell transplantation and tissue engineering. We investigated their biological characteristics and differentiation mediated by different methods. It is important to study the short-term fate of labeled allogeneic MSCs after subcutaneous implantation in rabbits in order to provide insights into the application of allogeneic MSCs for tissue regeneration. MATERIALS AND METHODS: Mesenchymal stem cells were labeled by two different methods in vitro and then were incubated with gelatin sponge. Autologous MSCs-Gelatin constructs and allogeneic MSCs-Gelatin constructs were subcutaneously implanted into 32 rabbits. The constructs were analyzed for the survival and migration of labeled MSCs at day 3, week 1, 3, and 5 post-implantation. RESULTS: EGFP was successfully expressed following transfection of MSCs with the retroviral vector pLEGFP-N1. In addition, EGFP-MSCs can be functionally induced into osteocytes, chondrocytes, and adipocytes in conditioned media. By weeks 3 after implantation, the labeled cells distributed extensively on the surface of gelatin sponge and gradually integrated into host tissues. EGFP-labeled MSCs were observed under fluorescence microscopy and BrdU-expressing cells were detected with immunohistochemical stain in allogeneic or autologous MSCs-Gelatin constructs during the initial five weeks after implantation. CONCLUSIONS: It is a simple and reliable way to trace the changes of MSCs in vivo by EGFP in cell transplantation and gene therapy. Allogeneic rabbit MSCs can survive for at least 5 weeks after subcutaneous implantation and maintain a strong ability of migration, indicating that allogeneic MSCs are of certain value in clinical application for temporary replacement.     

The reaction of posttransplant denervated liver on the hemorrhagic shock in rats

OBJECTIVE: The aims of the study were to determine the effects of denervation on the function of the liver transplantation as a blood reservoir and to define its vulnerability to ischemic-reperfusion (I/R) injury after hemorrhagic shock. MATERIALS AND METHODS: Hemorrhagic shock with a mean arterial blood pressure (MAP) of 40 to 50 mm Hg was induced by withdrawing blood at a rate of approximately 1 mL/min among 10 posttransplant denervated rats and 10 sham rats for 1 hour. The rats were then resuscitated by retransfusing the drawn blood with sacrifice under deep anesthesia at 1 hour after resuscitation. The total amount of blood required to achieve hemorrhagic shock was compared between groups as well as the vulnerability and reactions of the posttransplant denervated liver to I/R injury after hemorrhagic shock as assessed by gene expressions of c-jun, c-fos, tumor necrosis factor (TNF)-alpha, interleukin (IL)6, IL-10, and heat-shock protein 70 (HSP70). RESULTS: The volume of blood that had to be drawn to reach a MAP of 40 to 50 mm Hg was not significantly different between the groups. One hour of hemorrhagic shock followed by resuscitation resulted in significant increases in the genes expression of c-fos, TNF-alpha, IL-6, IL-10, and HSP70 in comparison to the control values, but no difference was observed between experimental and sham groups. CONCLUSION: We suggest that the function of the liver as a blood reservoir and the gene expressions of c-fos and pro- and anti-inflammatory cytokines, as well as the protective protein HSP70 in response to I/R injury, were not altered by liver transplantation.     

用SSH方法构建BTCC患者尿脱落细胞差异表达基因的cDNA消减文库

目的:应用抑制性消减杂交(SSH)方法构建膀胱移行细胞癌(BTCC)患者与正常人尿脱落细胞差异表达基因cDNA消减文库。方法:分别从BTCC患者与正常人尿液中提取总mRNA,用SMART技术反转录成cDNA,经过HaeⅢ酶切后将BTCC尿脱落细胞cDNA分为两组并接上接头,再与过量正常膀胱尿脱落细胞cD-NA进行两轮消减杂交及两轮抑制性聚合酶链反应(PCR),使得差异表达的DNA片段得以富集。PCR产物与T/A载体连接并转化大肠杆菌JM109构建成差异表达基因的cDNA消减文库。文库扩增后,随机挑取克隆进行酶切、测序及同源性分析。结果:PCR鉴定有317个克隆载有主要在200～900bp之间呈随机分布的插入片段,片段插入率达82.6%,证实建库成功。对20个质粒测序结果经同源性比对分析,其中20个片段源于17个已知基因,1个克隆在GenBank中未检索到与其有相似性的基因序列,表明它们可能为BTCC差异表达的新基因。结论:该消减杂交文库质量可靠,其成功构建为进一步筛选、克隆BTCC差异表达基因提供了依据。     

食管贲门癌患者术后早期肠内营养中输液增温器的应用

目的 观察输液增温嚣加温营养液对食管贲门癌患者术后早期肠内营养后胃肠功能的影响.方法 将104例食管贲门癌根治术后早期应用肠内营养支持的患者分为对照组(53例)和观察组(51例),对照组进行肠内营养时按常规经营养管输注营养液,观察组进行肠内营养时采用输液增温器对营养液予持续恒定加温,观察术后胃肠功能恢复情况和相关胃肠道并发症发生情况.结果 观察组术后首次肛门排气时间、首次排便时间较对照组显著提前(均P＜0.01),术后腹胀发生率减少(P＜0.05).结论 输注营养液时应用输液增温器予持续恒定加温,增温效果确切稳定,减少了因营养液温度不适造成的胃肠道反应,有利于促进胃肠功能.     

Inducible nitric oxide synthase expressions in different lung injury models and the protective effect of aminoguanidine

OBJECTIVE: Our aim was to study the expression of inducible nitric oxide synthase (iNOS) in 2 experimental models: (1) ischemia/reperfusion (I/R) of the lung tissues and (2) oleic acid infusion. The protective effect of an iNOS inhibitor, aminoguanidine, was evaluated in these 2 injury models. MATERIALS AND METHODS: Real-time polymerase chain reactions and Western blots were used to assess the mRNA and protein expressions of iNOS in lung tissues after applying 2 injury models. In the I/R model, ischemia was induced by clamping one branch of the pulmonary artery for 60 minutes and then reperfusing for 120 minutes. In the bone fracture model, lung injury was induced by intravenous (IV) infusion of oleic acid (0.1 mL/kg); analysis was performed 6 hours after injury. Blood samples were collected for the assay of 3 inflammatory parameters: tumor necrosis factor alpha, hydroxyl radicals, and nitric oxide (NO). The wet/dry lung weight ratio was used as a parameter reflecting the lung injury level. RESULTS: mRNA and protein expressions of iNOS were significantly increased in these 2 lung injury models compared with the controls. Blood concentrations of TNFalpha, hydroxyl radicals, NO, and wet/dry lung weight ratio were also significantly higher in the 2 experimental groups than in the sham-treated group. The iNOS inhibitor aminoguanidine (20 mg/kg) significantly attenuated the lung injury induced by these challenges. CONCLUSIONS: Reperfusion of the ischemic lung tissues or IV infusion of oleic acid can both induce lung injury by activating systemic inflammatory responses and inducing iNOS expression. Administration of aminoguanidine can significantly attenuate the injury, suggesting that iNOS expression may play a critical role in the lung injury induced in these 2 models.     

经皮激光椎间盘减压术治疗颈椎椎间盘突出症

颈椎椎间盘突出症是以颈肩痛、四肢乏力、行走不稳，或头痛及眩晕为一组症状的疾病，经皮激光椎间盘减压术（percutaneous laser disc decompression，PLDD）是椎间盘突出症的微创治疗方法，1986年美国的Choy及德国的Ascher首先将该方法应用到临床，现将2000年11月至2008年1月收治的231例用PLDD方法治疗的经验总结如下。     

白血病导致的阴茎异常勃起11例诊治

目的探讨自血病相关阴茎异常勃起的诊疗特点及预后。方法回顾性分析1992年2月至2005年1月我院11例白血病相关阴茎异常勃起患者的临床资料及随访记录。结果本组。11例均为慢性粒细胞白血病（CML）。年龄18～56岁，平均23岁。阴茎异常勃起均为低流量型，持续勃起时间8～72h，平均25．3h。11例经治疗后异常勃起均获缓解，其中非手术治疗4例，手术治疗7例，术后阴茎完全恢复疲软时间0H5d，平均2．8d。8例随访时间3～20个月，平均14．7个月，3例失随访。6例于术后7d～5月恢复勃起功能，平均26d，其中2例持续勃起≤12h，3例为13~24h，1例为25～48h。2例术后出现勃起功能障碍，其中1例持续勃起25～48h，1例〉48h。结论白血病导致的阴茎异常勃起以血液动力学分类主要为缺血型，为了避免阴茎缺血坏死及继发阴茎勃起障碍，应该尽可能地在24h内采取包括外科处理、化疗及血细胞分离等有效手段解除病理性勃起状态。