组织工程心脏瓣膜研究进展

目前组织工程心脏瓣膜研究已在支架的选材、种子细胞的选择、种子细胞的种植与瓣膜构建方法三个方面取得进展，并已构建出三种代表性组织工程心脏瓣膜。对它们各自的特点进行综述。     

体外血栓形成机理的实验研究

血栓形成与流体力学因素关系密切，用健康成人血样进行的实验表明，Chandler血栓环内血液呈现出三维流动和二次流动状态，在管壁处的剪切应力最大。体外血栓形成应考虑血栓环弯曲和内部血液回流因素。血栓环内下弯月面处血栓的形成可能是流速相对较高的流体元冲击下弯月面导致血小板和红细胞聚集所至。当血栓环旋转时间低于10min时，血栓形成不良。15min是血栓形成的最佳时间。转速为3．75rpm时，不能形成血栓。     

In Situ Thermal Denaturation of Proteins in Dunning AT-1 Prostate Cancer Cells: Implication for Hyperthermic Cell Injury

The in situ thermal protein denaturation and its correlation with direct hyperthermic cell injury in Dunning AT-1 prostate tumor cells were investigated in this study. The in situ thermal protein denaturation was studied using both Fourier transform infrared spectroscopy (FTIR) and differential scanning calorimetry (DSC). The FTIR spectra at different temperatures show changes in protein secondary structure (from alpha helix to extended beta sheet) during in situ thermal protein denaturation within AT-1 cells. Calorimetric studies using DSC show that endothermic heat release is associated with the in situ thermal protein denaturation. Furthermore, both the secondary structure changes detected by FTIR and the calorimetric changes detected by DSC were quantified and the kinetics of the overall in situ thermal protein denaturation was derived under different heating conditions. The onset temperature where the overall in situ thermal protein denaturation is first detectable was found to be scanning rate dependent (approximately 41 degrees C at 2 degrees C min(-1) and approximately 44 degrees C at 5 degrees C min(-1)). The kinetics of the overall in situ thermal protein denaturation was derived from both DSC and FTIR measurements and was fit using kinetic and statistical models. The kinetic data determined by FTIR and DSC under the same heating conditions match well with each other. The activation energy of the overall in situ thermal protein denaturation is found to be strongly dependent on the temperature range considered (the activation energy ranges from approximately 110 kJ mol(-1) between 44 and 90 degrees C to approximately 750 kJ mol(-1) between 44 and 50 degrees C). However, its dependence on heating rate is negligible. Several denaturation peaks, including a dominant one between approximately 62 and 65 degrees C, are identifiable from both the DSC and the FTIR results. To investigate directly the relationship between thermally induced cell injury and the in situ thermal protein denaturation, both acute (propidium iodide dye exclusion, assessed 3-h postthermal treatment) and chronic (clonogenics, assessed 7-day postthermal treatment) cell injury were quantified using AT-1 cells prepared under the same conditions as for the DSC protein studies. Comparisons of the results from the cell injury studies and the DSC protein denaturation studies show that the overall in situ thermal protein denaturation correlates well with both the acute and the chronic cell injury, which suggests that overall in situ thermal protein denaturation is an important mechanism of direct hyperthermic cell injury in AT-1 cells at the macromolecular level.     

山莨菪碱对家兔动脉粥样硬化的抑制作用

用65只日本兔喂高脂饲料,观察山莨菪碱对动脉粥样硬化形成的作用及其有关检测指标的影响。结果表明,山莨菪碱组主动脉内膜粥样硬化斑块面积、胆固醇含量、内膜通透性及血液TC、LDL-C、TG、LPO、TXA_2、5-HT、Pt聚集力,血液流变学等,均显著降低;PGI_2及SOD增高;组织光镜及电镜改变减轻。说明山茛菪碱对动脉粥样硬化的形成有显著抑制作用。     

经颅磁刺激安全性的实验研究

目的 :探讨重复经颅磁刺激的安全性。方法 :选用 3 6只健康Wistar大鼠 ,随机分为对照组 ,低频刺激组和高频刺激组 ,对低频组和高频组分别给予不同频率和强度的经颅磁刺激 ,然后对各组大鼠的行为、组织病理形态学、血清髓鞘碱性蛋白 (MBP)及神经元特异性烯醇化酶 (NSE)含量进行观察。结果 :低频刺激组 (5Hz)和高频刺激组 (2 0Hz)在刺激过程中均未出现异常活动 ,无肢体强直、阵挛等 ,脑组织形态学包括大体观察、普通光镜及电镜改变不明显 ,其血清MBP和NSE含量与正常对照组比较 ,差异无显著性意义 (P >0 0 5 )。结论 :在一定强度和频率内经颅磁刺激是一种比较安全的方法     

颞下颌关节与颅面指标的计算机相关及回归分析

本文用计算机分析统计了118例(236侧)颞下颌关节的12项骨性指标及10项颅面指标的正常值及相关关系。结果表明颞下颌关节各项指标之间、颞下颌关节与颅面各主要指标之间,均存在良好的相关关系。说明颞下颌关节,特别是关节窝和髁突的形态大小具有明显的规律性。由于颅面诸指标与颞下颌关节主要指标之间高度相关,因而本文用逐步回归方法,建立了由颅面特征指标推算髁突形态的回归方程。本文的结果可为该关节的形态研究及人工关节的设计和应用提供有益的依据。     

胎儿消化器官发育中的肥大细胞超微结构特点

实验对１０例不同胎龄肥儿消化器官的胎大细胞进行了超微结构观察，发现胎儿发育接近成熟时，其肥大细胞根据颗粒的超微结构可分ＴＣ肥大细胞和Ｔ肥大细胞两型；胎儿发育后期以大细胞有分泌活动呈活化状态；胎儿肥大细胞与成纤维细胞，上皮细胞，血管，神经等密切接触。     

雌激素对卵巢摘除大鼠心内神经节细胞Bcl-2和Bax表达的影响

本实验建立了去卵巢和雌激素替代疗法动物模型,用免疫组织化学SABC法结合图象分析方法,观察大鼠心内神经节细胞中Bcl-2和Bax的变化,探讨雌激素对卵巢摘除大鼠心内神经节细胞中Bcl-2和Bax表达的影响。去卵巢(OVX)大鼠心内神经节细胞中Bcl-2的表达较正常对照组明显减弱(P<0.05),雌激素替代治疗组大鼠心内神经节中Bcl-2的表达与正常对照组相比无显著性差异(P>0.05),而较卵巢摘除组显著增高(P<0.05);卵巢摘除后同时给予特异性雌激素受体阻断剂(TAM)和17β-雌二醇(OVX+TAM+ERT)组大鼠心内神经节中Bcl-2的表达较正常对照组显著减弱(P<0.05),但与OVX组无显著性差异(P>.05)。各组中Bax的表达无显著性差异(P>0.05)。实验结果提示雌激素能上调大鼠心内神经节细胞中Bcl-2的表达,但对Bax的表达无影响。     

RNA-binding protein is involved in aggregation of light neurofilament protein and is implicated in the pathogenesis of motor neuron degeneration

Abnormal protein aggregation is emerging as a common theme in the pathogenesis of neurodegenerative disease. Our previous studies have shown that overexpression of untranslated light neurofilament (NF-L) RNA causes motor neuron degeneration in transgenic mice, leads to accumulation of ubiquitinated aggregates in degenerating cultured motor neurons and triggers aggregation of NF-L protein and co-aggregation of mutant SOD1 protein in neuronal cells. Here, we report that p190RhoGEF, an RNA-binding protein that binds to a destabilizing element in NF-L mRNA, is involved in aggregation of NF-L protein and is implicated in the pathogenesis of motor neuron degeneration. We show that p190RhoGEF co-aggregates with unassembled NF-L protein and that co-aggregation is associated with down-regulation of parent NF-L mRNA in neuronal cells. Co-expression of NF-M increases NF assembly and reduces RNA-triggered aggregation as well as loss of solubility of NF-L protein. siRNA-induced down-regulation of p190RhoGEF not only reduces aggregation and promotes assembly of NF-L and NF-M, but also causes reversal of aggregation and recovery of NF assembly in transfected cells. Examination of transgenic models of motor neuron disease shows that prominent aggregates of p190RhoGEF and NF-L and down-regulation of NF-L expression occur in degenerating motor neurons of mice expressing untranslated NF-L RNA or a G93A mutant SOD1 transgene. Moreover, aggregates of p190RhoGEF and NF-L appear as early pathological changes in presymptomatic G93A mutant SOD1 transgenic mice. Together, the findings indicate that p190RhoGEF is involved in aggregation of NF-L protein and support a working hypothesis that aggregation of p190RhoGEF and NF-L is an upstream event triggering neurotoxicity in motor neuron disease.