骨髓基质细胞和内皮细胞联合种植构建组织工程化骨的初步研究

为阐明骨髓基质细胞和内皮细胞联合种植在生物复合材料上构建组织工程化骨 ,在促进成骨过程、加速局部血管生成中的作用 ,将大鼠骨髓基质细胞和人脐静脉内皮细胞联合种植在左旋聚乳酸 /β-磷酸三钙 (PL L A/β- TCP)多孔复合支架材料上作为实验组 ,仅种植骨髓基质细胞在该材料上作为对照组。将此种有活细胞的复合材料种植于裸鼠大腿后侧肌袋内 ,分别于种植后 1、4、8、12、16周处死动物 ,取出复合材料 ,行组织学检测 ,并用图像处理技术计算实验组和对照组的成骨面积百分比和材料面积百分比 ,观察其变化规律。结果显示 :实验组成骨面积百分比增加比对照组明显加快 ,而材料面积百分比减少比对照组迅速 ;其内毛细血管网形成情况也要明显优于对照组。表明骨髓基质细胞和内皮细胞联合种植于支架材料构建组织工程化骨不仅有利于成骨作用 ,促进新生骨区内部血管网形成 ,还有利于复合材料的降解吸收 ,这在构造组织工程化骨过程中具有重要意义。     

Th1 memory: implications for vaccine development

Summary: T‐helper 1 (Th1) cells play a critical role, via interferon‐γ (IFN‐γ) production, in mediating intracellular killing against a variety of infectious pathogens. Thus, understanding the regulation of Th1 responses could provide better insight into vaccine design for infections requiring Th1 immunity. The cellular and molecular mechanisms that control the induction of Th1 effector cells have been well characterized. More recently, there has been substantial progress in furthering our understanding of the factors that regulate the development of Th1 memory cells. It is clear that Th1 responses are functionally heterogeneous, as defined by their ability to produce IFN‐γ. Furthermore, this heterogeneity has profound implications for the capacity of distinct lineages of Th1 cells to develop into memory cells. This review emphasizes the mechanisms controlling the differentiation of naïve CD4⁺ T cells into effector and then memory cells in a progressive manner. It highlights the importance of IFN‐γ as a positive regulator for inducing Th1 responses but a negative regulator for sustaining Th1 effector cells. In conclusion, we discuss how this current understanding of Th1 differentiation will inform vaccine design and better define immune correlates of protection.     

Enhanced osteoinduction by intramuscular grafting of BMP-beta-TCP compound pellets into murine models.

The osteoinductive effects of bone morphogenetic protein (BMP, derived from murine osteosarcoma) were studied with regard to its use combined with beta-tricalcium phosphate (beta-TCP). BMP and beta-TCP were molded into pellets by the "pressure method", originated by us and transplanted to ddY mice. Control mice received interdorsal muscular implantations of either the BMP or beta-TCP pellets. The animals were sacrificed 1, 2 and 3 weeks after grafting, for radiological, histochemical, and ultrastructural observations. The BMP-beta-TCP compound pellets induced faster cartilage and bone formation, whereas these activities were slower when pellets made solely of BMP were used. The beta-TCP pellets demonstrated no osteoinductive properties. Observations revealed two types of beta-TCP resorbing multinuclear giant cells. One was osteoclastic, expressing calcitonin receptors, having numerous mitochondria and ruffled border-like structures; the other was not osteoclastic in nature. In animals grafted with the compound pellets, a great number of osteoclastic cells gathered on the pellets, much earlier than those grafted with the pellets made of BMP alone. Then, osteoblastic bone formation over the cement lines followed an osteoclastic resorption of both beta-TCP and newly formed bone. In contrast, BMP induced few osteoclastic cells, resulting in slower bone coupling. Furthermore, the faster bone formation induced by the compound pellets seemed to be associated with the presence of beta-TCP. Porous by nature, beta-TCP would entrap BMP within its micropores, and thus, the intrinsically diffusible BMP is retained and its action consequently prolonged. In addition, the compound pellet offered increased surface contact between BMP and mesenchymal cells. Therefore, BMP-beta-TCP compound pellets induce cartilage and bone formation more rapidly than does BMP alone.     

亚低温减少大鼠短暂性全脑缺血后皮质iNOS诱导的神经元凋亡

为研究亚低温对大鼠脑缺血再灌注后皮质iNOS表达、NO产生及神经元凋亡的影响及探讨亚低温的神经保护机制,用大鼠短暂全脑缺血模型,采用Nissl染色观察存活神经元、免疫组化法检测iNOS、硝酸还原酶法检测NOx-水平和TUNEL染色结合电子显微镜观察检测凋亡神经元。结果显示:常温缺血组额叶皮质iNOS表达、NOx-水平增高,出现凋亡神经元;低温缺血组iNOS表达、NOx-水平明显低于常温缺血组,未检测到凋亡神经元。上述结果提示,脑缺血后iNOS来源的NO参与了神经元的凋亡过程,亚低温可减少大鼠短暂性全脑缺血后iNOS诱导的神经元凋亡。     

特殊类型的小儿变态反应性亚败血症

变态反应性亚败血症(SA)是一种少见疾病，临床表现复杂多样，其基本特征是：①长期反复的弛张热：②一过性皮疹；⑧关节肿痛；④血培养阴性；①对抗生素治疗无效而对激素有反应．本文介绍SA几种特殊的临床峩现，包括：突出的中枢神经系境症状．大量的心包积掖，变应性血管炎，血液系境表现为骨髓增生异常综合征(MDS)并最终转变为白血病．等等，这些特殊的表现极为罕见，但它们一且成为突出的临床特征．本病的诊断将变得十分困难认识这些特殊的表现，对正确毋断本病具有较大价值的。本文就这具有特殊表现的SA的临床特征和诊断进行分析和探讨。     

海绵质骨螺旋钉拔出试验之生物力学分析

评估螺旋钉设计优劣的简便方法之一为拔出试验。虽然比较用之海绵质骨试件可取自相同部位，自同一方向植入螺旋钉，并具有相同基准。然而因各处海绵质骨骼结构不尽相同，至今尚未有人探讨如使用不同之海绵质骨结构，例如近似等向性之杆状结构，或是板与杆组合之有强列方向排列者，对于螺旋钉拔出之最大力量有多大影响？采用牛股骨远端部位及牛颈椎Ｃ２～Ｃ６作为不同结构特性之试体。并各由两相互垂直之方向旋入螺旋钉，来做拔出试验。最后并建立一三维有限元素模型，用以研究螺纹周围之变形模式及其预测拔出最大力量的准确性。模型分析中以应变能密度准则作为破坏之参考标准。     

TNF与急性早幼粒细胞白血病

１６例急性早幼粒细胞白自病患者血清ＴＮＦ活性明显高于正常对照（Ｐ＜０．０５），而经ＲＡ诱导分化治疗中期及治疗后明显降低（Ｐ＜０．０５），但仍高于正常对照组。各治疗时相的外周白细胞浆内ＴＮＦ平均水平及正常对照间均无明显差别（Ｐ＞０．０５），治疗前及治疗中期胞浆ＴＮＦ活性升高率明显高于治疗后或正常对照（Ｐ＜０．０５）。相关分析表明：血清ＴＮＦ活性水平与外周血ＷＢＣ总数或骨髓ＧＭ－ＣＦＵ无明显相关，而与     

化解冲剂对脓毒症大鼠神经肽及细胞因子的调节作用

为阐明传统中医学整体观与现代医学神经内分泌免疫网络学说的一致性。建立了大鼠用人感染模型；动态观察了脓毒症大鼠血浆中β－内啡肽、精氨酸加压素及血管活性肠肽的变化；同时观察了血中单个核细胞分泌肿瘤坏死因子α及白细胞介素６能力的改变；并观察了活化瘀代表方剂“化解冲剂”对上述改变的调节作用。     

HLA中部区域多态性反映单体型遗传保守性

对２８个代表１２种不同的ＨＬＡ单体型的细胞株同时进行Ｃ４、ＣＹＰ２１、ＢＡＴ３的ＲＦＬＰ检测，观察到了７种不同的Ｃ４－ＣＹＰ２１－ＢＡＴ３的ＲＦＬＰ结构形式。结果显示：Ｃ４－ＣＹＰ２１－ＢＡＴ３基因结构具有高度的多态性，且具有祖传单体型性质和祖传单体型特异性性质。本项研究表明，ＨＬＡ祖传单体型在遗传与进化过程中是高度保守的。本文还对祖传单体型研究的意义及随机个体单体型分型的可能性进行了探讨。