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。     

p63 deficiency activates a program of cellular senescence and leads to accelerated aging

The p53 tumor suppressor plays a key role in organismal aging. A cellular mechanism postulated to drive the aging process is cellular senescence, mediated in part by p53. Although senescent cells accumulate in elderly individuals, most studies have relied on correlating in vitro senescence assays with in vivo phenotypes of aging. Here, using two different mouse models in which the p53-related protein p63 is compromised, we demonstrate that cellular senescence and organismal aging are intimately linked and that these processes are mediated by p63 loss. We found that p63(+/-) mice have a shortened life span and display features of accelerated aging. Both germline and somatically induced p63 deficiency activates widespread cellular senescence with enhanced expression of senescent markers SA-beta-gal, PML, and p16(INK4a). Using an inducible tissue-specific p63 conditional model, we further show that p63 deficiency induces cellular senescence and causes accelerated aging phenotypes in the adult. Our results thus suggest a causative link between cellular senescence and aging in vivo, and demonstrate that p63 deficiency accelerates this process.     

一种测量视网膜锥体闪烁光ERG的改良方法：闪烁指数分析法

闪烁光ＥＲＧ是反映视网膜锥体活动的客观指标。但在诸如视网膜色素变性等一些视锥功能处于高度受累的疾病，反应波形呈现非窦状，使用以往在分析中采用的峰－峰值测量法，则不能有效地反应出波形所代表的真切含义。本文根据病理状态下闪烁光反应的波形特点，特此提出一项测量闪烁光ＥＲＧ振幅的改良方法，即闪烁指数（ｆｌｉｃｋｅｒｉｎｄｅｘｔ．ＦＩ）分析法，并通过数学方法推导出一项闪烁指数测量公式以代替方格卡尺测量法。应用本法已在实践中获得良好的验证，从而认为应用此项方法可以准确、客观、迅速地测量得锥体闪烁光的反应状态，特别是在对锥体功能呈病理状态的一些视网膜疾病的观测。通过计算机程序化处理，ＦＩ分析法可为临床视觉电生理研究提供一种有效的手段。