后成质的

Results It was demonstrated that β-TrCP expressed in oral epithelium, tooth bud, mesenchymal cell cytoplasm of ameloblast and edontoblast of different stage of tooth development.

结果β-TrCP在胚胎10.5、13.5、14.5、16.5、18.5d的小鼠牙胚上皮层与间充质层，以及出生后0、3、6d的小鼠成釉细胞与成牙本质细胞胞浆呈特征性表达。

When scales are proposed by nutrition solution, the information of bulblet is very regular: information of bulblet is almost located in inside 1—2mm of wound, the root is formed below of bulblet.

营养液浸种鳞片，小子球的分化很有规律性，据试验观察，小子球发生大都在伤口腹内侧1—2mm处，在沿切口呈线状排列，腹外侧和愈伤组织处只占1%左右，小子球形成后多在其下部生根；而一般基质无菌水培养的多先在鳞片下部生根，后形成小子球，即较前者推迟一周。

The histopathologic observations of corneas after penetrating keratoplasty in dogs: Thestructure of wholly transparent graft was the same as that of host cornea apart from the upperdonor-host junction where there was minimal irregularity of the corneal lamellae. However, thecorneal lamellae at the lower donor-host junction were neat. The graft with its central part beingtransparent only showed poor coaptation with recipient, in which the graft shifted inward and had marked wrinkles and folds in Descemet"s membrane. On the back of Descemet"s membranethere was hyperplastic stromal fibers that thickened the graft and partially adhered to iris.

5犬穿透性角膜移植术后角膜病理组织学观察完全透明的植片与植床结构一致，仅两者对合处上部纤维紊乱，而下方纤维排列整齐；中央透明的植片与植床对合不良，植片向植床方向嵌入，后弹力层皱缩、折叠，植片下方因有来自植床的基质纤维而增厚，部分对合处与虹膜粘连；浑浊的植片有比较完整的上皮层，植片约2／3深度的基质丧失原来纤维整齐排列结构，代以大量成纤维细胞增生。

A549 cells are more sensitive to CDDP-induced apoptosis(P.01) and less sensitive to THP andβ-Ele-induced apoptosis than A375p(P.01, P.05 respectively). Condensation and crack of nucleus and apoptotic bodies appeared in apoptotic cells of A549 and A375p cell lines in all treated groups and necrocytosis were to be seen in some groups. Fluorescence imaging experiments demonstrated that accumulation of iASPP in cytoplasm but little distribution in nucleus in all groups. untreated groups in two cell lines presented a bright-green colour,followed by CDDP-treated groups,and THP-treated groups is the darkest one in all groups.

免疫荧光显示，未加药物处理的A549和A375p细胞胞质染色均匀呈亮绿色，核区较暗；CDDP及β-Ele处理组细胞为暗绿色，其中可见皱缩的凋亡细胞；THP处理的细胞胞质荧光弱呈灰绿色，由于THP嵌入DNA自发红色荧光与二抗的绿色荧光中和，胞核被染成桔红色，结果提示药物处理后A549和A375p细胞中iASPP的表达有不同程度的下降。

Rat glioma cell C6 was infected by the deficiency recombinant retrovirus (named C6TK). The sensitivity of C6TK cells to GCV or ACV increased 450 or 10 times than that of C6 cells respectively. Rat C6 glioma model was successfully built, and SD rats inoculated intracerebrally C6TK cells had normal gliomas. The average survival periods of the rats were about 15 days. However, after treated with ACV, the growth of C6TK tumors obviously regressed, and the survival periods extended to 57.8±8.1 days, especially in rats injected with mixed PA317TK and C6 cells or in situ PA317TK cells, which the tumors nearly disappeared after ACV administration and the survival periods extended to over 120 or 71.4±36.1 days respectively, P＜0.001.

结果：构建了带有HSV-tk基因的反转录病毒载体GINaTK，应用脂质体转移方法将GINaTK导入反转录病毒包装细胞PA317，成为产病毒细胞PA317TK，用带有HSV-tk基因的复制缺陷型反转录病毒感染C6细胞，命名为C6TK细胞，对GCV和ACV的敏感性分别高于亲本450倍和10倍；成功地建立了大鼠脑胶质瘤模型，并证实转染细胞C6TK的成瘤效应未改变，存活期约为15天；而经ACV治疗后，含有C6TK细胞的肿瘤生长明显被抑制，大鼠生存期延长为57.8±8.07天，尤其是采用PA317TK细胞混和治疗组和原位治疗组，肿瘤基本消失，大鼠生存期显著延长，混和治疗组存活120天以上，原位治疗组存活至71.4±36.1天。t检验，P值均小于0.001。

Results: GINaTK retroviral vector containing HSV-tk was constructed and transduced into PA317 retrovirus packaging cell by lipofectin (named PA317TK). Rat glioma cell C6 was infected by the deficiency recombinant retrovirus (named C6TK). The sensitivity of C6TK cells to GCV or ACV increased 450 or 10 times than that of C6 cells respectively. Rat C6 glioma model was successfully built, and SD rats inoculated intracerebrally C6TK cells had normal gliomas. The average survival periods of the rats were about 15 days. However, after treated with ACV, the growth of C6TK tumors obviously regressed, and the survival periods extended to 57.8±8.1 days, especially in rats injected with mixed PA317TK and C6 cells or in situ PA317TK cells, which the tumors nearly disappeared after ACV administration and the survival periods extended to over 120 or 71.4±36.1 days respectively, P ＜0.001.

结果：构建了带有HSV-tk基因的反转录病毒载体GINaTK，应用脂质体转移方法将GINaTK导入反转录病毒包装细胞PA317，成为产病毒细胞PA317TK，用带有HSV-tk基因的复制缺陷型反转录病毒感染C6细胞，命名为C6TK细胞，对GCV和ACV的敏感性分别高于亲本450倍和10倍；成功地建立了大鼠脑胶质瘤模型，并证实转染细胞C6TK的成瘤效应未改变，存活期约为15天；而经ACV治疗后，含有C6TK细胞的肿瘤生长明显被抑制，大鼠生存期延长为57.8±8.07天，尤其是采用PA317TK细胞混和治疗组和原位治疗组，肿瘤基本消失，大鼠生存期显著延长，混和治疗组存活120天以上，原位治疗组存活至71.4±36.1天。t检验，P值均小于0.001。

Results:(1)NSCs form typical neurospheres under adequate concentration in vitro, which are immunoreactive to Vimentin. Typically and terminally differentiated mature neural cells could not be found without the stimulus of mitogen or only under NSCs self-regulation and self-induction;(2)NSCs derived from hippocampus maintain the character of stem cells much longer with better biological behavior; NSCs passed to the 2-3 passage are the best to graft since they have not differentiated;(3)NSCs cultured in vitro could self-regulate and differentiate into neurospheres and progenitors positively immunoreactive to specific antibodies representing neurons, astrocytes, oligodendrocytes and Schwann cells;(4)There are widespread synaptic contacts between various kinds of descendent clones and cells;(5)Neurospheres could be formed without the stimulus of mitogen when NSCs and OECs are cocultured. Many neurospheres and cells immunoreactive to Vimentin, GFAP, MAP2, 02, p75NGFR, GFAP, S-100, Synaptosis, Vimentin, Tau (Tau is only positive in cocultureof HNSCs+HOECs) could be found;(6)The supernatant fluid triturated from adult rat spinal cord stimulates NSCs to differentiate into neurons, but do not terminally differentiate;(7)Fibroblasts and O4 oligodendrocytes are not supported to grow under this culture medium.Part II: Isolation, culture and identification of rat and human olfactory ensheathing cellsOlfactory ensheathing cells/glials are the most powerful cells to enable the regeneration of axons in the central nervous system.

结果表明：①在适宜的浓度体外培养条件下，NSCs能形成典型的神经干细胞克隆球，Vimentin免疫荧光染色阳性，单靠丝裂原刺激或NSCs自我调节和分化诱导，不会产生典型的终末分化的成熟神经细胞；②海马源性的NSCs维持干细胞特性的时间更长，生物学特性更优；③传至第2～3代的NSCs尚未分化时移植最佳；④体外培养的NSCs能自我调控分化为神经元、星形胶质细胞、O2少突胶质细胞、雪旺氏细胞染色阳性克隆球和前体细胞；⑤各种子代克隆球和细胞存在广泛的突触联系；⑥NSCs与OECs联合培养时，不需丝裂原刺激即能形成克隆球，获得大量Vimentin、GFAP、MAP2、O2、p75NGFR、GFAP、S-100、Synaptosis、Vimentin、Tau(Tau只有人HNSCs+HOECs联合培养时出现阳染)染色阳性的克隆球和细胞；⑦脊髓研磨后的上清液刺激神经干细胞向神经元方向分化，但并不出现终末分化；⑧本研究培养条件不利于成纤维细胞、O4生长。

After osteoplastic induction, peripheral blood MSCs had strongly positive reactions for alkaline phosphatase staining, total collagen staining, alizarin red staining.

外周血间充质干细胞成骨诱导后，碱性磷酸酶染色、总胶原染色及茜素红染色均呈强阳性；成脂诱导后油红染色呈阳性，有一定数量的脂滴形成。

The SPECT imaging of ~(99)Tc~m-GEBP11 can show the tumor mass clearly and ~(131)I-GEBP11 has anti-tumor effect with weak toxicant and secondary effect, which is the foundation for them to develop nuclide probe or radiotherapeutics drugs targeting to tumor vasculature.3. GEBP11 can inhibit angiogenesis, which comes true probably through its inhibition effects on the proliferation, invasion, migration and adherence of ECs.

1、GEBP11具有活体内胃癌血管靶向结合的能力，它与胃癌血管内皮细胞膜受体特异结合后可被内化。2、~(99)Tc~m-GEBP11 SPECT成像能较好地显示体内肿瘤灶，~(131)I-GEBP11具有明显的抗肿瘤效应及较弱的毒副作用，为开发肿瘤血管成像核素探针及受体放射治疗新药奠定了基础。3、GEBP11具有抑制胃癌血管生成的作用，这可能通过抑制ECs增殖、基质降解及迁移、粘附能力实现。

Nerve and ligament tissues could be clearly observed from light and soft patch, and this might and prevent hurt by mistake, improve repairing operability, enhance correct putting of patch, and decrease incidence of pain.

超薄轻质补片更柔软、更透明、操作容易，透过网片能清楚地观察到网片后方的神经和韧带等组织，可预防误伤，提高了修补中的易操作性，并且便于网片的正确放置，减少了修补后疼痛的发生率，而且网片的结构更有利于成纤维组织的长入，能很好地适应患者修补后因体位变动和肌肉收缩而产生的纵向和横向移动，患者修补后的不适感也极大地降低等优点。

The split between the two groups can hardly be papered over.

这两个团体间的分歧难以掩饰。

This approach not only encourages a greater number of responses, but minimizes the likelihood of stale groupthink.

这种做法不仅鼓励了更多的反应，而且减少跟风的可能性。