粘细胞

The following methods were used in the study, such as viral inoculation of animal, pathological method, flow cytometry, RT-PCR, in situ hybridization, immunohistochemistry and terminal deoxy nucleotidyl transferase mediated dUTP nick end labling . Morphological changes of the infected chickling, dynamic changes of T, B cells and T subsets, changes of adhesion molecules on the lymphocyte surface, necrosis and apoptosis of lymphocyte and neurons, changes of MIP-1β and IL-8 producing cells in the brain, cell types of perivascular tuffing in cerebral tissue were systematically studied.

在研究过程中，采用了病毒接种技术、普通病理学研究方法、流式细胞仪技术、RT-PCR技术、原位杂交技术、免疫组化技术、凋亡细胞末端标记技术，系统研究了不同日龄的SPF雏鸡人工感染AEV-NH937株后的病理变化，T和B淋巴细胞、T淋巴细胞亚群的动态变化规律，淋巴细胞表面某些粘附分子的变化，淋巴细胞和神经元的坏死与凋亡，雏鸡脑组织中产生趋化因子MIP-1β和IL-8细胞的变化规律，脑组织中围官性细胞浸润的细胞类型。

The following methods were used in the study, such as viral inoculation of animal, pathological method, flow cytometry, RT-PCR, in situ hybridization, immunohistochemistry and terminal deoxy nucleotidyl transferase mediated dUTP nick end labling. Morphological changes of the infected chickling, dynamic changes of T, B cells and T subsets, changes of adhesion molecules on the lymphocyte surface, necrosis and apoptosis of lymphocyte and neurons, changes of MIP-1β and IL-8 producing cells in the brain, cell types of perivascular tuffing in cerebral tissue were systematically studied. The key research results were.(1)The average percentage of CD19+cell in blood, bursa and spleen, after 3, 5 days of inoculation, was significantly Phybridization revealed that the number of IL-8 and MIP-1βproducing cells was increased in the infected brain.

在研究过程中，采用了病毒接种技术、普通病理学研究方法、流式细胞仪技术、RT-PCR技术、原位杂交技术、免疫组化技术、凋亡细胞末端标记技术，系统研究了不同日龄的SPF雏鸡人工感染AEV-NH937株后的病理变化，T和B淋巴细胞、T淋巴细胞亚群的动态变化规律，淋巴细胞表面某些粘附分子的变化，淋巴细胞和神经元的坏死与凋亡，雏鸡脑组织中产生趋化因子MIP-1β和IL-8细胞的变化规律，脑组织中围官性细胞浸润的细胞类型。

According to the specialty of the structure,it may be predicted that the function of Kail gene come down to cell-cell adherence and cell-matrix connection.

结构分析提示它在细胞与细胞间粘附、细胞与基质的连接中可能起有一定作用，研究也证实它可以增强肿瘤细胞之间的聚集能力，降低其吞噬能力及侵袭能力，而不影响细胞的增殖力。

The results showed that cMSCs and EA.Hy926 endothelial cells could attach and proliferate on scaffold, and the cell did not appear obvious abnormity in morphology. So it was indicated that the scaffold could not disturb the biological behavior of cMSCs and EA.Hy926 endothelial cells. It also showed that cells in dynamic culture were growing more bloomingly and metabolizing more rapidly than those in static culture.

两组研究结果发现细胞能在支架材料上粘附、增殖，并且细胞形貌正常，说明材料的加入不影响细胞的生物学行为，同时发现，动态培养的细胞比静态培养的细胞生长旺盛，代谢快。

In PsNPV infected treatment, the color of the gland was purple-black dyed with eosin and the cells were distortedly squeezed together. The tracheae nearby showed grievous pathological changes and a lot of white granules deposited around it. The pathological changes in PsGV infected treatment showed another pattern. The gland body was relative small with smaller individual cells, most of which were red dyed with eosin. The cell limits were obscure.In coinfected treatment,there were few gland cells colorated by esoin.

结果表明，不同感染组粘虫前胸腺腺体都有不同程度的组织病变，PsNPV感染组在感染晚期与前胸腺相连的气管严重病变，出现大量白色颗粒状物累积，被伊红染成紫黑色，腺体细胞被挤压变形；PsGV感染组的前胸腺腺体变小，单个细胞也小，细胞界限不十分明显；两种病毒混合感染组的腺体细胞小，能被伊红染色的细胞极少。

PartⅡThe mechanism elucidation about effects ofα-(2,3)/(2,6)sialic acid on the Cx43gap-junction functions.(1) Westernblotting experiment showed that the decrease of sialic acid didn\'t changethe Cx43 expression and its phospholation level.(2) Westernblotting experiment showed sialidase didn,t change the ZO-1 expression,IP and confocal experiment showed sialidase improved the interaction of Cx43 andZO-1.(3) Westernblotting experiment showed sialidase didn\'t change N-cadherin expression,IP and confocal experiment showed sialidase promoted the complex formation ofCx43 and N-Cadherin.(4)Sialidase could increase the ERK1/2 phospholation level,and enchanedintercellular homotypic adhesion,Immunofluorometric assay showed sialidase couldpromote the N-cadherin cluster on the membrance.

第二部分：α—(2，3)／(2，6)唾液酸对肿瘤细胞CX43间隙连接功能影响的机制研究1、Westernblotting结果表明降低细胞膜表面唾液酸并不改变Cx43的表达及其磷酸化水平：但Cx43连接斑形成增多；2、Westernblotting结果表明唾液酸酶作用后细胞ZO—1表达没有改变，IP及免疫荧光共定位结果表明唾液酸酶作用后促进了Cx43与ZO-1的结合；3、Westernblotting结果表明唾液酸酶作用后细胞N-cadherin表达没有改变，IP及免疫荧光共定位结果表明唾液酸酶作用后促进了Cx43与N-Cadherin复合物的形成；4、唾液酸酶作用后细胞内ERK1／2磷酸化水平明显增加，细胞间同质粘附增加，以及免疫荧光表明唾液酸降低后可促进N-cadherin的膜成簇。

The proliferation stimulating effects on whole and nonadherent splenocytes of mice were assayed by MTT method; The cell cycles of whole splenocytes were tested with flow cytomytry.

通过MTT法测定小鼠全脾细胞或不粘附细胞的增殖活性，流式细胞仪检测小鼠全脾细胞的细胞周期。

One hand mechanical obstruct led to the increase of veinous resistance and the obstacle of microcirculation, the other hand the adhesive PMN was activated in excess, the white blood cells released a lot of enzymes, in which PMN-elastase can decompose the components of cell and many albumens, inclusive of immunoglobulin、alexin and fibrication. These components induced the injury of the pancreatic capillary vessels and cell and lysosome enzy made the tissue protein hydrolyze and produced unsaturated fatty acids, which destroyed the structure and function of cellar membrane. The inflammatory cellar factors activate other immunocytes to produce the injury and necrosis of tissue, which aggravated the pathological injury and led to shock、pyaemia and MODS. So ICAM-1 and LFA-1 played an important role in SAP. Frossard found that the expression of ICAM-1 in the rat model, especially in serum、pancreas and lung. All these showed ICAM-1 is an important factor in AP and concomitant lung injury.

胰腺小叶组织局部血管EC首先被激活，ICAM-1表达升高，与被激活的PMN表面表达的LFA-1相结合，&PMN-EC&相互作用加剧，一方面机械性阻塞毛细血管导致静脉阻力增加、微循环障碍；另一方面粘附的PMN过度吞噬或激活，当白细胞吞噬的颗粒不能被封闭隔离，连同细胞内的酶被释放出来，其中的PMN-elastase能够降解细胞基质中各种成分，水解多种蛋白，加重胰腺的毛细血管内皮细胞和腺泡的损伤；释放的溶酶体酶使组织蛋白水解，产生的不饱和脂肪酸引发脂质过氧化方应，破坏细胞膜的结构和功能；释放的炎性细胞因子，激发其他的免疫细胞的功能，导致进一步的组织损伤和坏死，加重SAP的病理损伤，最终导致休克、脓毒血症及多器官功能障碍等严重后果。

METHODS: The level of intracellular calcium of human microglia grown on coverslip,which was loaded by calcium-probe,Fluo-4,and then treated in various experimental processing,was detected by confocal microscopy with time resolution mode.The binding of gp120 to human microglia was determined with confocal microscopy or flow cytometry after treatment with gp120 and stained with anti-gp120-FITC antibody.Phosphorylation of ERK within human microglia with or without gp120 stimulation was analyzed with confocal microscopy following the direct immuno-staining with anti-phosphorylated ERK antibody.

用钙离子探针Fluo-4标记粘附在盖玻片上的人小胶质细胞，运用共聚焦显微镜以荧光强度为指标实时观察各种条件下的细胞内钙离子水平的变化；用gp120处理并用anti-gp120-FITC进行染色，运用共聚焦显微镜术和流式细胞术分析人小胶质细胞与gp120结合情况；用抗磷酸化ERK 抗体免疫荧光方法进行染色，运用共聚焦显微镜术和流式细胞术进行ERK磷酸化水平分析。

The two can cause ultrastructural pathogenesis widely in many organs and tissues such as hepar, pancreas, lien, ren, pulmo, cerebral, cerebellum, cor, muscular and so on, of them ,caused by i~olates YG97 and Y98 more obvious in epithelial cells of digestive tract and unobvious in epithelial cells of respiratory tract ,but ultrastructural pathogenesis caused by NDV strain F48E8 ,more obvious and more serious in glandularis and muscularis ventriaculi and in epithelial cells of respiratory tract .

将鹅源分离株YG_(97)、鸡源分离株Y_(98)和NDV强毒株F_(48)E_8感染SPF鸡，运用扫描电镜和透射电镜观察该二株病毒对机体细胞的影响，结果显示三株禽副粘病毒均引起机体肝、胰、脾、肾、肺、小脑、大脑、心和肌肉等实质器官组织细胞的超微病变，其中YG_(97)和Y_(98)引起消化道粘膜上皮细胞发生微绒毛脱落、纤毛脱落、分泌颗粒增多、细胞游离面破溃等显著的超微病变，引起气管粘膜上皮细胞的不显著超微病变；F_(48)E_8强毒株引起胃粘膜显著而严重的超微病变；还引起气管粘膜上皮严重的超微病变。

Plunder melds and run with this jewel!

掠夺melds和运行与此宝石！

My dream is to be a crazy growing tree and extend at the edge between the city and the forest.

此刻，也许正是在通往天国的路上，我体验着这白色的晕旋。