粘附的

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。

The method uses radiative immunity law to determine CV group, healthy group and content of the SIgA in taking secretion of bacterium group vagina, method of the conglutinate outside using system determines white beads bacterium is epithelial to the vagina (the conglutinate ability of VEC), the influence of VEC of conglutinate of white beads bacterium when observing SIgA standard.

方法采用放射免疫法测定CV组、健康组及带菌组阴道分泌物中sIgA含量，用体外粘附方法测定白念珠菌对阴道上皮细胞的粘附能力，观察sIgA水平时白念珠菌粘附VEC的影响。

Interestingly at l2h Cinnamylaldehyde could increase HUVEC adherence to THP-1.(5) At 4h and l2h Muscone decreased PMN-HUVEC adhesion, as well as inhibited ICAM-1, VCAM-1 and CD44 expression on TNF-primed HUVEC. But it markedly increased HUVEC adherence to THP-1 at 12h.

结果提示：黄芪多糖、川芎嗪、桂皮醛和麝香酮可以抑制PMN与HUVEC粘附并抑制HUVEC表面粘附分子的表达，桂皮醛和麝香酮能明显促进THP-1与HUVEC粘附。

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。

Results Salivary amylases can both enhance and competitively inhibit the adhesion of the strain to HA, while IgA degraded fragments and MW=13 000 protein only promote its adhesion.

结果 唾液IgA降解片段和相对分子质量为13 000的酸性蛋白仅促进变链粘附，唾液淀粉酶具有促进粘附及抗粘附双重作用。

P1 and a 117 000 surface protein of WD9463A both inhibit adhesion of the strain to IgA degraded fragments and salivary amylases.

结果 唾液IgA降解片段和相对分子质量为13 000的酸性蛋白仅促进变链粘附，唾液淀粉酶具有促进粘附及抗粘附双重作用。

Results:Berberine inhibited HUVEC adhesion for lymphocyte when pretreated HUVEC and antagonised IL-1 and TNF-induced upregulation of HUVEC adhesion for lymphocyte.Meanwhile,IL-1-stimulated lymphocyte adhesion to HUVEC was diminished in the presence of berberine.The main molecular mechanism of berberines function may be downregulating the expression of ICAM-1 on the HUVEC .

结果：小檗碱能抑制静息的及IL-1、TNF激活的内皮细胞与淋巴细胞间的粘附，其主要分子机制为下调内皮细胞表面粘附分子ICAM-1的表达；小檗碱能抑制IL-1激活的淋巴细胞与内皮细胞的粘附，对淋巴细胞表面粘附分子CD18的表达无影响。

Results:Berberine inhibited HUVEC adhesion for lymphocyte when pretreated HUVEC and antagonised IL-1 and TNF-induced upregulation of HUVEC adhesion for lymphocyte.Meanwhile,IL-1-stimulated lymphocyte adhesion to HUVEC was diminished in the presence of berberine.The main molecular mechanism of berberine's function may be downregulating the expression of ICAM-1 on the HUVEC .

结果：小檗碱能抑制静息的及IL-1、TNF激活的内皮细胞与淋巴细胞间的粘附，其主要分子机制为下调内皮细胞表面粘附分子ICAM-1的表达；小檗碱能抑制IL-1激活的淋巴细胞与内皮细胞的粘附，对淋巴细胞表面粘附分子CD18的表达无影响。

RESULTS:Berberine inhibited IL-1, TNF-induced HUVEC adhesion for PMN when pretreated HUVEC and antagonised IL-1, TNF-induced upregulation of ICAM-1 on HUVEC. Meanwhile, TNF-stimulated PMN adhesion for HUVEC and CD18 upexpression on PMN was diminished in the presence of berberine.

结果：小檗碱与IL-1或TNF共同处理HUVEC，能抑制IL-1、TNF诱导的PMN与HUVEC间的粘附增强，且能下调由IL－1、TNF诱导的HUVEC表面粘附分子ICAM-1表达的增高；小檗碱与TNF共同处理PMN，能抑制TNF诱导的PMN与HUVEC的粘附增强，亦能降低TNF诱导的PMN表面粘附分子CD18的表达。

Cellular adhesion molecule is a kind of glucoprotein expressed on the membrane surface of various cells,which mediate the conjunction and adhesion of cells and extracellular matrix.Vascular cellular adhesion molecule-1(VCAM-1) and intercellular adhesion molecule-1 (1CAM-1) are members of CAM.

细胞粘附分子(cellular adhesion molecule，CAM)是一类由多种细胞产生的，调节细胞和细胞间以及细胞和基质间相互结合并起粘附作用的膜表面糖蛋白，主要包括血管细胞粘附分子-1(vascular cellular adhesion molecule-1，VCAM-1)和细胞间粘附分子-1(intercellular adhesion molecule-1，ICAM-1)等。

What are your goals and strategies for growth?

你的成长目标和策略是什么？

And unto the angel of the church in Sardis write; These things saith he that hath the seven irits of God, and the seven star I know thy works, that thou hast a name that thou livest, and art dead.

3：1 你要写信给撒狄教会的使者，说，那有神的七灵和七星的，说，我知道你的行为，按名你是活的，其实是死的。