细胞坏死

Tumor necrosis factor-alpha may injure vascular endothelial cells by many ways, and the injury of vascular endothelial cella can accelerate the release of tumor necrosis factor-alpha, which can injure the vascular endothelial cells again.

肿瘤坏死因子α可通过多种途径损伤血管内皮细胞，血管内皮细胞的损伤又促使肿瘤坏死因子α的释放，再次损伤血管内皮细胞，两者互为因果，形成恶性循环。

The study of the histopathology showed that the haemolymph in the disease crab decreased sharply, and was replaced by large amount of parasites, which was observed in muscle, heart and hepatopancreas from the disease crab. The pathological characteristics mainly appeared as cells swelling, necrosis, nucleus condensation and collaspe.

组织病理学观察发现，病蟹血淋巴急剧下降，代之以大量的寄生原虫，该寄生虫在病蟹的肝胰腺、鳃、心脏、肌肉等部位大量侵袭，并引起这些组织发生以坏死为主的变质性病变，其病理特征主要表现为：细胞肿胀、变性、坏死，某些细胞的细胞核固缩、碎裂或崩解。

Results Cvb-D obviously lightened isoprenaline-induced myocardial pathological changes such as turbulence of myocardial fiber, plasmolysis of necrotic cell, inflammatory cell infiltration of necrotic interstitial region. Cvb-D remarkably inhibited myocardium cell apoptosis of myocardial ischemia rats caused by isoprenaline.

结果 Cvb-D可显著减轻Iso诱发的心肌缺血致心肌肌纤维排列紊乱，坏死细胞胞泉溶解，坏死间质区炎性细胞浸润等病理改变；Cvb-D可显著抑制Iso诱发的心肌缺血性模型大鼠心肌细胞凋亡。

Tumor necrosis factorαis a pleiotropic factor involved in diverse cellular responses, including inflammation,apoptosis and necrosis.

肿瘤坏死因子TNFα是一个多效性细胞因子，参与调节炎症反应、细胞凋亡和坏死等。

Using acupotomology incise and separate the hip joint articular capsule and ligament and the periosteum on the collum ossis femoris and the soft tissue nearby the joint can cause slight hurt and haemorrhage. The hurt factor is release from the local tissue. Human self-rebuilding system is activated, Building bone function of osteoblast is accelerated, new bone is built quickly. New blood vessel and nerve ending is rebirth. Local tissue's blood supply and nerve nourishment is improved. The developing of bone necrosis is prevented. The necrotic part is re-blood vessel. The conditions of the necrotic's absorbing tissue and the new bone's replacing are established.

针刀治疗股骨头无菌性坏死是通过针刀对髋关节囊、关节囊韧带、股骨颈的骨膜和髋关节相邻周遍组织切割分离铲拨松解可以产生轻微创伤、出血、局部组织释放创伤因子，激发人体自我修复重建反应，激活成骨细胞造骨功能，加速新骨生成，促进新血管和神经终端组织再生与重建，使局部组织血流加速，改善血液供应和神经营养状况，阻止坏死进一步发展，使股骨头颈坏死区域再血管化，为坏死组织吸收和为新骨再生爬行替代过程创造条件。

At high magnification, liquefactive necrosis of the brain demonstrates many macrophages at the right which are cleaning up the necrotic cellular debris.

高倍镜下，在右侧的脑组织液化性坏死灶中许多巨噬细胞清除了坏死的细胞碎片。

The number of DC is more in the cases of those that have more necrotic areas and lymphocytes infiltration.

树突状细胞形态不规则，绝大部分DC分布于坏死灶和汇管区间质中与淋巴细胞伴行，肝细胞内一般不常见，坏死灶越多，淋巴细胞浸润越多的病例中DC细胞也越多。

Results:(1) In clinical pathology, swelling, denatured, even necrosis and putrescence could be picked out; Collagen fibers in tendon remarkedly swelled, and tissue structure disarranged, and collagen even ruptured, broken and dissolved; Obvious denature, apoptosis and necrosis could be found in tendon cells. There appeared to be a big accumulation of inflammatory cells.

结果 （1）临床病理组织学观察发现：肌腱组织肿胀、变性、甚者坏死、腐败；肌腱内胶原纤维肿胀明显、组织结构紊乱，失去正常排列，甚者出现胶原断裂、破碎、溶解等现象；腱细胞可见明显的变性、凋亡和坏死；病变部位可见大量炎性细胞聚集。

The findings of the newly identified goose paramyxovirus strain GPMV/HBexperimental infection were as follows: The challenge caused high morbidity and highmortality.The clinical signs included severe depression, decreased appetite or anorexia,white,yellow and green diarrhea, with neural symptoms;pathological changes showed thathaemorrhage and ulceration of intestine mucosa, necrosis of spleen and pancreas,andedema of liver and kidney, uratic deposition in kidney.Eosinophilic inclusion bodies werefound in the cytoplasm of pancreas and a large quantities of fiber protein were found inintestine. Lots of hemosidefin was found in some area of liver and kidney. A number ofT、B lymphocytes reduced sharply in spleen,lymph nodes in dead geese. Transmissionalelectron microscope showed that some cells had the morphological characteristics ofmitochondria swelling, morphological changes were condensation of nuclear chromatininto dense masses,followed by its marginating against the nuclear envelope, andespecially concentration of cytoplasm association with lots of lipid droplet.

人工感染雏鹅实验中，雏鹅临床表现为高发病率和高死亡率，食欲和饮水减少，拉白色、黄绿色稀粪，伴有神经症状；常规组织学观察，脾脏和胰腺肿大，有白色坏死斑点，肠道出血和坏死，肝脏肿大变性，肾脏肿大变性有尿酸盐沉着等；用特殊染色和组织化学方法首次对人工感染鹅副粘病毒的雏鹅的重要脏器进行研究，结果表明：胰腺中发现病毒包涵体，肠道中大量纤维素以及胶原纤维增生，肾脏、肺脏大量含铁血黄素沉着，免疫器官如脾脏和淋巴结中T、B淋巴细胞大量减少；电镜下多种细胞呈现线粒体水肿，多种实质细胞的染色质固缩，染色质边集，特别是细胞内容物如脂肪滴增多的病理变化特征。

Materials and Methods Thirty SD rats, feeding in clearing grade standard, were classified into five groups at random. Application of transmission electron microscopy, scanning electron microscopy, light microscopy and immunohistological staining meth- ods, normal morphology of outflow pathways was observed and component of extra cel- lular matrix was defined. The effects of 50 IU of TNF-α given intracamerally on the morphology of outflow pathways and other tissues of anterior segments, expression of trabecular stromelysin and the change of components of trabecular extra cellular matrix were observed in 24h, 3days, 7days and 14days after injection.

中文题名TNFα对鼠眼房水外流影响的形态学观察副题名外文题名 The effect of TNFα on morphology of outflow pathways in rat eyes 论文作者王大博导师王竫华教授学科专业眼科学研究领域\研究方向学位级别博士学位授予单位青岛大学学位授予日期2002 论文页码总数90页关键词青光眼房水外流通道肿瘤坏死因子-α馆藏号BSLW /2003 /R775 /1 目的在观察SD大鼠眼房水外流通道形态及确定其房水外流通道细胞外基质成份的基础上，探讨房水中肿瘤坏死因子α浓度的增加是否能诱导小梁细胞基质溶解素的表达和分泌，进而启动小梁细胞外基质的重塑过程。

For a big chunk of credit-card losses; the number of filings (and thus charge-off rates) would be rising again, whether

年美国个人破产法的一个改动使得破产登记急速下降，而后引起了信用卡大规模的亏损。

Eph. 4:23 And that you be renewed in the spirit of your mind

弗四23 而在你们心思的灵里得以更新