细胞坏死

Was presented in 12 cases (24%) by bacterial isolation. By in-situ hybridization, PCV2 signals were chiefly distributed in interstitial and necrotic lesions, and the positive signals could be found in macrophages-like cells and necrotic debris. PRRSV signals were mainly located at interstitial lesions and alveolar wall, and the positive signals could be found in macrophages-like cells and epithelial cells of alveoli. Swine influenza virus could be found in interstitial and necrotizing lesions, and the signals could be found in macrophages-like cells, and epithelial cells of terminal bronchiole and alveoli.

另运用原位杂交法对PCV2、PRRSV及猪流行性感冒病毒进行检测，结果发现PCV2主要分布於PNP的间质及坏死病灶区，并能於肺泡及终末细支气管上皮细胞、巨噬细胞与坏死细胞碎片皆可见有病毒核酸；PRRSV则多分布於间质病灶区及肺泡壁处，能於巨噬细胞与肺泡上皮细胞见到病毒核酸；SIV则存在於间质及坏死病灶区，且能於肺泡及终末细支气管上皮细胞与巨噬细胞见有病毒核酸。

Morphological and flourescent changes were assessed using confocal microscopy in whole-mount organ of Corti preparations. Results (1) After the animals were exposed to broadband noise at 122 dB SPL in 4 h/day for 2 days, both apoptosis and necrosis appeared in OHCs. The single strand DNA in apoptotic OHCs were observed both in guinea pigs and mice.(2) In normal OHCs, EndoG was distributed outside of nuclei. EndoG translocated from outside to inside of the nuclei in both apoptotic and necrotic OHCs following noise exposure.(3) The MNNG cochlear perfusion and noise exposure both caused the transloctation of AIF from the mitochondria to the nuclei. The translocation of AIF took place in both apoptotic and necrotic OHCs.

结果 (1)暴露于120 dB SPL的白噪声环境中每天4小时，连续2天后引起豚鼠和小鼠耳蜗外毛细胞凋亡时，其细胞核内产生ssDNA，而在正常细胞内没有三ssDNA；（2）在正常情况下，EndoG分布于耳蜗毛细胞的细胞核外，在暴露于上述噪声后发生凋亡和坏死的豚鼠耳蜗外毛细胞中，EndoG从细胞核外转移到细胞核内，细胞核中的EndoG显著增加；（3）豚鼠耳蜗外淋巴灌流烷化剂MNNG后发生耳蜗外毛细胞凋亡和坏死，在凋亡和坏死的耳蜗外毛细胞中，AIF自线粒体转移到细胞核，其变化与噪声损伤引起耳蜗外毛细胞凋亡和坏死时一致。

We also have observed some organs pathological changes of juvenile Jian Carp, such as pancreas acinous gland and zymogen granules of acinous gland cell disappearing, intercellular substance hyperplasia and inflammatory cells soakage, hepatatrophia, liver cell granular or vacuolar degeneration and necrosis, karyolysis or pyknosis, glycogen granules decreasing, metanephros atrophy, metanephric canaliculus epithelium granular or vacuolar degeneration and necrosis, mitochondrion swelling and mitochondrion cristae disappearing, karyolysis, distal convolutal tubule microvilli desquamating, spleen marrow cell degeneration and necrosis, intercellular substance of spleen hyperplasia, spleen atresia, blood corpuscle disappearing.

后肾土黄色、淡褐色或苍白色，肾小管上皮细胞肿胀、颗粒或水泡变性、坏死，细胞内有大量血细胞流出，线粒体肿胀，嵴结构消失，细胞核溶解，肾间质甲状腺滤泡和拟淋巴细胞增生，远曲小管微绒毛脱落、管道细胞界限不清。心脏肌纤维肿胀、颗粒或空泡变性，严重的肌纤维溶解、变细或断裂，肌纤维间水肿、炎性细胞浸润，部分心肌细胞核浓缩。脾脏暗褐色，脾髓质细胞变性、坏死，拟淋巴细胞明显减少，淋巴细胞岛少见、岛中细胞成份减少，黑素巨噬细胞中心减少、体积缩小，脾脏网状基质水肿，脾窦闭锁，血细胞减少。

Pathology and ultrastructure detection revealed cell necrosis and collapse, sever nuclear damage was observed in the death cells. The early characteristics of necrosis such as margination of heterochromatin was also found in some tumor cells. Besides, well differentiated tumor cells, degenerative tumor cells and some lymphocytes were seen.

直形针给药组肿瘤组织早期表现为大片的组织坏死，晚期表现为存活区域的增加，坏死区域与存活区域界限分明，两者间多有移行带；弧形针分段扇形注药者早期、晚期组织均表现为大片坏死，肿瘤间质内可见淋巴细胞浸润和纤维结缔组织增生；各时间段的检测标本中都可见一定数量的凋亡细胞，但比例远远小于坏死的肿瘤细胞。

In treatment group, there was no progressive necrosis in stasis zone, and at 24 h post injury, capillary dilation, cell edema and inflammatory infiltration were lessened significantly. In control group, 2 wounds had progressive necrosis (accounted for 10% of the total). Cell edema, inflammatory infiltration and capillary thrombosis were serious, Until 72 hr post injury, cell edema did not subside and necrosis of the dermis worsened. 2. Pathological assessment of the stasis zone tissue: As compared with that in control group, in treatment group the dermis structure in stasis zone was intact and the collagenous fiber bundle was normal.

结果：①创面细胞形态学改变：伤后8h毛细血管扩张、细胞水肿，炎性浸润最明显；治疗组中央淤滞区无进行性坏死，伤后24h后毛细血管扩张、细胞水肿、炎性浸润减轻；对照组2个创面呈进行性坏死（占10%），中央淤滞区细胞水肿、炎性浸润明显，毛细血管血栓形成，伤后72h水肿仍明显，真皮坏死加重；②淤滞区组织病理学评分：治疗组与对照组相比，治疗侧淤滞区的表皮结构相对完整、胶原纤维束相对正常，粒细胞浸润小于5个/400倍视野。

N perifocal tissue intracerebral hemorrhage there were rarefaction neuron,cell spaces augmentation,cell diminution,distinct demarcation of cell membrane and surrounding,and we discovered a lot of degeneration and necrosis nerve cells,cell body collapsed,pycnosis anachromasis,nucleoli disappeared. In EPO group we discovered that center area of hemorrhage shinked,nerve cells of degeneration and necrosis decreased in perifocal tissue,majority cells morphous were normal and pathological changes were light.

CH对照组在术后皮层出血中心无神经元，仅见少量胶质细胞，细胞间质空泡样改变；出血边缘区神经元稀疏，细胞间隙增大，细胞缩小，胞膜与周围分界清楚，并可见大量变性及坏死的神经细胞，表现为胞体皱缩，核固缩深染，核仁消失。rhEPO治疗组出血中心区变小，边缘区神经细胞变性坏死减少，多数存活细胞形态相对正常，病变较轻。

The inflammation reaction hyperplactic stage and lymphatic nodular stage are of nonspecific morphological changes and should be diagnosed with the help of positive tuberculin test and obvious increase of adenosine deaninase ; tuberculous nodular stage has a great number of epithelioid cells,and Langhans cells, caseous necrosis stage is characterized by a great deal of necrotic tissue and debris,a small number of fragmented epithelioid cells, and mainly by antiacid bacteria fibrinous hyperplastic stage is featured by a few fibrous tissue, cells and mucous oweing to hardness to get puncture, neans tuberculous restoration,and scar formation.

结核初期-炎性增殖期60例，占5.5%；结核早期-淋巴结节期130例，占11.9%；结核中期-结核性结节期有590例，占54.1%；结核晚期-干酪样脓样坏死期有280例，占25.7%；结核恢复期-纤维素增殖期30例，占2.8%。炎性增殖反应期非特异性形态学变化，需要结合结核抗体阳性和腺苷酸脱氨酶明显增高有助于诊断，结核结节期主要可有较多类上皮样细胞及郎罕氏细胞；而干酪样脓样坏死主要见大量坏死组织及碎屑、少数残碎不全类上皮样细胞，此期主要能查到抗酸菌为特点；纤维增殖期，抽出物难取，仅见少数纤维组织、纤维细胞和黏液间质为其特征，提示结核恢复、瘢痕形成所致。

Aside from pancreatic enzymes activiation and autodigestive process, recent investigations have established that the upregulation of inflammatory mediator are believed to be the critical steps in the progression of mild pancreatitis to severe pancreatitis. Tumor necrosis factor-, ThyomboxaneA2 ,ProstaglandinsI2 are all important inflammatory mediator. TNF-( is one of cytokines. It is important to the over-production of ICAM-1,VCAM-1, TXA2 andPGI2. The ICAM-1 and VCAM-1 mediate both leukocytes adhesion and migration through the endothelium into tissues to connect with injuried target cells. The TXA2 and PGI2 are the production of arachidonic acid. They are responsible for the tissue ischaemia.

肿瘤坏死因子（Tumor necrosis factor-， TNF-、血栓素A2（ThyomboxaneA2，TXA2），前列环素（ProstaglandinsI2，PGI2）均是炎症反应中重要的炎性介质，其中肿瘤坏死因子-是非常重要的细胞因子之一，它由活化的单核细胞产生，在细胞间黏附分子（Intercellular adhesion molecule-1，ICAM-1）及血管细胞黏附分子(Vascular cell adhesion molecule-1，VCAM-1的表达、血栓素A2及前列环素过量生成方面起着重要的作用，前两者是介导白细胞与内皮细胞黏附，迁移于组织并与受损的靶细胞相结合的主要媒介，是炎症反应中的重要介质，后两者是花生四烯酸的代谢产物，亦是重要的炎性介质，参与构成血液循环障碍。

Results: In the first group of which pancreas was allotransplanted combining with spleen and duodenum: dropsy of stroma between pancreatic folia, light dropsy of gland alveolus cells and pancreatic islet cells were observed at 3 d post operation; Infiltration of inflammatory cells in pancreatic tissue and focus necrosis of the gland alveolus cells occurred at 5 d post operation; Necrosis and dissolve at part of gland alveolus cells and pancreatic islets were observed at 7 d after operation.

结果： 胰、脾、十二指肠联合移植组：术后3 d胰腺小叶间质水肿，腺泡细胞和胰岛细胞轻度水肿；术后5 d炎细胞浸润，腺泡细胞灶状坏死；术后7 d腺泡细胞和胰岛细胞部分坏死、自溶。

There were no statistically differences between the 8th~ 14thday, the 15th - 21th day post-BC and the control group. During the rt~24tkday post-BC , pycnosis degeneration or necrosis neurons of the locus cerebral cortex, dorsal hippocampus, dentate fornix were significantly increased, then decreased gradually, but recovered to normal by the 24thday after BC, and especially in parietal cortex and piriform cortex the necrosis neurons were significantly increased than temporal cortex , and there were no statistically difference berween the left and the right side. Pycnosis degeneration or necrosis neurons in the brainstem reticular formation were markedly increased in the 4thday after BC, and there were no statistically difference among the other groups and the control group.

与对照组相比，BC后在大脑皮质、背侧海马和齿状回部位，固缩变性和不完全坏死细胞数先显著增加(P＜0.05)，然后逐渐减少，至24d基本恢复正常；顶叶、梨状皮质比颞叶皮质变性坏死细胞多，差异有高度显著性(P＜0.01)；大脑左侧比右侧变性坏死细胞稍少但差异无显著性；在BC后4d，脑桥核、斜方体核平面的脑干网状结构中固缩变性和不完全坏死细胞数明显增多(P＜0.05)，其它组间无显著性差异。

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。