细胞坏死

Electron-microscopic observation: In stroke-prone spontaneous hypertension group, electron density was found increased in necrotic neurons; moreover, some nuclear membrane lost double-layer structure with ridges broken, even reduced or disappeared, displaying vacuolated changes. In losartan 30 mg/ group and losartan 10 mg/ group, most of neurons displayed basically normal morphology, with neuron chromatin evenly distributed and nuclear envelops regular, but there were still some neurons that had dense chromatin, with ridges broken and reduced.

3组大鼠脑组织电镜观察：易感型自发性高血压组大鼠坏死神经元电子密度增高，有的核膜失去双层结构，嵴断裂、减少甚至消失，呈空泡样改变；氯沙坦30mg/组和氯沙坦10 mg/组大多数神经元染色质分布均匀，核膜规整，细胞形态基本正常；少数神经元核染色质较致密，部分嵴断裂、减少。

Light microscope: hemorrhage, vacuolization, edema and necrosis were the most notable changes, but inflammatory cells infiltrating was few.

光镜下，出血、空泡形成、水肿、坏死是最显著的变化，而炎性细胞浸润较少。

Wagener FA, Eggert A, Boerman OC, Oyen WJ, Verhofstad A, Abraham NG, Adema G, van Kooyk Y, de Witte T, Figdor CG. Heme is a potent inducer of inflammation in mice and is counteracted by heme oxygenase. Blood 2001;98(6):1802-1811.11 McCoubrey WK Jr, Huang TJ, Maines MD.

推测其作用机制可能有以下几个方面：(1)研究证实，在EAE的发生和发展中，有多种炎性细胞因子，如白细胞介素-1、2，肿瘤坏死因子a和干扰素g发挥着重要作用，他们的存在进一步激发了HO-1的表达[17]。

Showed that inhibition of FLASH expression abolishes TNF (191160)-induced NFKB (164011) activation in embryonic kidney cells.

表明，抑制闪光的表达废除肿瘤坏死因子（ 191160 ）诱导nfkb （ 164011 ）激活在胚胎肾细胞。

At day 20, some of the acini collapsed, and the epithelial cells of the duct were damaged.

由10μg·L-1 B\P处理20d时，在鳃回血管中发现血细胞坏死后残留的固缩细胞核，鳃丝的上皮细胞排列不规则甚至断裂，部分消化腺泡崩解，鳃丝结构和消化导管上皮结构损害严重；消化盲囊组织结构的损伤比鳃更为严重。

After SE, DNA ladder was seen in nucleus amygdalae where neurons were morphologically necrotic, which suggests that programmed cell death mechanisms may be activated in this SE model.

结论癫痫持续状态后，形态学上表现坏死的神经元出现梯状DNA电泳带，提示在此模型中可能存在程序性细胞死亡的机制。

After SE, DNA ladder was seen in nucleus amygdalae where neurons were morphologically necrotic, which suggests that programmed cell death mechanisms may be activated in this SE model.

结论癫痫持续状态后，形态学上表现为坏死的神经元出现梯状DNA电泳带，提示在此模型中可能存在程序性细胞死亡的机制。

The cochleae of animals were dissected. propidium iodide, a dna intercalating fluorescent probe, was used to trace the morphological changes in ohc nuclei. f-actin staining was used to determine missing ohcs. the single strand dna in apoptotic ohcs of guinea pigs and mice, and apoptosis inducing factor and endonuclease g in ohcs of guinea pigs were examined by immunofluorescence method.

分离解剖耳蜗后，用碘化丙啶染色细胞核、pholloidin染色f-actin，免疫荧光抗体分别染色单链dna、核酸内切酶g和凋亡诱导因子（apoptosis inducing factors， aif），制备耳蜗铺片，激光共聚焦显微镜下观察凋亡和坏死毛细胞内的荧光信号变化。

Reduce the hoist of leucocytes of sinus coronaries blood of myocardial ischemia and reperfusion injury dogs;2. decrease the leakage of plasma CK, CK-MB and LDH;3. regulate the vaso-active substances such as ET, TXB〓 and PGI〓;4. decreased the inflammatory cell factors such as IL-1, IL-6 and TNF

综上，奥沙恩注射液可降低心肌缺血再灌注损伤模型犬冠状窦血白细胞总数，减少I／R后CK、CK-MB和LDH的释放，调节血管活性物质ET、〓和〓的产生，降低血清炎性细胞因子TNF-α、IL-1和IL-6的含量，抑制PMN的激活及对心肌的浸润，减轻心肌组织的病理改变，以及减轻心肌缺血及坏死程度、降低心肌耗氧量，从而显示出较强的对犬急性心肌缺血再灌注损伤的保护作用。

Hepatocytes which expressed VEGF positively mainly distributed in fatting areas. While in later periods (8 to I 2wk), the liver tissue inflammatory was light, but diseases in hepatocytes were significant.

乙肝肝细胞的变性坏死等与肝内血管病变导致的肝血供障碍密切相关，肝内血管病变主要有血管炎症、血管阻塞、血管破坏、血管增生及肝窦狭窄、阻塞、扩张和肝窦毛细血管化。

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。