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The results showed that the glandular epithelial cells of serous acinus,the epithelial cells of all gland ducts and parasympathetic ganglion cells appeared GnRH positive in immunoreaction.The positive substance was distributed in the cytoplasma with negative nuclei.

结果显示,大鼠颌下腺的浆液性腺泡的上皮细胞,各级导管的上皮细胞及副交感神经节细胞均呈促性腺激素释放激素免疫反应阳性,阳性反应物质分布在胞质,胞核呈阴性反应。

Results:The degenerative changes of articular cartilage in the manipulation group and the sodium hyaluronate group,such as vacuolar degeneration of cytoplasm,decreased quantity and degraded function of orginele,pycnosis of nuclear and necrosis even disintegration of cell,are lesser than that in the group without treatmnet.

结果:手法干预组和透明质酸钠组软骨细胞发生胞浆空泡化,细胞器数量减少,功能减退以及细胞核固缩甚至细胞坏死崩解等退变现象的程度较空白对照组轻,手法组与透明质酸钠组相当。

These abnormal changes mainly occurred at two stages:(1) at meiotic prophase, almost half of Peiai 64S microsporocytes exhibited aberration, with sparse free ribosomes, underdeveloped mitochondria and many swollen endoplasmic reticula.

这些变化主要发生在两个阶段:(1)减数分裂前期,约半数的小孢子母细胞的胞质出现异常,游离核糖体稀少,并具有不发育线粒体和大量泡状内质网。

After the cells dealt with GS-Rh2 of 13.0 mg/L, the typical apoptosis cells were discovered: showing disorganized, highly contracted and vacuolated, condensed cytoplasm, vanished karyotheca, ruptured cell nucleus and apoptotic body.

凋亡细胞吉姆萨染色检测:经13.0 mg/L人参皂甙单体Rh2处理后,HL60细胞出现核染色质浓缩、呈周边凝聚,核膜裂解形成凋亡小体、胞质出现空泡但胞膜完整的典型细胞凋亡形态学改变。

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。

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。

However, the membrane of toxopalsma in liver tissues was stickled out and broken, vacuole lied in cytoplasma, mitochondrion and endoplasic reticulum were swollen or broken, and dense granules were disappearing TEM ×10000

肝组织内弓形虫随扁桃酸作用时间的延长,其受损程度明显加重。在治疗早期(24、72h)肝组织内虫体胞膜突出、破裂,胞质中出现空泡,线粒体和内质网肿胀或破裂,致密颗粒消失,虫体电子密度降低(图2B)。

Lipid scrambling in resealed ghosts occurs in the absence of cell shrinkage and microvesicle formation, processes that are generally attributed to Ca(2+)-induced lipid scrambling in intact erythrocytes.

重封血影细胞中的脂质紊乱在细胞皱缩缺失和微泡形成时发生,此过程在完整的红细胞中通常归因于Ca(2+)诱导的脂质紊乱。

Blood-brain barrier in tumors and peritumoral oedematous regions had the same variations in ultrastructure.

瘤体和瘤周水肿区血脑屏障超微结构变化无明显差异,内皮肿胀,毛细血管腔狭小,胶面有稀疏的绒毛样突起,内皮为无孔型,胞质内胞饮泡较多,内皮紧密连接增长,细胞连接间隙增宽,基膜完整,胶质膜缺损。

Results After the treatment with 15 μmol·L~(-1) of evodiamine for(24 h,)A375-S2 cells exhibited typical characteristics of apoptosis:loss of membrane microvilli,cytoplasmic hyp...

结果经15μmol.L-1吴茱萸碱处理24 h的A375-S2细胞表现出典型的凋亡特征,即细胞表面微绒毛消失、胞质空泡化、染色质浓集、边聚。

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