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染色质溶解

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Light and electron microscopy showed central chromatolysis of motor neurons in the lumbar cord from 1 week after the start of compression.

研究结果:光学和电子显微镜检查表明从压迫1周后出现腰髓运动神经元的中心染色质溶解。3周后,在前角可见到一些神经元的凋亡。

Severance of nerve from muscle will induce retrograde changes in the body of the neuron, known as chromatolysis, which is a sign of dysfunction.

有很多的肌肉神经,会在神经元内减少,就是「色原溶解;核染质溶解;染色质溶解消失;色素溶解消失」也是代表了「官能障碍

Howeer, few studies hae looked at changes of neurons within the caused by disturbance of axonal flow, the axon reaction, chromatolysis, and cell death as a result of mechanical compression of the entral

但是, 很少有研究关注腹侧神经根机械性压迫所致的神经元改变,如轴流,轴索反应,染色质溶解,细胞死亡等。

Under transmission electron microscope, cellular swelling in brain tissue, nuclear membrane of neuron has incisures, some chromatic agglutination, group A mainly appears endoplasmic reticulum distention and glial cell endocytosis, while group B mainly appears histolysis; cardiac fibrous structure is chaotic, Z line concentrates, mitochondria swelling, nucleus deform; the ecphyma of podocyte becomes thinner and longer like villus, some mix together, plasma membrane infolding of renal cells decreases, mitochondria malformation, cells in lumens.

透射电镜观察显示,试验组动物脑组织细胞肿胀,神经元核膜出现切迹,部分染色质凝集,A组动物出现内质网扩张及胶质细胞吞噬现象,B组动物以组织溶解为主;心肌纤维结构紊乱,Z线聚集,收缩带形成,线粒体肿胀,核变形;肾小球足突细长,绒毛化,并可见足突融合,肾小管上皮细胞质膜内褶减少,线粒体畸形,管腔可见脱落细胞,上述改变均以B组为著。

Results (1)The permillage of myocyte apoptosis in infarct area in elder patients with sudden death caused by AMI was significantly higher than that in control group(663.00‰±117.12‰ vs 34.30‰±20.68‰,P<0 .01).However the permillage of myocyte apoptosis in 1-vessel,2-vessel,and 3 - vessel disease were 514.28±165.12‰,564.38‰±102.33‰ and 668.25‰±127. 19‰,respectiverly,significantly higher as compared to control group(All P< 0.01).But no significance was found among the three groups.(2)The size of DNA f ragment about 180~200 bp was found only in those patients with two and three ve ssels involoved.(3)The electron microscope showed the characteristics of myocyte apoptosis episodes,the others showed the characteristics of necrosis.

结果 TUNEL法发现,猝死者梗死区的心肌细胞凋亡千分数老年组(663.00‰±117.12‰)明显高于正常对照(34.30‰±20.68‰)(P<0.001);心肌细胞凋亡千分数在冠脉1支病变者(514.28‰±165.12‰)<2支病变者(564.38‰±102.12‰)<3支病变者(668.25‰±127.19‰),虽然均明显高于正常对照(均P<0.01),但三组之间比较则无统计学上的差别(均P>0.05);冠脉2~3支病变者梗死区的心肌细胞DNA电泳可见相差约180~220 bp的阶梯片段;电镜发现猝死者梗死区内的心肌细胞核膜完整、染色质浓集、电子密度增加的凋亡特征,有的则出现核膜破裂、染色质溶解成碎屑的坏死现象。

Most endothelial cells fell off, elastic fibre autolyze; the number of SMC decreased, some SMC nucleus contracted completely or depressed, typical apoptosis body were seen in later stage, muscle silk autolyzed and disappeared mostly; in outer layer saw much collagenic fiber, arranged unorderly; inflammation cells were seen in the aneurysm wall(hypertrophy cell et al.).

多数瘤壁的内皮细胞溶解脱落,不连续,弹力纤维自溶;动脉瘤血管壁均可见SMC明显减少,较多SMC染色质边聚、固缩,部分SMC核全部固缩或出现不规则凹陷,SMC核胞浆或胞核部分出现脱落或裂解成碎片,晚期可见典型的凋亡小体出现,肌丝大都自溶消失:外膜可见大量的胶原纤维,排列较紊乱;瘤壁还可见炎性细胞浸润。

The results indicated that the erythropoietic/granulopoietic ratio was markedly increased with megaloblastic morphology in all stage of erythrocyte.

结果表明:2例CDAⅠ型患者骨髓幼红细胞比例增加,各阶段细胞存在不同程度巨幼样变;原红细胞核不规则,早幼或中幼红细胞可见奶酪核,约半数晚幼红细胞有核溶解和破碎现象,晚幼红细胞核损伤有时伴胞质溶解,细胞间染色质桥少见;各阶段红细胞核膜和内质网同时出现不同程度溶解。

Results Microscopically, different degrees of hepatocytic degenerative changes and hyperplasic fibrous tissue and typical false lobule formation could be seen. Timm's staining result showed uneven distributed black granular deposits in the hepatocytes. No specific PAS staining was observed. Utrastructurally, the mitochondria were increased in volume and dramatically different in shape. The number of lysomes were increased.

结果 光镜下肝细胞表现为不同程度的退行性变,胶原纤维增生以及典型假小叶形成;Timm's染色阳性,发现不均匀分布黑色颗粒或团块样物质沉积;PAS染色则普遍缺乏特异性染色;超微结构显示线粒体形态多样,体积增大,溶酶体增多,粗面内质网管腔扩张,附着核糖体的脱颗粒,以及胞质水肿,质膜溶解。

All experimental piglets revealed the characteristic nonpurulent encephalomyelitis,such as hyperemia,hemorrhage,edema in little vein and capillary v...

发病猪出现脑、脊髓的小静脉和毛细管充血、出血、水肿,神经原水肿、急性肿胀、急性液化及中央染色质溶解,胶质细胞轻微增生等非化脓性脑脊髓炎特征。

Observations underelectron microscopy showed that YSV destroyed the structure of chromatin,damaged cell organelles of tumor cells, and induced apoptosis and necrosis intumor cells.

超微结构研究显示,YSV(320μg/kg/d)诱导人肝癌BEL-7402细胞的染色质溶解、固缩,细胞器的普遍崩解,细胞出现凋亡和坏死。

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