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髓化

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Antibodies including mouse antihuman neurofilament,rabbit anti-human myelin basic protein,rabbit anti-human Al,rabbit anti-human IgM,mouse anti-human IgG,mouse anti-human CD31,mouseanti-human GFAP,mouse anti-human Ki-67,rabbit anti-human serotonin(5-HT),rabbit anti-human SYN,and mouse anti-human c-fos protein were used for immu-nohistochemistry with S-P method.The colorant was brown yellow DAB.

免疫组化染色用S-P法,一抗分别为鼠抗人神经丝蛋白、兔抗人髓鞘碱性蛋白、兔抗人Al、兔抗人IgM、鼠抗人IgG、鼠抗人CD31、鼠抗人GFAP、鼠抗人Ki-67、兔抗人血清素(5-HT)、兔抗人SYN及鼠抗人C-fos蛋白,显色剂为棕黄色DAB。

Results The pathological changes in the nuclei mentioned above included the crimple and ruture of nucleus membrane,mitochondria degeneration and other degenerative structure such as plenty of primary lysosomes,agglomeration of lipochrome,Golgi complex degeneration and so on.

结果上述核团神经元的超微结构均发生病理性改变,神经细胞核膜皱缩,核膜凹凸不整,并有局部断裂;线粒体变性,基质浓度降低及空泡化;粗面内质网和高尔基复合体囊腔扩张变性;大量初级溶酶体及脂褐素集聚;出现了髓样体和多泡体等变性结构。

METHODS: A limb ischemia-reperfusion injury model in rats was established. The animals were randomly divided into three groups: control group, IR group and IPC group. The contents of diamide oxidase, nitric oxide, endothelin-1 (ET-1) and ratio of nitric oxide/endothelin-1 (NO/ET-1) in the plasma and the gut were measured. The leavels of myeloperoxidase, ratio of DNA chain, total nitric oxide synthase, inducible nitric oxide synthase and constitutive nitric oxide synthase in the gut were determined.

雄性Wistar大鼠18只,随机分为对照组,缺血再灌注组和缺血预适应组,每组6只,分别测定血浆和小肠组织二氨氧化酶、一氧化氮、内皮素-1(ET-1)、NO/ET-1比值的含量变化及小肠组织的髓过氧化物酶、DNA双链百分率(ratio of DNA chain %)、总一氧化氮合酶、诱导型一氧化氮合酶、结构型一氧化氮合酶的水平;免疫组化法检测小肠组织的诱导型一氧化氮合酶、内皮型一氧化氮合酶的表达。

Results: electronic microscope showed that in prednisone group heterochromatin increased in some cells, entoblast was not obvious in some cells, fat drops were small and few, mitochondria vacuole were common, and myelin figure was found in smooth endoplamic reticulum. the ultrastructure in yc group was almost normal and megamitochondrion formation was common. a large amount of fat drops were found in cytoplasm in gw group and little improvement was found compared with that in prednisone group.

结果: 电镜结果显示:激素组个别细胞异染色质增多,核仁不明显,脂滴显著变小变少,线粒体空泡化常见,有滑面内质网髓鞘样结构形成;养阴组电镜结构基本正常,其特征是细胞内有较多的巨大线粒体形成;桂附组较激素组改善不明显,其特征是胞质内可见大量脂滴。

Large numbers of experiments internal and external had confirmed both direct current and square pulse of distal end cathodal could improve peripheral nerve regeneration, because it could speed up transmigration, creeper, growth and development of cell Schwann, derivate growth of nerve fiber; it also increased blood capillary of epineurium, brood blood vessel, amendment ischemic of impaired nerve, it still could accelerate Wallerian

国内外大量的基础实验及临床研究都证实远端负极电流的直流电场及脉冲电场等均有促进周围神经再生的作用,认为其可加速Schwann细胞的游走、爬行及生长发育,诱导神经纤维的生长;电刺激还能促使神经外膜毛细血管数量增多,扩张血管,改善神经损伤段缺血状态,并加速Wallerian变性及崩解组织的清除,为Schwann细胞发育和髓鞘化过程提供充足的能量与物质,同时为神经轴突的再生提供良好的内环境;在神经断端出现瘢痕或神经瘤时,电刺激可增加神经纤维穿越瘢痕的能力。

SCI can cause hematomyel ia, dropsy, necrosis, capsular space, gummosis and so on, which can lead to neuron deprivation, demyelination of neurite. Clinical symptoms mainly manifest funct ion disorder of movement, sense, reflectance, and musculus sphincter below injury plan.

SCI后出现脊髓出血、水肿、坏死、囊腔形成、退变胶质化等一系列病理改变,以致神经元丧失、轴突脱髓鞘,临床表现为受损平面以下的运动、感觉、反射及括约肌功能的障碍。

Results: The main ultrastructural changes after Cd treatment included swelling or vacuolation of mitochondria, increase of myelin figures in GCT cells, and swelling of mitochondria in the endothelial cells of peritubular capillaries. The changes above were most prominent at 7~15d, and swelling of the cytoplasm and slight karyolysis were also found. The morphology of GCT cells didn't recovery to normal yet after 30d.

结果:镉注射后24h,GCT细胞内出现不同程度的线粒体肿胀和空泡化,胞质和线粒体内可见髓样结构,GCT周围毛细血管内皮细胞线粒体肿胀。7~15天后上述改变明显加重,部分GCT细胞见胞质广泛肿胀和轻度核溶解,30天后细胞形态仍未恢复正常。

From the commencement of week 3,the cartilage showed the characteristic of later OA morphologically with fibrosis of cartilage,sclerosis of sunchondral bone,amalgamation,opening and fibrosis of marrow cavity.

从第3周开始,正常的软骨细胞基本消失,呈纤维样变,软骨下骨硬化;髓腔融合、开放、纤维化,呈现晚期骨性关节炎的改变。

Methords After the KG1a cells had been treated by the demethylation kit, the DNA was drawn.

去甲基化试剂盒对急性髓性白血病细胞KG1a进行去甲基化处理,并提取其DNA。

In addition, DNA methylation profiles segregated patients with CEBPA aberrations from other subtypes of leukemia, defined four epigenetically distinct forms of AML with NPM1 mutations, and showed that established AML1-ETO, CBFb-MYH11, and PML-RARA leukemia entities are associated with specific methylation profiles.

此外,根据DNA甲基化的不同可将CEBPA基因畸变与其他亚型的白血病区分开来,并定义出四个不同表型的伴NPM1基因突变的急性髓系白血病,并且表明AML1-ETO, CBFb-MYH11,和 PML-RARA 三种白血病类型与特定的甲基化有关。

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