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Chronic hypoxia and MCT-induced pulmonary hypertension are associated with excess collagen deposition in pulmonary arteries; meanwhile, the muscularization of nonmuscular intra-aeinar arteries also plays an important role in maintenance of pulmonary hypertension.

1。在慢性缺氧和MCT诱发的肺动脉高压进展过程中,肺动脉壁胶原沉积过度,泡内动脉结构发生改变,动脉中层厚化,非肌性动脉肌性化。2.764-3能部分抑制胶原的过度沉积,降低缺氧性及野百合碱性肺动脉高压,从而逆转泡内动脉的结构改变。

In the past twelve years there have been hundreds of studies showing these nonthermal effects--- such as DNA damage and nonrepair, opening of the blood-brain barrier (allowing toxins and pathogens to reach the brain), lowered immunity, decreased melatonin levels, effects on stress proteins, formation of micronuclei (aberrations in cell nuclei which are often markers for cancer), changes in calcium metabolism affecting communication between cells, changes in brainwave patterns as seen on EEG's, plus effects observed on many different systems of the body.

在过去十二个月里,已有数以百计的研究表明这些非热效应---如DNA损伤和nonrepair ,开放血脑屏障(允许毒素和病原体到达大脑),降低免疫力,降低褪黑激素水平,对应激蛋白,形成的微(畸变细胞核往往是癌症的标志),改变钙代谢的影响细胞之间的沟通,改变脑电波模式脑电图上看到的,加上效果观察许多不同的系统的机构。

Results Oxygen metabolism abnormality was found after trauma, and it was correlated with ISS, RTS, injured organ or region and number of injured organs, shock, systemic inflammatory response syndrome and respiratory complications. It was more intense in the patients with MODS. There was marked difference in the ratio of change in oxygen metabolism between MODS and NMODS groups. Oxygen deficiency metabolic variables tended to deteriorate in the nonsurvival group. More marked changes in metabolic variables indicated severer organ dysfunction, reaching their peak values before death.

结果 氧代谢水平在创伤后即发生异常,与创伤严重度评分、RTS、损伤器官部位与数量、低血容量性休克、全身炎症反应综合征以及是否并发呼吸系统合并症等有关;并发MODS患者氧代谢水平变化更为明显,与轻伤对照组和NMODS组比较相关氧代谢比值改变差异均有显著性;死亡组乏氧代谢指标常呈持续恶化趋势,其代谢水平改变越显著,预示器官功能损害程度越严重,往往于死亡前达到峰值。

Cardiac hypertrophy and extracellular matrix remodeling happened as a result of chronic overrange of pressure in heart and hypervolaemia which lead to damage of relaxation and compliance of heart.Drugs including renin-angiotensin converting enzyme inhibitor,angiotensin receptor blocker,aderergic receptor blocker,aldrosteron antagonism,tatins endothelin receptor blocker pancreatic kiniogenase and calcalium channel blocker,can delay or reverse the remodeling by several mechanisms.

主要表现为心脏在慢性超负荷的压力、容量作用下发生的病理改变致使左室肥厚组织胶原结构发生改变,导致心肌顺应性降低,舒张功能受到损害;作用于肾素-血管紧张素系统的药物及肾上腺素受体阻滞剂、醛固酮拮抗剂、他汀类药物、内皮素受体拮抗剂、胰激肽原酶、钙通道阻滞剂等药物通过不同途径和机制延缓和逆转左心室重构。

Results; The injection of mixed bacteria caused a pathological alteration of oviductal wall, such as edema in mucous, shortened cilia of epithelium, inflammatory cell infiltrating, dilation and hyperraemia in blood capillary within lamina propria and obstruction of oviductal lumen. These pathological changes were recovered following the treatment of FGST intragastrically administrated.

结果 在使用混合菌接种后,小鼠输卵管管壁结构发生改变,主要包括黏膜层水肿、上皮细胞顶端纤毛变短或消失、固有层炎性细胞浸润、毛细血管充血、管腔狭窄甚至闭塞。;附归参汤;长期给药后明显使上述病理改变向正常组织转归。

The experimental group corneas were preserved by organ culture for 4 weeks, the corneal thickness was measured with ultrasonic corneal pachymeter. Then every corneas were divided into half -chip, there are 48 half-chip total. It was divided into 4 groups, there are 12 half-chip in every groups. The corneal endothelial cell density of 12 half-chip were counted through Alizarin Red-Trypan blue staining; 12 half-clip corneas were fixed with 4% neutral formalin solution, HE staining was performed, the expression of AQP-1 in corneal stroma and corneal endothelial cell were detected through immunohistochemical staining; Na~+-K~+-ATPase activities in 12 half-clip corneas were examined with Na~+-K~+-ATPase kit; the expression of AQP-1 mRNA were detected through real-time fluorescent quantitation PCR.

实验组经器官培养保存4周后以角膜测厚仪测量角膜厚度,然后每个角膜被分成两半,共48个半片角膜,再分成4组,每组12个半片。12个半片用茜素红-台盼蓝染色染色行角膜内皮细胞计数;12个半片角膜用4%中性福尔马林溶液固定行HE染色、应用免疫组化染色检测AQP-1在角膜基质和内皮细胞表达的改变;12个半片角膜用Na~+-K~+-ATP酶试剂盒测量角膜内皮细胞Na~+-K~+-ATP酶活性;12个半片角膜用实时荧光定量PCR检测AQP-1mRNA表达改变。

At 2 weeks following injury, hematoxylin-eosin staining showed that brain tissue breakage at damaged site as scar connection, remarkable porosis in the blank group; typical morphological changes as neural cells at the transplanted site in the control group; typical morphological changes as neural cells without cavity in the experimental group.

伤后2周苏木精-伊红染色空白组可见损伤处脑组织断裂,为瘢痕连接,有明显空洞形成;对照组在移植部位出现典型的神经细胞样形态学改变;实验组出现典型的神经细胞样形态学改变且空洞消失。

These changes were at least partly due to postsynaptic alterations in the response to glutamate, and apparently affected each synapse in proportion to its initial strength.

这些改变至少部分是由于在谷氨酸应答中突触后的改变,并按其最初的比例影响每个突触。

These changes were at least partly due to postsynaptic alterations in the response to glutamate, and apparently affected each synapse in proportion to its initial strength.

这些改变至少部分是由於在谷氨酸应答中突触后的改变,并按其最初的比例影响每个突触。

MTT assay FAK signaling pathway inhibitor genistein on human corneal epithelial cell cytotoxicity;RT-PCR detection of human corneal epithelial cells adhesion to fungus at different times,extracellular matrix protein including laminin,fibronectin,FN glass,Ⅳcollagen,transmembrane protein integrinαⅤ,integrinβ1(ITGβ1),as well as the FAK signaling pathway FAK1,FAK2 and Paxillin gene expression;Western blot detection of the signal transduction pathway adhesion-associated protein ITGβ1,FAK and PAX expression and the inhibition of genistein. Immunocytochemical method was used to observe the LN,FN and FAK expression in human corneal epithelial cells during interaction with the fungues;Laser scanning confocal microscope had a cell positioning on FN,FAK and PAX,observed the changing of the human corneal epithelial cytoskeleton after stimulated by fungues;Quantitatived by flow cytometry to detect of human corneal epithelial cells with PAX at ITGβ1 fungal expression after adhesion;Optical microscopy quantitied the fungues and human corneal epithelial cell adhesion and recorded to determination the integral optical density afrer adhesion;Scanning and transmitted electron microscope observed the changing of cell ultrastructure after fungues and human corneal epithelial cell adhesion.

第一部分真菌激活人角膜上皮细胞FAK信号转导通路的体外实验研究将三种常见致病真菌(白色念珠菌、烟曲霉菌和茄病镰刀菌)分别与人角膜上皮细胞共孵育,MTT法检测FAK信号通路抑制剂染料木黄酮的对人角膜上皮细胞的细胞毒性作用;RT-PCR检测真菌黏附人角膜上皮细胞后不同时间细胞外基质层连蛋白、纤连蛋白、玻连蛋白、Ⅳ型胶原、跨膜蛋白整合素αV、整合素β1(ITGβ1),以及FAK信号通路中FAK1、FAK2和桩蛋白基因的表达情况;Western blot的方法检测黏附信号转导途径相关蛋白ITGβ1、FAK和PAX的表达,以及染料木黄酮对真菌刺激人角膜上皮细胞FAK信息通路活化的抑制作用;免疫细胞化学方法观察人角膜上皮细胞与真菌相互作用过程中LN、FN和FAK的表达;激光共聚焦显微镜对FN、FAK和PAX进行了细胞定位,并观察真菌刺激后人角膜上皮细胞骨架的变化;流式细胞仪定量检测人角膜上皮细胞ITGβ1与PAX在真菌黏附后表达的改变;光学显微镜观察真菌与人角膜上皮细胞黏附数量,记录并测定了黏附后积分光密度值OD扫描及投射电镜观察了真菌与人角膜上皮细胞黏附后,细胞超微结构的改变。

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