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Electro-acupuncture could lower abnormally-increased plasma t-PA、PAI-1 amount, advance activity of rats blood fibrinolytic system, protect integrality of vascular endothelial cell, promote thromb elimination, relieve chronic angiospasm, improve collateral circulation, enhance recovery of ischemic and semidarkness region, consequently protect the brain tissue from injury.

电针能降低急性脑梗死大鼠血浆异常升高的t-PA及PAI-1含量,提高大鼠纤溶系统的活性,保护血管内皮细胞的完整性,促进机体清除血栓、缓解慢性血管痉挛、改善侧枝循环,促进缺血区及半暗带的恢复,从而发挥脑保护作用。

It can expedites proliferation and synthesizing active of cartilage cell and osteoblast too. Quicken ossification in the cartilagines and improving bone repair. But it has no influence to engendering blood vessel.

在骨愈合早期、中期,中药可加强巨核细胞的聚集及增强其活性,并可促进软骨细胞、成骨细胞的增殖及合成活性,加快软骨内骨化,促进骨愈合;而对血管形成无明显作用。

Activities of chymase and ACE were tested by radioimmunological method. Expressions of phosphoric extracellular signal regulated kinase 1/2 (p-ERK1/2) in hearts were measured by western blot. Results: As compared to the control group levels of GSP, myocardial enzymes and myocardial Ang Ⅱ were much lower in those of APS group.

心肌组织的血管紧张素Ⅱ含量;RT-PCR法检测心肌糜酶和血管紧张素转换酶 mRNA表达;放免法检测chymase和ACE的活性;免疫蛋白印迹法检测心肌磷酸化的细胞外信号调节激酶1/2(p-ERK1/2)含量。

Elastic fibers were well-distributed,and vascular endothelial cell did not immigrate.We suggested that expression of ectogenic VEGF triggered paracrine and autocrine of VEGF of chondrocyte and co-acted with VEGF receptor 2 to enhance permeability of chondrocyte and improve internal construct of engineering cartilage,and prevent vascularize proceed.

转VEGF基因软骨细胞作为组织工程的种子细胞与pluronic F-127复合后可于裸鼠体内形成转基因组织工程软骨,与对照组相比,转VEGF基因组织工程软骨具良好的生物学特性,结构均一且与正常软骨组织相似,软骨ECM的GAG、COLⅡ、COLⅩ增多,RunX2、Sox9表达增高,细胞处于增生期的肥大状态,初步分析其原因可能是转染后外源性的VEGF持续表达触发了软骨细胞VEGF自分泌,并通过VEGFR-2作用于软骨细胞,提高了软骨细胞活性,促进其存活与增殖,但未在软骨组织内引起血管内皮细胞的迁移及小血管形成。

But inner hair cell and tectorial membrane were normal.4. The quantities of nNOS and iNOS increased obviously in the cochlea of HIE rats.

1。缺氧缺血时,nNOS和iNOS在新生大鼠耳蜗的内、外毛细胞,血管纹,螺旋神经节等细胞的分布增多,但两者的活性变化不同,分别在缺氧缺血的早期和晚期时活性最强。

After administration of L-N〓-nitro-Arginine, a specific antagonist of NOS, it was found that the basal and stimulated NO release of blood vessels (aorta, internal carotid, renal and mensenteric artery) was decreased further. The increase of coronary blood flow stimulated by Ach was also reduced further, while the platelet aggregation degree and erythrocyte aggregation index increased significantly. Pathological examination indicated that aortic endothelium was destroyed, the blood vessels in cerebral, cardiac and renal tissues were hypertrophied further and some were almost occluded. The above fin dings resulted in SHR feeded with L-NNA having high incidence of stroke rate and high degree of renal cirrhosis when compared to control SHR. The infarct and hemorrhagic focuci in cerebral tissues, infarct focuci in cardiac tissues, atrophy and hyalinedegeneration of renal glomeruli and degeneration even necrosis of renal tubuli in renal tissues were al so found. The increase ratio of brain and heart to body weight and decrease ratio of kidney to body wei ght further demonstrated that the cerebral, cardiac and renal injuries were aggravated.

在上述结果的基础上进一步给予SHR NOS特异性拮抗剂左旋亚硝基精氨酸后,血管(胸主、颈内、肾及肠系膜动脉)NO基础释放及激动剂刺激释放进一步减少,Ach刺激冠脉流量的增加和胸主动脉内膜NOS活性也进一步减少,血小板聚集程度及红细胞聚集指数显著上升,病理切片显示胸主动脉内皮细胞破坏明显,脑心肾组织内的血管进一步增厚甚至几乎阻塞,导致饲L-NNA的SHR缺血性及出血性脑卒中发生率显著高于对照SHR,脑体重比显著升高;心肌内出现明显的缺血梗塞疤痕灶,心体重比显著升高;肾小球明显萎缩、玻璃样变性,肾小管也变性甚至坏死,使肾硬化程度显著增加呈颗粒性固缩肾,肾体重比也显著减少。

The biological characteristics of the CCM are mainly relevant to the unmaturity of the vessel wall. A series of angiogenic factors play an important role in the development of the lesion. The proliferative activity of the CCM needs to be studied further. The different clinical presentations of CCM was based on its pathological diversity.

CCM生物学特性主要与其血管壁组织结构的不成熟有关,各种血管因子发挥了相当重要的促进作用,CCM本身的增殖活性有待进一步研究;CCM不同的临床表现与其病理特点的差异密切相关。

ONOO〓 had direct vasoactive effect for relaxation of precontracted isolated pulmonary artery. Relaxing action of ONOO〓 was weak and was negtively regulated by endothelial cells, further supporting the notion that ONOO〓 may be involved in pulmonary hypertension in the early stage of ES.

用离体血管环检测张力方法,发现ONOO〓具有一定的舒张肺动脉作用,但舒张效应较弱,并受到血管内皮细胞的抑制性调节;抑制K〓通道和PARS活性可增强ONOO〓对离体兔肺动脉的舒张作用。

Immunohistochemistry method was used to determine the expression of thrombomodulin , it showed that TM was expressed in the endothelial cell surface and the intracellular bridge of normal nasopharyngeal squamous cells, but in NPC cells was negative.

血栓调节蛋白(Thrombomodulin,TM)为一种能与凝血酶结合的质膜蛋白,有广泛的生物学活性,主要分布于血管内皮细胞实体性肿瘤的血管形成是近十年来研究得较多的一个领域。

Screened with cOnidia of hauIthe mp, the bo of myce1iageednated frOm cOnidia of Prtubo mp was Observd Whe the mixtUr of CS-l l andcs-l2, aS well aS the COmPoUnd cs-7 were Presot. And the mtw of Cs-1l and cs-12shOwed grOWth-inhibitory activity ofendothlial cells and NIH-3T3 fibrobast in the.

稻瘟霉活性筛选结果显示CS-11和CS-12的混合物、CS-7具有使稻瘟霉孢子菌丝体变形的作用;体外药理实验显示,CS-11和CS-12的混合物具有显著的体外抑制血管内皮细胞生长作用及抑制血管成纤维细胞生长作用。

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