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Results Cvb-D obviously lightened isoprenaline-induced myocardial pathological changes such as turbulence of myocardial fiber, plasmolysis of necrotic cell, inflammatory cell infiltration of necrotic interstitial region. Cvb-D remarkably inhibited myocardium cell apoptosis of myocardial ischemia rats caused by isoprenaline.

结果 Cvb-D可显著减轻Iso诱发的心肌缺血致心肌肌纤维排列紊乱,坏死细胞胞泉溶解,坏死间质区炎性细胞浸润等病理改变;Cvb-D可显著抑制Iso诱发的心肌缺血性模型大鼠心肌细胞凋亡。

Discussion TNF-αis an inflammatory cell cytokine,with the properties of autocrine, produced by cadiocyte at the early age of MIRI,inducing myocardial function abnormal and cadiocyte necrosis in MIRI、pyaemia、chronic cardiac insufficiency、viral myocarditis and the homograft rejection of heart.

讨论 TNF-α是心肌缺血再灌注早期心肌细胞产生的炎性细胞因子,是一种自分泌的作用因子,在缺血再灌注损伤、脓毒症、慢性心功能不全、病毒性心肌炎以及心脏同种移植排斥反应中均能导致心肌功能能障碍和心肌细胞坏死。

The mice were sacrificed on 7, 10, 14, 21 and 28 days post-inoculation and then the hearts were aseptically removed. Pathological changes in the myocardium were observed by light microscopy and the expression of the CD4+ T lymphocyte in the myocardium was determined by immunohistochemistry. ResultsThe CD4+ T lymphocyte was found in the myocardium in the CVB3 infection group.

分别于接种病毒后第7、10、14、21、28d随机取正常对照组小鼠3只、病毒感染组小鼠8只断髓处死,无菌条件下取心脏,光镜下观察心肌组织的病理变化并计算心肌病理组织学积分,应用免疫组化方法检测CD4+ T细胞在心肌中的表达,并与心肌病理组织学积分作相关性分析。

Spontaneous differentiation of ESCs and iPSCs into cardiomyocytes is however limited. To elucidate the regulatory mechanisms and effectively differentiate these pluripotent cells into specific cardiomyocytes are crucial to obtain fundamental knowledge in cardiogenesis, screen drugs and promote the usage of these cells in replacement therapy. This review summarizes the current state of differentiation of cardiomyocytes from mouse and human ESCs and their regulatory factors.

但这些多能干细胞向心肌细胞自发分化的效率非常低,因此,如何有效地诱导这些多能干细胞向心肌细胞的定向分化对深入认识心肌发生发育的关键调控机制和实现其在药物发现和再生医学,如心肌梗塞、心力衰竭的细胞治疗以及心肌组织工程中的应用均具有非常重要的意义。

Spontaneous differentiation of ESCs and iPSCs into cardiomyocytes is however limited. To elucidate the regulatory mechanisms and effectively differentiate these pluripotent cells into specific cardiomyocytes are crucial to obtain fundamental knowledge in cardiogenesis, screen drugs and promote the usage of these cells in replacement therapy.

但这些多能干细胞向心肌细胞自发分化的效率非常低,因此,如何有效地诱导这些多能干细胞向心肌细胞的定向分化对深入认识心肌发生发育的关键调控机制和实现其在药物发现和再生医学,如心肌梗塞、心力衰竭的细胞治疗以及心肌组织工程中的应用均具有非常重要的意义。

Doetschman TC, Eistetter H, Kemler R, et al. The in vitro development of blastocyst-derived embryonic stem cell lines: formation of visceral yolk sac, blood islands and myocardium [J]. J Embryol Exp Morph, 1985,87:27~45.[2] Robbins J, Doetschman T, Jones WK, et al. Embryonic stem cell as a model for cardiogenesis[J]. Trends Cardiovasc Med, 1992,2:44~50.[3] Moreadith RW, Radford NB.

被诱导的心肌细胞的判定除常规指标外,我们还用了心脏特异性引物β-MHC对不同收缩时间的心肌细胞总RNA进行RT-PCR扩增和RNA斑点杂交,发现该心肌细胞不仅具有正常心肌细胞的特性,而且在分化早期就高度地表达心脏特异性基因。

Methods In APS group and diabetes mellitus control group, levels of serum glucose, insulin, C peptide, myocardial enzymes, glycosylated serum protein and angiotensin Ⅱ in plasma and myocardial were tested; Immuno-histochemistry was used to measure expression levels of type Ⅰ and type Ⅲ collagen; Expression levels of chymase Mrna and angiotensin-converting enzyme mRNA were detected by using fluorescent quantitative polymerize-chain-reaction; Activities of chymase and ACE were tested by radioimmunoassay.

检测APS治疗组和DM对照组仓鼠的血糖、胰岛素、C肽、心肌酶谱、糖化血清蛋白水平,血浆和心肌组织的AngⅡ含量;免疫组化法检测心肌Ⅰ、Ⅲ型胶原;荧光定量PCR法检测心肌chymase和ACE mRNA表达;放免法检测chymase和ACE活性。

In TUNEL assay it can be observed that cystamine can reduce myocardial cell apoptosis . At the same time Western Blot analysis to prove cystamine can reduce cardiac cell apoptosis and Deth receptor and Mitochondria through theses two pathsway, NF-κB protein expression significantly increased furthermore, it promots cell survival, which can reduce cardiac hypertrophy,apoptosis.

在TUNEL assay中可以观察到胱胺可以减少心肌细胞的凋亡,同时我们也利用Western Blot证明胱胺可以减少心肌细胞的凋亡是透过Deth receptor和Mitochondria这两条路径,而这样子降低凋亡的现象很有可能与NF-kB这讯息传递的分子上升有关,因此胱胺确实具有保护心肌细胞的作用,可改善心肌细胞肥大、凋亡的情形。

In recent animal studies intramyocardial transplantation of ESCs or their differentiated cardiac-like cells regenerated injured myocardium and improved heart function in infarcted animal models.

新近的研究表明,在心肌梗死动物模型中,心肌内移植胚胎干细胞或由其分化成的心肌样细胞,能导致已损伤心肌的再生,并改善心脏功能。

Immunofluorescence staining shows that, the CaN Aβ protein expression of intrapericardial injection group decreased in some myocytes under epicardium, while other groups show no decreased fluorescence.

三在体心肌CaN AβsiRNA表达质粒转染后,转染各组与心肌肥大模型组CaN AβmRNA水平比较无差异(P>0.05),但免疫荧光结果显示心包腔内途径CaN Aβ干扰组较心肌肥大模型组心外膜下部分心肌荧光减弱。

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