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There was an obvious increase of insulin receptor gene and protein in the cerebral ischemia reperfusion tissues in rats. The positive cells such as neuron, neuroglia cells, vascular endothelium cells possibly participated in regulating the processes of energy metabolism of cells and neovascularization. It implied that the high expressions of insulin receptors in vascular endothelium cells in ischemic zones possibly participated in regulating the pathophysiological changes of the blood vessels in ischemic zones; The higher expressions of insulin receptors in different cells were possibly one of the self-protective machanisms in which the ischemic tissues confront the anoxemia injury.

脑缺血再灌注大鼠脑组织胰岛素受体基因和蛋白水平表达增加;半暗带区神经元、部分神经胶质细胞及血管内皮细胞等阳染细胞可能参与脑缺血后组织细胞的能量代谢、促新生细胞形成等病理生理调节过程;胰岛素受体在缺血区血管内皮细胞高表达提示其可能在缺血区血管的病理生理变化中起某种调节作用;胰岛素受体在不同细胞中表达增高可能是缺血脑组织对抗缺血缺氧损伤的自身保护机制之一。

Human umbilical venous endothelial cells were cultured, and were exposed to different concerntrations of HCY with/or not with CuSO4; Cell counting of detached cells were performed with a hematocytometer; the cell survival was monitored by MTT assay and the cellular injury was evaluated by LDH release; Hoechst 33258 staining was used to observe nuclear morphological changes and the apoptosis was measured by DNA agarose gel electrophoresis ;the percentage of apoptosis was quantified by flow cytometry.

体外培养人脐静脉血管内皮细胞,用不同浓度的HCY伴/不伴生理浓度Cu~(2+)与内皮细胞作用;细胞计数板检测脱落细胞率;MTT法及乳酸脱氢酶释放率的测定来衡量细胞的存活与损伤;Hoechst 33258荧光染色观察细胞核形态变化和DNA琼脂糖凝胶电泳检测细胞凋亡,并采用流式细胞术定量测定细胞凋亡率。

HBV transplacental transmission route may be realized by cell to cell transfer in placenta, which means that HBVs in maternal blood and/or intervillous space infect DCEC and/or DC and/or TC, then transmit to VMC, then to VCEC, and finally to fetus.

HBV经胎盘感染胎儿的路径可能是通过胎盘细胞至细胞的传递而实现的。即母血和/或绒毛间隙HBV→蜕膜毛细胞管内皮细胞和/或蜕膜细胞和/或滋养层细胞→绒毛间质细胞→绒毛毛细血管内皮细胞→胎儿。

Methods Pterygial samples were extracted and collected and the pterygial endothelial cells and pterygial fibroblasts were cultured alone, conditional and co-cultured to form different culture systems. The methods included that to select the suitable intensity of ultraviolet by MIT, to detect the changes of curves of growth about two kinds of cells by MIT and to explore the developments of protein and RNA of vascular endothelial growth factor and fibroblast growth factor-basic in three culture systems under ultraviolet whose intensity is 20 mJ/cm^2 by ELISA and RT-PCR.

收集翼状胬肉标本,采用血管内皮细胞和成纤维细胞单独培养、条件培养和共同培养的方法构建体系,用MTT法选择紫外线照射细胞的适宜强度;采用MTT法绘制强度20mJ/平方公分紫外线照射下细胞生长曲线;采用ELISA和RT-PCR检测紫外线照射下3种体系中细胞上清液和细胞中血管内皮细胞生长因子和成纤维细胞生长因子的蛋白和RNA含量变化。

Immunofluorescence assay was used to detect endothelial cell uptake and absorption acetylated low density lipoprotein and ulex europaeus agglutinin-Ⅰ. EPCs quantitative detection of surface markers was performed by flow cytometry: CD133, CD34 antigen expression and KDR.

通过免疫荧光法观察内皮细胞吸收乙酰化低密度脂蛋白和荆豆凝血素Ⅰ情况,流式细胞仪定量检测血管内皮祖细胞表面CD133、CD34和KDR抗原表达阳性率来鉴定血管内皮祖细胞。

At least 0.1μg/ml of endotoxin can induce the morphologic changes and the decrease of F-actin in HUVECs. Endotoxin can injury HUVECs only when its concentration reaches 0.4μg/ml and incubates over 12 hours. It suggests there is a different molecule mechanism in VEC from the endotoxin-CD14 pathway in CD14 positive cells.

内毒素直接损伤血管内皮细胞须较大浓度(>0.4μg/ml),但在较低浓度下(0.1μg/ml)可直接引起内皮细胞的一些形态学变化和F-actin含量的变化,初步推测血管内皮细胞可能存在着与通常认识的内毒素—内毒素结合蛋白—CD14途径激活细胞不同的分子机制。

Results VEGF-C and VEGFR-3 are all expressed on both mesenchymal cells and vascular endothelium of the embryos during early period. In middle and latter period, VEGFR-3mRNA is mainly expressed on cell plasm of alimentary canal, but it has no expression on vascular and lymphatic endothelium; The expression of VEGFR-3 is extensive and positive expression is seen on the vascular and lymphatic endothelium.

在胚胎中、后期消化道组织中VEGF-C主要表达于消化管壁组织细胞以及肠系膜内,在血管和淋巴管内皮细胞则无表达;VEGFR-3亦表现为广泛的表达,于血管和淋巴管内皮细胞可见阳性表达,并随着胚胎的发育,其在淋巴管内皮细胞的阳性表达率明显增加。

The positive expression rates of Tissue Inhibitors of Metalloproteinase-2 protein in the cases of involuting groups were significantly higher than those in proliferating group and vascular malformation groups and normal skin group (P.05). Its difference was significant. Conclusions: Matrix MetallProtinase-2 and Tissue Inhibitors of Metalloproteinase-2 may play an important role in the pathogenesis of hemangiomas through angiogenesis. They may have no effect on vascular malformation and normal skin

血管瘤退化期,TIMP-2表达明显升高,说明 TIMP-2与血管瘤纤维化、消退有关,其机制可能是一方面通过抑制MMP-2介导的基底膜降解而在内皮细胞迁移、聚集中起作用,另一方面直接抑制内皮细胞的增殖及迁移,使内皮细胞高频率调亡,细胞外基质增多,组织出现纤维化,最终导致血管瘤的退化。2、血管畸形和正常皮肤小血管中MMP-2和TIMP-2不表达或表达较弱,说明血管畸形和正常皮肤小血管中并不存在异常的血管生成,据此可以对血管性疾病进行分型、分期,并指导临床治疗。

Some cell dropped into the cavity and became free. Thrombosis or part organization could be seen. The internal elastic layer became thin, disappear or broken. In internal and middle layer existed fibroblasts, fibrocytes and collagen. Some of the wall indicated hyaline change, soomth muscle cell decreased greatly. The massive inflammatory cells invaded the middle and external layer. There were many foam cells in the capsule tissue. Cytoplasm was filled with fatty tissue and cholesterol. some cavities were full of thrombosis. Some thrombosis was fibrosis, the bottom was organization. The surface of the thrombosis existed red blood cell and librae.(2)Elatic fibrila staining: the internal elastic menbrane almost completely disappeared, the intact internal elastic menbran could be seen in the new small vessels.

动脉瘤管壁厚薄明显不均,全层或局部区域显著变薄向外膨出,内皮细胞空泡变性或坏死脱落,部分内皮细胞剥离并突入管腔成游离状,可见血栓形成及部分血栓机化;内弹力板变薄、消失或突然中断;在内膜及中膜部位主要为纤维母细胞、纤维细胞和大片胶原;部分动脉瘤壁呈均质状玻璃样变,平滑肌细胞明显减少;中膜和外膜可见大量的炎性细胞浸润;瘤壁组织有纤维母细胞、纤维细胞、大片胶原成分及较多泡沫细胞,胞浆内充满脂类物质及胆固醇结晶;部分动脉瘤腔内充满血栓,有的血拴已经纤维化,血栓基部机化,血栓表面有红细胞和纤维素。

Vascular endothelial cell growth factoris a kind of glucoprotein ,which has separated by culturing stellate cells of bovine glandula pituitaria in vitro by Ferrara etc. in 1989.lt can express that anxo-act vascular endothelial cell growth specificly and induce vasotropic growth ,so it is called VEGF.

血管内皮细胞生长因子(Vascular endothelial cell growth factor)是1989年Ferrara等牛垂体星状细胞体外培养分离出的一种糖蛋白,其在体内外都表现出特异性地促进血管内皮细胞的生长并诱导血管生成作用,故此称为血管内皮细胞生长因子。

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