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肥大细胞

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Results The hind limb function of the injured rats recovered at different degrees, the most extent recovery occurred during the time site 1~2 week, recovery continued from 2 to 3 week and, BBB was up to 12 at the end of the third week, but there was no significance recovery during 3~4 week. the astrocyte caudal to the injury plane began hyperplasy and hypertrophy; astrocyte in which GFAP in expression was positive the gray matter increased obviously from 3 days to 14 days after hemisection. The expression of MBP is same as that of GFAP.

结果 伤后后肢均有不同程度的恢复,1~2周时恢复幅度最大,2~3周时后肢运动功能继续恢复,3周时BBB评分最高达12分,3~4周运动功能无显著性恢复,损伤后1 d损伤远端3~6 mm处GFAP阳性星形胶质细胞开始增生肥大,3~4 d灰质中星形胶质细胞明显增多,2周时达到高峰,损伤近端3~6 mm处少突胶质细胞的增生反应过程与星形胶质细胞相似。

Results一. Culturing and identification of human conjunctiva cells1. morphous of conjunctiva cellsCells were harvested by tissue cultivation after digestion. Ponderosus cells adhered after 48 hours. Cells were shown in shape of round, ellipse and polygon. Cell body was loose and lucency with nucleus in center, cell membrane was also clearly seen. Cells were arranged in inlay and fuse in film after 12-14 days.2. Immunochemistry testNomogeneous immunochernical positive granules against CK13 were observed in endochylema of human conjunctiva cells.3. growth curve of conjunctival cellsSubcultured cells were aged and feeble after 5th passage.

结果一、正常人结膜细胞的培养与鉴定1、活体细胞的形态消化后组织块培养法:48小时后见大量上皮细胞贴壁,细胞不规则呈圆形、椭圆形、多边形,细胞体肥大透亮,细胞核位于中央,胞膜清楚,约12-14天后细胞呈镶嵌状排列,融合成膜状。2、免疫组化鉴定培养的人结膜上皮细胞CK13免疫组化染色见阳性颗粒均匀分布于胞浆中。3、培养结膜细胞生长曲线传代培养多数样本于P5代以后开始出现衰老征象。

The cells in the cambial layer of the periostlum showed low or negative signal in the immediate injury response period. The osteoblasts differentiated from the periosteum cells stained strongly in the intramembranous ossification period, and the differentiated chondrocytes stained most strongly in the chondrogenesis period.

结果 在急性损伤反应期,血肿延伸范围内的骨膜内层细胞有少量表达;在膜内成骨期,成骨细胞表达量较高,骨膜细胞表达量少;在软骨形成期,成熟软骨细胞表达量最高;在软骨内成骨期,肥大软骨细胞不表达,成骨细胞表达量较高。

RESULTS: Twelve days after mandibular vertical functional positioning the condylar height increased. Nine days after mandibular vertical functional positioning the thickness of prechondroblast layer and chondroblast layer increased significantly compared with control groups. However the thickness of hypertrophic layer decreased significantly after 6 days' mandibular repositioning. No change was found in the thickness of mesenchymal layer during the experimental period.

结果:下颌垂直向功能性移位后12d,髁突高度较对照组显著增加,前斜面更倾斜;髁突后上区前成软骨细胞及成软骨细胞层厚度在实验第3~6天无明显差异,第9天开始出现显著变化,实验组较对照组显著增厚,这种变化持续到实验第12天;肥大软骨细胞层厚度在实验第3、9、12天,实验组与对照组无显著差异,在实验第6天较对照组显著减少,间充质细胞层变化不大。

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。

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。

Its pathologic mechanism has the close relation to high blood sugar, the excrescent of kidney blood dynamics and the household hereditary, etc. Following the improvement of molecular biology, in recent years, many people discovered that many varieties of cell factors take part in the process of DN and exertive important functions.

近年来随着分子生物学技术的进步,研究发现有多种细胞因子参与DN的发生发展过程,其中以转化生长因子、血小板衍化生长因子为核心因子,其作用涉及到肾小球血流动力学改变、细胞外基质代谢、细胞增殖和细胞肥大等诸多方面。

Receiving signals from any kinds of cascades, a number of transcription factors have been implicated as direct mediators of hypertrophic gene expression including SPl, Elk-1, SRF, MEF-2, GATA, and LIM proteins.

目前虽然认为心肌肥大的发病机制与细胞外的心肌肥大因子刺激、细胞内的信号转导和核内的某些基因活化有关,但其最本质的特征是心肌细胞基因表达的异常。

Results Positive staining for VEGF was distributed mostly in osteoblasts, osteoclasts and newly-born osteocytes. Vascular endothelial cells and bone marrow cells also showed VEGF positive reaction. Hypertrophic chondrocytes in calcifying region of chondroephysis were VEGF positive, but VEGF was absent from chondrocytes in other zones of chondroephysis.

结果 VEGF阳性反应主要见于成骨细胞、破骨细胞及新生骨细胞中,血管内皮细胞及骨髓细胞也呈阳性反应;骺软骨钙化区肥大的软骨细胞为VEGF阳性反应,但其它区域的软骨细胞中无VEGF表达。

RESULTS:(1) ET-1 could increase total protein production, surface area, ERKs activity and [Ca2+]i in cultured cardiomyocyte in dose-dependent manner at concentrations ranging from 10-9 to 10-7 mol/L. And this effect could be abolished by BQ123, an antagonist of ETA receptor, partly inhibited by PTX, but not by BQ788, an antagonist of ETB receptor.(2)The activation of ERKs and the increase of [Ca2+]i induced by ET-1 were obviously inhibited by PD98059, a selective ERKs kinase inhibitor, and nifedipine, a calcium channel blocker, respectively. Both antagonists partially inhibited ET-1-stimulated cardiomyocyte hypertrophic response.(3) Staurosporine, a selective PKC inhibitor, could inhibit ET-1-stimulated cardiomyocyte hypertrophic response and increase of [Ca2+]i, but not affect the activation of ERKs.

结果: ①ET-1浓度依赖性增加新生大鼠心肌细胞蛋白质含量和心肌细胞表面积、ERKs活性及[Ca2+]i浓度,以上作用可被ETA受体拮抗剂BQ123所完全抑制,被百日咳毒素部分抑制,而ETB受体拮抗剂BQ788则无效;②ERKs激酶特异性抑制剂PD98059可完全抑制ET-1激活ERKs的作用,钙通道拮抗剂硝苯地平可明显抑制ET-1介导的[Ca2+]i浓度增加,但二者皆仅部分抑制ET-1介导的心肌细胞肥大反应;③蛋白激酶C选择性抑制剂staurosporine并不能明显抑制ET-1介导的ERKs激活,但可抑制ET-1介导的的[Ca2+]i浓度增加及心肌细胞肥大反应。

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