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胶质细胞

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In recent years, bioresearch about ECM indicated that there some kinds of matrix effector cells play key roles in the formation of organic fibrosis and the activation of them is the main source of collagenation cells.

近年来关于ECM的生物学研究表明,在器官纤维化的形成过程中,往往有一些间质效应细胞发挥关键作用,它们的激活已成为胶原生成细胞的主要来源。

Results:Periodontal ligament cells formed confluent layer on Ti after 7 days .

结果 :牙周韧带细胞在纯钛表面生长良好,14天后形成单层,形成大量细胞基质,其成份主要为Ⅰ型胶原。

In the pathological proceeding of pulmonary fibrosis, myofibroblast plays an important role, such as: the abnormal extracellular matrix deposition causing by the remarkable capability of collagen synthesis, derogation of the lung compliance owning to the contractibility of myofibroblast,secreting many cytokines,which contribute to the damage of the alveolar epithelial cells.

肌成纤维细胞在PF的病理进程中扮演着重要的角色,其胶原合成能力强可造成细胞外基质的异常沉积、具收缩性使肺顺应性下降、分泌多种炎性介质加重肺泡上皮损伤。

It is composed of specialized cells called chondrocytes that produce a large amount of extracellular matrix composed of collagen fibers, abundant ground substance rich in proteoglycan , and elastin fibers.

它是专门组成所谓的软骨细胞以及产生大量细胞外的基质所组成的胶原纤维,含有丰富的蛋白多醣物质,以及弹性纤维。

Astragali many candies can be promoted into hyperplasia and collagenic formation of fibrous cells within the range of certain density, the ones that strengthened the wound ground substance are synthetic in order to promote the wound to heal.

细胞实验结果显示:黄芪多糖在一定的浓度范围内可促进成纤维细胞的增殖和胶原的合成,增强创伤基质的合成以促进伤口愈合。

Results Compared to those before treatment the volume of the implanted keloid of Group D began to decrease since 14 days after treatment time-dependently (all P 《 0.05), and the volumes of the other 3 groups continued to increase and peaked on days 21, 14, or 7 respectively (all P 《 0.05).Microscopy showed infiltration of a larger quantity of histiocyte in the keloid tissue, and more obvious collagen disorganization and apoptosis of fibroblasts in Group D than in the other 3 groups.The protein expression of Bcl-2 was more remarkable and the protein expression of BAX was less remarkable in Group D than iu the other 3 groups.

结果 用药前和用药后7、14、21、28、35 d,D组瘢痕疙瘩组织块体积(mm3)分别为173±5、172±5、147±5、125±6、112±7和84±9,从用药后14 d开始明显缩小(均P<0.05);而其他3组瘢痕疙瘩组织块体积均明显增大,从用约后7 d开始各时点测得的体积均明显大于D组(均P<0.05)。D组瘢痕疙瘩组织中有大量小鼠组织细胞浸润,胶原结构破坏和成纤维细胞凋亡明显重于其他3组,Bcl-2蛋门质表达明显弱于而Bax蛋白质表达明显强于其他3组。

E and Sirus red in supersaturated picric acid solution;the amount of HA in serum was measured with the method of radiative immunity;the quantitative expression of fibrosis factor—TGF、PDGF was measured with the method of immunity histochemistry.Results:Myocardial collagen in model group increased obviously compared with normal group from the results of electron microscope、H.E、Sirus red in supersaturated picric acid solution.

腹腔注射柯萨奇B3病毒建立病毒性心肌炎慢性期心肌纤维化小鼠模型,随机分为模型对照组、通心络低剂量组、中剂量组、高剂量组,并设正常对照组,用药四周后处死动物通过透射电镜观察心肌细胞超微结构;HE染色、苦味酸天狼星红染色观察心肌胶原数量;放免法测定血清透明质酸的含量;免疫组化染色观察致纤维化细胞因子—转化生长因子和血小板衍生生长因子的定量表达。

Methods:Establish the model of myocardial fibrosis in chronic stage of viral myocarditis by injecting CVB3 into Balb/c rats,divide these rats into model group、Tong xin luo low dose group、Tong xin luo medium dose group、Tong xin luo high dose group and set up normal group,after four weeks of giving medicine execute the animals and observe the ultrastructure of myocardial cell with tramission electron microscope,the quantity of myocardial collagen was observed by staining with H.E and Sirus red in supersaturated picric acid solution;the amount of HA in serum was measured with the method of radiative immunity;the quantitative expression of fibrosis factor—TGF、PDGF was measured with the method of immunity histochemistry.

腹腔注射柯萨奇B3病毒建立病毒性心肌炎慢性期心肌纤维化小鼠模型,随机分为模型对照组、通心络低剂量组、中剂量组、高剂量组,并设正常对照组,用药四周后处死动物通过透射电镜观察心肌细胞超微结构;HE染色、苦味酸天狼星红染色观察心肌胶原数量;放免法测定血清透明质酸的含量;免疫组化染色观察致纤维化细胞因子—转化生长因子和血小板衍生生长因子的定量表达。

Most endothelial cells fell off, elastic fibre autolyze; the number of SMC decreased, some SMC nucleus contracted completely or depressed, typical apoptosis body were seen in later stage, muscle silk autolyzed and disappeared mostly; in outer layer saw much collagenic fiber, arranged unorderly; inflammation cells were seen in the aneurysm wall(hypertrophy cell et al.).

多数瘤壁的内皮细胞溶解脱落,不连续,弹力纤维自溶;动脉瘤血管壁均可见SMC明显减少,较多SMC染色质边聚、固缩,部分SMC核全部固缩或出现不规则凹陷,SMC核胞浆或胞核部分出现脱落或裂解成碎片,晚期可见典型的凋亡小体出现,肌丝大都自溶消失:外膜可见大量的胶原纤维,排列较紊乱;瘤壁还可见炎性细胞浸润。

Results Microscopically, the tumor cells were epithelioid or short spindled and special nests of tumor cells separated by arboring fibrovascular septa. Such morphological variants of CCSK as myxoid degeneration, microcysts formation and sclerosing pattern of extracellular hyalined collagen simulating osteoid were present in some regions.

结果 镜下见瘤细胞为上皮样或短梭形,被分枝状纤维血管间质分隔成巢团状,部分区域见黏液样变性微囊肿和细胞外胶原玻璃样变类似骨样组织的硬化型等形态变异。

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