查询词典 plerosis

Outcome:(1) Acute ischemic damage may induce the expression of c-fos protein in Cerebral Cortex quickly. Also, the expression increases by the ischemia time delay. It may hint that ischemia injury can rise the ability of nerve cells to tolerate ischemia and anoxia. And the expression level of c-fos can be up-regulated by putting blood of 12 hand Jing Points. So we think that treated by this therapy can rise the irritability of brain to resist the development of ischemia and enhance the ability to plerosis.(2) Acute ischemic damage may induce the expression of HspVO in Cerebral Cortex quickly. Also, the expression increases by the ischemia time delay. It may hint that ischemia injury can rise the ability of nerve cells to tolerate ischemia and anoxia.

三 结果(1)急性缺血性脑损伤可快速诱导c-fos蛋白在皮层缺血区脑组织的表达，其表达有随缺血时间延长而逐渐增多的趋势，提示脑的缺血性损伤可应激性地增强神经细胞对缺血、缺氧的耐受和适应能力，而应用井穴放血的干预治疗可明显上调缺血区皮层脑组织c-fos的表达水平，进一步增强脑组织对抗缺血性损伤的应激能力，抵抗缺血性脑损害的进一步发展。

Previous studies have shown that the mechanisms of MDR involve Pgp, MRP, LRP, BCRP, GSH/GST, PKC, Topo DNA plerosis, genes related to apoptosis and changes of cellular environment (such as pH, hypoxia and temperature).

目前发现的肿瘤多药耐药机制主要涉及Pgp、MRP、LRP、BCRP、GSH/GST、PKC、TopoⅡ、DNA修复、多种凋亡相关基因和肿瘤细胞生活的内外环境变化。

Previous studies have shown that the mechanisms of MDR involve Pgp,MRP,LRP,BCRP,GSH/GST,PKC,Topo DNA plerosis,genes related to apoptosis andchanges of cellular environment (such as pH,hypoxia and temperature).

目前发现的肿瘤多药耐药机制主要涉及Pgp、MRP、LRP、BCRP、GSH/GST、PKC、TopoⅡ、DNA修复、多种凋亡相关基因和肿瘤细胞生活的内外环境变化。

The therapeutic mechanism of the method of nourishing qi, activating blood, dispersing phlegm and promoting the collaterals was supposed as that it intervened the airway remodeling and alleviated the progress of airflow obstruction of COPD by suppressing the chemo taxis of cytokines, regulating the proliferation of fibroblast cell and smooth muscle cell and preventing the proliferation and plerosis of extracellular matrix.

推测益气活血化痰通络法防治COPD的机制可能为：通过抑制炎症细胞的趋化、影响细胞因子的活性、调节成纤维细胞和平滑肌细胞的增殖、阻止细胞外基质的增生修复，从而达到干预COPD患者气道结构重塑，减缓COPD气流受限进展的作用。

The human cartilages are composed of chondrocyte and extracellular matrix,the form of chondrocytes are hypertrophy and the quantity are less;the ECM of cartilage are compised of type II collagen and proteoglycan. Articular cartilages are all hyaline with little fibers. Trauma and arthritis are the main cause of cartilage injury,the ommilayer injury ofcartilage can be recovered by marrow,but because of without stimulation mechanism,the new tissues are merely fibrocartilages,they can not be coincide with hyaline cartilage in menchanics;the purely damage of articular cartilage can not stimulate chondrocyte to regenerate because of without blood circulation,thus,the plerosis of articular catilage can not depend on the proliferation of local chondrocyte.Ever since,people tried their best to find a way to reconstruct articular cartilage.

造成人体关节软骨损伤的原因主要为创伤和关节炎，关节软骨全层损伤可由于骨髓中间充质干细胞的高速增殖修复，但这种修复由于缺乏相应的刺激机制，只能形成纤维软骨，而不能形成符合关节生理、力学要求的透明软骨；单纯软骨部分损伤软骨组织内无血管，软骨细胞迁移迟缓，无法使损伤区域软骨细胞再生，因此，关节炎及关节创伤后的软骨修复不能依赖于软骨细胞的增殖和迁移。

Both Fas and NO can lead chondrocyte apoptosis respectively and cause articular cartilage destruction. IGF-Ⅰ, TGF-β, bFGF, BMP and other growth factors are polypeptide agents that can influence cell activity by signal convection. They can accelerate chondrocyte proliferation and proteoglycan synthesis, play the local regulation action on formation and plerosis of bone and cartilage tissue by autocrine or paracrine. They have the ability to induce cartilage formation. Some investigations showed that growth factors can influence chondrocyte metabolism, synthesis of specific Ⅱ type collagen and proteoglycan by co-operation and inhibition. 1. 3 Situation of OA therapeutics The therapeutic methods of OA mainly comprised non-drug treatment, drug treatment, operation treatment, tissue and genetic engineering, et al. Drug treatment is the chief method among them.

若其活性发生改变，则将导致关节软骨基质成分的丢失和进行性破坏；软骨细胞凋亡与OA的发病密切相关，Fas与NO可各自独立介导软骨细胞凋亡，造成关节软骨破坏；IGF-Ⅰ、TGF-β、bFGF、BMP等生长因子是一组通过细胞间信号传递影响细胞活动的多肽因子，具有促进细胞生长、增殖与合成等作用，可通过自分泌或旁分泌方式对骨和软骨的形成和修复起局部调节作用，可促进软骨细胞增殖、分化与蛋白多糖的合成，具有较强的诱导软骨形成的能力，研究表明多种生长因子相互促进、相互抑制，以协同或拮抗方式影响软骨细胞代谢，影响软骨细胞特异性Ⅱ型胶原和蛋白多糖的合成分泌。

The human cartilages are composed of chondrocyte and extracellular matrix , the form of chondrocytes are hypertrophy and the quantity are less; the ECM of cartilage are compised of type Ⅱ collagen and proteoglycan. Articular cartilages are all hyaline with little fibers. Trauma and arthritis are the main cause of cartilage injury, the ommilayer injury ofcartilage can be recovered by marrow, but because of without stimulation mechanism, the new tissues are merely fibrocartilages, they can not be coincide with hyaline cartilage in menchanics; the purely damage of articular cartilage can not stimulate chondrocyte to regenerate because of without blood circulation, thus, the plerosis of articular catilage can not depend on the proliferation of local chondrocyte.

造成人体关节软骨损伤的原因主要为创伤和关节炎，关节软骨全层损伤可由于骨髓中间充质干细胞的高速增殖修复，但这种修复由于缺乏相应的刺激机制，只能形成纤维软骨，而不能形成符合关节生理、力学要求的透明软骨；单纯软骨部分损伤软骨组织内无血管，软骨细胞迁移迟缓，无法使损伤区域软骨细胞再生，因此，关节炎及关节创伤后的软骨修复不能依赖于软骨细胞的增殖和迁移。

The human cartilages are composed of chondrocyte and extracellular matrix , the form of chondrocytes are hypertrophy and the quantity are less; the ECM of cartilage are compised of type Ⅱ collagen and proteoglycan. Articular cartilages are all hyaline with little fibers. Trauma and arthritis are the main cause of cartilage injury, the ommilayer injury ofcartilage can be recovered by marrow, but because of without stimulation mechanism, the new tissues are merely fibrocartilages, they can not be coincide with hyaline cartilage in menchanics; the purely damage of articular cartilage can not stimulate chondrocyte to regenerate because of without blood circulation, thus, the plerosis of articular catilage can not depend on the proliferation of local chondrocyte. Ever since, people tried their best to find a way to reconstruct articular cartilage.

中文题名人骨髓基质干细胞成软骨诱导及多孔复合材料作为细胞载体的体外实验研究副题名外文题名 Cartilage induction of human mesenchymal stem cells and experiment on compound porous materials as cells' scaffold in vitro 论文作者刘晓岚导师周江南学科专业外科学研究领域\研究方向学位级别博士学位授予单位中南大学学位授予日期2003 论文页码总数68页关键词骨组织工程软骨细胞骨髓基质干细胞壳聚糖高分子外消旋聚乳酸馆藏号BSLW /2003 /R68 /10 造成人体关节软骨损伤的原因主要为创伤和关节炎，关节软骨全层损伤可由于骨髓中间充质干细胞的高速增殖修复，但这种修复由于缺乏相应的刺激机制，只能形成纤维软骨，而不能形成符合关节生理、力学要求的透明软骨；单纯软骨部分损伤软骨组织内无血管，软骨细胞迁移迟缓，无法使损伤区域软骨细胞再生，因此，关节炎及关节创伤后的软骨修复不能依赖于软骨细胞的增殖和迁移。

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我尽力帮你找人帮忙。

At first I only know bruck is the idol of American younglings, afterwards I returned back to Taiwan ,even in Beijing last year ,I saw her poster everywhere, I was so surprised at her charm.

起初我只晓得布鲁克雷德丝是美国少男少女崇拜的偶像，后来回台湾，甚至去年在北京，居然也四处看见她的海报，才惊讶她的魅力之大。