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DATA SYNTHESIS: Il-17 exerted the biological function after combines with its receptor maybe induced the occurrence and the development of the osteoarthritis by the way of increasing the chondrocyte, expression of inducible nitricoxide synthase and nitrogen monoxide, boosting up the tbe chondrocyte and the expression of MMP-1/3/13, boosting up the activation of the aggrecanase and the collagenase, boosting the decompose of the cartilage proteoglycan and collagen, boosting up the monocyte evocable breakage of the cartilaginous matrix.

资料综合:白细胞介素17通过与其受体结合发挥生物学作用,其可能通过增加关节软骨细胞诱导性一氧化氮合酶表达和一氧化氮产量,增强软骨细胞基质金属蛋白酶(MMP-1/3/13)的表达,增强蛋白聚糖酶和胶原酶活性,促进软骨蛋白多糖及胶原降解,并增强单核细胞对软骨基质的破坏,从而诱导和加速骨关节炎的发生和发展。

Vascular endothelial growth factor is an important angiogenine. There is accumulating evidence shows that expression of VEGF in mature chondrocyte can promote cell redifferentiation and caryocinesia activity. VEGF plays a key role for chondrocyte to survival and proliferation during the chondrogenesis.

对成熟软骨细胞分泌表达蛋白的研究发现,软骨细胞表达一定水平的VEGF以提高软骨细胞有丝分裂活性并促进其再分化,在软骨发生发育过程中,对软骨细胞的存活与增殖起着重要的作用。

After 24 weeks,the operation area of group A was more smooth,and the surrounding normal cartilage naturally straight flush,transparent form new cartilage,subchondral bone formation in good condition;Group B restoration surgery the basic integrity of the cartilage tissue, center is not yet fully integrated,there was slight depression;CollagenⅡimmunohistochemistry of cartilage that was new brown area.Group C has no formation of articular cartilage.The growth and the intergration of subchondral bone of group A and B were better.

术后24周取材,见A组山羊手术区关节表面较为光滑,与周边正常软骨自然连续平齐,透明的新生软骨组织形成,软骨下骨形成完好;B组山羊手术区修复的软骨组织基本完整,中心部位仍未完全融合,有微小凹陷;Ⅱ型胶原免疫组化示新生软骨组织呈棕黄色。C组术区关节凹陷,无关节软骨组织形成。A组和B组,软骨下骨的生长及与周围组织的结合均较好,无植入物脱落现象的发生。

These include inflammatory arthritides such as rheumatoid arthritis, ankylosing spondylitis and reactive arthritis,99 101 synovial impingement,meniscoid entrapment, chondromalacia facetae, pseudogout,synovial inflammation, villonodular synovitis, and acute and chronic infection.102 106 Intrafacetal synovial cysts can be a source of pain because of distension and pressure on adjacent pain-generating structures, calcification,and asymmetrical facet hypertrophy.107 110 In a retrospective review of MRI scans in 303 consecutive patients with LBP, Doyle and Merrilees111 found that9.5% had facet joint synovial cysts, the large majority of which were located posteriorly.

包括炎症性关节炎如类风湿性关节炎,强直性脊柱炎及反应性关节炎等,还有滑液撞击,关节软骨版卡压,关节面软骨软化,假性痛风,滑液炎症,绒毛结节性滑膜炎和急慢性感染。小关节内滑囊囊肿可由于拉伸和压缩临近的疼痛发生结构,骨化及不对称关节增生等原因引起疼痛。在一项303例连续患者的MRI研究中,Doyle 和 Merrilees发现其中9.5%存在小关节囊肿,大部分发生于关节囊后部。

Therefore to study the molecule regulation mechanism of development and maturation of condylar cartilage in embryo, can not only discover the mechanism of its physiological rebuilding and restoration to set up the academic base for related treatment in clinic, but possiblely supply new treatment methods for trauma and destruction to articular cartilage. Histological and immunohistochemistry methods have been used to state the feature of development of the mandibular condylar cartilage, and molecule mechanism of its endochondral ossification.

目前对四肢关节软骨、生长板软骨的发生及再生修复的研究较为深入,而髁突软骨的发生、生理改建及再生修复机制的研究尚处于起步阶段,因此研究胚胎期髁突软骨发育及形成的分子调控机制,可望揭示其生理性改建及损伤修复的机制,为临床有关治疗奠定理论基础,并可能为关节软骨的损伤及破坏提供新的治疗手段。

The process of osteoarthritis mesochondrium degradation is possibly attributed to the synergistical consequence of MMPs and other factors. Pilose antler peptide can promote the proliferation of OA chondrocytes of rabbits ,inhibit the overexpression of MMPs of OA chondrocytes.It can possibly play a effective role in the treatment of OA.

结论骨性关节炎软骨细胞在骨性关节炎发病过程中,软骨细胞正常分化及增殖发生改变;骨性关节炎软骨基质降解过程可能是金属蛋白酶与其它因子协同作用的结果;鹿茸多肽可促进骨性关节炎软骨细胞增殖,并可抑制骨性关节炎软骨细胞中金属蛋白酶的过度表达,可能对治疗骨性关节炎有较好的作用。

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。

Based on these MRIs, researchers determined how much cartilage loss occurred over time at the two joints of the knee: the tibiofemoral joint, where the thigh bone meets the lower leg bone; and the patellofemoral joint, behind the kneecap.

基于这些,磁共振成像,研究人员确定有多少软骨发生损失随着时间的推移,两个关节膝关节:胫股关节,大腿骨会见小腿骨骼;及髌股关节,后面膑。

A slipped disc occurs when the jelly-like disc of cartilage that acts as a cushion between two vertebrae in the spine, slips or prolapses so it is pressing on the nerves causing the muscles of the back to go into spasm.

椎间盘脱出是由于脊柱两块椎骨中的起缓冲冲击作用的胶状椎间盘软骨发生滑动或脱垂时,压迫椎管内神经引起后背痉挛。在严重的情况下椎间盘软骨不得不通过手术的方法移走,在一些情况下脊柱的骨头被熔合了避免进一步的移动。

Of hereditary multiple exostoses and solitary osteochondromas, 9% and 1.3% to 4.1%, respectiely, occur in the spine. In either case, neurologic symptoms are not common.

遗传性多发性外生骨疣病和孤立骨软骨瘤发生于脊柱的比率分别是9%及1.3%~4.1%,两种情况(发生于脊柱的遗传性多发外生骨疣及孤立骨软骨瘤)下,神经系统症状并不常见。

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