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The degradating and redistributing of ECM were migration of VSMC and vascular remodeling through inhibiting the production of PDGF-BB and the activation of MMPs so to prevent the vascular stenosis.⑤Orthotopic hybridism in situ: The expression of MMP-3 increased after operation, the tendency and intensity were parallel to the expression of NF-κB. Tongxinluo could decrease the expression of MMP-3 and NF-κB. The study showed that the producting and activating of MMP-3 were modulated by NF-κB. The inhibition to the producting and activating of MMp-3 of Tongxinluo was mediated by inhibiting the activating of NF-κB. Conclusion ①The rabbit vascular stenosis model could be established successfully by plain balloon damage, the operation process was easy, economical and practical.

①单纯球囊损伤可成功建立典型家兔血管狭窄模型,操作方法简单,经济实用;②以VSMC增殖、迁移为主的内膜增厚以及以ECM降解、合成与再分布所致的血管重构是导致受损血管狭窄的根本原因;③通心络能明显抑制VSMC的增殖、迁移和ECM降解、合成,阻止血管内膜增生和血管重构,防止受损血管狭窄;该作用可能与其减少和阻止PDGF-BB的产生和活性,以及抑制MMPs的表达和恢复MMPs/TIMPs平衡有关;④通心络能显著抑制球囊损伤后血管内膜增生和血管重构,可能与其保护血管内皮,改善内皮功能,增加血清NO含量有关;⑤通心络抑制内膜增生和血管重构,减轻受损血管狭窄,还可能是通过抑制NF-κB的活化途径而起作用的。

In the following up for 24 month of 34 cases, patency rate of sacculus proprius expanded was 79.7% and endoluminal stent was 85.7% respectively.

结果: 动脉血管再管化即时成功46例。34例随访24个月,血管腔内球囊扩张及球囊扩张加支架移植再管化24个月通畅率分别为78.57%及85%。

Objective To study the relationship of endangium proliferation and the expression of metalloproteinases and tissue inhibitors of metalloproteinases after angioplasty of iliac artery in rabbits to investigate the probable mechanism of composite Danshen pill in prevention and treatment of restenosisMethods 30 white male rabbits of Japan (the average body weight was 25~30 kg)were randomly divided into 3 groups:normal control group,model group (intima destroyed by balloon and given hypercholesterol diet),CDP group (intima destroyed by balloon and given hypercholesterol diet plus drug CDP 150 mg/d),10 ones each groupResults The results of iliac artery angiogram and the analysis of pathology:there were lumens stenosis,thinner intima,smaller intima area,in CDP group compared with those in model group,and ratio of intima and tunica media thickness and area among each group (P<001)Immunohistochemistry analysis:the MMP2,MMP9,TIMP1,TIMP2 in model group significantly increased than those in control group (P<001)The CDP group had lower MMP2 and MMP9 expression,higher TIMP1 and TIMP2 expression,and increased MMP2/TIMP1,MMP9/TIMP2 than model group (P<001)The thickening of vascular neointima and stenosis degree of vascular lumen were relevant to MMP2 and MMP9 (r=0896,P<001)Conclusions MMP and TIMP play the very important role in the restenosis process of arteryCDP could inhibit the thickness of vascular neointima after balloon injury,the probable mechanism of which may be inhibiting collagen formation,smooth muscle immigration and decreasing hyperplasia of intima by interfering expression of MMPs and TIMPs

目的 研究兔髂动脉成形术后血管内膜增生和基质金属蛋白酶及其抑制物表达之间的关系,探讨复方丹参滴丸预防再狭窄的可能机制。方法健康成年二级雄性日本大耳白兔30只,平均体重25~30 kg。随机分为3组:正常对照组10只,模型组10只(球囊内膜剥脱加高胆固醇饮食),治疗组10只(球囊内膜剥脱加高胆固醇饮食以及复方丹参滴丸150 mg/d)。结果兔髂动脉造影、血管病理图像分析检测结果:①复方丹参滴丸组较模型组血管造影示管腔直径狭窄、内膜厚度减少、内膜面积减少、内膜厚度和中膜厚度比、面积比,各组之间有显著性差异(P<001)。②免疫组化分析:模型组MMP2、MMP9、TIMP1、TIMP2表达均高于对照组(P<001);复方丹参滴丸组MMP2、MMP9的表达低于模型组,而TIMP1、TIMP2的表达高于模型组;TIMP1/MMP2、TIMP2/MMP9明显增加,差异有显著性(P<001)。③内膜的增生以及管腔的狭窄程度与MMP2、MMP9有很好的相关性(r=0896,P<001)。结论 MMP和TIMP在再狭窄形成中起重要作用;复方丹参滴丸能够明显抑制血管损伤后的内膜增生,可能的机制是通过影响金属蛋白酶MMP2、MMP9及其抑制物TIMP1、TIMP2的表达从而抑制胶原的生成、平滑肌的迁移、增生,而减少内膜的增生。

An endodermal sinus tumor of the testis is shown composed of primitive germ cells that form glomeruloid or embryonal-like structures.

睾丸的内胚层窦肿瘤由原始生殖细胞构成,这些细胞形成血管球或胚芽样结构。

It is not uncommon to see lymphocytes accompany just about any chronic renal disease: glomerulonephritis , nephrosclerosis , pyelonephritis .

在一些慢性肾脏疾病中通常可以观察到一些淋巴细胞,如:血管球性肾炎、肾硬化、肾盂肾炎。

Special staining methods, such as Masson and the Van Gieson staining were used to study the distribution of collogen fibers and elastic fibers. ResultsBy HE staining, the subepithelial connective tissues and vessels in the pterygium were more prominent than normal conjunctival tissues. An amorphous subepithelial superficial hyalinized zone and coarse eosinophilic granular materials were observed in the pterygia, but they were not found in normal conjunctival specimens. Coarse fibers were visible only in the deeper subepithelial connective tissues of pterygial samples. With Masson′s staining, the dense staining of collagen fibers was also more prominent in the pterygium than in the subepithelial connective tissues of normal conjunctiva. Abnormal collagen fibers were visible in the deeper sub-epithelial connective tissues of pterygial samples. With Van Gieson staining, abnormal collagen fibers were visible in the deeper subepithelial connective tissues. Dark coarse elastic fibers were found in the abnormal fibers only in the subepithelial deep connective tissues of pinguecula in the pterygia but not in the conjunctiva. With immunohistochemistry staining, MMP-3 was strong in the pterygial epithelium, moderate in fibroblast and absent from pterygial vascular walls. LN was strongly expressed in the blood vessel wall, moderately in the epithelial basement membrane and absent from the entire stroma.

结果HE染色:翼状胬肉组织上皮下基质中存在结缔组织的增生和血管形成;基质浅层存在一无定形物质透明区及粗糙的颗粒样嗜酸性物质,在翼状胬肉体部深层基质中存在粗糙的纤维组织;正常球结膜组织细胞排列整齐;基质为疏松结缔组织,胶原纤维平行排列,其间可见成纤维细胞,散在少量中性粒细胞、毛细血管;Masson染色:翼状胬肉浅层基质中存在致密的胶原纤维染色,深层基质中的胶原纤维存在变性样改变;VG染色:翼状胬肉组织深层基质中存在大量变性的胶原纤维,其间夹杂黑色的弹性纤维;免疫组化染色法:MMP-3在翼状胬肉上皮细胞中呈强表达,成纤维细胞中呈中等强度表达,血管内皮细胞中未见表达;LN在血管壁中呈强表达,在上皮细胞基底膜中呈中等强度表达,在整个基质中未见明显表达;col Ⅲ在整个翼状胬肉基质中呈强表达。

The expression of AT2R gene can be regulated efficiently in vivo by local delivery of MSC with dual-stable expression of AT2R gene, thus reduces the formation of intimal hyperplasia.④AT2R gene can influence the expression of ECM and significantly promote the cellular apoptosis in the injury rat carotid artery.⑤These data demonstrate the clinical potential of AT2R regulatable expression to prevent restenosis after PCI.

研究结论:(1)与VSMC直接接触可以诱导MSC向血管成分细胞分化;(2)构建的Dox-on可调控的MSC细胞株诱导活性可靠,使外源AT2R基因的表达处于有效的主动控制下;(3)局部导入MSC不影响球囊损伤后大鼠颈动脉新生内膜增生;(4)由MSC介导的AT2R可调控表达受到Dox的良好调控,可有效抑制球囊损伤后大鼠颈动脉新生内膜增生;(5)AT2R影响血管损伤后修复时ECM成分的表达,并促进细胞凋亡的发生,可能是AT2R介导抑制新生内膜形成的机制。

The results are unsure for experimental use;The rabbit's corneas that were removed with upper-half of corneal limbal epithelium lamella and erased the center corneal epitheliums were transparent with intact corneal epithelium;In the approach,the corneal and limbal epitheliums were burned with a cotton swab socked in 1 mol/L NaOH,there were 4 rabbits' corneal stroma happened perforation or ulcer and symblepharon,and the other one presented corneal epithelium phenotype.This is an applicable method to create the pathological model of corneal limbal stem cell total deficiency.

结果表明,处理后4周,全周角膜缘上皮板层手术切除,中央角膜上皮层用1 mol/L NaOH擦除的5只试验家兔角膜表面全部血管化、结膜化,未发生睑球粘连,角膜基质胶原纤维完整未见溃疡、穿孔等病变,细胞印迹学检查为结膜表型,可作为实验性角膜缘干细胞移植的病理模型;全周角膜缘上皮板层手术切除,中央角膜上皮用生理盐水擦除的5只试验家兔,有2只为结膜表型,另3只为角膜表型,观察期内结果不稳定;半周角膜缘上皮板层手术切除,中央角膜上皮层用生理盐水擦除的5只试验家兔,角膜表面透明,全部为角膜表型;直接用1 mol/L NaOH擦除角膜缘和中央角膜上皮的试验家兔,有4只角膜基质胶原纤维断裂、溶解,并伴有严重的溃疡、穿孔、睑球粘连等病变,不能用于移植试验,另1只角膜表面透明,未见结膜和新生血管长入,细胞印迹学检查为角膜表型。

Conventional imaging technique which unsubtracted bone was used first,use 3D treatment on workstation to reconstruct cerebral vessels,to diagnose aneurysm,vascular malformation and tumor as well as to evaluate the preoperative and postoperative efficacy.Subtract bone techniques including one by one slice subtraction,semi-automatic digital subtraction radiography,matched mask bone elimination and control tube exposure light spot imaging technique can show the vessels more clear without the interference of bone as well as the relationship between vessel and pathological changes more accuracy.

首先是未去骨的常规成像技术,利用工作站进行多平面重建技术、最大密度投影、容积再现、表面遮盖法等多种三维处理得到头部血管及肿瘤图像,对动脉瘤、血管畸形及肿瘤血管进行病变诊断及术前、术后评价;其次是近年出现的逐层减影、半自动数字减影、匹配蒙片骨去除法及控制球管曝光点的减影等去除颅骨的减影技术,没有颅骨的干扰血管显示更加清楚,血管与病变关系显示更准确。

The oral administration of the Cu2+ chelator TM could reduce neointimal thickening after balloon injury in the rat. And the expression and activity of MMP9 were significantly suppressed by moderate copper deficiency induced by TM.

TM诱导的适度铜缺乏能够显著抑制MMP9的表达和活性,这可能是起抑制血管球囊损伤术后再狭窄的机制之一。

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