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inflammatory相关的网络例句

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与 inflammatory 相关的网络例句 [注:此内容来源于网络,仅供参考]

We previously demonstrated that intravenously administered arginine attenuates the inflammatory response, whereas the simultaneous administration of arginine and an NOS inhibitor, i.e., L-NMMA, might not improve hypermetabolic and inflammatory responses in peritonitic rats.

先前的实验证实,以静脉给予arginine可减缓腹膜炎大鼠的发炎反应,但同时给予arginine及NOS抑制剂未改善其高度代谢及发炎现象。

On the one hand, the inflammatory cells and inflammatory mediators phagocytize necrosis cells and impaired cell debris; on the other hand, they activate muscle satellite cells (locate among the basilar membrane and sarcolemma, and in dormancy state when quite) by secreting growth factor to proliferate to form new myotube cells which develop muscle fiber, repair impaired muscle fiber and accomplish muscle regenerative process.

炎症因子在损伤部位发挥着双重作用,一方面吞噬坏死细胞和损伤的细胞碎片,另一方面通过分泌生长因子激活肌卫星细胞(安静时处于休眠状态的,位于基底膜和肌膜之间),使其增殖形成新的肌管细胞进而发育成肌纤维,修复损伤的肌纤维,完成肌肉的再生过程。

Affect on the liver pathological state after XIEZHIPING treated: the golden hamster hepatic tissue morphous structure of normal control was normal, which had regular hepatic lobules and no lipid droplet;that of model control manifested diffuse heavy adipose degeneration and heavy ballooning degeneration with inflammatory cell infiltrate which mainly composed of lympholeukocyte;that of high dose group showed midrange ballooning degeneration with chronic inflammatory cell infiltrate which mainly composed of lympholeukocyte and plasmocyte;that of media dose group indicated slight focus ballooning degeneration with a small quantity normal hepatic cells in some locals;that of low dose group appeared midrange adipose degeneration with a few lympholeukocyte cell infiltrate in the parts of central veins and port area.

泻脂平治疗后对肝脏病理状况的影响:空白对照组金黄地鼠的肝组织形态结构正常,肝小叶规则,无脂滴发现;模型对照组肝脏弥漫性重度脂肪变性,发生重度气球样变,伴见以淋巴细胞为主的慢性炎性细胞浸润;泻脂平高剂量组肝细胞呈现中度气球样变,伴见以淋巴细胞、浆细胞为主的慢性炎性细胞浸润;中剂量组肝细胞轻度灶性气球样变,局部可见少量正常肝细胞;低剂量组肝细胞呈中度脂肪变性,可见中央静脉及汇管区些许淋巴细胞浸润。

Thus, in polyarthritic rat, a model of chronic inflammatory pain, we demonstrated that herpes simplex irus ector mediated oerexpression of proenkephalin A in primary sensory neurons at the lumbar leel elicited both antihyperalgesic and anti-inflammatory actiities.

在一个慢性炎症性疼痛模型-多关节炎鼠上,我们证明单纯疱疹病毒媒介介导的前脑啡肽在腰水平初级神经原的过度表达引起了抗痛觉高敏和抗炎症活动。

Result: Porosis and inflammatory cell infiltration in the spinal cord, rupture of muscle bundles, hypertrophia and over growth of muscle cells and collagens, and inflammatory cell infiltration in the bladder wall could been seen under HE dyeing. Nissal dyeing showed the decrease of neurons at the injured segment, upper and lower segments of the spinal cord. Result of immunohistochemistry showed there were caspase-3 positive expression in all the segments. The injured spinal cord and bladder expressed significantly more caspase-3 positive results (P.0l), upper and lower segments were lower than the injured segments (P.01), but higher than the control team (P.0l).

结果:HE染色发现脊髓损伤后脊髓内空洞形成、炎性细胞浸润等病理学变化,膀胱壁中可见到肌束断裂、肌细胞肥大增生、胶原增生、炎性细胞浸润等病理学改变;Nissal染色显示脊髓损伤后损伤节段及其上、下节段均出现神经元数量的减少;免疫组化结果表明3组均有不同程度的caspase-3表达,损伤组脊髓和膀胱内膜caspase-3表达较正常组显著增加(P.01),损伤上段及下段caspase-3表达较损伤节段为少(P.01),但均高于正常对照组(P.01)。

The body's inflammatory response to traumatic injury or infection is designed to protect it and return it to the preinjury state, but excessive inflammatory responses can seriously injure tissues and organs.

身体对于创伤或感染的炎症反应是为了保护身体,将其恢复到受伤前的状态,但过度的炎症反应会严重伤害组织和器官。

to use spinal lateral approach under the guidance of the c-arm x-ray machine, the needle position will be part of the disc, after successful percutaneous insert the plasma sword to melt herniated nucleus pulpous with the power, and then enter the moderate ozone to further expand the scope of ablation, and strengthen the inter-disk degradation and inhibition of the release of inflammatory mediators to eliminate protrusion of nerve roots caused by the oppression and inflammatory stimulation.

采用脊柱后外侧入路,在c型臂x线机引导下,将穿刺针定位于椎间盘部位,经皮穿刺成功后先插入等离子刀,通电后消融髓核使髓核皱缩,再打入适量臭氧,进一步扩大消融范围,加强降解间盘和抑制炎性介质的释放,来消除因间盘突出引起的对神经根的压迫和炎性刺激。

Results(1) Group of electroacupuncture in Shu and dense wave can significantlyreduce the degree of ankle swelling(P<0.05, P<0.01), which shows thatelectroacupuncture has obvious anti-inflammatory and repercussive roles;(2) Theresults of HE staining showed that group of electroacupuncture in Shuand dense wave can significantly reduce inflammatory cell infiltration,inhibit synovial cell proliferation, and decrease proliferation of granulationtissue in rats joints;(3) group of electroacupuncture in dense-wave can increase the pain thresholdof experimental rats (P<0.05, P<0.01), reduce the content of peripheral painmediums, such as K~+, DA and 5-HT(P<0.05, P<0.01), which shows thatelectroacupuncture has significant analgesic effect;(4) In the local lesion of joints, electroacupuncture can significantly reducethe content of IL-1β, IL-8, TNF-a, increase IL-4 content, decrease theexpression of COX-2mRNA, and significantly promote the expression ofHSP-70 protein in synovial tissues of acute gouty arthritis rats (P<0.05,P<0.01),thus restrain the occurrence of synovial tissue inflammation.

结果:(1)电针疏密波组能显著减轻踝关节肿胀度(P<0.05,P<0.01),表明电针有明显的抗炎消肿作用;(2)HE染色显示:电针疏密波组可使大鼠关节炎症细胞浸润明显减轻,滑膜细胞增生明显被抑制,肉芽组织增生明显减少;(3)电针密波组能提高实验性大鼠痛阈(P<0.05,P<0.01),降低外周疼痛介质K~+、DA、5-HT的含量(P<0.05,P<0.01),表明电针有明显的镇痛作用;(4)在病变关节局部,电针能显著降低急性痛风性关节炎大鼠滑膜组织IL-1β、IL-8、TNF-α含量(P<0.05,P<0.01),升高IL-4的含量(P<0.05,P<0.01),并降低关节滑膜内COX-2mRNA的表达(P<0.05,P<0.01),可促使急性痛风性关节炎大鼠滑膜内HSP-70蛋白表达显著增加(P<0.05,P<0.01),从而抑止滑膜组织炎症发生。

PTX at tenuates the ALI induced by LPS or sepsis in rat. The therapeutic effects of PTX include:improve oxygenation, at tenuate pulmonary edema formation, enhance animal survival in sepsis-induced ALI. The mechanisms may related with the effects of PTX inhibiting the chemotaxis, migration, activation of inflammatory leukocytes, diminishing the production of active oxygen, and inhibiting inflammatory cytokine release partly.

4PTX对大鼠内毒素性ALI及脓毒症性ALI均有一定的防治作用,主要表现在改善动脉血氧合,减轻肺水肿形成,提高脓毒症性ALI大鼠的存活率等方面,其机理可能与抑制白细胞趋化与激活,减少肺内白细胞渗出及活性氧产生,一定程度上抑制炎性细胞因子生成等有关。

RESULTS: During 10 - 12 weeks, in cuntrol group: The defect area was repaired by white and soft tissue that had no resistance to press. The repaired tissue was still lower than the surrounding articular surface with clear boundary. By histological observation, it was found that the defect was repaired by the mechanism similar to inflammatory reaction and the defect is ultimately filled by the hyperplasia of hyaline degenerative fibrous tissues. In filling group: the defect was repaired by semi-transparent, smooth, textured tissues with polish that had resistance to press as well as elasticity. The repaired tissue was almost similar to the shape of the surrounding cartilage,difficult to be distinguished. After histological observation, it was found that there was no inflammatory reaction, but active hyperplasia of inner bonetissue and cartilage tissues; a lot of osteoid tissues and trabeculation were found. Newlborn cartilage was fused with surrounding cartilage tissue and connected with surrounding tissues.

结果:10~12周,对照组:缺损区由白色、质软、按压无阻抗的组织修复,修复组织仍低于周围关节面,边界仍清晰可辨,组织学以类似炎症反应的机制修复缺损,最终以透明变性的纤维组织的增生来填补缺损部位;填充组:缺损区由半透明状、质韧光滑有光泽,按压有阻抗并有弹性的组织修复,修复组织与周围软骨外形上已基本相似,不易区分,组织学未见有炎症反应的过程,内骨组织和软骨组织增生活跃,并可见大量类骨组织和骨小梁形成,新生软骨和周围软骨组织融合,并与周围组织连接。

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我不懂得羞怯和惧怕,我的