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lps相关的网络例句
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The Western blot results were consistent with those of immunohistochemical method. CONCLUSION: p38 MAPK expression increases in alveolar and airway epithelial cells in LPS induced acute lung injury rat models. The activation of p38 MAPK is found in most lung tissues, suggesting that p38 MAPK participates in the signal transduction in inflammatory and noninflammatory cells.

LPS诱发的大鼠急性肺损伤模型中,磷酸化p38 MAPK在气道和肺组织内表达增加,p38 MAPK的激活见于肺组织内多数细胞,提示肺内炎性和非炎性细胞均有p38 MAPK信号分子的激活。

Thus our study indicates that impaired immunity against nontyphoidal Salmonella bacteremia in HIV infection results from excess inhibitory antibodies against Salmonella LPS whereas serum killing of Salmonella is induced by antibodies against outer membrane proteins.

他们的发现意味着HIV所造成的缺陷不止是细胞介导的免疫,而体液免疫(是由分泌的抗体所介导的)在以LPS蛋白为标靶的免疫反应中也受到了相当大的损害。

The endotoxin also named as lipopolysaccharide in the outer membrane of Gram-negative bacteria is the primary constituent of pathopoiesis. LPS which has extensive biological activity can induce severe inflammation in cascade and lead to sepsis、systemic inflammatory response syndromes、multiple system organ failure.

细菌壁外膜的内毒素又称脂多糖(lipopolysaccharide,LPS)是其主要致病成分,具有广泛的生物活性,能引起严重的炎症级联反应,是导致脓毒症、系统性炎症反应综合征、多脏器功能衰竭的主要致病因子。

Three hours after an administra-tion of LPS peritoneally, the number and staining intensity of positive structures were not obviously changed.

LPS免疫刺激后,阳性细胞的数量和染色强度无明显变化。

Furthermore, we demonstrated that macrophages harvest from rats peritoneally injected LPS exhibits increase of c-Src expression as compared to those derived from PBS-injected control.

最后,我们更证明了腹腔注射 LPS 老鼠的巨噬细胞较诸对照组,不但呈现活化而且其 c-Src 表现量也明显增加。

LPS is recognized as a main promotor in the pathophysiology of sepsis.

LPS通过其活性中心Lipid A与细胞表面的受体结合,介导脓毒症的发生。

ConclusionThese results suggested that scutellarin has markedly protective effect on immune hepatic injury induced by BCG plus LPS in mice.

结论灯盏乙素对BCG+LPS诱导的小鼠免疫性肝损伤有明显的保护作用。

Objective and Methods To evaluate mechanisms of drugs commonly used in the treatment of septicemia, giving antibiotics including Minocycline (10 mg/kg), Clindamycin (10 mg/kg), Cyclosporin (15 mg/kg) and Platonin (10 mg/kg) to septicemic rat injected with LPS. Clinical improvement, blood pressure, heart rate, survival time are assessed, and the amount of endogenous NO production is determined.

本实验之目的是要探讨在临床上常用於治疗败血症的数种药物,可能的作用机转;藉由注射老鼠LPS模拟败血症前,先给予Minocycline,Clindamycin,Cyclosporin,Platonin等药物治疗,评估药物的改善状况,同时观察血压、心跳、动物存活时间及侦测体内NO的生成量,来比较给药与否之差异,且针对变化的可能原因来探讨。

It was found that levels of IFN-γ and NO in splenocyte supernatants stimulated by PRBC or LPS from DBA/2 mice were remarkably higher than those of 1640 culture group,and they increased gradually with culture time.

结果表明以PRBC或LPS刺激后,DBA/2小鼠脾细胞上清液中IFN-γ和NO水平随培养时间的延长均有不同程度的提高,但BALB/c小鼠48h培养组的IFN-γ和NO水平仅比24h培养组略有升高。

Results After 2 or 6 hours of LPS intravenous administration, severe lung injury and positive signals of NT occurred with the latter located in the pulmonary macrophages, endothelia, subendothelial and muscular layers of the pulmonary artery.

结果 LPS静脉注射2 h和6 h 后,肺脏有明显损伤及硝基酪氨酸产生的阳性信号,该信号主要分布于肺泡壁巨噬细胞、肺小血管和细小支气管周围的巨噬细胞以及部分肺动脉的内皮细胞、内皮下层及肌层。

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