Conclusion LPS can stimulate expression of ESM 1 in endothelial cells.
结论 LPS对ECV304中ESM1的表达有促进作用.
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The ultrastructure of Clara cells damaged significantly 24 h post LPS injection.
LPS致伤后24h,Clara细胞的超微结构明显受损.
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NF - κ B inhibitor CAPE suppressed LPS - induced these effects.
NFκB抑制剂咖啡酸苯乙酯(CAPE)抑制了LPS介导的上述效应.
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Conclusion LPS can inhibit the apoptosis of PMNs.
结论LPS对PMNs的凋亡有抑制作用.
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Conclusion LPS could involve bone tissue in inflammation and inhibit the differentiation of osteoblast.
结论LPS刺激骨组织发生炎症反应、抑制成骨细胞分化.
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Conclusion: The role of LPS in caries - induced reparative dentin might be a significant determinant.
结论: 提示适度的LPS在牙髓对龋病的防御反应过程中起着一定调节作用.
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In addition , apoptosis did occur in AEC isolated from TNF KO mice following LPS stimulation.
在TNF基因剔除(knockout,KO)小鼠,LPS仍 可明显诱导AEC凋亡.
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ACP, GOT, GPT, CHE, CK, LPS and LDH activities had little correlation with fiber digestibility and Met, Cys digestibility ( P & gt; 0.05 ).
酸性磷酸酶(ACP) 、 谷草转氨酶(GOT) 、 谷丙转氨酶(GPT) 、 胆碱酯酶(CHE) 、 肌酸激酶(CK) 、 脂肪激酶(LPS)和乳酸脱氢酶(LDH)的活性与营养物的消化率呈弱相关 ( P & gt; 0.05 ).
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In this reaction, PS was decomposed into polysilane of low molecu - lar weight ( LPS ) containing Si - C skeleton and Si - H bonds.
在这一反应中, PS裂解为含Si—H键的低分子聚硅烷 ( LPS ).
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PurposeTo study extraction, purification and physicochemical analysis of Laminaria polysaccharide sulfate ( LPS ).
目的研究海带硫酸多糖 ( LPS ) 的提取制备及其组分的纯化和理化性质.
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Notably, treating mice with GSK - 3 inhibitor showed a decrease in LPS - induced renal cell apoptosis in vivo.
除了抗发炎作用, GSK -3 抑制剂可以降低体内LPS诱发小鼠肾脏组织中的细胞凋亡现象.
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CONCLUSION: LPS induces liver IL - 6 expression , which might activate BEC proliferation through STAT 3 pathway.
结论: LPS刺激导致肝组织IL-6分泌增加, 后者可能通过STAT3介导BEC增殖.
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There were 76 ODPs and 285 LPs covering the HKSAR.
年底时,全港共有76份发展大纲图和285份发展蓝图.
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At the end of 1998, there were 85 ODPs and 336 LPs.
迄一九九八年底, 已拟备的发展大纲图有85肺垃发展蓝图则有336份.
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MAP , PaO _ 2 , pH and serum TNF - α concentrations were recor ded every hour after LPS.
5h内观察动物的MAP、PaO2 、 pH,血清TNF - α.
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