1、

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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2、

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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3、

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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4、

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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5、

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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6、

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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7、

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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8、

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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9、

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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10、

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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11、

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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12、

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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13、

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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14、

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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15、

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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16、

Conclusion IL-12, IL-2 and LPS may promote lck gene express in renal tubular epithelial cells and only IL-12 can induce p38 phosphorylation through lck uniquely, and they can play biologic role in renal tubular epithelial cells via lck/ p38 signaling pathways.

结论IL-12、IL-2、LPS促进肾小管上皮细胞中lck基因表达,并只有IL-12唯一通过lck诱导p38磷酸化,它们皆可通过lck/p38信号传递途径参与对肾小管上皮细胞发挥生物学作用。

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17、

LPS also lead to a drop in plasma H 2 S concentration, lung CSE activity and CSE mRNA expression.

血浆H2S含量 、 肺组织CSE活性及CSEmRNA表达下降.

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18、

XBJ has the effect of protecting the lung damage caused by LPS.

血必净注射液对于内毒素所致肺损伤有保护作用。

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19、

Conclusion: QLG has protective effect on immunologic liver injury induced by BCG plus LPS, which might be related with anti-lipid peroxidation.

结论:QL对BCG加LPS致小鼠免疫性肝损伤有保护作用。其护肝作用与抗脂质过氧化等因素有关。

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20、

Semi-quantative RT-PCR was used to determine the effect of PrG on mRNA expression of COX-1 and COX-2 in RAW murine macrophage cell line stimulated by LPS.

半定量RT-PCR法检测PrG对LPS刺激的Raw小鼠巨噬细胞COX-1、COX-2mRNA表达的影响。

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