Showing 18,181 - 18,200 results of 123,020 for search '(( 2 e decrease ) OR ( 5 ((point decrease) OR (((mean decrease) OR (a decrease)))) ))', query time: 2.35s Refine Results
  1. 18181

    TPX2 selectively regulates the levels of H4K16ac during G1-phase. by Gernot Neumayer (77179)

    Published 2014
    “…Note that the statistically significant (i.e. p<0.05) increase in γ-H2AX levels and decrease in H4K16ac levels upon TPX2 depletion is attenuated at the G1/S transition (i.e. 13 h after release). …”
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    Image_1_Increased NOX2 expression in astrocytes leads to eNOS uncoupling through dihydrofolate reductase in endothelial cells after subarachnoid hemorrhage.TIF by Shu-Hao Miao (14367141)

    Published 2023
    “…</p>Discussion<p>The increased level of NOX2 in astrocytes contributes to decreased DHFR in endothelial cells, thus aggravating eNOS uncoupling, which is an essential mechanism underlying acute vasoconstriction after SAH.…”
  12. 18192

    Image_3_Increased NOX2 expression in astrocytes leads to eNOS uncoupling through dihydrofolate reductase in endothelial cells after subarachnoid hemorrhage.TIF by Shu-Hao Miao (14367141)

    Published 2023
    “…</p>Discussion<p>The increased level of NOX2 in astrocytes contributes to decreased DHFR in endothelial cells, thus aggravating eNOS uncoupling, which is an essential mechanism underlying acute vasoconstriction after SAH.…”
  13. 18193

    Table_1_Increased NOX2 expression in astrocytes leads to eNOS uncoupling through dihydrofolate reductase in endothelial cells after subarachnoid hemorrhage.docx by Shu-Hao Miao (14367141)

    Published 2023
    “…</p>Discussion<p>The increased level of NOX2 in astrocytes contributes to decreased DHFR in endothelial cells, thus aggravating eNOS uncoupling, which is an essential mechanism underlying acute vasoconstriction after SAH.…”
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    AMPK activity and cell proliferation in HCC cell lines, PLC/PRF/5 and HepG2. by Jidong Cheng (548009)

    Published 2014
    “…(D): BrdU incorporation was significant decreased in both of PLC/PRF/5 and HepG2 cells by metformin treatment for 24 h (E): Metformin inhibited cell proliferation and the growth inhibition was rescued by AMPKα1 siRNA and compound C (an AMPK inhibitor) treatment (cell count method). …”
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