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These results agree with previous observations regarding induction of NO production after A2AAR/A2BAR stimulation in porcine carotid artery endothelial cells (PCAEC) [ 44], human iliac arterial endothelial cells (HIAEC) [ 45], and HUVEC [ 27, 29, 46, 47], as well as with others indicating adenosine mediated augmentation in the VEGF expression in many endothelial cells [ 29, 40, 41, 48– 53].
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The mechanism for mitochondrial dysfunction in βIRKO cells is multifactorial and includes reduced glucose-mediated augmentation in mitochondrial membrane potential and reduced ATP levels that could be due either to decreased synthesis or to increased consumption in order to maintain the membrane potential.
Pre-treatment of PANC-1 cells with 250 μ M NAC effectively prevented BD-mediated augmentation in the expression of p22phox and p67phox NADPH oxidase.
Nevertheless, combination of L-NAME and MRS-1754 reduced in 43 ± 1% and 29 ± 1% the NECA-mediated augmentation in cell proliferation in normal and preeclamptic HUVEC, respectively (data not shown).
Moreover, functional presence of A2BAR leading to activation of NO/VEGF signaling pathway in cells derived from normal pregnancy is suggested because the NECA-mediated augmentation in cell proliferation, nitrotyrosine formation, and VEGF protein abundance is inhibited by MRS-1754 coincubation.
Together, the data indicate that Ncf1 is required for the TGFβ mediated augmentation of ROS.
This study has examined the TLR mediated augmentation of innate and adaptive immune responses to a candidate vaccine antigen for a respiratory pathogen.
The amount of recombinant RT (35 fmoles per reaction) and the template RNA (0.04∼0.4 fmoles/reaction) was optimized to detect IN-mediated augmentation of RT activity.
Furthermore, at 72 and 48 h, this zinc-mediated augmentation was greater in zinc-deficient persons (p = 0.006), although the similar trend at 24 h was not statistically significant.
The putative molecular events occurring in mitochondria for BSO-mediated augmentation of ATO-induced apoptosis are summarized in Figure 9.
This is the first report showing the involvement of ROS-mediated mitochondrial injury in BSO-mediated augmentation of ATO-induced apoptosis.
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