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The increasing total amount of desorbed hydrogen, ν*H = (νoffH + νH), as τoff becomes longer is the cause of the observed augmentation of the IS, microdeformation and decrease of microhardness.
Samples stimulated with and without TGFβ demonstrated no significant differences in expression indicating that the observed augmentation of ROS by TGFβ was not due to enhanced gene expression.
The observed augmentation of IL-1 cytokine levels in animals during graft rejection is in accordance with the observations of others.
Since MPTP formation has been proposed to function as a Ca2+ release mechanism (Elrod et al., 2010; Bernardi and von Stockum, 2012), the observed augmentation in baseline Ca2+ in Bax/Bak-deficient mitochondria, and their greater uptake capacity further suggest that Bax/Bak are required for MPTP-dependent Ca2+ release.
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Measures of arterial stiffness did not change from baseline after either walnut supplementation or control, and there were no differences observed in augmentation index (−6.6±6.5 % versus −8.4±6.3 %), or augmented pressure (−2.2±2.1 mmHg versus −2.7±2.4 mmHg) or at the end of each 4 week period.
This might result from an increased mineral density, as usually observed after augmentation, and the concomitant higher bone-to-implant contact [20].
In addition, we observed the augmentation of inhibitory action against MMP-9 enzymatic activity by 4′-demethylated nobiletin, which is a major metabolite of nobiletin.
Correspondingly, we observed an augmentation of MHC class II-expressing cells following WNV infection.
Importantly, we also observed similar augmentation of TGF β1-induced EMT in these TAK1-knockdown cells.
Moreover, we observed an augmentation of TAA-LP-specific T helper type 1 cell responses and tumor antigen-spreading in HNSCC patients vaccinated with TAA-SPs.
When CskAS OTI CD8+ T cells were stimulated by APCs preloaded with peptides of different agonist potency during strong CskAS inhibition (5 μM), we observed marked augmentation of CD69 expression in responses to weak (T4, Q4H7, G4) agonists, contrasting with only slight enhancement of the responses to strong (OVA, Q4R7) agonists.
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