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We have previously demonstrated a role for serotonin (5-HT) as one potential modulator of respiratory recovery following cervical hemisection, a mechanism that likely occurs via 5-HT2A and/or 5-HT2C receptors.
In conclusion, the present results suggest that the SDHB gene is targeted by a somatic mutational mechanism that likely involves the activity of a cytidine deaminase enzyme expressed in PBMCs and leukemic T cells.
We demonstrate that such alcohols inhibit growth and protein synthesis at high concentrations via a mechanism that likely results from a targeted regulation of eIF2B.
A fundamental aging mechanism that likely contributes to chronic diseases and age-related dysfunction is cellular senescence (Kirkland, 2013b, a; Tchkonia et al., 2013; Kirkland & Tchkonia, 2014).
Unlike human alveolar macrophages which only produce EGF, type II pneumocytes of adult rats produce EGF and express EGFR which use an autocrine mechanism that likely regulates pneumocyte differentiation and growth [ 17, 18].
In conclusion, activation of AMPK with AICAR in H441 cell monolayers is associated with inhibition of two distinct amiloride-sensitive Na+-permeable channels by a mechanism that likely reduces channel open probability.
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We have previously demonstrated separate therapeutic roles for theophylline, and more recently serotonin (5-HT) as modulators to phrenic nerve motor recovery; mechanisms that likely occur via adenosine A1 and 5-HT2 respectivelyespectively.
Characterization of the activity of a regulatory polymorphism of the APP gene points towards understanding mechanisms that likely underlie the majority of AD cases and may contribute to promoter-based drug design.
Potential mechanisms that likely influence the functions of NS1 include: (i) post-translational modifications [10], [11], [12]; (ii) strain-specific polymorphisms [13], [14], [15], [16], [17], [18]; and (iii) spatio-temporal distribution [19], [20].
The ongoing studies continue to further our understanding of the fundamental mechanisms that likely underlie the therapeutic benefits of this treatment.
Our data provide insights into mechanisms that likely operate to promote collagen fibril fragmentation, which is a defining feature of the pathophysiology of human skin aging.
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