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In particular, the FMN heme IET is essential in coupling electron transfer in the reductase domain with NO synthesis in the heme domain by delivery of electrons required for O2 activation at the catalytic heme site.
Some reports have shown that the amebicidal activity of activated macrophages is mainly associated with NO synthesis [ 54– 54].
Its direct relationship with NO synthesis [ 47] and its function as indicator of endothelial stress [ 48] point at a probably direct correlation between adipocyte size, growth, and/or energy availability, direct correlated of NO synthesis [ 49] possibly being mediated by WAT itself by means of VEGF-A.
The α-thalassemias are classified into the α-thalassemia with no synthesis of α-chains and α+-thalassemia with a reduction in synthesis of α-chains.
ADMA is also able to interfere with NO synthesis by competing with arginine and SDMA for cellular transport across cationic amino acid transporters (CATs).
ADMA interferes with NO synthesis by competing with arginine and symmetric dimethylarginine (SDMA); the latter is not biologically active, for cellular transport across CAT.
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Increased ADMA levels are associated with reduced NO synthesis as assessed by impaired endothelium-dependent vasodilation.
This review will provide an overview of the interplay between NO and epigenetics as well as emphasize the unprecedented importance of these pathways to explain phenotypic effects associated with biological NO synthesis.
In metabolic disorders associated with atherosclerosis, NO synthesis and/or stability is reduced [ 5, 6, 14].
With impaired NO synthesis, as expected, we found a reduced abundance of S-nitrosylating species.
In these two studies, L-arginine in premature infants was supplemented with the intention of increasing NO synthesis with the rationale that NO's role as a vasodilator would be protective to the gut through prevention of ischemic injury [ 30, 31].
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