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This prompts the question, do some of these substitutions provoke compensatory NA mutations to maximize viral fitness?
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During the pathogenesis of T2DM, insulin resistance of peripheral tissues (liver, skeletal muscle, and adipose tissue) provokes compensatory increments in insulin secretion by pancreatic β-cells.
During the pathogenesis of type 2 diabetes, peripheral tissues, such as liver, skeletal muscle, and adipose tissue, develop insulin resistance which provokes compensatory increments in pancreatic insulin secretion.
The double hit of intrinsic mitochondrial dysfunction and age-related impairment provokes compensatory mitochondrial biogenesis, manifested as mitochondrial proliferation.
From this constellation of findings, it was concluded that loss of mitochondrial fusion causes instability in mitochondrial DNA and provokes compensatory mitochondrial proliferation.
This analysis revealed a broad peak of correlation spanning approximately 400 ms in the recent past, during which steering errors provoke a compensatory response.
An increase in mtDNA degradation is expected to either directly increase heteroplasmy variance if mtDNA populations are weakly controlled, or to provoke a compensatory, population-maintaining increase in mtDNA replication, thus increasing mtDNA turnover, which also acts to increase variance if mtDNA populations are subject to feedback control.
As a consequence, cellular free cholesterol content drops, which, in turn, provokes a compensatory SREBP-2-mediated induction of cholesterol synthesis [32], [33] that is reflected by an increased expression of cholesterogenic genes and increased cholesterol synthesis.
Distinguishing the network abnormalities that provoke dystonia from compensatory changes remains a challenge.
We did, however, observe that in A375 R1 tumors, vermurafenib provoked the MAPK pathway via compensatory increases in c-RAF and Ksr; this likely lead to induction of Hif-1α and Sp1 transcription factors (independent of c-Myc), resulting in increased levels of hexokinase II, membrane GLUT-1 and, thereby, subsequent FDG uptake [39, 40] (Figures 3B 4B and 5; Additional file 6: Figure S6).
Exposure of Saccharomyces cerevisiae to alkaline pH provokes a stress condition that generates a compensatory reaction.
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