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Endothelin-1 (ET-1) may mediate increased resistance to hepatic sinusoidal blood flow.
Although their expression did not change in BCC1617, by just being functionally expressed they may mediate increased resistance to antibiotics.
The data support the idea that TBC1D4 is a nexus for insulin- and exercise-responsive signals that may mediate increased insulin action after exercise.
For example, activity in the medial postcentral cortex may mediate increased difficulty in finding a random-looking sequence, or other differences related to task processing such as the amount of information that was taken into consideration for the number choice.
Therefore, we propose that chronic exposure to alcohol vapor affected the DA and 5-HT systems in the ACCS of the mesoaccumbens reward pathway, which may mediate increased voluntary alcohol-drinking behavior.
The mild enhancement of inflammatory/immune response indicated by these gene changes is reflected in the pathophysiologic responses of the two groups (Penn et al. 2007) and raises concern that ETS may mediate increased inflammatory injury or alter immune response upon initial exposure to an infectious agent such as respiratory syncytial virus (Phaybouth et al. 2006).
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At the same time, there is emerging evidence that stresses other than hypoxia may mediate increases in genes that are normally considered hypoxia responsive.
Interactions between bone and vitamin D may also mediate increased deposition of calcium in the arterial wall mediated by molecules and hormones released by bone (30).
LSCC cells harbouring wild-type p53 were significantly radiosensitised by Nutlin-3 (P<0.0001; log-rank scale), and displayed increased cell cycle arrest and significantly increased senescence (P<0.001) in the absence of increased apoptosis; thus, our data suggest that senescence may mediate this increased radiosensitivity.
Moreover, these findings suggest that epigenetic changes serve as a steward of cellular memory of aberrant intrauterine environments, and that site-specific changes in DNA methylation may mediate the increased susceptibility to age-related diseases observed later in life.
Thus, defective IL-12 induction may mediate the increased susceptibility of PD-1−/− mice to T. gondii infection.
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