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The data demonstrated that A. montana and A. absinthium extracts protected NCTC cells against oxidative damage, supported cell proliferation and showed no alterations in cell cycle caused by H2O2-induced oxidative stress.
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Muse cells are inherently resistant to cellular stress, and genetically resilient to DNA damage, supporting their application for the investigation of age-related and degenerative diseases.
Regardless, these findings in conjunction with our results demonstrating a crucial role for MutS and DinB in coping with ROS-induced DNA damage support an alternative model for pathoadaptation of P. aeruginosa colonizing the CF airways.
We observed a decrease in the absolute number of monocytes with minocycline treatment with no further CNS damage, supporting the notion that monocyte expansion is required to drive disease.
Notably, erythrocyte counts did not decrease in dependency of other parameters indicative of liver damage (Supporting Fig. 2A-C).
MUSTN1 expression was also upregulated in correlation to exercise-induced muscle damage, supporting its possible involvement in muscle damage repair [ 93].
Further, kinetic analysis of serum ALT levels revealed that the lack of IL-17RA led to sustained protection from hepatocellular damage (Supporting Fig. 2L).
Oestrogens directly promote cellular proliferation in the lung and can induce direct DNA damage (supporting a role in lung cancer development).
Our results demonstrate that the PCI technique enhances the bleomycin effect under appropriate conditions, and importantly we show that PCI-bleomycin treatment leads to increased levels of DNA damage supporting that the observed effect is due to increased bleomycin uptake.
The database of dichloromethane-induced chromosomal instability and DNA damage supports a mutagenic mode of carcinogenic action for dichloromethane, with a primary role for the GST metabolic pathway in carcinogenesis.
The finding that patients with shock displayed the strongest correlations between catecholamines and endothelial damage supports the notion that a threshold level exists above which catecholamines exert deleterious effects on the endothelial glycocalyx and cells.
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