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We measured levels of damage to lymphocyte DNA as evaluated by comet and micronuclei assays, plasma MDA concentration, and plasma LDH activity (Table 3).
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To further understand how age-related CMA failure and the lack of compensatory response by other proteolytic systems with age impact protein quality control in older organisms, and whether it could led to accumulation of damage, we measured levels of oxidatively modified proteins in vivo.
To further investigate the possibility that MSH2 selectivity of agents such as methotrexate and menadione could be explained by oxidative damage, we measured levels of the most prevalent product of DNA oxidation, the oxidized base 8-hydroxy-2'-deoxyguanosine (8-OHdG).
However, in the current study we measured levels of 8-oxoguanine, a specific marker of oxidative DNA damage formed during free radical damage to DNA.
However, it is possible to evaluate the biological significance of exposure to genotoxic chemicals at the time of exposure by measuring levels of genetic damage in exposed populations.
As comet analysis is capable of measuring 0.06 to 3 breaks per 10 daltons, the lowest level of sensitivity would be approximately 100 breaks per equine genome; this is more than adequate to measure levels of background DNA damage in control cells [ 68].
To evaluate the effect of patent ductus arteriosus (PDA) on the myocardium by measuring levels of cardiac troponin T (cTnT), a marker of ischemic myocardial damage.
However, to evaluate a possible contribution of the initial steps on the measurable levels of DNA damage (possible DNA repair), a dose response for the initial DNA damage levels was measured in agarose-embedded cells.
An assessment of the vulnerability of the networks has been given by measuring the level of damage introduced by a controlled removal of links.
We measured the levels of DNA damage induced by bleomycin alone and by PCI-bleomycin using the comet assay.
The high sensitivity of the γ-H2AX foci assay has enabled researchers to measure low levels of DNA damage.
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