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Different cytotoxic effects of cladribine-triphosphate are known: direct DNA effects are caused by incorporation of cladribine-triphosphate as a fraudulent base into DNA, leading to a termination of DNA chain elongation and to DNA breakages that cannot be repaired because of the interference of cladribine and DNA repair mechanisms.
The studies mentioned above about DNA effects were carried out both in vitro and under light.
There is also little evidence for indirect DNA effects, including alterations in gene expression, cell proliferation, or apoptosis (Laszlo et al, 2005; Chauhan et al, 2006; Lixia et al, 2006; Qutob et al, 2006; Joubert et al, 2007).
As the techniques to obtain transmitochondrial cybrids involve complex manipulations and also do not entirely eliminate nuclear DNA effects on mitochondrial function, interpretations derived from this experimental model are not straightforward [ 27].
Using this methodology, McGregor et al. (2006) determined that all of the mode-of-action elements (i.e., cytotoxicity, cell proliferation, and DNA effects) for formaldehyde-induced nasal tumors are highly non-linear and do not occur unless a particular threshold dose (6ppm) has been exceeded.
Most studies of the non-thermal effects of RF EMF indicate no direct DNA effects such as mutagenicity or genotoxicity of RF EMF exposure in the range of 800 1900 MHz and an SAR of less than 2 W kg−1.
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After 24 h, biofilm mass was similar to the uncoated control (Fig. 3B), indicating that the observed DNA effect is not related with the initial adherence process.
Structural properties of DNA effecting indirect readout by proteins include flexibility, elasticity, bending and kinking, major and minor groove widths, and hydration[ 8- 10].
Third, while LV modulates FU by enhancing its anti-DNA effects via the inhibition of thymidylate synthase, MTX modulates FU primarily by increasing the incorporation of fluorouracil triphosphate into RNA, adding pharmacodynamic interest to the comparison (Sobrero et al, 1997).
In MRL- lpr/lpr mice, the administration of a synthetic G-rich DNA (named ODN 2114) known to block CpG-DNA effects led to less autoimmune tissue injury in the lungs and kidneys, accompanied by decreased serum levels of anti-dsDNA IgG2a Abs and of IFN-α [ 61].
Prodigiosin treated bacterial cells exhibited extremely high DNA damaging effects.
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