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Thus, comparison of actual gene regulation values by both treatments using statistical approaches and correlation of these M-values are clearly superior in such a setting since they directly compare gene regulations caused by treatment with either synthetic GC.
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This study was designed to evaluate gene regulation caused by US-mediated destruction of microbubbles in the heart.
It has been shown that UI, R and Otx are sufficient to resemble the regulation caused by module A and B during the same developmental period [10].
Taken together, these findings suggest adverse effect on epidermal homeostasis and hair-cycle regulation caused by disruption of the RASSF9 gene.
This suggests that DNA methylation is involved in the regulation of NR2B gene; based on this, we hypothesized that the NR2B gene up-regulation caused by CIE and 5'AZA treatments may share the same mechanism, i.e. DNA demethylation.
In the present study, we sought to determine the functional significance of Cav-1 up-regulation caused by treatments with DNA damaging agents, a phenomenon that was also observed by others [33], [34], [43].
In addition, a selected subset of samples from CXCR4-tropic SHIVKu1-infected macaques was included with objective to compare the differences in CC-chemokine down-regulation caused by the two SHIVs.
Cis-regulation caused by mutations in the promoter sequence upstream from the CHS transcriptional start site is most consistent with the solitary nature of the CHS expression difference among the eight ABP-related loci examined.
Based on measurable and significant CC-chemokine gene down-regulation caused by SHIVSF162P4 that is known to be less pathogenic in term of its ability to deplete the peripheral CD4+ T cells than other SHIVs, SIV or HIV, a subset of samples obtained from SHIVKu1-infected macaques (PID 0 and 14) was included in this study.
In addition, we included a selected subset of samples from SHIVKu1-infected macaques in order to compare the differences between the extent of CC-chemokine down-regulation caused by CCR5-tropic SHIVSF162P4 and more pathogenic CXCR4-tropic SHIVKu1 at the acute stage of infection.
This may represent negative-feedback-induced up-regulation caused by effector cell resistance.
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