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We have taken advantage of the fact that the hippocampus continuously generates new dentate granule cells (GCs) to probe morphofunctional development of GCs expressing different variants of hAPP in a healthy background.
Both types of responses can result in the development of GCs.
miR-375, miR-203, and miR-193b methylation might be host adaptation to the development of GCs.
We also observed methylation changes in miR-200b, miR-193b, miR-203, and miR-210 CpG islands in the development of GCs that has not been previously reported.
Because significant correlation between miR-375 methylation and H. pylori infection was not observed among the tested gastric samples, we suggest that miR-375 methylation might be a unique host adaptation to the development of GCs.
According to the possible cause effect relationship between H. pylori infection and the development of GCs, miR-210 inactivation by DNA methylation may play a role in gastric carcinogenesis.
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The immunosuppressive effect of Nef on the B-cell response to SIV was previously suggested by the work of Chakrabarti et al, who showed that Nef-deleted SIV strain induced a more rapid development of GC and circulating SIV-specific Ab than pathogenic SIV strain [52].
It seems that the development of GC before the age of 50 is likely to be accompanied by familial susceptibility.
Development of GC-adverse metabolic effects has mainly been studied with high doses (30 to 60 mg) [ 18, 19].
Originally such genes were postulated to be responsible for the development of GC-induced side-effects [ 18, 19].
To identify potential molecular markers for GC and to better understand the development of GC at the molecular level, comprehensive gene expression analysis is useful.
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