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Although bioaccumulation of ACPNs has not been studied in particular, the distribution of HANs in mouse organs was studied via intravenous administration.
RNA from mouse organs was prepared as previously described using a single step isolation protocol [51].
The infection of different mouse organs was monitored by demonstrating the presence of bacterial DNA by nested PCR (Table S1 and S2).
To estimate the specificity of the hypertrophic gene signature, an additional dataset monitoring gene expression in healthy mouse organs was also used.
The elastin preparation procedure for mouse organs was modified due to the small amount of material (0.02 0.10 g from Pcft-deficient mice [ 27] and 0.04 0.54 g from other mice).
Overall, the long duration from the time of detection of cancer cells in the organs (by PCR and/or histological staining) to the development of visual macrometastasis in mouse organs was similar to the delay in development of measurable metastasis in breast cancer patients following diagnosis of primary breast tumors [ 46, 47].
Similar(54)
Mouse organs were examined histopathologically by veterinary pathologists (MR, HP, LM) using formalin-fixed, paraffin-embedded sections stained with hematoxylin and eosin (H&E).
After perfusion, xenograft tumors and mouse organs were removed and homogenized.
Mouse organs were fixed in 4% paraformaldehyde overnight and embedded in paraffin.
To assess the overall ratios of ERM protein expression, various mouse organs were analyzed by western blot.
These results demonstrate that the failure of the mutant to grow and persist in mouse organs is due to the mutant's inability to withstand oxidative and nitrosative stresses even in resting macrophages, and is not due to its induction of marked inflammatory responses.
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