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To evaluate CSC-induced tumor promotion in other mouse skin models, male DBA/2 mice were treated with N-methyl-N′-nitro-N-nitrosoguanidine (MNNG) (300 μg) or DMBA (75 or 150 μg) followed by promotion with 1R4F CSC at concentrations ranging from 9 to 45 mg "tar"/application.
Two mouse skin models were used.
In mouse skin models, COX-2 deficiency significantly protects against chemical carcinogen- or UV-induced NMSC while overexpression confers endogenous tumor promoting activity.
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The response variables flux and skin retention were determined in in vitro hairless mouse skin model.
In a mouse skin model of VEGF-driven pathological angiogenesis, transduction with active Cdc42 (L28Cdc42) markedly improved VEGF neovessels, as measured by increased lumen formation, enlarged vessel diameter, and enhanced perfusion of macromolecular tracers.
As demonstrated here with a mouse skin model of VEGF-driven angiogenesis, expression of an established DN mutant of calpain-I reduced vascular blind ends and markedly improved network integration and vascular perfusion.
In a mouse skin model of VEGF-driven angiogenesis, retroviral transduction with dominant-negative (DN) calpain-I promoted neovessel integration and lumen formation, reduced blind ends, and improved vascular perfusion.
Finally, we evaluated the toxicity of the AuC liposome hydrogel by using a mouse skin model.
Furthermore, an interaction between the HB-EGF carboxy-terminal region (HB-EGF-C) and PLZF occurs in a mouse skin model of keratinocyte hyperplasia.
Our laboratory has shown that arsenite markedly increased the cancer rate caused by solar-simulation ultraviolet radiation (UVR) in the hairless mouse skin model.
The mouse skin model has been extensively used to study molecular changes associated with the dysregulated signaling that occurs in the different stages of tumor development.
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