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All mouse work described in this study have been conducted according to Animals Act, 2006 (China) and approved by the Institutional Animal Care and Use Committee IACUCC approval ID #M07015) of the East China Normal University.
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Many of the concepts of multistage carcinogenesis have been developed and refined using the mouse skin model system and the work described in this article has been carried out in an attempt to analyze the molecular changes that are associated with the initiation of tumor development, the selection of initiated cells to form papillomas, or the progression of premalignant tumors to carcinoma.
Such experiments will require an accurate genomic map of the mouse Psg locus, which we undertook to produce in the work described herein.
Therefore, the estimated cost for the histopathology work described here is ≤US$1200 per mutant line (≤US$300 per mutant mouse).
The work described herein involved the use of several independent cohorts of GhrR KO and WT mice over the course of two years.
The work described in this study was aimed to examine the relationship between DNA methylation, radiosensitivity and delayed genomic instability in mouse embryonic stem cells.
The work described here directly tests the hypothesis that there is a block in autophagy in Fig4 and Vac14 mutant mice.
Furthermore, our work describes the first mouse model of mitochondrial myopathy with exercise intolerance associated to CoQ deficiency, providing new insights to understand the genotype phenotype disparity associated to CoQ deficiency.
Furthermore, our work describes the first mouse model of mitochondrial myopathy with exercise intolerance associated to CoQ deficiency, providing new insights to understand the genotype phenotype disparity associated to CoQ deficiency and may have a potential impact on the treatment of this mitochondrial disorder.
This work describes X-ray imaging of mouse using a colloid solution of silica-coated Au (Au/SiO2) nanoparticles.
This work describes the first double transgenic mouse model bearing both human FcRn and HSA genes (hFcRn+/+, hAlb+/+) under the control of an endogenous promoter.
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