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Enhanced cathepsin expression and activity in cystatin C-deficient mice contributed to the progression of dysplasia by altering premalignant tissue epithelial proliferation, apoptosis, and neovascularization.
We further hypothesized that the increased bone remodeling in Arf-/ mice contributed to OS development and provide evidence that zoledronic acid, a bisphosphonate inhibitor of bone resorption, prevented or delayed onset of OS in Tax+Arf-/ mice.
Taken together, the data indicated that both impaired BMMSCs and activated osteoclast activity in CD4+CD25−CD45RB+hi T cell-treated OVX-immunocompromised mice contributed to the osteoporosis phenotype.
AI designed and performed all experiments with mice, contributed to data analysis and paper writing.
JH performed surgery on mice, contributed to study design, histopathology and data interpretation, and drafted the manuscript with XC.
XC performed surgery on mice, contributed to study design, histopathology and data interpretation, and drafted the manuscript with JH.
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Determine if impaired intestinal barrier function and low-grade chronic inflammation in Zip14 KO mice contribute to ZIP14-associated parkinsonism.
Could the excessive incidence of tumorigenesis in p53-deficient mice contribute to our understanding of the threshold vs nonthreshold issue in genotoxic carcinogenesis?
Based on these results, it is suggested that overexpression of GABAA receptor β2 subunit in BALB/cByJ mice relative to C57BL/6j mice contributes to the dysfunction in GABAA transmission in regions of brain known to regulate responses to stress.
ESL degradation in apoE deficient mice contributes to reduced increased urinary protein excretion without significant changes in renal morphology.
Moreover, we investigate whether the deregulated hemostasis in HRG-deficient mice contribute to the elevated angiogenic switch, previously reported in these mice.
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