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Since CD59a is the principal regulator of the membrane attack complex in mice, we evaluated the impact of CD59a gene deletion upon maintenance of bone architecture.
Specifically, our DNA/RNA analysis was limited in that rather than analyzing complete groups of mice, we evaluated 8 animals.
As the number of B lymphocytes and plasma cells were similar in uninfected WT and galectin-3 mice, we evaluated these niches only in infected mice.
Knowing that only P140 controls lupus disease in MRL/lpr mice, we evaluated conformational characteristics of both peptides by 1H-NMR spectroscopy and molecular dynamics calculation.
To determine whether FSH could potentiate osteoclast differentiation in ITAM-adapter deficient mice, we evaluated the effect of FSH during in vitro osteoclastogenesis.
To further characterize the elongated growth plate phenotype in Col2a1-ΔTβR1 transgenic mice, we evaluated markers of chondrocytes differentiation by in situ hybridization.
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In the present study, by using Cdc42 conditional KO mice, we evaluate how postnatal disruption of Cdc42 in excitatory neurons affects structural plasticity of dendritic spines and synaptic plasticity.
Because of the increased plasma lipids in Paigen diet fed PDZK1/apoE dKO compared to apoE KO mice, we next evaluated atherosclerosis in the aortic roots and coronary arteries of these mice.
To investigate potential defects in neuronal functions of the JAM-C SC KO mice, we initially evaluated their electrophysiological properties.
To uncover the physiological relevance in the livers of fasted and refed WT mice, we first evaluated general gene expression profiles under different nutritional conditions.
Because many of the cells did not clearly segregate into these two discrete populations (particularly in mdx and mdx-CCR2−/− mice), we also evaluated the mean fluorescent intensities of iNOS and CD206 expression (Fig 6D G) in all MPs.
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