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Alternatives to GM mice lie in the use of genetically altered cells and tissues or donated human diseased tissue.
We also compared the sexually dimorphic genes in murine and human diseased kidneys.
While autophagy has been recently studied in experimental models of human disease [42], very few studies have examined this process in clinical samples of human diseased tissue.
These same reagents have been used in numerous studies as confirmatory tools to establish the presence of NB in human diseased tissues.
Moreover, this analysis was further justified by the many studies published to date relying on these same antibody reagents to produce identification of NB in human diseased tissues.
Based on our results it would appear that all earlier published studies using γ-FBS to demonstrate and implicate NB and CNP in human diseased tissues are fundamentally flawed.
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Further linkages between this mouse model of disease, healthy mice, healthy humans, and diseased humans simply do not exist at present but are clearly justifiable for future research.
More than 90% of B cells recovered from human periodontal diseased tissues express RANKL, as opposed to about 54% of T cells [ 10].
Here, we show that EndoG displays cytotoxic nuclear localization in dopaminergic neurons of human Parkinson-diseased patients, while EndoG depletion largely reduces α-synuclein-induced cell death in human neuroblastoma cells.
Both Nox2 and Nox4 have been shown to be localized within the plaque of diseased human coronary arteries, and we have previously demonstrated that in diseased human coronary arteries mRNA expression of Nox2 correlated with NADPH oxidase activity.
Studying how the diseased human cells develop in a mouse could offer treatment insights.
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