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The essential nature of NPC1 for infection in cells derived from mammals of multiple species, including bats, and for infection and in vivo pathogenesis in lethal EBOV infection mouse models argues against the existence of alternative filovirus entry receptors (Carette et al., 2011; Miller et al., 2012; Herbert et al., 2015).
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Our data on this first C9orf72 mouse model argues in favor for a gain-of-function pathological mechanism in C9orf72 associated ALS and FTD.
However, also less destructive variants of IAV are able to induce lethal synergism in a mouse model [10] arguing for additional mechanisms.
It is often argued that data from mouse models may not directly translate to humans.
The similarities to RA and other mouse models of autoimmune arthritis outlined above would strongly argue in favor of this scenario.
Indeed, it had been demonstrated that proteasome activity is correlated with mitochondrial malfunction and oxidative stress in a mouse model of neurometabolic disease, arguing for a role of mitochondria dysfunction in ROS-mediated proteasome activation.
Therefore it could be argued that in the hepatic GH resistant mouse models there may be a disproportionate influx of lipids relative to hepatic mass.
Now, of course, one can easily argue that mice are not people, and that mouse models of Lyme disease do not adequately reproduce what happens in people.
The latter study argues for two different NF-κB signaling pathways being involved in these two mouse models.
It has been argued that due to these differences between murine and human CLCA orthologs, the value of mouse models for mucus cell metaplasia in translational medicine is questionable.
Thus, our combined analysis of the mouse model and the human samples argues for COX activity as a common mechanism co-opted by cancer cells to promote immune escape across species.
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