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Thus, the atrophic lymphoid organs and accompanying reduced lymphocyte development and maintenance in the Lmna-/ mice may result from the overall poor health of the mice.
As such, the reduced HIC status of schistosomiasis infected mice may result in a decreased level of HSC activation, which in turn results in lower deposition of collagen.
Thus, the obese and hyperphagic phenotypes of Leptin145E/145E mice may result in part from attenuated leptin action in the hypothalamus.
Hence, those fragmented and mislocated mitochondria in the cumulus cells of diabetic mice may result in subcellular energy depletion and even cell death [23], [37], [38].
This difference was insignificant among PTX-treated groups, suggesting that memory decline in APP/PS1 mice may result from changes in synaptic protein levels through homeostatic mechanisms.
Reactive oxygen species (ROS) production by mitochondria plays a critical role in many physiological processes and therefore over quenching of ROS in ob/ob mice may result in pathological conditions.
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Later onset disease in the mouse may result from differences between species in neuronal vulnerability to loss of PLA2G6.
This has important implications as studies have demonstrated that deleting a gene in a mouse may result in the death of one strain but not another.
There were also signs of DNA damage in spinal cord motor neurons of AR100 mice, which may result from downregulation of DNA repair genes and/or mitochondrial dysfunction.
Together, our results indicate a perturbance of hippocampal plasticity in adolescent APP23 mice which may result in the development of memory deficits later during disease progression.
Analysis of cell counts show that MPTP treatment of A53T transgenic mice (65%) may result in a slightly lower number of dopaminergic neurons than with the non-transgenic littermates (70.4%) (Fig. 2C).
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