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The immunosuppressive properties of mTOR inhibitors, coupled with their efficacy for tumor prevention in mouse models, suggested that modulation of the immune system is important for mutant K-Ras mediated lung tumorigenesis.
Research done in mouse models suggested that insulin resistance and the resultant type 2 diabetes can be prevented by disabling the macrophage inflammatory pathway (19, 20).
These studies in HCC mouse models suggested that NF- κB plays a proinflammatory role in macrophages during early stages of the tumor growth.
The HD mouse models suggested that the accumulation of the mutant protein impairs neurogenesis in the hippocampus (Fedele et al. 2011).
Studies in mouse models suggested that the environment for the production of anti-RHA was distinct from that of anti-small nuclear ribonucleoproteins (anti-snRNPs) or anti-Su (Ago2) [ 12, 18].
Interestingly, a recent analysis of imatinib and nilotinib effects in SSc mouse models suggested that high activation status and expression pattern of TKI targets was predictive of the potential response to therapy [ 8].
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Experimental evidence in mouse models suggests that the degradation of the extracellular matrix by matrix metalloproteinases (MMPs) plays an important role in infarct rupture.
These observations along with experimental evidence in cellular and mouse models suggest that TG2 can contribute to the abnormal aggregation of disease causing proteins and consequently to neuronal damage.
However, chronic gastrointestinal dysfunction suffered by a subset of patients after surgery as well as studies in HSCR mouse models suggest that aberrant NC segregation and differentiation may be occurring in ganglionated regions of the intestine.
As an example, ciliopathies like BBS are associated with diabetes mellitus and obesity, and mouse models suggest a role for cilia in controlling hyperphagia [25].
Studies on human samples indicate that the cell-of-origin is likely a cone photoreceptor [35, 36] whereas studies in mouse models suggest a horizontal cell [37], or a Müller glia cell [38].
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com