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The big question now is whether the mouse model does, in fact, reflect what's happening in human PIH.
However, mouse is not a naturally menstruating animal, and the mouse model does not truly reflect the occurrence and development of the human menstrual process.
Nonetheless, the tipsy mouse model does not allow us to test this mechanism biochemically.
While biologically interesting, this mouse model does not fully recapitulate the physiological activity of FL ERBB4.
This mouse model does not develop amyloid plaques but APP-derived intracellular Aβ aggregates and synapse loss [ 12].
Although the adoptive mouse model does not accurately reflect all the features of human MM, it recapitulates many major characteristics of the disease.
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Initial descriptions of the inflammatory profile in this mouse model did not detect serum IL-1β [8].
A recent study found that conditional inactivation of KDM6A in a mouse model did not change global levels of H3K27me3, though it did contribute to a MDS-like phenotype and reduced migration of HSCs (Thieme et al., 2013).
However, the mouse model did not support a role of CTLA-4 in enhancing pathology.
Induction of β2-overexpression in this mouse model did not affect overall single L-VDCC gating significantly.
Even though the mouse model do not reproduce actual clinical manifestation of the disease, in our previous studies, selection did influenced the outcome of inflammation and tissue damage [2], [3].
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com