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At a histopathological level, fibrosis and myocyte hypertrophy are features of cardiac tissue from both humans and animals with impaired kidney function that are thought to mediate the abnormal relaxation properties of the left ventricle in CKD [25], [43], [44].
Accordingly, either estrogen action or progesterone action or both, resulting from overexpression of PR-A, may mediate the abnormal mammary phenotype of PR-A transgenics.
This process is believed to mediate the abnormal recruitment and dysregulation of additional factors including extracellular matrix (ECM) proteins resulting in brain vessel dysfunction.
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Our previous study demonstrated that the activation of Akt and JNK in SD-Mg mediates the abnormal production of MIP-1α, as evidenced by a decrease in MIP-1α production by treatment with the pharmacological inhibitors [11].
Analysis of the underlying mechanism suggests that this phenomenon depends on the activation of the pseudo-hypoxic pathway — most probably mediated by the abnormal stabilization of HIF-2α following VHL inactivation — and the loss of the p53/TIGAR pathway.
Figure 5 demonstrates that the suppressive effect of mature α/β TCR transgenes on DN cell proliferation is mediated by the abnormal activation of PKD2 catalytic activity.
DLK-1 was not required to mediate all of the abnormal phenotypes caused by ptrn-1 loss of function, however: the ectopic accumulation of mCherry::RAB-3 in the PLM posterior process was similar in the dlk-1 ju476 dlk-1 ju4765597) double mutant to that of the ptrn-1 tm5597) ptrn-1 tm5597.
The structural characterization of binding geometries is therefore of interest as a basis for the construction of mimetics that can mediate the effects of abnormal immune response.
Previous studies of mice lacking RIM1 α (RIM1 α−/− throughout the brain showed that deletion of RIM1 α results in multiple behavioral abnormalities. In an effort to begin to delineate the brain regions in which RIM1 deletion mediates these abnormal behaviors, we used conditional (floxed) RIM1 knockout mice (fRIM1).
Therefore, we reasoned that studying protein protein interactions that involve SP1 would provide insight into the abnormal signals that mediate transcriptional down-regulation of p120ctn in NSCLC.
A common feature of SDH and VHL mutations is their capacity to mediate a pseudo-hypoxic response, i.e. the abnormal stabilization of HIFs under normoxic conditions.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com