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35 Our data, demonstrating a strong relationship between p53, p16 and pRb suggest cooperative effects for RB/p16 dysfunction and mutations in the TP53 gene.
Our data demonstrating that lamellocytes can originate from plasmatocytes sheds new light on hemocyte lineages.
Our data demonstrating opposing effects of p53 in different cell types may hold several possible explanations.
Our data, demonstrating that curcumin induces mitotic catastrophe in part through induction of CUGBP2 expression is consistent with this observation.
Our data demonstrating that RAPA enriches for CD4+CD25high T cells with a high expression level of Foxp3 are consistent with this paradigm.
Our data demonstrating decreased Pcsk1 levels in the yolk sac after hyperglycemia insult suggests that Pcsk1 KO mice may have an unappreciated inducible vascular phenotype.
Our data demonstrating increased phosphorylation of mTOR and S6K paralleling that of IRS-1 Ser636/639 phosphorylation in response to a hyperandrogenic, hyperinsulinemic stimulus are consistent with these prior studies.
Our data demonstrating that BMP4 propagates mesendoderm-inducing signals in differentiating EBs via the induction of endogenous TGF and Wnt growth factors are also consistent with the autoregulatory induction loops proposed to initiate and maintain gastrulation in mouse embryos [55].
Our data demonstrating CHST3 expression in the murine endocardial cushion suggests that this may be a conserved mechanism to regulate mesenchyme production, although further studies are required to confirm this hypothesis.
Our data demonstrating early, more drastic changes in the actin cytoskeleton validate these observations and suggest that the early disorganization of the actin cytoskeleton may be a key element that facilitates further dysregulation of the cytoskeleton in ovarian cancer.
Our data, demonstrating a significant association between hyperamylasemia and cholelithiasis, are in agreement with both theories.
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