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Timely transfer to rehabilitation is supported by recent reports demonstrating outcome benefits 5 and cost-effectivity 6 of a continuous chain of care from the intensive care unit to inpatient rehabilitation to discharge.
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Furthermore, CD38 inhibition by SFA provides additional insight into recent reports demonstrating SFA's capacity to abrogate bioactive IL-12 production in vitro and in vivo.
Together, these results are consistent with recent reports demonstrating calsyntenin-1 cleavage by ADAM10/17, but not by BACE1 (Hata et al., 2009).
This finding supports recent reports demonstrating a very high negative predictive value of the IFN-γ-based IGRAs (reviewed by Diel et al 19).
This apparent developmental change in the source of Ca2+ required for EGABA depolarization is supported by a recent report demonstrating the NMDAR-dependence of EGABA depolarization induced in mature (DIV 19 22), but not young, cultures with bath perfusion of glutamate [30].
These results are supported by a recent report demonstrating that MSCs reside in the limbal niche [48].
This hypothesis is further supported by a recent report demonstrating that systemic inhibition of miR-92a expression prevents ox-LDL-dependent EC activation and subsequent atherosclerotic plaque progression.
One way this could occur is suggested by a recent report demonstrating that the environment of the peritoneal cavity may recruit Th1 cells, because the peritoneal cavity appears to be dominated by IFNγ+CXCR3+ T cells in naïve mice [ 73].
This notion is supported by a recent report demonstrating that DAF-12 and DAF-16/FoxO mutually influence target gene expression in animals lacking a germline (McCormick et al. 2011).
This concept is further supported by a recent report demonstrating that tumor stroma restrains pancreatic cancer progression and that pharmacological HH pathway activation in stromal cells can actually slow down in vivo tumorigenesis (Lee et al., 2014).
Generally, this suggestion is supported by a recent report demonstrating that p38 participates in oxidative stress-induced senescence via an alternative ATM-independent pathway, implicating lamin B1 accumulation [ 49].
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com