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Conclusions: Our studies of iLIRKO mice suggest a liver-pancreas endocrine axis in which IGF-1 functions as a liver-derived growth factor to promote compensatory pancreatic islet hyperplasia through IR-A.
While no definitive observation of in vivo porcine endogenous retrovirus (PERV) transmission in humans has been reported, the in vitro ability of PERV to infect human cells and the observation of PERV transmission to immunodeficient mice suggest a need for ultra-sensitive techniques to monitor porcine xenograft recipients and contacts for possible PERV transmission.
Now, experiments with mice suggest a possible new treatment: drugs that fend off cell suicide.
Two new studies of mice suggest a surprising reason why these people may not have the right mixture of bacteria in their guts.
Our results, using adult mice, suggest a different mechanism.
The ovarian phenotypes of heterozygous GATA6 knockout mice suggest a causative role for the loss of GATA factors in ovarian tumorigenesis.
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Findings in this cohort of mice suggest an intermediate outcome between that of pre- and post-cohorts.
Gene knockout experiments in mice suggest an important role for the α1B adrenoceptor in the control of vascular tone.
Collectively, the severe hematopoietic defects observed in Mx1-cre/Flox-Apc mice suggest an important role for APC in the maintenance of the hematopoietic stem and progenitor compartments.
Furthermore, results from caveolin-1 KO mice suggest an important role of caveolin-1 in hepatocyte lipid droplet formation and liver regeneration [30] [32].
After exposure to UVB, Cbl-b−/− mice showed a reduced epidermal thickening compared to WT mice, suggesting a lower degree of overall cell injury (Fig. 1c).
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