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To this end, we hypothesized that the iron-deprived mice would exhibit a sleep wake circadian pattern characteristic of the human syndrome: increased wakefulness during the hours immediately preceding the sleep-predominant period.
We hypothesized that muscles of meltrin β−/− mice would exhibit aberrant gene expression patterns related to their defects in NMJ formation.
Since AKAP5 is most highly expressed in the ventral and dorsal striatum where it colocalizes with RIIβ [6] we tested whether AKAP5 mice would exhibit deficiencies similar to those seen in RIIβ KO mice.
If one administered a muscle relaxant by itself, treated mice would exhibit LORR while remaining fully aware.
mice would exhibit a more drastic phenotype, and we had hoped that the presence of the Ncadk.i.i
As inhibition of TRPV1 results in hyperthermia, it was expected that TRPV1 knockout (KO) mice would exhibit altered thermoregulatory pathways.
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Because obese people in western cultures where liver disease is prevalent typically consume a diet that contains high amounts of saturated fat, we hypothesized that mice consuming SAFA would exhibit the greatest degree of NASH.
Consequently, mice expressing mutant p53 would exhibit phenotypes similar to those observed in the TAp63-/ mice.
They described that human or mouse cells lacking AIF would exhibit high lactate production and enhanced dependency on glycolytic ATP production due to severe reduction of ETC complex I activity.
Because the tumorspheres exhibited stem-like properties, it might be expected that tumors in mice derived from the tumorspheres would exhibit similar morphology as the patient tumors.
Given that most of the aforementioned signaling pathways are critical for certain developmental processes and patterning events, one might have predicted from the in vitro studies that secreted sulfatase-deficient mice would have exhibited profound developmental defects in a multitude of organ systems.
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