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The activity levels of testicular steroidogenic enzymes, 3β-hydroxysteroid dehydrogenase (3β-HSD) and 17β-hydroxysteroid dehydrogenase (17β-HSD) were significantly decreased in treated mice indicating decreased steroidogenesis after organotin compounds administration.
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DMTS accuracy also was maintained during the sessions initiated 24 h after compound administration.
This reduction may be achieved by non-invasive imaging allowing repeated, longitudinal probing in each animal post-compound administration.
We tested the feasibility of detecting proximal tubule kidney toxicity and phospholipidosis with metabonomics techniques after single compound administration as an early safety pharmacology approach.
Estimation of TRK inhibitor potency in a cellular context is required for drug discovery programs and is measured by receptor phosphorylation levels upon compound administration.
The left femoral artery and vein were cannulated for compound administration and continuous measurement of arterial blood pressure (MABP).
Details of various routes of compound administration, measurement of food consumption and body weight were described in Supplemental Methods S1.
As well, HHT is able to block translation in mice bearing Tsc2+/−Eμ-Myc lymphomas as revealed by polysome analysis of tumors two hours following compound administration (Fig. S5C).
From 16 and 24 hours after compound administration, HSP90-p23 complexes reassembled in the BT-474 xenografts.
After compound administration, the operated rats were placed on a heating pad maintained at 37°C.
Plasma concentrations were below levels of quantitation 48 hours after compound administration.
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