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Decreased p-Akt and VEGF levels were observed in O β−/−MI mice compared with O β−/−S mice, while OSM treatment could not reverse the alteration as those detected in WT mice and 6(c)).
When cells treated wither with FFA or hydrogen peroxide were concomitantly exposed to 300 μM of NAC, the ROS level decreased to 1.22 ± 0.12 and 1.07 ± 0.16 (P = NS) fold respectively, indicating that the addition of NAC was able to reverse the alteration in redox state induced by both FFA treatment and hydrogen peroxide.
Second-site suppressor mutations at Val510 to less hydrophobic residues such as aspartic acid may reverse the alteration in the local structure of the protein caused by the ΔF508 mutation or prevent intermolecular interactions that lead to retention in the endoplasmic reticulum or increased turnover at the cell surface.
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Paeonol administration could effectively reverse the alterations in the concentrations of 5-HT, NE and reduce the IL-6 and TNF-α levels.
EOPF administration could effectively reverse the alterations in the concentrations of 5-HT and 5-HIAA; reduce the IL-6, IL-1β, and TNF-α levels.
TPs administration could effectively reverse the alterations in the concentrations of 5-HT and NE, elevate the activities of SOD and CAT as well as the level of GSH, reduce the MDA level and inhibit lipid peroxidation.
Pretreatment with fluoxetine (20 mg/kg) or PAH (60 and 120 mg/kg) could effectively reverse the alterations in the concentrations of 5-HT and NE, and attenuate LPS-induced increases in TNF-α and IL-6 levels.
The significant role of MED23 in gluconeogenesis and Chol synthesis led us to speculate that acute liver deletion of Med23 could reverse the alterations associated with insulin resistance.
In animal studies, fish proteins lowered blood pressure in spontaneously hypertensive rats [ 26- 28], while in rats that had developed hypertension after sucrose administration, fish oils were able to reverse the alterations on metabolic parameters and blood pressure [ 29].
The administration of DHF (50 mg/kg b.wt. daily for 21 day) to rats exposed to either ACR or IR significantly reversed the alteration in all studied parameters.
Thus, JNK-specific inhibition with D-JNKI1 significantly reversed the alteration of LTD observed in transgenic mice.
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