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Since mitochondrial DNA damage is also a source of ROS due to the production of 8-oxoG, the ability of the Klotho overexpressing transgenic mouse to decrease circulating levels of 8-oxoG, and its activation of mitochondrial MnSOD suggests that these Klotho activities may be a part of the mechanism of resistance to oxidative stress [ 15].
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To evaluate the role of elevated extracellular adenosine in hyperoxic lung injury, we used CD73−/− mice to decrease adenosine production and then measured inflammation and alveolar development.
After injection of 20% CCl4, the levels of ALT, AST, and TBIL dramatically increased as a result of enzyme release caused by massive hepatocyte damage, indicating acute and massive death of hepatocytes, which also caused the body weight of the mice to decrease.
A recent study demonstrated that the probiotic VSL#3 caused mice to decrease food intake 67.
Prior administration of vitamin E or vitamin C in the fipronil exposed mice led to decrease in lipid peroxidation and significant increase in activities of antioxidants, viz., glutathione, total thiol, superoxide dismutase and catalase.
The fatty acid changes in the fat-1 mice appear to decrease ROS production from both sites in Complex I.
The GSH level in blood of As-treated mice appeared to decrease at all fixation intervals, as compared to that of Dw-controls.
In a pathological state, for example, the degree of osteoporosis accelerates causing the degree of BAp orientation in mice femora to decrease [ 23].
The 8‐oxo‐dG levels in the adipose tissues of KK‐ A y and Min mice tended to decrease following the 500 mg/L apocynin treatment (Fig. S3).
Whereas resistance then stabilized in CD1 mice, resistance continued to decrease by 38% to E17.5 in B6 mice (Table 3).
Inbred 9 to 10-week-old female BALB/c OlaHsd mice of 18 to 20 g (Harlan Laboratories B.V., Venray, The Netherlands) mice were used to decrease experimental variability.
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