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In group 1, DST caused a higher ΔEM, ΔmPAP/ΔCO, ΔPVR, and ΔTAPSE than group 2, with a lower IVA increase and a negative ΔSV (p < 0.05).
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Hepatic triacylglycerol content was lower in IVA-PLA2-knockout mice than in wild-type mice under normal dietary conditions.
The degree of the HF diet-induced increase in hepatic TG content was lower in IVA-PLA2-knockout mice than in wild-type mice.
Although high-fat diets increased hepatic triacylglycerol content in both genotypes, the degree was lower in IVA-PLA2-knockout mice than in wild-type mice.
Furthermore, as shown in Table 2, we confirmed that the serum level of PGE2 was significantly lower in IVA-PLA2-knockout mice than in wild-type mice under the dietary conditions.
The serum level of prostaglandin E2, which has a fat storage effect, was lower in IVA-PLA2-knockout mice than in wild-type mice, irrespective of the kind of diet.
Our recent [2] and the present studies showed that hepatic TG content was lower in IVA-PLA2-knockout mice than in wild-type mice under normal dietary conditions, suggesting a physiological role of IVA-PLA2 in the regulation of TG accumulation in the liver.
Considering our recent finding that hepatic TG content is lower in IVA-PLA2-knockout mice fed normal chow diets than in wild-type mice [2], it is possible that a suppression of IVA-PLA2 protects against the development of fatty liver under HF dietary conditions.
Fourth, when the proposed subband approach is used alone (FIVA-S), the average performance is already higher than other compared IVA algorithms (IVA, FIVA, IVA-C).
DST unmasked a significant lower increase of IVA of PAH group 1 with respect to PAH group 2 (5.9 ± 0.7 vs. 9.9 ± 1.5 m ⋅ s-2) (Table 3).
Our findings suggest that a deficiency of IVA-PLA2 alleviates fatty liver damage caused by high-fat diets, probably because of the lower generation of IVA-PLA2 metabolites, such as prostaglandin E2.
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