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Specifically, of the 40 gene transcripts "normalized" statistically by IL-6 administration, 28 (70%) were significantly modulated within the SBR50/IL-6/NS rat hearts compared to the SBR50/IL-6/GQ rat hearts in the direction consistent with the hypothesis that IL-6 "normalized" SBR50/P-induced changes in gene transcript levels through activation of Stat3.
Sorbitol and fructose content increased in Type 2 diabetic rat hearts compared to non-diabetic rat hearts (Fig 1A & 1B).
However, fatty acid oxidation was significantly reduced in infarcted rat hearts compared to shams, but not in EPO-treated infarcted hearts.
In contrast, glycolytic rates in the presence of insulin were significantly decreased by 17% in 15 mg/kg type 2 diabetic rat hearts compared with control hearts.
Second, the percentage of SNO-modified mtCx43 was increased by 41.6 ± 1.7%% (n = 17, p < 0.05) in preconditioned rat hearts compared to control perfused hearts (Fig. 7c, d).
Oxygen consumption, measured using chemiluminescence, was reduced to the same extent in all infarcted rat hearts compared with shams (p < 0.05).
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By calculation, total cardiac LPL activity was increased 90% for CA-rat hearts compared with corresponding euthermic controls (P < 0.01: Fig. 7).
Mitochondrial UCP3 and MTE-1 levels were both increased by 20% in high fat-fed rat hearts when compared with controls, with no significant change in ATP synthase or ANT levels, or citrate synthase activity.
The flow rate of perfused hearts compared to normal rats was shown to be increased by 1 μM CAPA from 11.8 ± 1.0 mL/min to 15.6 ± 1.2 mL/min.
Levels of nitric oxide, which is indicative of nitrosative stress (μmol/L), increased significantly in diabetic rat heart when compared to control (STZ 259.3 ± 29.3 vs. control 21.3 ± 4.4, P < 0.05).
Genes encoding sarcomeric proteins, collagens, extracellular matrix proteins, calcium regulating proteins, and proteins of energy metabolism in immunized rat hearts were upregulated, compared to controls.
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