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They showed that both conditions are associated with enhanced AGE deposition and myocardial inflammation.
They showed that hypovitaminosis D is not associated either with enhanced AGE accumulation or with markers of inflammation.
Summarizing, our cross-sectional study suggests that in diabetic subjects hypovitaminosis D is not associated with enhanced AGE accumulation and sufficient vitamin D levels are not linked with a lower AGE accumulation.
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This theory predicts that in an older animal (or human), the activity of tumor suppressors would be associated with enhanced aging phenotypes.
Its action is tightly regulated in multiple steps of activation and inhibition and, when dysregulated, results in organ atrophy with enhanced ageing or cancer progression.
We expected that low levels of vitamin D could be associated with an enhanced AGE formation, while, in the presence of sufficient vitamin D, lower concentrations of AGEs should occur.
Based on linear models with explanatory variables (muscle cross-sectional area, age, RA status and sex), we found that patients with RA showed a greater age-related decrease in cortical thickness with a concomitant increase in outer bone circumference consistent with an enhanced aging pattern [ 4].
Despite the large number of AGEs produced during the Maillard reaction, recent focus is on the major non-crosslinking AGE Nε-carboxymethyllysine. Kneyber and colleagues focused on sepsis-induced cardiac dysfunction and investigated whether myocardial inflammation is associated with enhanced cardiac AGE deposition and whether this is further enhanced by mechanical ventilation.
PBHT at 1150 °C, which is lower than the solvus temperature of the borides, for 12 h resulted in boride-free joint with uniform chemical composition and enhanced aging response.
The supersaturated degree of both the dissolved solute atoms and vacancies in the α-Mg matrix was expected to be increased, resulting in an enhanced age-strengthening, compared with normal solution and aging treatments.
However, the statistically significant association of PA with enhanced cognition at age 60 69 years in our final model suggests that the association of PA with enhanced cognition in the younger non-ɛ4 carriers is likely independent of mobility limitation and chronic medical illnesses.
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