SUMMARYBackground and aims: Increased levels of advanced glycation end-products (AGE) and their precursors, such as methylglyoxal (MG), in patients with diabetes may account for impaired response to heart ischemia. Pyridoxamine is a derivate of vitamin B6, which has been shown to reduce AGE formation. Our goal was to assess the role of pyridoxamine in protecting from MG-induced impaired heart response to ischemia. Methods: Wistar rats were subjected to MG administration (WM), MG plus pyridoxamine (WMPyr), or no treatment (W). Half of the hearts from each group were submitted to ischemia and the other half were perfused as control. The levels of CEL, Bcl-2, Bax, and total and phosphorylated forms of JNK and Akt were determined. Results: Methylglyoxal led to higher levels of AGE and AGE receptor (RAGE) than in the W group. During ischemia, MG caused an impairment of survival pathways and Bcl-2/Bax ratio, a marker of apoptosis. Pyridoxamine treatment decreased glycation and restored the activation of JNK and Akt during ischemia. These events were followed by levels of Bcl-2/Bax ratio similar to W group. Conclusion: Methylglyoxal-induced AGE accumulation impairs the activation of cell survival pathways during ischemia. Pyridoxamine-induced decrease of glycation inhibited the effects of MG accumulation in the heart, suggesting that it can be of added value to usual diabetic therapy.
Research shows that nighttime social media is negatively associated with sleep quality and that it might be utilized to cope with aversive psychological states related to cognitive pre-sleep arousal (i.e., transdiagnostic psychopathology variables, referring to maladaptive repetitive thought), namely Fear of Missing Out (FoMO). The use of nighttime social media to cope with other aversive cognitive states (i.e., worry/rumination), their relationship with FoMO, and these variables' association with sleep are not fully understood. This study explored the relationships between nighttime social media, sleep quality, FoMO, cognitive pre-sleep arousal, and maladaptive cognitive emotion regulation (i.e., worry/rumination). The present correlational study followed a cross-sectional design. Participants were 525 university students, ranging in age from 18 to 64 (M = 22.39, SD = 5.62). Measures of sleep quality, morningness/eveningness, cognitive pre-sleep arousal, worry, rumination, FoMO, nighttime screen, and social media use were collected online or in pencil-paper format. Multiple linear regression analyses were performed. Nighttime social media and FoMO were associated with rumination, worry (H1) and cognitive pre-sleep arousal. Both FoMO and worry predicted higher levels of cognitive pre-sleep arousal (H2) and nighttime social media use (H3). Nighttime social media use independently predicted poor sleep quality (H4). These results suggest that worry and FoMO may potentially affect sleep quality by increasing cognitive pre-sleep arousal and nighttime social media. A possible explanation for these findings is that nighttime social media might be used as a strategy to cope with aversive cognitive states. These conclusions may contribute to improving sleep intervention in this population.
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