The Effects of Preoperative Pain Education on Pain Severity in Cardiac Surgery Patients: A Pilot Randomized Control Trial.

BACKGROUND: There is minimal research on the effect of individualized preoperative education on postoperative pain and postoperative pain medication intake. AIM: The study objective was to assess the effect of individually tailored preoperative education on postoperative pain severity, number of pain breakthroughs, and use of pain medication in participants receiving the intervention compared to controls. METHODS: A pilot study with 200 participants was conducted. The experimental group received an informational booklet and discussed their ideas surrounding pain and pain medication with the researcher. Controls received no intervention. Postoperative pain severity was measured by a Numerical Rating System (NRS), which was divided into mild (NRS 1-3), moderate (NRS 4-6), and severe (NRS 7-10). RESULTS: In the participant cohort, 68.8% of participants were male, and the average age was 60.48±10.7. Average postoperative 48-hour cumulative pain scores were lower in those who received the intervention compared to controls; 50.0 (IQR 35.8-60.0) vs. 65 (IQR 51.0-73.0; p < .01) participants who received the intervention had less frequent pain breakthroughs when compared to controls (3.0 [IQR 2.0-5.0] vs. 6.0 [IQR 4.0-8.0; p < .01]). There was no significant difference in the amount of pain medication taken by either group. CONCLUSIONS: Participants who receive individualized preoperative pain education are more likely to have decreased postoperative pain.

Alteration of autophagy-related protein 5 (ATG5) levels and Atg5 gene expression in diabetes mellitus with and without complications.

BACKGROUND: Autophagy is a catabolic mechanism that involves lysosomal-dependent degradation of unnecessary intracellular components and responsible for normal cellular homeostasis. Autophagy pathway and its key participant ATG5/LC3 are associated with several pathologies such as diabetes mellitus and its complications. METHODS: Levels and expression of autophagy key components ATG5 and LC3B were analyzed in both human model and murine tissues. One hundred and twenty human subjects were divided into four groups: Healthy (control), diabetes mellitus without complications, diabetic nephropathy, and diabetic retinopathy. Additionally, we used kidneys from WT healthy and diabetic nephropathy mice. Lysate derived from human peripheral blood mononuclear cells and murine renal cortex lysates were subjected to western blot and immunohistochemical analysis. RESULTS: Western blot and immunohistochemical analysis demonstrate that ATG5 protein levels were significantly decreased in diabetes mellitus, diabetic nephropathy (DN), and diabetic retinopathy patients versus healthy controls and in DN mice compared to healthy mice (0.65 ± 0.04; 1.15 ± 0.13 A.U. units, respectively). Quantification of staining area (%) of ATG5 mice tissue expression also decreased in DN versus healthy mice (4.42 ± 1.08%; 10.87 ± 1.01%, respectively). LC3B LEVELS AND EXPRESSION: Significant reduction in peripheral blood mononuclear cells in diabetic patients (with or without complications) vs. healthy controls. Renal LC3B levels were lower in DN versus healthy mice (0.36 ± 0.03; 0.68 ± 0.07 A.U. units). Renal LC3B staining quantification revealed significant reduction in DN versus healthy mice (1.7 ± 0.23%; 8.56 ± 1.7%). CONCLUSION: We conclude that ATG5, as well as LC3B, are down regulated in diabetic patients with or without complications. This diminution contributes to deficiencies in the autophagy process.