Perioperative care based on roy adaptation model in elderly patients with benign prostatic hyperplasia: impact on psychological well-being, pain, and quality of life.

PURPOSE: This study aimed to assess the impact of perioperative care based on the Roy Adaptation Model (RAM) on psychological well-being, postoperative pain, and health-related quality of life (HRQoL) in elderly patients with benign prostatic hyperplasia (BPH) undergoing transurethral resection of the prostate (TURP). METHODS: A total of 160 elderly patients diagnosed with BPH between June 2021 and June 2022 and scheduled for TURP were randomly assigned to either the routine care group (n = 80) or the RAM group (n = 80). The RAM group received standard care supplemented with interventions based on the RAM model. Negative emotions measured by the Hospital Anxiety and Depression Scale (HADS), pain intensity by the Visual Analog Scale (VAS), and HRQoL by the 36-Item Short Form Health Survey (SF-36) were measured at the preoperative visit (T0), at 30 days (T1), and at 3 months of (T2) follow­up. RESULTS: Repeated measures ANOVA revealed significant differences in psychological well-being, postoperative pain intensity, and HRQoL within both the routine care and RAM groups across the three time points. Holm-Sidak's multiple comparisons test confirmed significant differences between each time point for both groups. The RAM intervention led to significant reductions in anxiety and depression levels, alleviation of postoperative pain intensity, and improvements in various domains of HRQoL at T1 and T2 compared to routine care. CONCLUSION: Incorporating the RAM model into perioperative care for elderly patients undergoing TURP for BPH has shown promising results in improving psychological well-being, reducing postoperative pain intensity, and enhancing HRQoL.

Rapamycin regulates Akt and ERK phosphorylation through mTORC1 and mTORC2 signaling pathways.

Numerous studies have shown that mammalian target of rapamycin (mTOR) inhibitor activates Akt signaling pathway via a negative feedback loop while inhibiting mTORC1 signaling. In this report, we focused on studying the role of mTORC1 and mTORC2 in rapamycin-mediated Akt and ERK phosphorylation, and the antitumor effect of rapamycin in cancer cells in combination with Akt and ERK inhibitors. Moreover, we analyzed the effect of mTORC1 and mTORC2 on regulating cell cycle progression. We found that low concentrations rapamycin increased Akt and ERK phosphorylation through a mTORC1-dependent mechanism because knockdowned raptor induced the activation of Akt and ERK, but higher doses of rapamycin inhibited Akt and ERK phosphorylation mainly via the mTORC2 signaling pathway because that the silencing of rictor led to the inhibition of Akt and ERK phosphorylation. We further showed that mTORC2 was tightly associated with the development of cell cycle through an Akt-dependent mechanism. Therefore, we combined PI3K and ERK inhibitors prevent rapamycin-induced Akt activation and enhanced antitumor effects of rapamycin. Collectively, we conclude that mTORC2 plays a much more important role than mTORC1 in rapamycin-mediated phosphorylation of Akt and ERK, and cotargeting AKT and ERK signaling may be a new strategy for enhancing the efficacy of rapamycin-based therapeutic approaches in cancer cells.