Application of Ward Noise Management in Perioperative Hepatobiliary Surgery: A Retrospective Study.

OBJECTIVE: To explore the application effect of ward noise management during the perioperative period of hepatobiliary surgery. METHODS: The clinical data of 295 patients undergoing hepatobiliary surgery admitted to People's Hospital of Zunyi City Bo Zhou District from March 2020 to March 2023 were retrospectively analyzed. In accordance with different perioperative management programs, patients were divided into the control (implementation of perioperative routine management) and observation (implementation of perioperative routine management + ward noise management) groups. Patients' general data were matched through propensity score matching, and 55 cases were allocated to each group. After matching, the clinical indicators of the two groups were compared to evaluate the effect of ward noise management on patients undergoing hepatobiliary surgery. RESULTS: No significant difference in general data was found between the two groups (P > 0.05). After management, the postoperative recovery indicators, such as feeding time, exhaust time, defecation time, first time to get out of bed, and incidence of postoperative complications, did not significantly differ between the observation and control groups (P > 0.05). The Hamilton Anxiety Scale, Hamilton Depression Scale and Pittsburgh Sleep Quality Index scores of the observation group were lower than those of the control group (P < 0.05). The average noise decibel values during the day, night, and over 24 hours of the observation group were lower than those of the control group (P < 0.05). CONCLUSIONS: Ward noise management can improve the negative emotions of patients undergoing hepatobiliary surgery, enhance sleep quality, and promote recovery. Therefore, it has a certain clinical promotion value.

Palmitic acid-induced apoptosis in pancreatic ß-cells is increased by liver X receptor agonist and attenuated by eicosapentaenoate.

Saturated fatty acids are implicated in the development of diabetes via the impairment of pancreatic islet ß-cell viability and function. Liver X receptors (LXRs) and eicosapentaenoate (EPA) are known regulators of fatty acid metabolism. However, their roles in the pathogenesis of diabetes remain incompletely understood. The aim of this study was to determine the effects of EPA and the LXR agonist T0901317 on saturated fatty acid (palmitic acid)-induced apoptosis in the insulinoma ß-cell line INS-1, a model for insulin-secreting ß-cells. T0901317 significantly promoted palmitic acid-induced apoptotic cell death in the INS-1 cells. Consistent with these results, caspase-3 activity and BAX and sterol regulatory element binding protein-1c (SREBP-1c) mRNA levels were markedly increased in INS-1 cells co-administered palmitic acid and T0901317. The production of reactive oxygen species was considerably higher in the cells cultured concurrently with T0901317 and palmitic acid than in the cells incubated with either agent alone. EPA treatment attenuated the cellular death promoted by palmitic acid and T0901317 in the INS-1 cells, disclosing a possible mediating mechanism involving the inhibition of SREBP-1c. Finally, T0901317 up-regulated the palmitic acid-induced expression of p27(KIP1), transforming growth factor beta 1, and SMAD3 proteins in INS-1 cells. These results demonstrate that palmitic acid-induced apoptosis in ß-cells is enhanced by T0901317 via the activation of LXRs and is blocked by EPA via the inhibition of SREBP-1c, suggesting that the regulation of lipogenesis and lipotoxicity affecting pancreatic ß-cell viability and insulin production may be a unique strategy for diabetes therapy.

Knockdown of RAGE expression inhibits colorectal cancer cell invasion and suppresses angiogenesis in vitro and in vivo.

The receptor for advanced glycation end-products (RAGE) is a transmembrane receptor in cells, and the interaction of RAGE with ligands results in pro-inflammatory gene activation. Aberrant RAGE activation was reported to promote the pathogenesis of colorectal cancer. This study aimed to investigate the effects of RAGE on the regulation of cell viability, invasion, and angiogenesis, as well as the underlying molecular mechanisms regulating these interactions in colorectal cancer cells. The RAGE mRNA and protein were evaluated in five colorectal cancer cell lines and in 45 cases of colorectal cancer tissue specimens (using immuohistochemistry). RAGE expression was then knockdown using RAGE shRNA for assessing cell viability and invasion assays as well as for tube formation and CAM assays in human umbilical vein endothelial cells and chick embryos, respectively. RAGE was highly expressed in colorectal cancer tissues, and was associated with increased microvessel density. Two of the four RAGE shRNA constructs were able to significantly knockdown RAGE expression in SW480 cells. RAGE knockdown inhibited invasion capacity of SW480 cells, but did not significantly affect cell viability. Furthermore, the conditioned growth medium from stable RAGE shRNA-transfected cells suppressed tube formation of human umbilical vein endothelial cells and angiogenesis of chicken embryos. Knockdown of RAGE inhibited expression of VEGF and SP1 protein in colorectal cancer cells. In summary, these data suggest that silence of RAGE expression could effectively inhibit colorectal cancer angiogenesis in vitro and in vivo.