The fast-track rehabilitation program results in fewer complications, less postoperative pain, a reduction in the hospital length of stay, and quicker return to work and normal activities after esophagectomy.
Background
Non-steroidal anti-inflammatory drugs (NSAIDs) are among the most widely prescribed drugs worldwide. However, the effect of NSAIDS on postoperative renal function is still unclear. Few studies have assessed the effects of parecoxib on renal function. Our aim is to investigate a correlation between parecoxib and the presence or absence of AKI postoperatively after a breast cancer surgery operation.
Methods
This was a retrospective cohort study that we performed on our hospitalized database. From January 2012 to August 2021, 3542 female patients undergoing radical mastectomy were enrolled, all data including the patients' information and laboratory results were obtained from electronic medical system. The main outcome was the incidence of AKI postoperatively. AKI was defined in accordance with the KDIGO criteria. Study groups were treated with or without parecoxib. Univariable and multivariable logistic regression analyses were performed.
Results
In our study, about 5.76% experienced AKI. The incidence rate of postoperative AKI (3.49%) within 7 days in the parecoxib group was lower than that in the control group (6.00%, P = 0.05). Compared to the control group, the AKI’s incidence was reduced by 49% (OR = 0.46; 95%CI 0.27–0.97) in parecoxib group in multivariable logistic regression analysis. There was a reduction in the incidence of postoperative AKI in other three subgroups: preoperative eGFR < 90 mL/min·1.73/m2 (OR = 0.52; 95%CI 0.27–0.97), blood loss < 1000 ml (OR = 0.48; 95%CI 0.24–0.96) and non-diabetes (OR = 0.51; 95%CI 0.26–0.98).
Conclusions
Parecoxib was associated with incidence of postoperative acute kidney injury.
Background
Exposure to anesthesia leads to extensive neurodegeneration and long‐term cognitive deficits in the developing brain. Caenorhabditis elegans also shows persistent behavioral changes during development after exposure to anesthetics. Clinical and rodent studies have confirmed that altered expression of the regulators of G protein signaling (RGS) in the nervous system is a factor contributing to neurodegenerative and psychological diseases. Evidence from preclinical studies has suggested that RGS controls drug‐induced plasticity, including morphine tolerance and addiction. This study aimed to observe the effect of propofol exposure in the neurodevelopmental stage on learning and memory in the L4 stage and to study whether this effect is related to changes in rgs‐3 expression.
Methods
Caenorhabditis elegans were exposed to propofol at the L1 stage, and learning and memory abilities were observed at the L4 stage. The expression of rgs‐3 and the nuclear distribution of EGL‐4 were determined to study the relevant mechanisms. Finally, RNA interference was performed on rgs‐3‐expressing cells after propofol exposure. Then, we observed their learning and memory abilities.
Results
Propofol time‐ and dose‐dependently impaired the learning capacity. Propofol induced a decline in non‐associative and associative long‐term memory, rgs‐3 upregulation, and a failure of nuclear accumulation of EGL‐4/PKG in AWC neurons. Inhibition of rgs‐3 could alleviate the propofol‐induced changes.
Conclusion
Inhibition of the expression of rgs‐3 alleviated propofol‐induced learning and memory deficits in Caenorhabditis elegans.
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