Objective:Acute kidney injury(AKI) is a common complication after cardiac surgery, and associated with increased risk of development of chronic kidney disease and mortality in the long term. Neutrophil percentage-to-albumin ratio(NPAR) is a new inflammatory marker that has been used to predict the poor prognosis of patients with cardiovascular disease or shock. However, the relationship between NPAR and AKI in patients with cardiac surgery has not been established. The aim was to evaluate the relationship between NPAR and AKI after cardiac surgery.Methods:Data of all adult patients underwent cardiac surgery with cardiopulmonary bypass from January 1, 2006 to December 31, 2018 were extracted from electronic medical record system of the Guangdong Provincial People's Hospital and retrospectively analyzed. The outcome of interest was AKI diagnosed by using the criteria of Kidney Disease Improving Global Outcomes. Logistic regression was used to assess the relationship between NPAR and postoperative AKI while adjust for potential confounders. In addition, restricted cubic spline(RCS) was utilized to provide a flexible description of the association of the preoperative NPAR and AKI. Results:Totally, 24 178 patients were analyzed. The incidence of AKI was 30.1%. Compared with patients without AKI, those with AKI were older and had higher rates of males, left ventricular ejection fraction(LVEF) less than or equal to 0.60, estimated glomerular filtration rate less than 90 ml·min -1·1.73 m -2, hypertension, diabetes, emergency surgery, preoperative critical illness, and reoperation. The baseline serum creatinine, serum uric acid, cardiopulmonary bypass time and postoperative mechanical ventilation time were higher or longer in AKI patients than those in none AKI patients. Then, patients were divided into four groups based on NPAR quartiles. After adjusting for confounding factors using logisitc regression, compared with patients with NPAR in group 3(1.551.97), respectively. The RCS showed a U-shaped nonlinear relationship( P for nonlinear less than 0.001) between NPAR and AKI after adjusting for potential confounding factors. RCS indicated the NPAR of 1.77 was the lowest risk for AKI. When NPAR less than 1.77, per 1-standard deviation(SD) increase in NPAR, the risk of AKI decreased by 23.2%( OR=0.768, 95% CI: 0.687, 0.859). Conversely, when NPAR above 1.77, per one SD increase in NPAR, the risk of AKI increased by 25.9%( OR=1.259, 95% CI: 1.166, 1.36). Conclusion:A U-shaped relationship between NPAR and AKI after cardiac surgery was shown. The appropriate value for NPAR might be 1.77. The risk of AKI might be increased, when less or above this value. NPAR might be used as an effective and economical tool to identify AKI risk among individuals with cardiac surgery, as well as to formulate individualized prevention and intervention strategy.

Objective To identify key safety hazards in the logistics department of a tertiary hospital in Nanjing,analyze their root causes,and implement targeted measures to reduce risk occurrence.Methods Hospital logistics hazard records were reviewed,and risk assessments were conducted.Root cause analysis(RCA)was used to identify proximal and root causes of risks,followed by corresponding countermeasures.Results Proximal causes of hazards included lack of knowledge/skills and imperfect operational procedures,while root causes involved inadequate risk management frameworks and limited inspection cate-gories.By clarifying management structures,optimizing inspection processes,and strengthening incentive mechanisms,the sam-ple hospital achieved significant increases in hazard detection and reductions in adverse events.Conclusion The study demon-strates that systematic safety inspections and hazard rectification mechanisms can effectively mitigate hospital logistics safety risks.

Objective To investigate the protective effect and mechanism of RhoE overexpression in angiotensin Ⅱ-induced myo-cardial fibrosis.Methods Primary cardiomyocytes were cultured in vitro using angiotensin Ⅱ-induced myocardial fibrosis model,and transfected with M-RhoE-carrying overexpressing adenovirus and overexpressing RhoE according to subgroup.α-SMA and Smad3 ex-pression distribution in primary cardiomyocytes were detected by immunofluorescence.The protein expression levels of RhoE,GAPDH,α-SMA,Smad3 and p-Smad3 in primary cells were detected by Western blotting.Results Ang Ⅱ interferes with primary cardiomyo-cytes.Western-blot analysis showed that compared with the control group,the expression levels of p-Smad3 and α-SMA in Ang Ⅱgroup were increased,while the expression levels of RhoE were decreased(P＜0.05).After transfection of RhoE overexpressing adenovi-rus,Western blot results showed that the α-SMA expression level in Ang Ⅱ group was increased compared with that in the control group(P＜0.05).Compared with Ang Ⅱ group α-SMA expression level in Ang Ⅱ+Ad-RhoE group was significantly decreased(P＜0.05).Immunofluorescence detection showed that the α-SMA fluorescence intensity in Ang Ⅱ group was increased compared with that in control group(P＜0.05).Compared with Ang Ⅱ group α-SMA fluorescence intensity in Ang Ⅱ+Ad-RhoE group was significantly decreased(P＜0.05).Effects of overexpression of RhoE gene on TGF-β1/Smad3 pathway.Western blot results showed that compared with the control group,the p-Smad3/Smad3 ratio in Ang Ⅱ group was increased(P＜0.05).Compared with Ang Ⅱ group,the p-Smad3/Smad3 ratio in Ang Ⅱ+Ad-RhoE group was significantly decreased(P＜0.05).Immunofluorescence nuclear translocation showed that compared with the control group,the red fluorescence in myocardial nucleus of Ang Ⅱ group was significantly increased(P＜0.05).Compared with Ang Ⅱ group,the red fluorescence in myocardial nucleus of Ang Ⅱ+Ad-RhoE group was significantly decreased(P＜0.05).Conclusion The process of Ang Ⅱ-induced myocardial fibrosis is accompanied by the activation of TGF-β1/Smad3 sig-naling pathway,and RhoE can inhibit Ang Ⅱ-induced myocardial fibrosis by inhibiting TGF-β1/Smad3 signaling pathway.

Patients with diabetes mellitus are at a significantly elevated risk of developing cognitive impairment,which adversely impacts their quality of life and imposes a substantial burden on the healthcare system.Novel antidiabetic agents,including sodium-glucose cotransporter 2 inhibitors(SGLT-2i),dipeptidyl peptidase-4 inhibitors(DPP-4i),glucagon-like peptide-1 receptor agonists(GLP-1RAs),and dual glucagon-like peptide-1 receptor/glucose-dependent insulinotropic polypeptide receptor agonists(e.g.,Tirzepatide),have been shown to not only effectively regulate glycemic control but also mitigate cognitive decline by inhibiting inflammation,reducing oxidative stress,preventing apoptosis,attenuating amyloid β-protein(Aβ)deposition,and suppressing tau protein phosphorylation.

Objective To identify key safety hazards in the logistics department of a tertiary hospital in Nanjing,analyze their root causes,and implement targeted measures to reduce risk occurrence.Methods Hospital logistics hazard records were reviewed,and risk assessments were conducted.Root cause analysis(RCA)was used to identify proximal and root causes of risks,followed by corresponding countermeasures.Results Proximal causes of hazards included lack of knowledge/skills and imperfect operational procedures,while root causes involved inadequate risk management frameworks and limited inspection cate-gories.By clarifying management structures,optimizing inspection processes,and strengthening incentive mechanisms,the sam-ple hospital achieved significant increases in hazard detection and reductions in adverse events.Conclusion The study demon-strates that systematic safety inspections and hazard rectification mechanisms can effectively mitigate hospital logistics safety risks.

Objective To investigate the protective effect and mechanism of RhoE overexpression in angiotensin Ⅱ-induced myo-cardial fibrosis.Methods Primary cardiomyocytes were cultured in vitro using angiotensin Ⅱ-induced myocardial fibrosis model,and transfected with M-RhoE-carrying overexpressing adenovirus and overexpressing RhoE according to subgroup.α-SMA and Smad3 ex-pression distribution in primary cardiomyocytes were detected by immunofluorescence.The protein expression levels of RhoE,GAPDH,α-SMA,Smad3 and p-Smad3 in primary cells were detected by Western blotting.Results Ang Ⅱ interferes with primary cardiomyo-cytes.Western-blot analysis showed that compared with the control group,the expression levels of p-Smad3 and α-SMA in Ang Ⅱgroup were increased,while the expression levels of RhoE were decreased(P＜0.05).After transfection of RhoE overexpressing adenovi-rus,Western blot results showed that the α-SMA expression level in Ang Ⅱ group was increased compared with that in the control group(P＜0.05).Compared with Ang Ⅱ group α-SMA expression level in Ang Ⅱ+Ad-RhoE group was significantly decreased(P＜0.05).Immunofluorescence detection showed that the α-SMA fluorescence intensity in Ang Ⅱ group was increased compared with that in control group(P＜0.05).Compared with Ang Ⅱ group α-SMA fluorescence intensity in Ang Ⅱ+Ad-RhoE group was significantly decreased(P＜0.05).Effects of overexpression of RhoE gene on TGF-β1/Smad3 pathway.Western blot results showed that compared with the control group,the p-Smad3/Smad3 ratio in Ang Ⅱ group was increased(P＜0.05).Compared with Ang Ⅱ group,the p-Smad3/Smad3 ratio in Ang Ⅱ+Ad-RhoE group was significantly decreased(P＜0.05).Immunofluorescence nuclear translocation showed that compared with the control group,the red fluorescence in myocardial nucleus of Ang Ⅱ group was significantly increased(P＜0.05).Compared with Ang Ⅱ group,the red fluorescence in myocardial nucleus of Ang Ⅱ+Ad-RhoE group was significantly decreased(P＜0.05).Conclusion The process of Ang Ⅱ-induced myocardial fibrosis is accompanied by the activation of TGF-β1/Smad3 sig-naling pathway,and RhoE can inhibit Ang Ⅱ-induced myocardial fibrosis by inhibiting TGF-β1/Smad3 signaling pathway.

Patients with diabetes mellitus are at a significantly elevated risk of developing cognitive impairment,which adversely impacts their quality of life and imposes a substantial burden on the healthcare system.Novel antidiabetic agents,including sodium-glucose cotransporter 2 inhibitors(SGLT-2i),dipeptidyl peptidase-4 inhibitors(DPP-4i),glucagon-like peptide-1 receptor agonists(GLP-1RAs),and dual glucagon-like peptide-1 receptor/glucose-dependent insulinotropic polypeptide receptor agonists(e.g.,Tirzepatide),have been shown to not only effectively regulate glycemic control but also mitigate cognitive decline by inhibiting inflammation,reducing oxidative stress,preventing apoptosis,attenuating amyloid β-protein(Aβ)deposition,and suppressing tau protein phosphorylation.

Objective:Acute kidney injury(AKI) is a common complication after cardiac surgery, and associated with increased risk of development of chronic kidney disease and mortality in the long term. Neutrophil percentage-to-albumin ratio(NPAR) is a new inflammatory marker that has been used to predict the poor prognosis of patients with cardiovascular disease or shock. However, the relationship between NPAR and AKI in patients with cardiac surgery has not been established. The aim was to evaluate the relationship between NPAR and AKI after cardiac surgery.Methods:Data of all adult patients underwent cardiac surgery with cardiopulmonary bypass from January 1, 2006 to December 31, 2018 were extracted from electronic medical record system of the Guangdong Provincial People's Hospital and retrospectively analyzed. The outcome of interest was AKI diagnosed by using the criteria of Kidney Disease Improving Global Outcomes. Logistic regression was used to assess the relationship between NPAR and postoperative AKI while adjust for potential confounders. In addition, restricted cubic spline(RCS) was utilized to provide a flexible description of the association of the preoperative NPAR and AKI. Results:Totally, 24 178 patients were analyzed. The incidence of AKI was 30.1%. Compared with patients without AKI, those with AKI were older and had higher rates of males, left ventricular ejection fraction(LVEF) less than or equal to 0.60, estimated glomerular filtration rate less than 90 ml·min -1·1.73 m -2, hypertension, diabetes, emergency surgery, preoperative critical illness, and reoperation. The baseline serum creatinine, serum uric acid, cardiopulmonary bypass time and postoperative mechanical ventilation time were higher or longer in AKI patients than those in none AKI patients. Then, patients were divided into four groups based on NPAR quartiles. After adjusting for confounding factors using logisitc regression, compared with patients with NPAR in group 3(1.551.97), respectively. The RCS showed a U-shaped nonlinear relationship( P for nonlinear less than 0.001) between NPAR and AKI after adjusting for potential confounding factors. RCS indicated the NPAR of 1.77 was the lowest risk for AKI. When NPAR less than 1.77, per 1-standard deviation(SD) increase in NPAR, the risk of AKI decreased by 23.2%( OR=0.768, 95% CI: 0.687, 0.859). Conversely, when NPAR above 1.77, per one SD increase in NPAR, the risk of AKI increased by 25.9%( OR=1.259, 95% CI: 1.166, 1.36). Conclusion:A U-shaped relationship between NPAR and AKI after cardiac surgery was shown. The appropriate value for NPAR might be 1.77. The risk of AKI might be increased, when less or above this value. NPAR might be used as an effective and economical tool to identify AKI risk among individuals with cardiac surgery, as well as to formulate individualized prevention and intervention strategy.

Stroke is a prevalent acute cerebrovascular disease associated with significant morbidity and mortality,which highly demand effective prevention and treatment strategies.Glucagon-like peptide-1 receptor agonists(GLP-1RA)is a novel type of antidiabetic drug that exerts hypoglycemic and weight loss effects on GLP-1 receptors.Additionally,GLP-1RA possess the potential to reduce infarction size and promote nerve recovery by inhibiting inflammation,oxidative stress,apoptosis,and improving blood-brain barrier permeability and other pathologies.This paper provides a comprehensive summary of the role of GLP-1 in stroke occurrence while also explores the underlying mechanisms by which GLP-1RA influences stroke pathogenesis.Furthermore,it briefly reviews the therapeutic efficacy of GLP-RA in managing stroke.

Objective:To explore the role and mechanism of exogenous active peptide spexin in regulating insulin resistance in adipose tissue.Methods:High-fat diet induced obesity model(DIO) mice and diabetic model(db/db) mice were given intraperitoneal injection of spexin(50 μg/kg) for 3 consecutive weeks, while each control group was given an equal volume of saline. After the intervention, the body weight, visceral fat weight and plasma biochemical indexes of the mice in each group were analyzed. Real-time fluorescence quantitative PCR was used to detect mRNA levels of Krüppel-like transcription factor 9(KLF9), peroxisome proliferator-activated receptor γ coactivator-1α(PGC-1α) and glucose transporter 4(GLUT4); Western blotting was used to detect the protein levels of KLF9, PGC-1α, GLUT4 and p-p38/p38 in adipose tissue.Results:Compared with DIO control mice, spexin-treated DIO mice showed a significant reduction in body weight ( P=0.043), adiposity ( P<0.001), glucose ( P<0.001), insulin ( P=0.008), HOMA-IR ( P<0.001) and elevation in glucose tolerance ( P=0.006) and insulin tolerance levels ( P=0.002). Compared with db/db control mice, spexin-treated db/db mice showed a significant reduction in body weight ( P<0.001), adiposity ( P<0.001), glucose ( P=0.041), insulin ( P=0.009), HOMA-IR ( P=0.007) and elevation in glucose tolerance ( P=0.008) and insulin tolerance levels ( P=0.031). In addition, the gene and protein levels of KLF9, PGC-1α and GLUT4 were significantly increased in the adipose tissue of spexin-treated DIO mice compared with DIO control mice [genes ( P<0.001, P<0.001, P=0.005); proteins ( P=0.047, P=0.022, P=0.001)], while p-p38/p38 protein levels were significantly decreased in the adipose tissue of spexin-treated DIO mice compared with DIO control mice ( P=0.002). Moreover, the gene and protein levels of KLF9, PGC-1α and GLUT4 were significantly increased in the adipose tissue of spexin-treated db/db mice compared with db/db control mice [genes ( P<0.001, P<0.001, and P=0.005); proteins ( P=0.001, P=0.004, and P<0.001)], while p-p38/p38 protein levels were significantly decreased in the adipose tissue of spexin-treated db/db mice compared with db/db control mice ( P=0.001). Conclusion:These results suggested that spexin may play a role in ameliorating adipose tissue insulin resistance in DIO mice and db/db mice through regulating p38MAPK-mediated inflammation and KLF9-PGC-1α-GLUT4 pathway-mediated glucose uptake.