Sepsis is a systemic inflammatory response triggered by infection and often leads to acute kidney injury(AKI).The pathogenesis of sepsis-associated AKI is complex,involving multiple factors such as renal ischemia,inflammation and oxidative stress.In recent years,pyroptosis,a pro-inflammatory form of programmed cell death,has gradually attracted the attention of researchers.Pyroptosis is activated by inflammasomes(e.g.,the NOD-like receptor pyrin domain-related protein 3 inflammasome,NLRP3 inflammasome),accompanied by Gas-dermin D(GSDMD)-mediated formation of cell membrane pores and release of cellular contents,which leads to exacerbation of local and systemic inflammatory responses.The mechanism of pyroptosis in sepsis-associated AKI has not been fully elucidated,but AKI is directly involved in the process of renal functional impairment by indu-cing the death of renal tubular epithelial cells and exacerbating the local inflammatory response.Blockade of key molecules in the pyroptosis pathway,such as GSDMD or NLRP3 inflammasome,can significantly alleviate renal injury,suggesting that the pyroptosis pathway may be a potential therapeutic target for sepsis-associated AKI.This review summarizes the recent research progress on pyroptosis in sepsis-associated AKI,and discuss its cen-tral role in the pathogenesis,particularly focusing on the inflammasome and GSDMD pathways.Additionally,this paper analyzes the potential of focal death inhibition as a therapeutic strategy and proposes future research direc-tions with the expectation of providing references for the treatment of sepsis-related AKI.

Objective To investigate whether Danlou tablet-containing serum ameliorates lipid deposition in HepG2 cells by regulating oxidative stress.Methods Optimal treatment conditions,including concentration and exposure time of Danlou tablet and concentration of oleic acid,were determined,and their effects on cell viability were assessed using the CCK-8 assay.An in vitro model of lipid depo-sition was established by inducing HepG2 cells with oleic acid.HepG2 cells were divided into control,model(treated with oleic acid),and Danlou tablet groups(treated with oleic acid and Danlou tablet).Intracellular lipid droplets were visualized using oil red O staining.Lipid content including non-esterified fatty acid(NEFA)and triglyceride(TG),as well as oxidative stress markers in the cell supernatant,were quantified by enzyme-linked immunosorbent assay.Ultimately,reactive oxygen species(ROS)levels were measured using a fluores-cent probe.Results The optimal conditions were 10％Danlou tablet,24-hour treatment,and 800 μmol/L oleic acid.Compared with the control group,the model group exhibited significantly increased lipid droplet number and size,elevated supernatant levels of NEFA,TG,malondialdehyde,cyclooxygenase-2,and ROS(P＜0.01),and decreased levels of catalase and superoxide dismutase(P＜0.01).Compared with the model group,the Danlou tablet group showed reduced lipid deposition and oxidative stress markers,and increased antioxidant enzyme activity.Conclusion Danlou tablet may ameliorate oleic acid-induced lipid deposition in HepG2 cells by regulating oxidative stress response.

Objective:To investigate the prevalence and risk factors of overweight and obesity among Chinese children aged 3-18 years from 11 provinces, antonomous regions, or municipalities.Methods:This national cross-sectional community health survey utilized a multistage stratified cluster-random sampling method to recruit 193 997 nationally representative participants from 11 provinces, autonomous regions, or municipalities between January 2017 and December 2019. All participants underwent physical examinations, and their caregivers completed questionnaires assessing participants′ dietary, lifestyle, familial, and perinatal information. Multilevel multinomial logistic regression models were employed to identify the potential risk factors.Results:The cohort comprised 193 997 children (102 178 boys, 91 819 girls),aged (10±4) years. Overall prevalence rates were 30 574(15.8%)overweight children and 17 217(8.9%) obesity children. Boys exhibited higher overweight and obesity rates than girls (17.0% (17 368/102 178) vs. 14.4% (13 206/102 178), 11.3% (11 553/91 819) vs. 6.2% (5 664/91 819), χ2=249.12,1 578.69,both P<0.001). The detection rates of obesity in Tanner stage 2 and 3 were the highest in boys and girls, with 13.4%(2 231/16 665) and 8.6%(880/10 221) respectively. Risk factors for obesity included parental overweight (paternal OR=2.34 and maternal OR=2.29), annual household income of 100 000-200 000 yuan (compared with<100 000 yuan, OR=1.04), higher paternal education (compared with below high school,high school and a college education OR=1.09,1.14), birth weight >4.0 kg (≤5 and>5 years old OR=1.74, 1.44,respectively), and western food consumption≥1 time/month (compared with<1, 1-2, 3-4,>4 times/month OR=1.36, 1.30, 1.67(≤5 years), 1.19, 1.16, 1.15 (>5 years), respectively) (all P<0.05). Conversely, coarse grain intake≥1 times/week (compared with<1 times/week, every day, 3-4, 1-2 times/week OR=0.74, 0.80, 0.71 (≤5 years), 0.75, 0.87, 0.90(>5 years), respectively, all P<0.05) was associated with reduced obesity risk. Conclusions:Obesity epidemiology in children demonstrates significant heterogeneity across age, gender, geographic regions, and pubertal stages. It is necessary to establish a personalized prevention and control strategy.

Sepsis is a systemic inflammatory response triggered by infection and often leads to acute kidney injury(AKI).The pathogenesis of sepsis-associated AKI is complex,involving multiple factors such as renal ischemia,inflammation and oxidative stress.In recent years,pyroptosis,a pro-inflammatory form of programmed cell death,has gradually attracted the attention of researchers.Pyroptosis is activated by inflammasomes(e.g.,the NOD-like receptor pyrin domain-related protein 3 inflammasome,NLRP3 inflammasome),accompanied by Gas-dermin D(GSDMD)-mediated formation of cell membrane pores and release of cellular contents,which leads to exacerbation of local and systemic inflammatory responses.The mechanism of pyroptosis in sepsis-associated AKI has not been fully elucidated,but AKI is directly involved in the process of renal functional impairment by indu-cing the death of renal tubular epithelial cells and exacerbating the local inflammatory response.Blockade of key molecules in the pyroptosis pathway,such as GSDMD or NLRP3 inflammasome,can significantly alleviate renal injury,suggesting that the pyroptosis pathway may be a potential therapeutic target for sepsis-associated AKI.This review summarizes the recent research progress on pyroptosis in sepsis-associated AKI,and discuss its cen-tral role in the pathogenesis,particularly focusing on the inflammasome and GSDMD pathways.Additionally,this paper analyzes the potential of focal death inhibition as a therapeutic strategy and proposes future research direc-tions with the expectation of providing references for the treatment of sepsis-related AKI.

Objective:To clarify the current status of mechanical ventilation management in critically ill patients and identify prognostic risk factors in Xinjiang Uygur Autonomous Region, thereby providing evidence for targeted training programs and quality improvement initiatives.Methods:A cohort study was conducted across multiple ICUs in Xinjiang Uygur Autonomous Region from January 31 to February 1, 2024. Patients receiving mechanical ventilation during the study period were enrolled, with clinical outcomes followed up until February 28, 2024. Statistical analyses included demographic characteristics, therapeutic interventions, laboratory parameters, and medication regimens.Results:A total of 77 ICUs and 727 patients were screened in the study, and 253 (34.80%) patients who received mechanical ventilation were ultimately included. Among these patients, 177 patients (69.96%) were treated in tertiary hospitals, and 76 patients (30.04%) in secondary hospitals. Significant differences were observed between tertiary and secondary hospitals regarding ventilator mode selection and mechanical ventilation parameter settings (all P<0.05). No significant differences were found in the 28-day mortality rate between tertiary hospitals and secondary hospitals (33.9% vs. 43.4%, P=0.194). Compared with patients in the survival group, death group patients were older and had more severe disease severity. Multivariate Cox regression analysis demonstrated that body temperature ( HR=1.573, 95% CI: 1.173-2.110, P=0.003), white blood cell count ( HR=1.048, 95% CI: 1.012-1.084, P=0.008), pH ( HR=0.019, 95% CI: 0.001-0.349, P=0.007), age > 65 years ( HR=1.817, 95% CI: 1.086-3.041, P=0.023), and fraction of inspired oxygen ≥ 60% ( HR=2.072, 95% CI: 1.143-3.757, P=0.016) were independent influencing factors for 28-day mortality in mechanically ventilated patients. Conclusions:Mechanically ventilated patients are a major component of the ICU population in Xinjiang Uygur Autonomous Region, with the characteristics of high risk of death. The clinical practice of mechanical ventilation in this region is heterogeneous. In the future, it is urgent to strengthen the improvement of medical quality and related training to improve the success rate of patients with mechanical ventilation.

Inflammatory bowel disease(IBD)is a chronic and recurrent intestinal disease,and has become a major global health issue.Individuals with IBD face an elevated risk of developing colorectal cancer(CRC),and recent studies have indicated that mitochondrial dysfunction plays a pivotal role in the pathogenesis of both IBD and CRC.This review covers the pathogenesis of IBD and CRC,focusing on mitochondrial dysfunction,and explores pharmacological targets and strategies for addressing both conditions by modulating mitochondrial function.Additionally,recent advancements in the phar-macological modulation of mitochondrial dysfunction for treating IBD and CRC,encompassing mitochondrial damage,release of mitochondrial DNA(mtDNA),and impairment of mitophagy,are thoroughly summarized.The review also provides a systematic overview of natural compounds(such as flavonoids,alkaloids,and diterpenoids),Chinese medicines,and intestinal microbiota,which can alleviate IBD and attenuate the progression of CRC by modulating mitochondrial function.In the future,it will be imperative to develop more practical methodologies for real-time monitoring and accurate detection of mitochondrial function,which will greatly aid scientists in identifying more effective agents for treating IBD and CRC through modulation of mitochondrial function.

Inflammatory bowel disease (IBD) is a chronic and recurrent intestinal disease, and has become a major global health issue. Individuals with IBD face an elevated risk of developing colorectal cancer (CRC), and recent studies have indicated that mitochondrial dysfunction plays a pivotal role in the pathogenesis of both IBD and CRC. This review covers the pathogenesis of IBD and CRC, focusing on mitochondrial dysfunction, and explores pharmacological targets and strategies for addressing both conditions by modulating mitochondrial function. Additionally, recent advancements in the pharmacological modulation of mitochondrial dysfunction for treating IBD and CRC, encompassing mitochondrial damage, release of mitochondrial DNA (mtDNA), and impairment of mitophagy, are thoroughly summarized. The review also provides a systematic overview of natural compounds (such as flavonoids, alkaloids, and diterpenoids), Chinese medicines, and intestinal microbiota, which can alleviate IBD and attenuate the progression of CRC by modulating mitochondrial function. In the future, it will be imperative to develop more practical methodologies for real-time monitoring and accurate detection of mitochondrial function, which will greatly aid scientists in identifying more effective agents for treating IBD and CRC through modulation of mitochondrial function.

Objective To summarize the best evidence for the evaluation,implementation,and assess-ment of early rehabilitation exercise for patients with severe traumatic brain injury,provide evidence-based support for clinical nursing and reduce disability and mortality rates.Methods Relevant evidence on early re-habilitation exercise of patients with severe traumatic brain injury from 14 databases or official websites inclu-ding BMJ Best Practice,UpToDate,BMJ Clinical Evidence,the official website of the World Health Organiza-tion(WHO),International Guidelines Collaboration Network(GIN),National Guidelines Library(NGC)in the United States,Scottish Inter Collegiate Guidelines Network(SIGN),JBI Evidence Based Healthcare Knowledge Base,Cochrane Library,PubMed,Embase,Cumulative Index of Nursing and Allied Health Litera-ture(CINAHL),China National Knowledge Infrastructure(CNKI),and Wanfang were retrieved,the latest clinical decisions,guidelines,evidence summaries,expert consensus,systematic reviews,clinical practices,and review results were integrated,the best evidence were extracted,and quality evaluation and classification were conducted.Results A total of 15 articles were included,summarizing 26 best pieces of evidence from six as-pects:early rehabilitation exercise assessment,early awakening rehabilitation treatment therapy,early respira-tory and airway management,early limb activity and muscle joint rehabilitation training,early bladder function training,and early nutritional management.Conclusion This study integrates the best evidence of early reha-bilitation exercise for patients with severe traumatic brain injury,providing evidence-based support for further clinical nursing practice,promoting the rehabilitation process of patients with traumatic brain injury,and im-proving their quality of life.

Objective To investigate the effects of acteoside in a rat model on of diabetic nephropathy(DN)and high-glucose-induced glomerular mesangial cells(GMCs),focusing on the role of acteoside in the silent information regulator 1(SIRT1)/nuclear factor eryth-roid 2-related factor 2(Nrf2)signaling pathway.Methods GMCs were cultured under normal glucose conditions or stimulated with high glucose.Fibrosis,oxidative stress,SIRT1 and Nrf2 protein expression,and mitochondrial structure were assessed in four groups:normal glucose,high glucose,high glucose+acteoside,and high glucose+acteoside+SIRT1 inhibitor(hsa62).DN was induced in rats via intraperitoneal streptozotocin injection,and animals were divided into control,model,and acteoside-treated groups.Pathological kidney changes,blood glucose changes,renal function indices,and protein expression of SIRT1 and Nrf2 were evaluated.Results Compared with controls,DN model rats showed significantly elevated fasting blood glucose,serum creatinine,blood urea nitrogen,and 24-h urinary protein levels of rats in the model group were significantly increased(P＜0.01).GMCs exhibited increased fibrosis,oxidative stress,and mitochondrial damage.Acteoside treatment significantly improved all measured parameters(P＜0.01);and mitigated mitochondrial injury.In vitro,acteoside reduced high-glucose-induced fibrosis and oxidative stress in GMCs,effects that were reversed by SIRT1 inhibition.Western blotting confirmed upregulation of SIRT1 and Nrf2 expression in both treated rat kidney tissues and GMCs(P＜0.01).Conclusion Acteoside alleviates glomerular fibrosis and oxidative stress in DN by activating the SIRT1/Nrf2 signaling pathway,suggesting its potential therapeutic agent for DN.

Objective To investigate whether Danlou tablet-containing serum ameliorates lipid deposition in HepG2 cells by regulating oxidative stress.Methods Optimal treatment conditions,including concentration and exposure time of Danlou tablet and concentration of oleic acid,were determined,and their effects on cell viability were assessed using the CCK-8 assay.An in vitro model of lipid depo-sition was established by inducing HepG2 cells with oleic acid.HepG2 cells were divided into control,model(treated with oleic acid),and Danlou tablet groups(treated with oleic acid and Danlou tablet).Intracellular lipid droplets were visualized using oil red O staining.Lipid content including non-esterified fatty acid(NEFA)and triglyceride(TG),as well as oxidative stress markers in the cell supernatant,were quantified by enzyme-linked immunosorbent assay.Ultimately,reactive oxygen species(ROS)levels were measured using a fluores-cent probe.Results The optimal conditions were 10％Danlou tablet,24-hour treatment,and 800 μmol/L oleic acid.Compared with the control group,the model group exhibited significantly increased lipid droplet number and size,elevated supernatant levels of NEFA,TG,malondialdehyde,cyclooxygenase-2,and ROS(P＜0.01),and decreased levels of catalase and superoxide dismutase(P＜0.01).Compared with the model group,the Danlou tablet group showed reduced lipid deposition and oxidative stress markers,and increased antioxidant enzyme activity.Conclusion Danlou tablet may ameliorate oleic acid-induced lipid deposition in HepG2 cells by regulating oxidative stress response.