BACKGROUND Living donor liver transplantation (LDLT) is an important treatment method for end-stage pediatric liver diseases, e.g. , biliary atresia (BA). Acute kidney injury (AKI) after transplantation is a common and serious complication in clinical practice that significantly influences patient mortality and survival rate. AIM To construct a clinical prediction model for AKI after pediatric LDLT based on machine learning (ML). METHODS This study included 340 children with BA who underwent LDLT at our center between December 2022 and December 2024. Complete clinical data were collected, including baseline characteristics, preoperative assessments, intraoperative variables, and postoperative recovery indicators. Least absolute shrinkage and selection operator regression was used for feature selection, and nine ML models were developed for model training and evaluation. After training on the training set, the predictive performance of each model was tested and compared. Finally, the best-performing model was interpreted and visualized using the SHapley Additive exPanations (SHAP) algorithm. RESULTS Excluding postoperative creatinine (Cr) levels, this study identified a total of six potential predictors associated with AKI after LDLT. The random forest model showed comprehensive and optimal predictive performance after 10-fold cross-validation, with an area under the curve of 0.875 (95% confidence interval: 0.805-0.944). In addition, the importance of predictors for AKI occurrence was ranked by SHAP analysis, and preoperative Cr level was identified as the most important predictor. CONCLUSION This study employed ML algorithms to construct a predictive model for early AKI following pediatric liver transplantation. The developed model is expected to assist doctors in performing timely treatment interventions, thereby reducing the occurrence of post-transplant complications and improve the survival time and quality of life in children undergoing liver transplantation.

Phosphatidylcholine （PC） and lysophosphatidylcholine （LPC） homologues are closely associated with coronary atherosclerosis. Accurate determination of their contents can provide an important basis for the clinical diagnosis and prognosis of coronary artery disease （CAD）. In this study， an analytical method based on liquid chromatography-tandem mass spectrometry was established， which enabled the simultaneous and accurate determination of 30 PC and LPC homologues using only 10 μL of human serum. Methanol-acetonitrile-methyl tert-butyl methyl ether-water was used as the extraction system， and an XBridge C18 column was selected as the stationary phase. The mobile phase consisted of an acetonitrile-water mixture （1∶1， volume ratio） and isopropanol， both containing 7.5 mmol/L ammonium formate and 0.15% （volume ratio） formic acid， and gradient elution was adopted for separation. Detection was performed using an electrospray ionization source in the positive ion mode with multiple reaction monitoring. Method validation results showed that the method exhibited a good linear relationship， with an average linear correlation coefficient of ≥0.999 7 over a linear range of 0.125-100 μg/mL. The limits of detection and limits of quantification were 0.01-1.94 μg/mL and 0.03-6.48 μg/mL， respectively. The recoveries ranged from 85.4% to 114.3%， while the intra-day precision and inter-day precision were no more than 4.6% and 12.6%， respectively. Serum samples from 110 clinical volunteers who underwent coronary angiography were determined using this method. The average population concentration of PC homologues was 526.80 μg/mL， and that of LPC homologues was 73.67 μg/mL. Spearman correlation analysis revealed that PC and LPC homologues were closely correlated with the severity of CAD， as well as with related clinical biochemical and lipid metabolism indicators， suggesting that they could serve as potential CAD-related metabolites in clinical practice. Designed to meet clinical analysis needs， this method features small serum sample volume， simple operation， and excellent response. It can efficiently determine 30 PC and LPC homologues in human serum， providing an important reference for exploring the association between these two lipid classes and CAD， as well as the translational application of related biomarkers.

BACKGROUND Living-donor liver transplantation (LDLT) is the definitive treatment for end-stage paediatric liver disease; however, acute kidney injury (AKI) occurs in 40%-70% of cases and significantly affects mortality and clinical outcomes. Esketamine has demonstrated anti-inflammatory and organ-protective properties in preclinical studies, but its renoprotective effects in paediatric LDLT have not been established. AIM To determine whether intraoperative administration of esketamine reduces perioperative AKI and attenuates the inflammatory response in paediatric LDLT. METHODS This randomised, double-blind, placebo-controlled trial was conducted at a tertiary transplant centre in China. Sixty paediatric patients (aged 5-15 months) undergoing LDLT were randomly assigned (1:1) to receive intraoperative esketamine (group E; 0.5 mg/kg at induction followed by 0.5 mg/kg/hour infusion) or placebo (group C). Blood samples were collected at five time points to measure serum creatinine (Scr), tumour necrosis factor, interleukin (IL)-18, IL-10, and neutrophil gelatinase-associated lipocalin (NGAL). Between-group comparisons used independent t-tests or Mann-Whitney U tests. RESULTS Group E demonstrated lower Scr at 3 hours post-reperfusion (40.56 +/- 15.4 mu mol/L vs 60.37 +/- 15.4 mu mol/L, P < 0.05), 24 hours postoperatively (36.35 +/- 8.96 mu mol/L vs 58.93 +/- 12.57 mu mol/L, P < 0.05), and 72 hours postoperatively (34.64 +/- 5.66 mu mol/L vs 53.51 +/- 8.69 mu mol/L, P < 0.05). Serum tumour necrosis factor, IL-18, and NGAL levels were also reduced in group E at time points T2-T5 (P < 0.05). Mechanical ventilation duration was shorter in group E (168.55 +/- 69.64 minutes vs 264.55 +/- 73.64 minutes, P < 0.001). CONCLUSION Intraoperative administration of esketamine attenuates the increase in Scr levels following ischemia-reperfusion injury and attenuates the systemic inflammatory response in paediatric LDLT recipients.

Background:Postoperative thrombosis is the most serious and common complication for children. The Sonoclot device is used to monitor coagulation function in transplant patients. However, no Sonoclot-based threshold for identifying children at risk of thrombosis has been established. This study aimed to identify the Sonoclot parameter and its optimal cutoff value for predicting early postoperative thrombosis in pediatric living-donor liver transplantation. Methods:This was a single-center, prospective and observational study. The study was performed in Tianjin First Central Hospital, Tianjin, China, between September 2019 to May 2021. Clinical data of 200 children with living-donor liver transplantation (LDLT) were collected and observed. The effects of coagulation function monitoring by Sonoclot devices at 1 h after ischemia-reperfusion on early thrombosis were analyzed. Receiver operating characteristic (ROC) analysis was used to obtain the sensitivity and cutoff value of Sonoclot parameters for the diagnosis of thrombosis. Results:A total of 38 cases (19%) had thrombosis complications. Twenty-three cases (11.5%) had postoperative hepatic artery thrombosis and 15 cases (7.5%) had portal vein and hepatic vein thrombosis. Univariate and multivariate analyses showed that whole blood activated clotting time (ACT) was independent risk factor for early postoperative thrombosis. ROC analysis found that the area under the curve (AUC) of ACT for the diagnosis of postoperative thrombosis was 0.918 (95% confidence interval: 0.872-0.954), and the cutoff value to predict early postoperative thrombosis was 228.5 s. The lower-ACT group had a higher incidence of overall thrombosis and hepatic artery thrombosis. Conclusions:ACT after ischemia-reperfusion was a risk factor for early postoperative thrombosis. Maintaining ACT above 228.5 s was associated with a lower incidence of early thrombosis in this cohort. Prospective randomized studies are needed to confirm a causal therapeutic target.

BACKGROUND:Myocardial injury is common during liver transplantation and is associated with poor outcomes. The development of a reliable prediction system for this type of injury is crucial for reducing the incidence of cardiac complications in children receiving living donor liver transplantation (LDLT). However, establishing a practical myocardial injury prediction system for children with biliary atresia remains a considerable challenge. AIM:To create and validate a nomogram model for predicting myocardial injury in children with biliary atresia who received LDLT. METHODS:Clinical data from pediatric patients who received LDLT for biliary atresia between November, 2019 and January, 2022 were retrospectively analyzed. The complete dataset was randomly partitioned into a training set and a validation set at a ratio of 7:3. Least absolute shrinkage and selection operator regression was used to preliminarily screen out the predictors of myocardial injury. The prediction model was established via multivariable logistic regression and presented in the form of a nomogram. RESULTS:This study included 321 patients, 150 (46.7%) of whom had myocardial injury. The participants were randomly allocated into two groups: A training group consisting of 225 patients and a validation group comprising 96 patients. The predictors in this nomogram included the preoperative neutrophil-to-lymphocyte ratio, high sensitivity C-reactive protein level, pediatric end-stage liver disease score and postreperfusion syndrome. The area under the curve for predicting myocardial injury was 0.865 in the training set and 0.856 in the validation set. The calibration curve revealed that the predicted values were very close to the actual values in the two sets. Decision curve analysis revealed that the prediction model offered a favorable net benefit. CONCLUSION:The nomogram developed in this study effectively predicts myocardial injury in pediatric LDLT patients, showing good accuracy and potential for clinical application.

Background: To evaluate the safety of propofol and sevoflurane for general anesthesia in elderly. Materials and Methods: All studies on sevoflurane, propofol, and hyperamylasemia from the establishment of Embase, Ovid, Cochrane Library, and Google Scholar from database establishment to December 2024 were searched. Literatures were screened, and data were extracted on the grounds of inclusion and exclusion criteria. Review Manager (RevMan) (Version 5.4. The Cochrane Collaboration.) was used for statistical analysis. Outcomes assessed included time to spontaneous eye opening, extubation time, incidence rate of postoperative cognitive dysfunction (POCD), postoperative delirium, agitation, nausea and vomiting. Results: Fourteen trials were identified and included in this meta-analysis. The results showed no significant difference in time to spontaneous eye opening (P = 0.54), the incidence of POCD (P = 0.07), postoperative delirium (P = 0.37), and postoperative nausea and vomiting (P = 0.8) between the sevoflurane and propofol groups. Compared with propofol groups, extubation time (P < 0.0001) was significantly shortened by sevoflurane groups. Conversely, compared with sevoflurane, the incidence of postoperative agitation in the propofol group was significantly reduced (P = 0.04). Conclusion: There was no difference in time to spontaneous eye-opening, the incidence of POCD, postoperative delirium, postoperative nausea, and vomiting between the sevoflurane and propofol groups. However, compared with propofol, sevoflurane can significantly shorten intubation time. The incidence of postoperative agitation (P = 0.04) was significantly lower in the propofol group compared with sevoflurane.

BACKGROUND:As a heterogeneous clinical syndrome, acute respiratory distress syndrome (ARDS) is caused by infection-associated inflammation with limited treatment options. Esketamine possesses antiinflammatory properties, and it is effective in treating lung diseases. OBJECTIVE:This study aimed to unveil the efficacy and mechanism of esketamine in ARDS. METHODS:Lipopolysaccharide (LPS) is widely used to induce inflammatory response in lung injury. The mice model of ARDS in this study was established through the inhalation of LPS. Hematoxylin-eosin (H&E) staining was used to evaluate the pathological changes in the lung tissues of ARDS mice, and the histological index of lung damage was employed. Bicinchoninic acid (BCA) assay kits were utilized to assess the total proteins in bronchoalveolar lavage fluid (BALF), and a hemocytometer was used to count the number of total cells. The pulmonary vascular permeability was detected using Evans blue staining. Western blot was carried out to detect the expressions of tight junction proteins, and enzyme-linked immunosorbent assay (ELISA) detected the release of inflammatory cytokines in BALF and serum. Dihydroethidium (DHE) staining was used to detect reactive oxygen species (ROS) production, and the levels of myeloperoxidase (MPO) and oxidative stress markers were measured using corresponding assay kits. Apoptosis was assessed through terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) and Western blot. Immunostaining detected the FUN14 domain-containing 1 (FUNDC1) and light chain 3B (LC3B) in lung tissues, and the expressions of autophagy-related proteins were detected using Western blot. RESULTS:Our data showed that esketamine treatment alleviated LPS-stimulated lung damage, improved pulmonary vascular permeability, and inhibited inflammatory response, oxidative stress, and apoptosis in ARDS mice. Mechanically, esketamine activated mitophagy through UNC-52-like kinase 1 (ULK1)/FUNDC1 signaling pathway. These findings, for the first time, revealed the therapeutic potential of esketamine in treating ARDS. CONCLUSION:Collectively, this study revealed the protective role of esketamine against lung injury, inflammation, oxidative stress, and apoptosis in mice with ARDS and revealed the reaction mechanism related to mitophagy.

ABSTRACT Liver ischemia reperfusion (IR) injury significantly impacts clinical outcomes by increasing the risk of hepatic dysfunction after liver surgery. Fatty livers are more susceptible to IR stress. Recent studies have demonstrated that S100A9 plays a crucial role in both IR injury and the progression of liver steatosis. Nevertheless, the precise mechanisms underlying these effects remain unclear. In our study, transcriptome analysis of fatty livers subjected to IR insult in mice identified S100A9 as an important mediator. Employing loss-of-function approaches, we investigated the immune regulatory function of S100A9 and its downstream signaling in fatty liver IR injury. As expected, S100A9 emerged as one of the most significantly upregulated genes during the reperfusion stage in fatty livers. Genetic knockdown of S100A9 markedly ameliorated liver pathological damage, evidenced by reduced macrophage/neutrophil infiltration as well as the decreased expression of proinflammatory factors. Transcriptome/functional studies revealed that S100A9 triggered liver inflammatory response via regulating toll-like receptor 2 (TLR2)/activating transcription factor 4 (ATF4) signaling. Additionally, TLR2 expression was notably increased in macrophages from ischemic fatty livers. In vitro, recombinant S100A9-stimulated macrophages exhibited the elevated production of proinflammatory factors and TLR2/ATF4 pathway activation. Intriguingly, S100A9 facilitated ATF4 nuclear translocation and enhanced NEK7/NLRP3 inflammasome activation in macrophages. In conclusion, our study identified S100A9 as a key regulator responsible for macrophage NLRP3 inflammasome activation and subsequent inflammatory injury in fatty liver IR process. Targeting TLR2/ATF4 signaling may offer a novel therapeutic strategy for mitigating S100A9-mediated liver injury.

OBJECTIVE:The aim of this study was to evaluate whether the pretransplant neutrophil-lymphocyte ratio (NLR) is associated with postreperfusion syndrome (PRS) after paediatric living-donor liver transplantation (LDLT) and the impact of different pretransplant NLR values on short-term outcomes. METHODS:Clinical data from paediatric patients who underwent LDLT for biliary atresia were retrospectively analysed. Receiver operating characteristic (ROC) curve analysis was used to evaluate the predictive value of the pretransplant NLR for PRS. The paediatric patients were stratified into two cohorts according to the optimal cut-off value, and their perioperative clinical indices were subsequently compared. RESULTS:This retrospective study included 313 paediatric patients who had been diagnosed with biliary atresia. Based on ROC analysis, the area under the curve (AUC) of the NLR was 0.738, with a sensitivity of 73.1% and a specificity of 68.2% when predicting PRS. Paediatric patients were split into two groups according to the optimal NLR cut-off: NLR-Low (n = 158) and NLR-High (n = 155). Compared with the NLR-Low group, the NLR-High group had significantly more postoperative intensive care unit and hospitalisation days (p < 0.05). Furthermore, patients in the NLR-High group demonstrated a notably lower 1-year survival rate than their counterparts in the NLR-Low group did. An elevated NLR, a prolonged graft cold ischaemic time, and the occurrence of hypothermia before reperfusion are independent risk factors for PRS. CONCLUSION:The pretransplant NLR is associated with postreperfusion syndrome in paediatric LDLT patients, and an elevated NLR is correlated with unfavourable short-term postoperative outcomes in paediatric patients after LDLT.

Neuropathic pain, attributed to its intricate pathogenesis, remains challenging to treat effectively. This study delineates neuroimmune-glial cell interactions within the ganglia as a pivotal mechanism initiating nerve damage, thereby contributing to neuropathic pain. Utilizing a chronic constriction injury (CCI) mouse model, we explored the pro-inflammatory molecule S100A9, secreted by myeloid cells, in the context of neuropathic pain development. Our findings revealed an upregulation of S100A9 in the dorsal root ganglia (DRGs) of CCI mice, predominantly due to neutrophil infiltration. Notably, S100A9 knockout significantly mitigated mechanical pain hypersensitivity and inflammation induced by CCI. We further elucidated the role of S100A9 in mechanical pain hypersensitivity using inhibitors and recombinant S100A9 proteins. Transcriptome sequencing indicated that S100A9 potentially influenced neuropathic pain by modulating the expression of orphan G protein-coupled receptor 153 (GPR153) and potassium channel Kcnk16 on the DRG neuron membrane. Collectively, our research underscores the significant role of S100A9 in neuropathic pain pathogenesis and presents it as a promising therapeutic target. KEY INNOVATIONS.

Rationale: Renal fibrosis is commonly recognized as the ultimate pathway for most chronic kidney diseases (CKD). Renal tubular epithelial inflammation drives the initiation and progression of renal fibrosis. Follistatin-like 1 (FSTL1) is a small matricellular protein, whose expression pattern, function and underlying mechanism in regulating renal inflammation and fibrosis remains largely unknown. Methods: We utilized two Fstl1-deficient genetic mouse models: heterozygous Fstl1+/- mice and whole-body Fstl1 conditional knockout mice, and a mouse model with FSTL1 overexpression via adenoviral vector infection. These mice were subjected to unilateral ureteral obstruction (UUO). We used an Fstl1 lineage tracing mouse to investigate the expression and location of induced FSTL1 in the obstructed kidney. We investigated the effect of FSTL1 on TNF-α induced epithelial inflammation and the NF-κB pathway by overexpression or knockdown of FSTL1 in human kidney epithelial cells (HK2). Results: We observed increased expression of FSTL1 in kidneys from patients with CKD, and UUO mouse model of renal injury and fibrosis. Deletion of Fstl1 in mice aggravated UUO-induced inflammatory kidney injury and subsequent fibrosis. Conversely, overexpression of FSTL1 by adenoviral vector infection in mice mitigated expression of proinflammatory cytokines and the fibrotic phenotype. Mechanistically, we identified that increased FSTL1 was mostly derived from the tubular epithelium of the obstructed mouse kidney. FSTL1 inhibited human renal epithelial cell inflammatory responses, as assessed by reducing the NF-κB pathway, release of IL-1β and IL-6, expression of intercellular adhesion molecule 1 (ICAM-1), and monocyte adhesion to kidney epithelial cells. Conclusions: These findings suggest that FSTL1 plays a protective role against kidney fibrosis by inhibiting renal epithelial inflammation via the NF-κB pathway in epithelium, thereby offering a potential novel strategy for treating progressive CKD.

The incidence of brain injury in sepsis patients has been as high as 70 %, which has been a significant cause of septic patients' death. However, the pathophysiology of brain injury in sepsis is multifactorial and inconclusive. There are no clear reasons or effective treatments for brain injury induced by sepsis. The experiment aims to research how Hydrogen sulfide (H2S) affects sepsis-induced brain injury. Male ICR mice developed sepsis via cecal ligation and puncture (CLP). Isodose H₂S was administered before operation and at 1、12 h post-operation. Zinc protoporphyrin IX (ZnPPIX, a HO-1 inhibitor) was intraperitoneally injected 1 h before surgery. After an operation, the survival rate of 7 days was observed and recorded. Morris water maze and Y-maze were applied to evaluate cognitive function. The expression level of Bad and Bcl-2 and neuronal apoptosis by TUNEL assay in the hippocampus were assessed. We used different methods to measure the protein expression and mRNA levels of heme oxygenase-1(HO-1), high-mobility group box 1 (HMGB1) and the activity of HO-1 in hippocampus neurons. The rate of survivors and cognitive impairment of septic mice were markedly improved after H2S treatment, and the brain injury in septic mice such as pathological damage and the expression change of Bad and Bcl-2 significantly alleviated. We discovered that the useful effects of H2S on brain injury in septic mice were related to the decreased level of HMGB1 in the hippocampus. In addition, H2S treatment alleviated brain injury of septic mice by promoting the expression and activity of HO-1. Moderate exogenous H2S treatment would be a potential treatment to relieve sepsis brain injury.

BACKGROUND AND AIMS:Myofascial pain syndrome (MPS), driven by dysfunction in myofascial trigger points (MTrPs), remains mechanistically unclear. This study aimed to explore miR-15 b's function in MTrP pathogenesis, focusing on its regulation of iron-sulfur (Fe-S) cluster synthesis and mitophagy. METHODS:A rat MTrP model was established using repetitive mechanical injury and eccentric exercise. Skeletal muscle tissues and primary satellite cells were analysed for miR-15b expression, Fe-S cluster-related proteins (NFS1, NDUFS3, and SDH B), and mitophagy markers (FUN14 structural domain-containing protein 1 (FUNDC1) and LC3-II/I). In vitro, tumour necrosis factor-alpha (TNF-α)-induced inflammation and miR-15b modulation (mimics/sponges) and NFS1 modulation (overexpression/knockdown) were used to assess mitochondrial functions. In vivo, the therapeutic effect on normal and MTrP model rats was evaluated by intramuscular injection of transiently transfected complexes of NFS1 plasmid, miR-15b plasmid or sponge constructs. RESULTS:MTrP rats exhibited miR-15b, suppressed NFS1, and impaired Fe-S-dependent complexes. Dual luciferase assays verified miR-15b targeting NFS1. Rescue experiments further validated that miR-15b directly inhibits NFS1, increase reactive oxygen species (ROS), lowering mitochondrial membrane potential (MMP), triggering FUNDC1-mediated mitophagy. TNF-α stimulation elevated miR-15b levels, exacerbating mitochondrial dysfunction, whereas miR-15b inhibition restored NFS1 and normalised mitophagy. In normal rats, miR-15b overexpression recapitulated MTrP-like pathology in healthy rats. Moreover, in the MTrP model rats, miR-15b overexpression exacerbated these manifestations, sponge and NFS1 treatment attenuated or even reversed certain pathological changes. CONCLUSIONS:miR-15b drives MTrP progression by suppressing NFS1, disrupting Fe-S homeostasis, and activating FUNDC1-dependent mitophagy. Targeting miR-15b mitigates mitochondrial dysfunction and pain hypersensitivity, underscoring its therapeutic potential in MPS.

BackgroundAccurately predicting the depth of anesthesia is essential for ensuring patient safety and optimizing surgical outcomes. Traditional regression-based approaches often struggle to model the complex and dynamic nature of patient responses to anesthetic agents. Machine learning techniques offer a promising alternative by capturing intricate relationships within physiological data. This study proposes a hybrid model integrating Long Short-Term Memory (LSTM) networks, Transformer architectures, and Kolmogorov-Arnold Networks (KAN) to improve the predictive accuracy of anesthesia depth.MethodsThe proposed model combines multiple deep learning techniques to address different aspects of anesthesia prediction. The LSTM component captures the sequential nature of drug administration and physiological responses. The Transformer architecture utilizes attention mechanisms to enhance contextual understanding of patient data. The KAN models nonlinear relationships between drug infusion histories and anesthesia depth. The model was trained and evaluated on patient data from a publicly available anesthesia monitoring database. Performance was assessed using Mean Squared Error (MSE) and compared against other models.ResultsThe hybrid model demonstrated superior predictive performance compared to conventional regression approaches. Tested on the VitalDB database, the proposed framework achieved a MSE of 0.0062, which is lower than other methods. The inclusion of attention mechanisms and nonlinear modeling contributed to improved accuracy and robustness. The results indicate that the combined approach effectively captures the temporal and nonlinear characteristics of anesthesia depth, offering a more reliable predictive tool for clinical use.ConclusionsThis study presents a novel deep learning framework for anesthesia depth prediction, integrating sequential, attention-based, and nonlinear modeling techniques. The results suggest that this hybrid approach enhances prediction reliability and provides anesthesiologists with a more comprehensive analysis of factors influencing anesthesia depth. Future research will focus on refining model robustness, exploring real-time applications, and addressing potential biases in predictive analytics to further improve clinical decision-making.

Background:We aimed to whether esketamine induction and maintenance of general anesthesia could reduce the incidence of perioperative neurocognitive dysfunction (PND) in elderly patients undergoing gastrointestinal tumor surgery and explore the related mechanisms preliminarily. Patients and methods:A total of 153 elderly patients were divided into two groups: a control group (group C, n = 75) and an esketamine group (group K, n = 78). In group K, 0.3 mg/kg esketamine was injected intravenously during anesthesia induction, and 0.3 mg·kg-1·h-1 was injected intravenously to maintain anesthesia. In group C, esketamine was replaced with an equal volume of normal saline. The Pittsburgh Sleep Quality Index (PSQI) was used to evaluate sleep quality 1 day before surgery and at 1, 3, 7, and 30 days after surgery. A battery of neurological tests was used to assess cognitive function 1 day before surgery and 7 and 30 days after surgery. Serum IL-6, TNF-α, NSE and Aβ1-42 concentrations were tested by enzyme-linked immunosorbent assay before surgery, at the end of surgery and 1 day after surgery. Results:The incidence of PND in group K at 7 days after surgery was lower than that in group C (P < 0.05). Compared with that in group C, the PSQI score in group K was lower at 1 and 3 days after surgery (P < 0.05). Compared with those in group C, the TNF-ɑ concentration in group K were lower both after surgery and 1 day after surgery (P < 0.05), and the IL-6, NSE and Aβ1-42 concentration were lower at 1 day after surgery (P < 0.05). Conclusion:The use of esketamine for anesthesia induction and maintenance in elderly patients undergoing gastrointestinal tumor surgery inhibited inflammation, alleviated neuronal injury and degeneration, improved postoperative sleep quality and cognitive function, and reduced the incidence of PND.

Acute lung injury (ALI) is a common postoperative complication, particularly in pediatric patients after liver transplantation. Hepatic ischemia–reperfusion (HIR) increases the release of exosomes (IR-Exos) in peripheral circulation. However, the role of IR-Exos in the pathogenesis of ALI induced by HIR remains unclear. Here, we explored the role of exosomes derived from the HIR-injured liver in ALI development. Intravenous injection of IR-Exos caused lung inflammation in naive rats, whereas pretreatment with an inhibitor of exosomal secretion (GW4869) attenuated HIR-related lung injury. In vivo and in vitro results show that IR-Exos promoted proinflammatory responses and M1 macrophage polarization. Furthermore, miRNA profiling of serum identified miR-122-5p as the exosomal miRNA with the highest increase in young rats with HIR compared with controls. Additionally, IR-Exos transferred miR-122-5p to macrophages and promoted proinflammatory responses and M1 phenotype polarization by targeting suppressor of cytokine signaling protein 1(SOCS-1)/nuclear factor (NF)-κB. Importantly, the pathological role of exosomal miR-122-5p in initiating lung inflammation was reversed by inhibition of miR-122-5p. Clinically, high levels of miR-122-5p were found in serum and correlated to the severity of lung injury in pediatric living-donor liver transplant recipients with ALI. Taken together, our findings reveal that IR-Exos transfer liver-specific miR-122-5p to alveolar macrophages and elicit ALI by inducing M1 macrophage polarization via the SOCS-1/NF-κB signaling pathway.