OBJECTIVE To screen and quantitatively analyze the quality marker （Q-Marker） associated with anti-renal fibrosis in Shenqi shenshuai mixture （SQSS）， so as to provide references for the analysis of pharmacodynamic substances and new drug transformation of SQSS. METHODS The chemical components of SQSS were characterized by untargeted metabolomics. Combined with network pharmacology， gene expression omnibus （GEO） and connectivity map （CMAP） databases， the anti-renal fibrosis Q-Markers of SQSS were screened. HPLC-MS/MS was applied to determine the contents of Q-Markers in 10 batches of SQSS. RESULTS A total of 1 319 compounds were identified from SQSS via untargeted metabolomics，and 84 active ingredients with anti-renal fibrosis activity were further screened out， such as formononetin. Nine anti-renal fibrosis Q-Markers were obtained by network pharmacology and GEO database， including berberine， quercetin， honokiol， nicotinamide， daidzein， coumarin， kaempferol， formononetin and amygdalin. The quantitative results showed that the average contents of the above components （excluding amygdalin） in 10 batches of SQSS were 2.523， 1.942， 26.848， 1.415， 0.692， 0.171， 0.374， 7.401 μg/mL， respectively. CONCLUSIONS Nine anti-renal fibrosis Q-Markers of SQSS were screened in this study， and the contents of eight among them were determined. The results can provide a basis for elucidating the pharmacodynamic material basis and promoting the new drug transformation of SQSS.

OBJECTIVE To screen and quantitatively analyze the quality marker （Q-Marker） associated with anti-renal fibrosis in Shenqi shenshuai mixture （SQSS）， so as to provide references for the analysis of pharmacodynamic substances and new drug transformation of SQSS. METHODS The chemical components of SQSS were characterized by untargeted metabolomics. Combined with network pharmacology， gene expression omnibus （GEO） and connectivity map （CMAP） databases， the anti-renal fibrosis Q-Markers of SQSS were screened. HPLC-MS/MS was applied to determine the contents of Q-Markers in 10 batches of SQSS. RESULTS A total of 1 319 compounds were identified from SQSS via untargeted metabolomics，and 84 active ingredients with anti-renal fibrosis activity were further screened out， such as formononetin. Nine anti-renal fibrosis Q-Markers were obtained by network pharmacology and GEO database， including berberine， quercetin， honokiol， nicotinamide， daidzein， coumarin， kaempferol， formononetin and amygdalin. The quantitative results showed that the average contents of the above components （excluding amygdalin） in 10 batches of SQSS were 2.523， 1.942， 26.848， 1.415， 0.692， 0.171， 0.374， 7.401 μg/mL， respectively. CONCLUSIONS Nine anti-renal fibrosis Q-Markers of SQSS were screened in this study， and the contents of eight among them were determined. The results can provide a basis for elucidating the pharmacodynamic material basis and promoting the new drug transformation of SQSS.

Objective To systematically evaluate the risk prediction models for postoperative pulmonary infection in patients with esophageal cancer, providing an objective basis for clinical selection and optimization of models. Methods A systematic search was conducted in Chinese and English databases such as VIP, Wanfang, CNKI, CBM, PubMed, Cochrane Library, Embase, and Web of Science for studies related to the risk prediction models of postoperative pulmonary infection in patients with esophageal cancer from the inception to September 30, 2024. The PROBAST tool was used to assess the quality of prognostic model research, and the RevMan 5.4 software was used for meta-analysis of predictive factors. Results A total of 17 articles were included, containing 26 pulmonary infection risk prediction models. The area under the receiver operating characteristic curve (AUC) ranged from 0.627 to 0.942, among which 21 models had good predictive performance (AUC>0.7). Quality assessment through the PROBAST tool revealed that all 17 articles had a high risk of bias. Meta-analysis results showed that common predictive factors for postoperative pulmonary infection in esophageal cancer included smoking history (OR=1.97), smoking index ≥200 (cigarettes-years) (OR=4.38), smoking index ≥400 (cigarettes-years) (OR=2.00), age (OR=1.27), comorbid diabetes (OR=2.13), comorbid emphysema or chronic obstructive pulmonary disease (OR=1.55), low plasma albumin levels (OR=1.17), prognostic nutritional index (OR=4.45), history of related lung diseases (OR=2.10), tumor location (OR=2.32), surgical approach (OR=2.21), operation time (OR=1.73), preoperative serum procalcitonin levels (OR=3.06), anastomotic leakage (OR=3.39), reduced forced expiratory volume in the first second/forced vital capacity ratio (OR=0.86), and hoarseness (OR=2.23). Conclusion At present, the risk prediction models for postoperative pulmonary infection in esophageal cancer are still in the stage of continuous development and optimization, and their research quality needs to be further improved. Future research can refer to the predictive factors summarized in this study based on meta-analysis, combined with clinical practice, to select appropriate methods to construct and validate the risk prediction models for postoperative pulmonary infection in esophageal cancer, thus providing early targeted preventive strategies for high-risk patients.

Objective: To investigate the distribution patterns and risk factors for multidrug-resistant bacterial pulmonary infections in patients with oral squamous cell carcinoma (OSCC) undergoing flap reconstruction surgery, and to provide evidence for infection prevention and treatment in this population. Methods: This study was approved by the institutional medical ethics committee. We retrospectively analyzed sputum culture results, antimicrobial susceptibility testing data, and clinical records of 109 OSCC patients undergoing flap reconstruction. Chi-square tests were employed to identify pathogens and risk factors for multidrug-resistant bacteria (MDR) in postoperative pulmonary infections. Multivariate logistic regression analysis was conducted to determine MDR risk factors and establish a nomogram prediction model. The model’s discriminatory power, accuracy, and clinical utility were evaluated using receiver operating characteristic (ROC) curves, calibration curves, and decision curve analysis (DCA). Results: Among the 109 patients, 52 had negative sputum cultures and 57 tested positive, of whom 14 developed multidrug-resistant (MDR) pulmonary infections. Chi-square analysis revealed that blood transfusion, pre-existing pulmonary diseases, operation time ≥ 490 min, intraoperative blood loss ≥ 400 mL, and abnormal BMI were significant risk factors for postoperative MDR infections (P < 0.05). Multivariate logistic regression identified pre-existing pulmonary diseases, intraoperative blood loss ≥ 400 mL, abnormal BMI, and operative duration ≥ 490 min as independent risk factors for MDR infections (P < 0.05). The nomogram prediction model for MDR infections demonstrated an area under the ROC curve (AUC) of 0.874 (95% CI: 0.775-0.973). The calibration plot showed good agreement between predicted and observed outcomes. DCA indicated a net clinical benefit when the threshold probability for high-risk MDR infections ranged from 0.000 to 0.810. Common MDR pathogens included MDR Pseudomonas aeruginosa, MDR Klebsiella pneumoniae, carbapenem-resistant Acinetobacter baumannii (CRAB), and methicillin-resistant Staphylococcus aureus (MRSA). Conclusion Among OSCC patients undergoing flap reconstruction, MDR pulmonary infections were predominantly caused by gram-negative bacteria (including CRAB, MDR Pseudomonas aeruginosa, and MDR Klebsiella pneumoniae along with the gram-positive pathogen MRSA. Pre-existing pulmonary comorbidities, prolonged surgery duration (≥ 490 min), significant intraoperative blood loss (≥ 400 mL), and abnormal BMI were confirmed as independent risk factors for these MDR infections. The nomogram predictive model incorporating these four variables demonstrated clinically reliable accuracy in risk stratification for postoperative MDR pulmonary infections in this patient population.

OBJECTIVE To investigate the effects of calcitriol on sepsis-induced immunosuppression and its potential mechanism. METHODS A sepsis-induced immunosuppression mice model was established using cecal ligation and puncture （CLP）. The 7-day survival rate， serum levels of tumor necrosis factor- α （TNF- α）， interleukin-6 （IL-6）， and IL-1β were determined in sham operation group， CLP group and calcitriol group （1 μg/kg）； the morphological changes of lung tissue in mice were observed. Lipopolysaccharide （LPS） tolerance macrophage models （representing sepsis-induced immunosuppression） were established using mice macrophage cell line RAW264.7 cells. The levels of TNF-α and IL-6 in cell supernatants as well as mRNA expressions of IL-1β， nucleotide-binding domain leucine-rich repeat and pyrin domain-containing receptor 3 （NLRP3）， IL-18 and caspase-1 were assessed in culture medium group， LPS group， LPS tolerance group， and calcitriol （5 μmol/L） group. The following parameters were measured： propidium iodide （PI）-positive cell ratio， caspase-1 activity， lactate dehydrogenase （LDH） release， and Ca2+ levels. RESULTS Compared with CLP group， 7-day survival rate and serum levels of TNF-α， IL-6 and IL-1β were increased significantly in calcitriol group （P＜0.05）. Additionally， pulmonary tissue damage was markedly attenuated in calcitriol group. Compared with LPS tolerance group， the levels of TNF-α and IL-6 in cell supernatants， mRNA expressions of IL- 1β， NLRP3， IL-18 and caspase-1， PI-positive cell ratio， caspase-1 activity， LDH release， and Ca2+ levels were all increased significantly in calcitriol group （P＜0.05）. CONCLUSIONS Calcitriol can reverse sepsis-induced immunosuppression， and the mechanism of action may be E-mail：yarfwy@163.com achieved by the binding of calcitriol to vitamin D receptor，which promotes the release of Ca2+ from the endoplasmic reticulum， thereby driving the NLRP3/caspase-1-mediated pyroptosis pathway.

Hepatic stellate cells (HSCs) are the primary fibrogenic cells in the liver, and their activation plays a crucial role in the development and progression of hepatic fibrosis. Here, we report that retinoid X receptor-alpha (RXRα), a unique member of the nuclear receptor superfamily, is a key modulator of HSC activation and liver fibrosis. RXRα exerts its effects by modulating calcium/calmodulin-dependent protein kinase kinase β (CaMKKβ)-mediated activation of AMP-activated protein kinase-alpha (AMPKα). In addition, we demonstrate that K-80003, which binds RXRα by a unique mechanism, effectively suppresses HSC activation, proliferation, and migration, thereby inhibiting liver fibrosis in the CCl₄ and amylin liver NASH (AMLN) diet animal models. The effect is mediated by AMPKα activation, promoting mitophagy in HSCs. Mechanistically, K-80003 activates AMPKα by inducing RXRα to form condensates with CaMKKβ and AMPKα via a two-phase process. The formation of RXRα condensates is driven by its N-terminal intrinsic disorder region and requires phosphorylation by CaMKKβ. Our results reveal a crucial role of RXRα in liver fibrosis regulation through modulating mitochondrial activities in HSCs. Furthermore, they suggest that K-80003 and related RXRα modulators hold promise as therapeutic agents for fibrosis-related diseases.

Osteoarthritis (OA) causes chronic pain that significantly impairs quality of life, with current treatments often proving insufficient and accompanied by adverse effects. Recent research has identified the dorsal root ganglion (DRG) and its resident macrophages as crucial mediators of chronic OA pain through neuroinflammation driven by macrophage polarization. We present a novel injectable thermo-sensitive hydrogel system, KAF@PLEL, designed to deliver an anti-inflammatory peptide (KAF) specifically to the DRG. This biodegradable hydrogel enables sustained KAF release, promoting the reprogramming of DRG macrophages from pro-inflammatory to anti-inflammatory phenotypes. Through comprehensive in vitro and in vivo studies, we evaluated the hydrogel's biocompatibility, effects on macrophage polarization, and therapeutic efficacy in chronic OA pain management. The system demonstrated significant capabilities in preserving macrophage mitochondrial function, suppressing neuroinflammation, alleviating chronic OA pain, reducing cartilage degradation, and improving motor function in OA rat models. The sustained-release properties of KAF@PLEL enabled prolonged therapeutic effects while minimizing systemic exposure and side effects. These findings suggest that KAF@PLEL represents a promising therapeutic approach for improving outcomes in OA patients through targeted, sustained treatment.

Objective To investigate the clinical characteristics of inguinal abscess caused by Actinotignum schaa-lii(A.schaalii),and improve the clinical recognition and attention on skin and soft tissue infection caused by this bacterium.Methods Clinical data of a patient with inguinal abscess caused by A.schaalii were reviewed.Biologi-cal characteristics of the bacterium were observed,and antimicrobial susceptibility testing was conducted.PubMed database was retrieved using"Actinobaculum schaalii"and"Actinotignum schaalii"as keywords.Meanwhile,Chi-na National Knowledge Infrastructure,Wanfang,and VIP databases were retrieved using corresponding Chinese re-trieval terms.Clinical data of skin or soft tissue infections caused by A.schaalii were summarized and analyzed.Results After literature retrieval and screening,38 cases from 13 literatures were finally included,out of which 33 patients with A.schaalii infection were treated with antimicrobial agents and/or incision drainage,and the treat-ment effect was good.Conclusion A.schaalii is an opportunistic pathogen.There are few reports on skin or soft tissue infections caused by it.Currently,the identification of this bacterium relies on mass spectrometry technology or gene sequencing.Clinical attention should be paid to the detection of this bacterium,and appropriate antimicrobial agents should be selected for its treatment.

Robot-assisted surgery with its advantages such as three-dimensional high-definition vision, dexterous robotic arms, and tremor filtration, is increasingly being applied to complex radical gastrectomy. However, the role of the surgical assistant remains crucial during the procedure. The assistant is responsible for tasks outside the console, including adjusting robotic arms, changing instruments, exposing the surgical field, and addressing unexpected situations. The technical proficiency of the assistant and their collaboration efficiency with the primary surgeon directly impact the smoothness of surgery and patients' outcomes. With the expansion of robot-assisted surgical indications, the establishment of a standardized training system and the optimization of team collaboration models have become urgent challenges to address. This article draws on the author's practical experience as an assistant in robot-assisted gastric cancer surgeries, conducting an in-depth analysis of the responsibilities and operational skills of surgical assistants in robot-assisted procedures. The aim is to develop a relatively comprehensive set of operational guidelines for surgical assistants in robot-assisted radical gastrectomy, providing valuable references for enhancing the overall efficiency of surgical teams and improving surgical outcomes.

IL-32 is a multifunctional cytokine with both pro-inflammatory and anti-inflammatory properties.It has been proved that expression of IL-32 increases with progression of gastric mucosal diseases and severity of gastric cancer(GC),thus participating in process of gastric"inflammation-cancer"transformation.However,how IL-32 affects malignant transformation of gastric"inflamma-tion-cancer"and finally leads to adverse outcome of GC invasion and migration is still controversial.In order to better clarify regulatory effect and possible mechanism of abnormal expression of IL-32 on different histopathological stages of gastric"inflammation-cancer"transformation,and to explore new directions and breakthroughs in molecular mechanism of early truncation and treatment of gastric precancerous lesion(GPL),we searched literatures related to IL-32 in six authoritative databases at home and abroad,such as Pubmed,Web of Science and CNKI,in past 30 years.It was found that pathogenicity or protective function of IL-32 in different histo-pathological stages of gastric"inflammation-cancer"transformation depended on its different subtypes,secretory forms,surrounding cytokine environment,disease status and genetic factors.IL-32 may regulate polarization of macrophages through NF-κB,MAPK,COX2,PR3,IDO,NOD,PKCδ,FAK and STAT3,amplify or inhibit chronic inflammatory stimulation of gastric mucosa,and thus participate in process of gastric"inflammation-cancer"transformation.Our new understanding of role of IL-32 in different stages of Cor-rea cascade may contribute to development of cytokine-directed therapy,and therapy aimed at regulating different alternative splicing subtypes of IL-32 and targeting IL-32 signals can be used as a new strategy for medical treatment of GPL and GC in future.