With the improvement of living standards， the incidence rate of metabolic dysfunction-associated fatty liver disease （MAFLD） is gradually increasing with a younger age of onset， and MAFLD has become a global health problem， while its specific pathogenesis remains unclear. Macrophages， as one of the important cells involved in the pathogenesis of MAFLD， have the ability to present antigens， eliminate pathogenic microorganisms， and promote liver inflammatory responses， thereby attracting wide attention for a long time. The latest studies have shown that macrophages may become a new therapeutic target for MAFLD. This article systematically reviews the role of intrahepatic macrophages in liver inflammation caused by MAFLD， including their activation， polarization， recruitment mechanisms， and interactions with other cells， in order to provide new ideas and perspectives for the clinical prevention and treatment of MAFLD.

Objective To construct machine learning models based on preoperative inflammatory and radiological features for the prediction of glioma grading and isocitrate dehydrogenase (IDH) mutation status, and to analyze application values of these models and identify the optimal predictive models. Methods A retrospective analysis was conducted on the data of pathologically confirmed glioma patients admitted to Tongji Hospital Affiliated to Tongji University from March 2019 to March 2023. LASSO regression was used to screen feature variables, and predictive models were constructed based on logistic regression (LR), random forest (RF), support vector machine (SVM), gradient boosting decision tree (XGBoost) and K-nearest neighbor (KNN) algorithms. The model performance was comprehensively evaluated using metrics including discrimination ability, area under the precision-recall curve (AUC), accuracy, F1 score and Brier score. The DeLong test was adopted to compare the AUC values among different models; Friedman rank-sum test was used to determine the overall performance differences of the models, with the Nemenyi test applied for multiple comparison correction. Results In the task of glioma grading prediction, the LR model achieved the highest comprehensive score (0.726), and no significant difference was observed between the LR model and the other four models; age was positively correlated with glioma grading (P=0.003). In the task of IDH mutation status prediction, the XGBoost model obtained the highest comprehensive score (0.832), which was superior to the LR (0.762, P=0.035) and KNN models (0.754, P=0.025), while no statistical differences were found between the XGBoost model and the RF or SVM models. Conclusions The LR model for glioma grading prediction and XGBoost model for IDH mutation prediction constructed based on a task-oriented strategy achieve a favorable interpretability while ensuring optimized performance, thereby providing reliable decision support for the individualized diagnosis and treatment of glioma.

Retinitis pigmentosa （RP） is the most common hereditary blinding eye disease in clinical practice， with the pathogenesis remaining unclear. Patients experience progressive apoptosis of retinal photoreceptor cells， accompanied by degeneration of retinal pigment epithelium （RPE） cells. Current Western medical treatments mainly focus on gene therapy and stem cell transplantation， showing limited efficacy. In contrast， clinical observations have confirmed the therapeutic effects of traditional Chinese medicine （TCM） treatments. Establishing an RP animal model that aligns with the diagnostic features of both TCM and Western medicine could help combine the strengths of both approaches， thereby broadening the treatment options for RP. This study categorizes and summarizes the existing RP animal models in terms of classification， types， inheritance patterns， and alignment with clinical manifestations. It is found that current RP models are primarily derived from natural animal models such as RD mice and RCS rats， transgenic animal models like RPE-65 knockout mice and rhodopsin gene knockout mice， and chemically induced models such as those created by monochromatic light exposure or N-ethyl-N-nitrosourea （ENU） administration. These three categories of models focus more on detecting RP-related histopathological， molecular biological， and cellular immunological indicators， but offer limited observation of the overall characteristics of the disease and lack insight into syndrome differentiation. Although RP is a congenital genetic disease， its progression is influenced by acquired factors such as environment， constitution， emotions， and care. Current models do not fully capture the characteristics of this disease. Therefore， establishing an RP animal model based on the diagnostic features of both TCM and Western medicine will have significant implications for future experimental and clinical research.

Retinitis pigmentosa （RP） is the most common hereditary blinding eye disease in clinical practice， with the pathogenesis remaining unclear. Patients experience progressive apoptosis of retinal photoreceptor cells， accompanied by degeneration of retinal pigment epithelium （RPE） cells. Current Western medical treatments mainly focus on gene therapy and stem cell transplantation， showing limited efficacy. In contrast， clinical observations have confirmed the therapeutic effects of traditional Chinese medicine （TCM） treatments. Establishing an RP animal model that aligns with the diagnostic features of both TCM and Western medicine could help combine the strengths of both approaches， thereby broadening the treatment options for RP. This study categorizes and summarizes the existing RP animal models in terms of classification， types， inheritance patterns， and alignment with clinical manifestations. It is found that current RP models are primarily derived from natural animal models such as RD mice and RCS rats， transgenic animal models like RPE-65 knockout mice and rhodopsin gene knockout mice， and chemically induced models such as those created by monochromatic light exposure or N-ethyl-N-nitrosourea （ENU） administration. These three categories of models focus more on detecting RP-related histopathological， molecular biological， and cellular immunological indicators， but offer limited observation of the overall characteristics of the disease and lack insight into syndrome differentiation. Although RP is a congenital genetic disease， its progression is influenced by acquired factors such as environment， constitution， emotions， and care. Current models do not fully capture the characteristics of this disease. Therefore， establishing an RP animal model based on the diagnostic features of both TCM and Western medicine will have significant implications for future experimental and clinical research.

OBJECTIVE To investigate the ameliorative effect and mechanism of short-acting exenatide on diabetic cognitive dysfunction. METHODS Spontaneously diabetic db / db mice were randomly divided into model group （normal saline） and exenatide group （50 μg/kg）， with db / m mice as the normal control group （normal saline）， with 8 mice in each group. Mice in each group were subcutaneously injected with corresponding drugs or normal saline twice daily for 8 consecutive weeks. Body weight and fasting blood glucose were measured at a fixed time every week. Cognitive function was evaluated by Morris water maze test. The levels of oxidative st ress indicators [malondialdehyde （MDA）， superoxide dismutase （SOD）， glutathione （GSH） ] ， cyclic adenosine monophosphate （cAMP） and protein kinase A （PKA） were detected in hippocampus tissue of mice. The hippocampal neuronal HT22 cells of mice were divided into control group （25 mmol/L glucose）， high glucose group （125 mmol/L glucose）， high glucose+exenatide group （125 mmol/L glucose+20 nmol/L exenatide）， high glucose+exenatide+H89 （PKA inhibitor） group （125 mmol/L glucose+20 nmol/L exenatide+10 μmol/L H89）， and high glucose+H89 group （125 mmol/L glucose+10 μmol/L H89）. After 48 h of intervention with corresponding solutions/culture medium， the levels of oxidative stress indicators， cAMP and PKA， the activities of mitochondrial respiratory enzymes Ⅱ and Ⅳ， and the phosphorylation level of dynamin-related protein 1 （Drp1） were measured. RESULTS Animal experiments showed that compared with the normal control group， the model group exhibited significantly increased body weight， fasting blood glucose and MDA level in the hippocampus （ P ＜0.05）， as well as significantly prolonged escape latency （ P ＜0.05）； swimming speed significantly slowed down， the time spent in the target quadrant， the number of platform crossings， and the levels of SOD， GSH， cAMP and PKA in the hippocampus were significantly decreased （ P ＜0.05）. Compared with model group， all the above indicators （except for swimming speed） in the exenatide group were significantly reversed （ P ＜0.05）. Cell experiments showed that compared with high glucose group， the high glucose+exenatide group had significantly decreased MDA level （ P ＜0.05）， and significantly increased levels of SOD， GSH， cAMP and PKA， the activities of mitochondrial respiratory enzymes Ⅱ and Ⅳ， and phosphorylation level of Drp1 （ P ＜0.05）. Compared with high glucose+exenatide group， the above indicators in the high glucose+exenatide+H89 group were significantly reversed （ P ＜0.05）. CONCLUSIONS Short-acting exenatide can activate the cAMP/PKA pathway， promote Drp1 phosphorylation， and increase the activities of mitochondrial respiratory enzymes， thereby maintaining mitochondrial stability， reducing oxidative stress injury， and ultimately improving diabetic cognitive dysfunction.

ObjectiveTo investigate the mechanisms by which Mahuang Lianqiao Chixiaodoutang （MLC） improves obesity-type polycystic ovary syndrome （PCOS） through the phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt） signaling pathway. MethodsThirty-six female Sprague-Dawley （SD） rats were randomly divided into a blank control group （Con） and an obesity-type PCOS model preparation group. The model was induced by gavage with letrozole （1 mg·kg^-1） combined with a high-fat diet （HFD）. After model establishment， the obesity-type PCOS model preparation group was further divided into the model group （Mod， normal saline）， metformin group （Met， 0.3 g·kg^-1）， low-dose MLC group （MLC-L， 4.3 g·kg^-1）， medium-dose MLC group （MLC-M， 8.6 g·kg^-1）， and high-dose MLC group （MLC-H， 17.2 g·kg^-1）. Active components of MLC and targets of obesity-type PCOS were screened from databases， a protein-protein interaction （PPI） network was constructed， and gene ontology（GO）and Kyoto Encyclopedia of Genes and Genomes （KEGG） pathway enrichment analysis was performed. The gut microbiota structure was analyzed based on 16S rRNA sequencing and correlated with network pharmacology pathways. Body weight and estrous cycle were dynamically monitored. Ovarian morphology was observed by hematoxylin-eosin （HE） staining. Cell apoptosis was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling （TUNEL）. Enzyme-linked immunosorbent assay （ELISA） was used to detect levels of follicle-stimulating hormone （FSH）， luteinizing hormone （LH）， anti-Müllerian hormone （AMH）， testosterone （T）， and estradiol （E₂）. Western blot was used to detect the protein expression levels of phosphorylated PI3K/PI3K （p-PI3K/PI3K）， phosphorylated Akt/Akt （p-Akt/Akt）， B-cell lymphoma-2 （Bcl-2）， and Bcl-2-associated X protein （Bax）. ResultsNetwork pharmacology screening identified 124 active components of MLC and 408 overlapping targets between the herbal formula and the disease. Core targets such as Akt1 and Bcl-2 were revealed. As indicated by 16S rRNA sequencing， the abundances of Lachnospiraceae， Lachnoclostridium， and Dorea were increased in the MLC groups （P<0.05）， while the abundance of Veillonella was decreased （P<0.05）. KEGG correlation analysis integrating network pharmacology and gut microbiota data showed significant enrichment of the PI3K/Akt signaling pathway. Animal experiments showed that， compared with the Mod group， body weight decreased to normal levels in the Met， MLC-M， and MLC-H groups. The estrous cycle became regular. The number of corpora lutea increased and cystic follicles decreased. Serum levels of T， FSH， and LH/FSH were reduced （P<0.05， P<0.01）， while the E₂ level was increased （P<0.01）. Ovarian cell apoptosis was reduced （P<0.01）， and the protein expression levels of p-PI3K/PI3K， p-Akt/Akt， and Bcl-2 in ovarian tissue were significantly increased， whereas Bax protein expression was significantly decreased （P<0.05， P<0.01）. ConclusionMLC can regulate gut microbiota structure， effectively improve ovarian pathology in rats with obesity-type PCOS， and inhibit ovarian granulosa cell apoptosis. The mechanism may be associated with upregulation of the PI3K/Akt signaling pathway.

ObjectiveTo investigate the mechanisms by which Mahuang Lianqiao Chixiaodoutang （MLC） improves obesity-type polycystic ovary syndrome （PCOS） through the phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt） signaling pathway. MethodsThirty-six female Sprague-Dawley （SD） rats were randomly divided into a blank control group （Con） and an obesity-type PCOS model preparation group. The model was induced by gavage with letrozole （1 mg·kg^-1） combined with a high-fat diet （HFD）. After model establishment， the obesity-type PCOS model preparation group was further divided into the model group （Mod， normal saline）， metformin group （Met， 0.3 g·kg^-1）， low-dose MLC group （MLC-L， 4.3 g·kg^-1）， medium-dose MLC group （MLC-M， 8.6 g·kg^-1）， and high-dose MLC group （MLC-H， 17.2 g·kg^-1）. Active components of MLC and targets of obesity-type PCOS were screened from databases， a protein-protein interaction （PPI） network was constructed， and gene ontology（GO）and Kyoto Encyclopedia of Genes and Genomes （KEGG） pathway enrichment analysis was performed. The gut microbiota structure was analyzed based on 16S rRNA sequencing and correlated with network pharmacology pathways. Body weight and estrous cycle were dynamically monitored. Ovarian morphology was observed by hematoxylin-eosin （HE） staining. Cell apoptosis was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling （TUNEL）. Enzyme-linked immunosorbent assay （ELISA） was used to detect levels of follicle-stimulating hormone （FSH）， luteinizing hormone （LH）， anti-Müllerian hormone （AMH）， testosterone （T）， and estradiol （E₂）. Western blot was used to detect the protein expression levels of phosphorylated PI3K/PI3K （p-PI3K/PI3K）， phosphorylated Akt/Akt （p-Akt/Akt）， B-cell lymphoma-2 （Bcl-2）， and Bcl-2-associated X protein （Bax）. ResultsNetwork pharmacology screening identified 124 active components of MLC and 408 overlapping targets between the herbal formula and the disease. Core targets such as Akt1 and Bcl-2 were revealed. As indicated by 16S rRNA sequencing， the abundances of Lachnospiraceae， Lachnoclostridium， and Dorea were increased in the MLC groups （P<0.05）， while the abundance of Veillonella was decreased （P<0.05）. KEGG correlation analysis integrating network pharmacology and gut microbiota data showed significant enrichment of the PI3K/Akt signaling pathway. Animal experiments showed that， compared with the Mod group， body weight decreased to normal levels in the Met， MLC-M， and MLC-H groups. The estrous cycle became regular. The number of corpora lutea increased and cystic follicles decreased. Serum levels of T， FSH， and LH/FSH were reduced （P<0.05， P<0.01）， while the E₂ level was increased （P<0.01）. Ovarian cell apoptosis was reduced （P<0.01）， and the protein expression levels of p-PI3K/PI3K， p-Akt/Akt， and Bcl-2 in ovarian tissue were significantly increased， whereas Bax protein expression was significantly decreased （P<0.05， P<0.01）. ConclusionMLC can regulate gut microbiota structure， effectively improve ovarian pathology in rats with obesity-type PCOS， and inhibit ovarian granulosa cell apoptosis. The mechanism may be associated with upregulation of the PI3K/Akt signaling pathway.

Objective To study the correlation between Periostin, interleukin-33 (IL-33), and chronic cough after thoracoscopic lobectomy in patients with coronary artery bypass grafting (CABG) combined with lung cancer. Methods A total of 102 lung cancer and coronary heart disease patients at Tianjin Chest Hospital from January 2022 to January 2024 were prospectively enrolled, and they were divided into a chronic cough group (n=42) and a non-chronic cough group (n=60) based on whether chronic cough occurred after surgery. Serum levels of Periostin and IL-33 were measured on the 1st, 7th, and 14th days post-lobectomy. The Pearson method was employed to analyze the correlation between Periostin and IL-33 levels and the severity of cough. Univariate and multivariate logistic regression analyses were conducted to identify factors influencing the occurrence of chronic cough. Additionally, receiver operating characteristic (ROC) curve analysis was utilized to assess the potential value of serum Periostin and IL-33 levels in predicting postoperative chronic cough. Results In patients with chronic cough, the peripheral blood Periostin and IL-33 levels measured on days 7 and 14 were significantly higher than those in patients with non-chronic cough, and the interactions between the two groups and at different time points were significant (P<0.001). The degree of cough was positively correlated with the levels of Periostin and IL-33 on days 7 and 14 (P<0.05), but had no significant correlation with the levels on day 1 (P>0.05). In patients with lung cancer, after thoracoscopic lobectomy, Periostin [OR=1.619, 95%CI (1.295, 2.025)] and IL-33 [OR=1.831, 95%CI (1.216, 2.758)] on day 7 and Periostin [OR=1.952, 95%CI (1.306, 2.918)] and IL-33 [OR=1.742, 95%CI (1.166, 2.603)] on day 14 were identified as risk factors for chronic cough. ROC curve analysis showed that the sensitivity of Periostin on day 7 was 69.05%, the specificity was 71.67%, and the area under the curve (AUC) was 0.756 [95%CI (0.616, 0.893)]. The sensitivity of Periostin on day 14 increased to 71.43% and the specificity was 76.67%, AUC was 0.762 [95%CI (0.633, 0.898)]. At the same time, the critical value of IL-33 on day 7 was 45.03 pg/mL, the sensitivity and specificity were both 83.33%, the AUC was 0.884 [95%CI (0.789, 0.980)], and the critical value of IL-33 on day 14 was 56.01 pg/mL, the sensitivity was 85.71%, the specificity was 80.00%, and the AUC was 0.899 [95%CI (0.799, 0.999)]. Joint logistic regression analysis of Periostin and IL-33 levels on days 7 and 14 showed showed that the sensitivity was 95.24%, the specificity was 95.00%, and the AUC reached 0.993 [95%CI (0.979, 1.000)]. Conclusion Periostin and IL-33 levels, measured at various time points, are abnormally elevated following thoracoscopic lobectomy in patients with combined CABG and lung cancer. These levels significantly correlate with cough severity. Given their predictive potential for chronic cough, these markers are deemed valuable biomarkers.

Objective To isolate pathogenic bacteria from the skin of a nude mouse exhibiting squamous skin scurfs, and perform bacterial identification, traceability analysis, and pathogenicity studies to provide a new approach for the diagnosis of pathogens in nude mice with squamous skin scurfs. MethodsSkin swab samples were collected from a nude mouse exhibiting squamous skin scurfs for nucleic acid testing, bacterial isolation and culture, biochemical identification, 16S rDNA gene amplification and sequencing, and whole genome sequencing to construct a phylogenetic tree. Fifteen BALB/c nude mice were randomized into a saline-treated control group, a high-concentration group treated with 1.8×10⁸ CFU/mL of the isolated bacterial suspension, and a low-concentration group treated with 1.8×10⁷ CFU/mL of the isolated bacterial suspension. Pathogenicity was assessed by animal infection experiments and observation of histopathological changes in skin tissue using HE staining. Results The nucleic acid test for Corynebacterium bovis was negative, excluding infection by this organism. The pathogen isolated on mannitol salt agar and blood agar, combined with Gram staining, suggested a Gram-positive Staphylococcus species. The isolated strain was identified by 16S rDNA sequencing and a fully automated microbial identification system as Staphylococcus xylosus. Phylogenetic tree analysis based on whole genome sequencing showed that the strain was most closely related to an isolate from leafy vegetables in South Korea (GenBank GCA_00207825.1). In the high-concentration group, squamous skin scurfs appeared on the head, neck, and back of nude mice on the 17th day post-infection, while in the low concentration group, similar symptoms appeared on the 20th day post-infection and gradually spread to other areas. The scaling symptoms were transient, lasting for 7 days in the high-concentration group and 3 days in the low-concentration group, after which the skin returned to normal. The infection rate was 33.33% in both the high- and low-concentration groups. No significant pathological changes were observed in the skin tissues of infected mice compared to the control group, indicating marked individual differences in the pathogenicity of the strain in nude mice. Conclusion A strain of Staphylococcus xylosus was isolated from the skin of a nude mouse exhibiting squamous skin scurfs. The strain is an opportunistic pathogen that causes transient squamous skin scurfs without significant histopathological changes, and there are individual differences in the sensitivity of nude mice to this strain. These findings can provide valuable data for pathogen identification in immunodeficient or gene knockout mice.

Objective To isolate pathogenic bacteria from the skin of a nude mouse exhibiting squamous skin scurfs, and perform bacterial identification, traceability analysis, and pathogenicity studies to provide a new approach for the diagnosis of pathogens in nude mice with squamous skin scurfs. MethodsSkin swab samples were collected from a nude mouse exhibiting squamous skin scurfs for nucleic acid testing, bacterial isolation and culture, biochemical identification, 16S rDNA gene amplification and sequencing, and whole genome sequencing to construct a phylogenetic tree. Fifteen BALB/c nude mice were randomized into a saline-treated control group, a high-concentration group treated with 1.8×10⁸ CFU/mL of the isolated bacterial suspension, and a low-concentration group treated with 1.8×10⁷ CFU/mL of the isolated bacterial suspension. Pathogenicity was assessed by animal infection experiments and observation of histopathological changes in skin tissue using HE staining. Results The nucleic acid test for Corynebacterium bovis was negative, excluding infection by this organism. The pathogen isolated on mannitol salt agar and blood agar, combined with Gram staining, suggested a Gram-positive Staphylococcus species. The isolated strain was identified by 16S rDNA sequencing and a fully automated microbial identification system as Staphylococcus xylosus. Phylogenetic tree analysis based on whole genome sequencing showed that the strain was most closely related to an isolate from leafy vegetables in South Korea (GenBank GCA_00207825.1). In the high-concentration group, squamous skin scurfs appeared on the head, neck, and back of nude mice on the 17th day post-infection, while in the low concentration group, similar symptoms appeared on the 20th day post-infection and gradually spread to other areas. The scaling symptoms were transient, lasting for 7 days in the high-concentration group and 3 days in the low-concentration group, after which the skin returned to normal. The infection rate was 33.33% in both the high- and low-concentration groups. No significant pathological changes were observed in the skin tissues of infected mice compared to the control group, indicating marked individual differences in the pathogenicity of the strain in nude mice. Conclusion A strain of Staphylococcus xylosus was isolated from the skin of a nude mouse exhibiting squamous skin scurfs. The strain is an opportunistic pathogen that causes transient squamous skin scurfs without significant histopathological changes, and there are individual differences in the sensitivity of nude mice to this strain. These findings can provide valuable data for pathogen identification in immunodeficient or gene knockout mice.