Abstract:Objective：Alzheimer’s disease（AD）is a progressive and irreversible neurodegenerative disorder characterized by pathological features including abnormal β-amyloid（Aβ）deposition，glial hyperactivation，synaptic impairment，and myelin dysfunction. The enriched environment（EE），a non -pharmacological intervention，has garnered attention for its potential to enhance neuroplasticity. However，the effects of EE on social behavior and associated neuropathology during the early stages of AD remain insufficiently explored. This study utilized the 5×FAD mouse model to systematically investigate the impact of EE on early pathological progression in AD，providing new evidence to support the application of EE in the prevention and treatment of AD. Methods：Two-month-old 5 × FAD mice were randomly assigned to a standard environment（SE）group or an EE group（5 mice per cage）and maintained in their respective housing conditions for four weeks. Behavioral tests，including the Y-maze，open field，elevated plus maze，and three-chamber social interaction assays were conducted. Subsequently，immunohistochemistry and Western blot were used to detect the distribution and expression of postsynaptic density protein-95（PSD-95），synaptophysin（SYP）and myelin basic protein （MBP）in the medial prefrontal cortex（mPFC）. Immunofluorescence staining and transmission electron microscopy were combined to observe the changes in neuronal，synaptic structure and myelin morphology to evaluate neuropathological changes. Results：EE did not affect short-term spatial memory or anxiety-like behaviors in 5 × FAD mice but significantly enhanced their social interaction capabilities. Pathologically，5× FAD mice exhibited marked Aβ deposition and glial activation in the mPFC. Compared with the SE group，EE mice showed significantly reduced Aβ accumulation and glial activation in the mPFC. Furthermore，EE improved myelin structural integrity in this region，while no significant effects were observed on synaptic proteins，synaptic ultrastructure，or neuronal survival. Conclusion：EE effectively mitigates AD-related pathology in 5 × FAD mice and alleviates social behavioral deficits， highlighting its potential for addressing AD-associated social dysfunction. These findings suggest that environmental interventions may exert neuroprotective effects by modulating neuroinflammation，reducing Aβ deposition，and preserving myelin homeostasis during AD progression.

Abstract:Objective：To investigate the effects and molecular mechanisms of Nao Tan Qing（NTQ）on neural stem cell（NSC） proliferation in Alzheimer’s disease（AD）mice. Methods：Transgenic mice with five familial Alzheimer’s disease（5 × FAD）were randomly assigned to two groups，the AD group treated with ddH2O and AD + NTQ group administered with NTQ by gavage. Immunofluorescence staining，real -time quantitative PCR（RT -qPCR），and Western blot were used to evaluate NSC proliferation in hippocampus. In vitro，embryonic NSCs of C57/BL6J mice were isolated and cultured with PBS or NTQ. Cell proliferation was detected by CCK -8 method and cell apoptosis was analyzed by TUNEL. Immunofluorescence staining was used to detect the number of sex - determing region of Y chromosome（SOX2）- box transcription factor 2（SOX2）positive，5 - bromo - 2 - deoxy uridine（BrdU）positive， and doublecortin（DCX）positive cells. The mRNA and protein levels of SOX2 and DCX were measured by RT-qPCR and Western blot. The expressions of cyclin D1，p27/Kip1 and GATA2 were detected by RT-qPCR and Western blot. The expression level of SOX2 was detected by RT-qPCR and Western blot after the in vitro treatment of NSC using cyclin D1-cyclin-dependent kinase（CDK）inhibitor. Results：In the AD+NTQ group，the number of SOX2+ cells in hippocampus significantly increased，with a marked elevation in SOX2 mRNA and protein levels compared with the AD group. In vitro，the diameter of neurospheres treated with NTQ was significantly larger， along with the increased number of BrdU+ ，SOX2 + ，and DCX+ cells. Moreover，SOX2 and DCX mRNA levels，as well as SOX2 protein level，were notably elevated. Mechanistically，the expression of GATA2 and its downstream molecule p27/Kip1 were decreased in the hippocampus of AD+NTQ mice，and the inhibitory effect on cyclin D1 was weakened in NSC proliferation. Addition of cyclin D1-CDK inhibitor attenuated the increase in SOX2 and DCX expression triggered by NTQ. Conclusion：NTQ maintains NSC proliferation and alleviates cognitive deficits in AD mice by modulating the GATA2-p27/Kip1-cyclin D1 signaling pathway.

Abstract:Objective：This study aimed to investigate the therapeutic effect of burdock polysaccharide on Alzheimer’s disease（AD） using Caenorhabditis elegans（C. elegans）pathology model. Methods：Burdock polysaccharide made in our lab was used at varying concentrations（62.5，125.0，and 250.0 μg/mL）on transgenic C. elegans AD models（CL4176，CL2355，and CL2006 strains）to study the effects on nematode amyloid beta（Aβ）deposition，chemotaxis，5-hydroxytryptamine sensitivity，paralysis，growth and development， locomotor activity，feeding ability. Oxidative stress and cholinergic neuron-related indexes were measured，and the expression levels of related genes in nematodes were examined by RT -PCR. Results：Burdock polysaccharide exhibited multiple biological activities， thus reducing the level and deposition of Aβ protein，reducing 5-hydroxytryptamine sensitivity，strengthening nematode chemotaxis and learning memory，delaying paralysis，promoting development，increasing swing and pharyngeal vibration frequency，increasing antioxidant enzyme activity and reducing acetylcholinesterase（AChE）activity. Meanwhile，it reduced the expression of age-1 and akt-1 genes，enhanced the expression of daf-16 gene，promoted the expression of skn-1，gst-4，sod-1 and sod-2，exert antioxidant effects，and alleviated AD symptoms. Concurrently，it attenuated AD pathology by inhibiting ace -1/ace -2 expression，and reducing AChE activity. Conclusion：Burdock polysaccharide may alleviate and improve AD-related pathological processes by regulating the age-1/akt-1/daf-16 signaling pathway to reduce oxidative stress levels while inhibiting AChE activity.

Abstract:Objective：To explore the potential causal relationship between Helicobacter pylori（HP）infection and esophageal cancer （EC）. Methods：The analysis incorporated genome-wide association study（GWAS）data with HP infection as the exposure and EC as the outcome. A variety of Mendelian randomization（MR）methods were utilized，including inverse - variance weighted analysis， weighted median，MR - Egger，Simple mode，and Weighted mode to investigate the association between HP and EC. Additionally， Bayesian-weighted MR was introduced and the results were corrected using the false discovery rate（FDR）to enhance precision. The study also involved outlier detection，heterogeneity testing，sensitivity analysis，and pleiotropy assessment，as well as removing single nucleotide polymorphisms（SNP）potentially affected by confounding factors. For results that were particularly contentious，a meta - analysis was performed to provide a broader perspective. Potential reverse causation was assessed using Steiger testing and reverse MR. Furthermore，linkage disequilibrium score regression（LDSC）was utilized to evaluate the genetic correlation between HP and EC. Results：The comprehensive analyses showed that both traditional two -sample MR and Bayesian -weighted MR after FDR correction indicated no statistically significant causal association between HP and EC（P ＞ 0.05）. No pleiotropy was evident（P ＞ 0.05），and the robustness of the results was confirmed by the leave-one-out test. However，genetic correlation analyses of anti-HP IgG serum positivity and HP GroEL antibody levels suggested a potential genetic link with esophageal adenocarcinoma（P ＜ 0.05）. Conclusion：Despite the use of advanced statistical methodologies，the current evidence is insufficient to support a definitive causal association between HP and EC. This finding underscores the need for larger-scale GWAS data and more detailed subtype-specific analyses to further explore the association between these two conditions. Future research should include a broader range of populations and geographical areas to enhance the generalizability and applicability of findings，while also investigating the specific impacts of different HP strains and possible biological mechanisms，providing a stronger scientific support for the prevention and treatment of EC.

Abstract:Objective：Bioinformatics methods were used to screen obesity - related genes and preliminarily explore their effects on adipocyte lipid metabolism. Methods：We obtained the C57BL6/J mouse white adipose tissue（WAT）datasets GSE30247，GSE37218， and GSE138632 from the Gene Expression Omnibus（GEO）. The transcriptome data of mice fed with a normal diet in GSE37218 and GSE30247 were set as the control group，and the transcriptome data of mice fed with a high-fat diet（HFD）were set as the experimental group. The NCBI official GEO2R tool was used to screen the differential genes of the two datasets after HFD，and P ＜ 0.05，log2FC＞1.5 were used as the screening criteria to obtain the common differential genes of the two datasets. Perform gene ontology（GO），mammalian phenotype ontology（MP），and human phenotype ontology（HPO）enrichment analysis on differentially expressed genes. Construct protein - protein interaction（PPI）networks using STRING database，screen and obtain hub genes using Cytoscape. The transcriptome data of mice fed with normal diet in the GSE138632 dataset were set as the control group，and the transcriptome data of mice fed with HFD were set as the experimental group for differential analysis. Gene predictive diagnostic analysis was performed using receiver operating characteristic（ROC）curve to further validate hub genes. Using lentivirus to construct a stable overexpressed 3T3-L1 cell line with STAM binding protein like 1（Stambpl1），oleic acid（OA）was used to induce lipid droplet accumulation in 3T3-L1 cells.；BODIPY staining and triglyceride（TG）content detection were used to determine lipid droplet accumulation. Results：After performing differential analysis on the GSE37218 and GSE30247 datasets，we found 57 genes were commonly upregulated in the epididymal white adipose tissue（eWAT）of mice fed withHFD compared to those fed with normal diet. Further analysis using multiple algorithms in Cytoscape identified 13 hub genes. The expression of these 13 hub genes was validated using the GSE138632 dataset， leading to the screening of Stambpl1. RT -PCR results showed that Stambpl1 was upregulated in the adipose tissue of HFD -induced obese mice. BODIPY staining and TG content assays revealed that overexpression of Stambpl1 in 3T3-L1 cells alleviated OA-induced lipid droplet accumulation. Conclusion：This study used bioinformatics to screen the obesity-related gene Stambpl1，and preliminarily confirmed that Stambpl1 inhibits lipid accumulation in adipocytes in vitro.

Abstract:Objective：This study aimed to investigate the expression of fibroblast-derived galectin-3（LGALS3）in lung tissue of a silicon dioxide（SiO₂）-induced pulmonary fibrosis mouse model and its relationship with extracellular matrix（ECM）deposition，further elucidating the role of LGALS3 in the mechanism of silicosis fibrosis. Methods：A pulmonary fibrosis mouse model was established by silica exposure，and collagen deposition and structural changes in lung tissues were observed using Sirius red staining and polarized light microscopy. Then，single - cell clustering analysis was performed to classify cells into 20 clusters，and differentially expressed genes upregulated in fibroblasts after 56 days of SiO₂ treatment were identified. Gene ontology（GO）enrichment analysis using Metascape was conducted to identify genes associated with ECM binding. In vitro，human lung fibroblasts（HPF - a）and mouse lung fibroblasts（MLg）were stimulated with transforming growth factor - β1（TGF - β1），and the expression levels of LGALS3 and its deposition on the ECM were detected by Western blot and immunofluorescence staining. Results：Single - cell clustering analysis showed a significant increase in fibroblast numbers after 56 days of SiO₂ treatment，with the top ten upregulated genes identified as Ccl6，Lyz2，Ftl1，Spp1，Lgals3，Cxcl2，Fth1，Psap，S100a9，and Ctss. GO enrichment analysis indicated that these genes were closely associated with ECM binding，with Ctss，Lgals3，and Spp1 being the core related genes. Dot plots demonstrated that the expression level of Lgals3 was significantly higher in the SiO₂ 56-day group compared to the control group. Sirius red staining and polarized light microscopy revealed significantly increased collagen deposition and dense structure in the lung tissues of the SiO₂ - exposed group， exhibiting typical pathological features of pulmonary fibrosis. Western blot results showed that LGALS3 expression in HPF - a cells exhibited a time-dependent increase after TGF-β1 stimulation，peaking at 12 hours（P ＜ 0.05）. Animal model validation confirmed that LGALS3 expression in lung tissues of the SiO₂ - exposed group was significantly higher than in the control group（P ＜ 0.001），and immunofluorescence staining revealed enhanced co -localization signals of LGALS3 with the fibroblast marker Vimentin（P ＜ 0.01）. Furthermore，after seeding TGF -β1- stimulated MLg cells onto ECM，LGALS3 expression levels significantly increased（P ＜ 0.05）； even after cell removal，LGALS3 expression on the ECM remained higher than in the control group（P ＜ 0.05）. Conclusion：This study confirms that fibroblast - derived LGALS3 is significantly upregulated in lung tissues of a silica - induced pulmonary fibrosis mouse model and participates in ECM deposition. The expression of LGALS3 is regulated by TGF-β1 and shows persistent accumulation on the ECM. These findings reveal the critical role of LGALS3 in pulmonary fibrosis and provide new theoretical insights into the pathological mechanisms of silicosis and potential therapeutic targets.

Abstract:Objective：This study explored the effects of knocking down apolipoprotein E（APOE）on the proliferation，migration， invasion，and other malignant characteristics of prostate cancer cells through in vitro experiments，and validated them through nude mouse in vivo experiments. Methods：The expression levels of APOE in three human prostate cancer cell lines LNCap，DU145，and PC - 3 were downregulated by transfecting small interfering RNA（siRNA）. Cell viability and sensitivity to anticancer drugs were detected through CCK-8 experiments，cell proliferation ability was detected through clone formation assay，cell migration and invasion were detected using transwell assay，the EdU assay was used to detect the proliferation of prostate cancer cells，and the effects of knocking down APOE and using androgen receptor inhibitor on prostate cancer tumor growth were investigated in vivo by nude mouse tumorigenesis experiments. Results：siRNA - induced downregulation of APOE expression significantly reduced the viability， proliferation，migration，and invasion ability of LNCap，DU145，and PC - 3 cells，increased cell sensitivity to anticancer drugs，and reduced the percentage of cells with relative polarization fluorescence. The results of in vivo experiments also showed that knocking down APOE significantly slowed down the growth rate of tumors，and the addition of androgen receptor inhibitor showed a more significant anti-cancer effect. Conclusion：APOE could regulate a series of malignant behaviors such as proliferation and metastasis of prostate cancer cells，and the expression regulation of APOE may play a crucial role in inhibiting the malignancy and progression of prostate cancer.

Abstract:Objective：To analyze the characteristics and pregnancy outcomes of pregnant women with gestational diabetes mellitus （GDM）combined with thrombocytopenia，and to explore the influencing factors of the main adverse pregnancy outcomes. Methods： Pregnant women with GDM combined with thrombocytopenia who delivered in the First Affiliated Hospital of Nanjing Medical University from January 2015 to December 2024 were systematically screened. Maternal characteristics，including baseline，previous medical history，prenatal laboratory examinations，as well as maternal and neonatal outcomes，were analyzed. Logistic regression analysis was employed to identify the factors influencing the main adverse pregnancy outcomes. Results：A total of 233 women with GDM combined with thrombocytopenia were screened，accounting for 3.8‰ of all pregnant women. The mean maternal age was 31.95 years. Among them，51.5% had a history of miscarriage，and 30.5% had other co -morbidities. In terms of pregnancy outcomes，there were 132 cases（56.7%）of cesarean section，38 cases（16.3%）of premature rupture of membranes，30 cases（12.9%）of postpartum hemorrhage，and 26 cases（11.2%）of preterm delivery. In terms of neonatal outcomes，there were 24 cases（10.3%）of macrosomia，13 cases（5.6%）of low birth weight，12 cases（5.2%）of neonatal asphyxia，17 cases（7.3%）of hyperbilirubinemia，and a total of 43 cases （18.5% ）were transferred to the neonatal intensive care unit（NICU）. The multivariate logistic regression analysis showed that comorbidities（OR=4.71，P=0.014）and fasting blood glucose（OR=2.48，P=0.044）were independent risk factors for preterm delivery in pregnant women with GDM combined with thrombocytopenia. Prenatal D-dimer（OR=1.25，P=0.005）and platelet levels（OR=0.98， P=0.012）were significantly correlated with the risk of postpartum hemorrhage. In addition，higher body mass index in late pregnancy （OR=1.22，P=0.039）and fasting blood glucose（OR=1.93，P=0.047）independently impacted the risk of macrosomia. Conclusion： Pregnant women with gestational diabetes mellitus combined with thrombocytopenia are at higher risk of adverse maternal and infant pregnancy outcomes such as postpartum hemorrhage，preterm delivery，and macrosomia. For such pregnant women，comprehensive measures should be actively taken to control blood glucose，correct thrombocytopenia，and choose an appropriate mode of delivery to improve maternal and infant outcomes.

Abstract:Objective：This study aims to explore the safety and efficacy of utilizing indocyanine green near -infrared（ICG -NIR） fluorescence imaging to guide lymph node（LN）dissection during Da Vinci robotic gastrectomy（RG）. Methods：The patients who underwent RG at the General Surgery Department of Affiliated Hospital of Nanjing University of Chinese Medicine from January 2021 to January 2024 were retrospectively analyzed. Among them，60 patients underwent ICG fluorescence navigation - guided lymphadenectomy（ICG group），while 117 received conventional LN dissection（non-ICG group）. Propensity score matching（1∶1）was performed to balance baseline characteristics. The number of retrieved LNs，surgical outcomes，postoperative complications，hospital stay，and recovery data were compared between two groups. Results：After matching，each group comprised 60 patients with comparable baseline characteristics，including age，sex，body mass index，nutritional risk screening scores，tumor diameter，tumor location，differentiation，vascular invasion，and Lauren type（all P ＞ 0.05）. All patients completed D2 lymphadenectomy，and there were no fluorescent LNs remaining after surgery. The ICG group had a significantly higher mean number of retrieved LNs（33.73± 12.66）than the non-ICG group（26.15±6.31，P ＜ 0.05）. Nevertheless，there was no significant difference in the number of positive LNs detected by postoperative pathology between two groups[1（0，6）vs. 0（0，4），P ＞ 0.05]. The ICG group demonstrated superior LN retrieval in both D1 and D2 regions（all P ＜ 0.05），particularly at stations 3，4d，6，7，8a，and 12a. No significant differences were found in operative time，intraoperative blood loss，postoperative hospital stay，complication rates，or postoperative inflammatory indicators on day 3（including CRP、WBC、Alb、AST/ALT）（all P ＞ 0.05）. A statistically significant difference in postoperative ventilation time was observed between the two groups（P ＜ 0.05），the ventilation time in the ICG group was found to be superior to the non - ICG group. Conclusion：ICG - NIR fluorescence imaging significantly improves the precision and completeness of LN dissection in RG without compromising perioperative safety.

Abstract:Objective：To construct a model for predicting pelvic lymph node metastasis in early - stage cervical squamous cell carcinoma. Methods：The clinical data of patients in the department of gynecology，Affiliated Hospital of Southwest Medical University from January 2019 to October 2023 were retrospectively analyzed. A univariate logistic analysis was performed based on the pathological examination results of pelvic lymph nodes as the outcome indicator. Two models were developed by univariate logistic analysis as well as forward and backward stepwise regression analysis. The Akaike information criterion（AIC），continuous net reclassification improvement index（NRI），and integrated discriminant improvement index（IDI）were used to determine the optimal model. The optimal model was then converted into a nomogram，and its efficacy was evaluated by the area under the receiver operating characteristic curve（AUC），Hosmer-Lemeshow test，calibration curve and decision curve analysis（DCA）. Bootstrap method was used for internal validation. Results：A total of 221 patients were enrolled. Forward and backward stepwise regression methods were used to establish model 1 and model 2，respectively. According to the results of AIC，serial NRI and IDI，model 2 was the optimal model [indicators：age，squamous cell carcinoma antigen（SCCA），carbohydrate antigen（CA）125 and lymph node status on magnetic resonance imaging]. The AUC was 0.818；the Hosmer-Lemeshow test results were χ² =0.942 and P=0.332，and the adjusted AUC was 0.800. DCA results showed that when the threshold probability was 0.03-0.50，the clinical net benefit was relatively high. The AUC of the internal verification of Bootstrap was 0.784. Conclusion：Models based on age，SCCA，CA125，and lymph node status in magnetic resonance imaging can help predict pelvic lymph node status for cervical cancer before surgery.

Abstract:Objective：To investigate the predictive value of clinical features combined with intravoxel incoherent motion diffusion- weighted imaging（IVIM-DWI）parameters for early pregnancy outcomes in patients undergoing frozen-thawed embryo transfer（FET）. Methods：This prospective study enrolled 70 infertile women who underwent FET at the Reproductive Center of the First Affiliated Hospital of Nanjing Medical University between December 2023 and January 2025. All participants underwent standardized pelvic magnetic resonance imaging（MRI）scans on the day of embryo transfer. Clinical and laboratory indicators，as well as conventional MRI features and IVIM-DWI parameters were collected. IVIM-DWI parameters（diffusion coefficient D，pseudodiffusion coefficient D* ，and perfusion fraction f）were extracted using FireVoxel software，with histogram data generated via SPSS. Student’s t-test，Pearson’s chisquare test，or Fisher’s exact test were employed to compare differences in clinical characteristics，MRI features，and IVIM - DWI parameters between the clinical pregnancy group and the non - pregnant group . Receiver operating characteristic（ROC）curves were constructed to quantify diagnostic performance using area under the curve（AUC）measurements，with statistical comparisons performed by DeLong’s test. Multivariate logistic regression was used to analyze the relationship between relevant indicators and clinical pregnancy outcomes. Results：The clinical pregnancy group comprised 42 cases，while the non - pregnanct group had 28 cases. The proportion of high-quality embryos in the clinical pregnancy group was higher than that in the non-pregnanct group［76.2% vs. 46.4%， P=0.011］. The junctional zone D* _mean was significantly higher in the clinical pregnancy group than that in the non - pregnancy group （45.233 ± 7.930 vs. 41.223 ± 6.369，P=0.029）. ROC analysis revealed that embryo quality（high-grade embryos）predicted pregnancy success with an AUC of 0.65（sensitivity 53.6%，specificity 73.2%），while junctional zone D* _mean achieved an AUC of 0.68（sensitivity 73.8%，specificity 67.9%）. The combination of embryo quality and junctional zone D* _mean demonstrated superior predictive efficacy （AUC=0.73，sensitivity 82.1%，specificity 60.0%）. Junction zone D* _mean 43.33×10^-3 mm² /s was identified as an independent risk factor for successful clinical pregnancy（OR=0.2，P=0.003）. Conclusion：IVIM - DWI enables noninvasive assessment of microcirculatory perfusion characteristics of FET patients. Combining embryo quality with junctional zone D* _mean enhances the prediction of clinical pregnancy outcomes.

Abstract:Objective：To investigate the impact of obesity on left ventricular mechanical contraction synchrony parameters in patients with normal myocardial perfusion imaging（MPI）. Methods：A retrospective analysis was conducted on patients who underwent cadmium zinc telluride single photon emission computed tomography（CZT SPECT）MPI at the First Affiliated Hospital of Nanjing Medical University from January 2023 to August 2024. A total of 133 patients with both normal MPI results and normal left ventricular ejection fraction（LVEF）were selected. They were divided into three groups based on body mass index（BMI）：normal group（18.5 kg/m² ≤ BMI＜24.0 kg/m² ，n=40），overweight group（24.0 kg/m² ≤BMI＜28.0 kg/m² ，n=45），and obese group（BMI≥28.0 kg/m² ，n=48）. The differences in left ventricular function parameters such as phase histogram bandwidth（PBW），phase standard deviation（PSD），end - diastolic volume（EDV），end-systolic volume（ESV），and LVEF among the three groups were compared. The relationship between BMI and these parameters was analyzed. Results：Both overweight and obese groups showed significantly higher PBW（22.00 ± 4.24）vs. （17.10±3.20），P ＜ 0.001；（26.13±5.74）vs（. 17.10±3.20），P ＜ 0.001）and PSD values（5.04±1.05）vs.（3.74±0.68），P ＜ 0.001；（6.34± 1.43）vs.（3.74±0.68），P ＜ 0.001）compared with the normal group. The obese group demonstrated significantly greater PBW（26.13± 5.74）vs.（22.00±4.24），P ＜ 0.001）and PSD（6.34±1.43）vs.（5.04±1.05），P ＜ 0.001）than the overweight group. PBW（r=0.446，P ＜0.001）and PSD（r=0.477，P ＜ 0.001）showed significant positive correlations with BMI in overweight and obese patients. Conclusion： Obese patients are more likely to develop left ventricular mechanical dyssynchrony（LVMD），and the novel CZT SPECT phase analysis technique can effectively evaluate left ventricular mechanical synchrony in obese patients at an early stage，providing important clinical guidance for early detection and intervention of LVMD to reduce cardiovascular events in this population.

Abstract:Objective：To investigate the predictive efficacy of laboratory indexes for the 30 - day risk of death in extracorporeal cardiopulmonary resuscitation（ECPR）patients prior to receiving support. Methods：A retrospective analysis was performed on 113 patients who received ECPR transfer for more than 24 hours at the Emergency and Critical Care Medicine Department of the First Affiliated Hospital of Nanjing Medical University between January 2018 and December 2023. The patients were categorized into two groups based on their 30-day survival rate：the survival group（n=44）and the death group（n=69）. The laboratory test indicators before ECPR enrollment were examined using univariate analysis and Kaplan -Meier analysis for each of these groups. Cox’s proportional hazards regression model was used in multivariate analysis to examine the laboratory test markers that showed statistically and clinically significant differences. Receiver operating characteristic（ROC）curves were used to plot the subject characteristics，and the area under the ROC curvewas calculated. Results：According to the multifactorial Cox analysis，lactate[HR（95%CI）：1.318（1.185- 1.467），P ＜ 0.05]，PaCO[2 HR（95%CI）：1.008（1.001-1.013），P ＜ 0.05]，Na[HR（95%CI）：1.068（1.022-1.116），P ＜ 0.05]， creatinine[HR（95%CI）：1.003（1.001-1.004），P ＜ 0.05]and activated partial thromboplastin time（APTT）[HR（95%CI）：1.001 （1.001-1.002），P ＜ 0.05]were among the risks associated with 30-day mortality in ECPR patients. Moreover，there may be preventive benefits for pH[HR（95%CI）：0.161（0.027-0.961），P ＜ 0.05]and fibrinogen（FIB）[HR（95%CI）：0.823（0.688-0.986），P ＜ 0.05]. Conclusion：In patients receiving ECPR，the primary risk factors linked to 30-day death are lactate，PaCO₂，Na，creatinine，and APTT，while pH and FIB may have a potential protective role.

Abstract:Cancer-associated fibroblasts（CAFs）are mainly derived from quiescent normal fibroblasts，and partially originate from mesenchymal stem cells，epithelial cells，and endothelial cells. As an important part of the tumor microenvironment（TME），CAFs play a key role in the metastasis process of breast cancer. In recent years，researchers have paid more attention to the biological properties of CAFs and their interactions with breast cancer cells，which promote breast cancer cell invasion and metastasis by secreting various cytokines and exosomal microRNA（miRNA），altering extracellular matrix compositions，regulating intercellular signaling，and remodeling the TME. Although a large number of studies have revealed the importance of CAFs in breast cancer metastasis，their specific mechanisms of action need to be further explored. In this paper，we systematically review the latest research progress of CAFs in breast cancer metastasis，and explore the core mechanism and function of CAFs in it，with a view to providing new ideas for future research.

Abstract:As a key link in tumor metabolic reprogramming，lactate metabolism plays an important role in the occurrence， development and treatment resistance of pancreatic cancer. Beyond being a glycolytic byproduct，lactate functions as a key signaling molecule that regulates tumor proliferation，invasion，immune escape，and drug tolerance. Recent advances have identified lactate dehydrogenase A（LDHA）and monocarboxylate transporters（MCTs）as promising therapeutic targets in pancreatic cancer. Preclinical studies have shown that targeting lactate metabolism can suppress tumor growth and remodel the immunosuppressive tumor microenvironment. Moreover，lactate-associated biomarkers can also assist in the diagnosis and prognosis of pancreatic cancer. Despite these advances，current lactate -targeted therapies are limited by poor specificity，suboptimal safety，and pharmacological instability. This review outlines the mechanistic underpinnings of lactate metabolism in pancreatic cancer，highlights emerging therapeutic targets and strategies，and discusses the potential of integrating lactate-targeted approaches with immunotherapy to improve clinical outcomes.

Abstract:Early gastrointestinal cancer（EGC）has subtle early symptoms and low screening rates，which leads to most patients being diagnosed at the middle or advanced stages，resulting in poor prognoses. Therefore，early diagnosis and timely treatment are crucial for improving patient outcomes. In recent years，artificial intelligence（AI）technology has been able to enhance the detection rate and diagnostic accuracy of early lesions through high-precision image analysis and data processing，thereby achieving early detection，early diagnosis，and early treatment to improve patient prognoses. However，AI also faces challenges such as insufficient training data，algorithm bias，and uneven development across regions，which need to be addressed in future advancements. This review aims to provide a comprehensive overview of the current applications of AI in the diagnosis and treatment of EGC，exploring its advantages，challenges，and future directions to offer valuable references for researchers and clinicians in related fields.

Abstract:The extracellular matrix（ECM）generates multiple bioactive fragments，termed matrikines，which play pivotal roles in ECM functions. Acetylated proline-glycine-proline（AcPGP）is a matrikine derived from collagen. By binding to the C-X-C chemokine receptor type 1 and 2，AcPGP exhibits complex biological effects such as inflammatory responses，vascular permeability，tissue repair and remodeling. In the lungs，the dys - regulation of AcPGP contributes to a variety of respiratory diseases，and serves not only as a biomarker for diagnosis and assessment but also as a potential therapeutic target. This article reviews the regulatory mechanisms， biological functions of AcPGP in the lungs，and its role in respiratory diseases such as chronic airway inflammation diseases，acute lung injury，and pulmonary fibrosis.