Hepatocellular carcinoma (HCC) is a lethal cancer with high morbidity rates worldwide. It is a major threat to public health in China, due to the combination of known and new risk factors, such as endemic hepatitis B virus (HBV), dietary aflatoxin exposure, and the occurrence of metabolic dysfunction-associated steatotic liver disease (MASLD). Although many methods for surveillance and multimodal therapies, such as surgery, local ablation, transarterial therapy, and new systemic agents, have been available, the survival rates of HCC remains poor. They have very limited durable responses, long post-treatment recurrence rates, and high resistance to treatment. This reflects an imperfect picture of the biological cause of the disease and a need for new mechanistic or targeted techniques. A significant characteristic of HCC, in common with other aggressive cancers, is the presence of reprogrammed, hyperactive cell metabolism. Tumor cells hijack metabolic pathways to promote their uncontrolled growth, stress survival, invasion and metastasis. While classical mechanisms such as the Warburg effect, lipid metabolism and glutamine utilization have been understood, the lysosome, which was once viewed as a static “waste disposal unit” to remove old organelles and proteins, is instead a dynamic signaling and metabolic core. The lysosomes incorporate nutrients, energy and stress signals by master regulators such as mTORC1 (activated on its surface) that balance anabolic growth and catabolic recycling to the cellular demands. In HCC, lysosomes are not passive, but are highly active and dysregulated. HCC cells upregulate lysosomes, which scavenge intracellular components via enhanced autophagy and engulf extracellular proteins via macropinocytosis, crucial for survival in the nutrient-poor, hypoxic tumor microenvironment. In addition to metabolism, lysosomes exhibit pro-invasive functions by secreting hydrolases to remodel the extracellular matrix, promote angiogenesis, and suppress stromal immune cells to foster a pro-tumor microenvironment. In a clinical context, lysosomes play an important role in therapeutic resistance: they sequester and inactivate chemotherapeutics via lysosomal sequestration, and enhanced autophagic flux protects the cell from therapy-induced damage, contributing to relapse, as lysosomal dysfunction is a key cause of treatment failure. This makes lysosomes promising yet challenging therapeutic targets in HCC. Recent preclinical and early clinical studies investigate multiple strategies to exploit the susceptibility of lysosomes: lysosome-specific agents, alkalinizing the lysosome lumen or inducing membrane permeabilization and lysosome-dependent cell death; pharmacological inhibition of key lysosomal enzymes or autophagy to impair nutrient recycling and stress adaptation; smart nanotherapeutic agents or antibody-drug conjugates, specifically activated in the acidic lysosomal environment or utilizing lysosomal pathways for efficient intracellular drug release; and combination strategies of lysosome-targeting agents with tyrosine kinase inhibitors or immunotherapy to overcome resistance and achieve synergistic antitumor effects. In summary, our review systematically presents the role of lysosomes in HCC, from metabolic reprogramming and microenvironmental adaptation to therapeutic resistance. By synthesizing the latest mechanistic insights and preclinical advances, this review highlights the indispensable role of lysosomes in the complex HCC biological network, emphasizing that an in-depth understanding of this dynamic organelle holds great promise for developing innovative, targeted therapies, offering new hope for improving the poor prognosis of global HCC patients.

ObjectiveTranscranial magneto-acoustic stimulation (TMAS) is an emerging non-invasive neuromodulation technique that may provide a novel non-pharmacological intervention strategy for Parkinson's disease (PD). PD is characterized by the progressive degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNc), leading to motor impairments such as bradykinesia, tremor, and rigidity. Increasing evidence indicates that mitochondrial dysfunction and impaired mitochondrial quality control are central mechanisms underlying dopaminergic neuronal loss. In particular, abnormalities in mitophagy and mitochondrial fission-fusion balance contribute substantially to oxidative stress, energy metabolic failure, and neuronal injury. At present, most clinical treatments for PD mainly alleviate symptoms but do not effectively halt disease progression. Therefore, exploring new interventions targeting the core pathological mechanisms is of considerable significance. This study aims to investigate whether TMAS can improve neural damage and motor dysfunction in PD mice by regulating mitophagy and the fission/fusion dynamic balance, thereby providing theoretical and experimental support for its application in PD treatment. MethodsMale C57BL/6 mice were used in this study. A PD model was established by intraperitoneal injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) for 7 consecutive days. After model induction, mice in the intervention group received TMAS once daily for 14 consecutive days, whereas the corresponding control group received sham stimulation. The stimulation target was positioned over the primary motor cortex (M1). Motor performance was evaluated using the pole test and the open-field test. To verify the activation effect of TMAS on the target cortical region, c-Fos immunohistochemistry was performed in the M1. To assess nigral dopaminergic neuronal injury, tyrosine hydroxylase (TH) immunohistochemistry was used to quantify TH-positive neurons in the SNc. Mitochondrial function was evaluated by measuring reactive oxygen species (ROS) levels and adenosine triphosphate (ATP) content in the SNc. Western blot was further performed to determine the expression of mitophagy-related proteins, including PINK1, Parkin, LC3-II, and p62, as well as mitochondrial dynamics-related proteins, including Drp1 and Opa1. ResultsTMAS significantly increased the number of c-Fos-positive cells in M1 (P<0.000 1), indicating effective activation of neurons in the targeted cortical region. Compared with the control group, MPTP-treated mice exhibited marked motor dysfunction, including a significant reduction in total distance traveled in the open-field test (P<0.000 1) and mean speed (P=0.000 1), as well as significant prolongation of turn time and total climbing time in the pole test (P<0.000 1). These behavioral impairments were accompanied by a substantial loss of TH-positive dopaminergic neurons in the SNc, whereas TMAS significantly increased TH-positive neuron survival (P<0.000 1). In parallel, MPTP induced a pronounced increase in ROS levels and a significant reduction in ATP content, indicating severe mitochondrial dysfunction and energy metabolism impairment (P<0.01). TMAS treatment significantly improved motor performance, as reflected by the reversal of MPTP-induced impairment in the open-field and pole tests, and significantly reduced ROS accumulation (P<0.01) while restoring ATP production (P<0.001). At the molecular level, MPTP markedly downregulated PINK1 and Parkin, decreased p62 expression, increased LC3-II accumulation, elevated Drp1 expression, and reduced Opa1 expression, whereas TMAS significantly reversed these abnormalities, suggesting restoration of mitophagy-related mitochondrial quality control and re-establishment of mitochondrial fission-fusion balance. Collectively, these findings indicate that TMAS ameliorates MPTP-induced neurotoxicity and restores mitochondrial homeostasis and energy metabolism. ConclusionTMAS effectively attenuates neural damage and improves motor dysfunction in MPTP-induced PD mice. Its neuroprotective effects are closely associated with multidimensional regulation of the mitochondrial quality control system, including restoration of PINK1/Parkin-mediated mitophagy and rebalancing of Drp1/Opa1-related mitochondrial dynamics. Rather than acting only as a symptomatic neuromodulatory intervention, TMAS may influence a key pathological axis of PD by improving mitochondrial homeostasis in SNc and protecting nigral dopaminergic neurons. These findings provide experimental evidence supporting TMAS as a promising non-invasive physical intervention for PD.

ObjectiveTranscranial magneto-acoustic stimulation (TMAS) is an emerging non-invasive neuromodulation technique that may provide a novel non-pharmacological intervention strategy for Parkinson's disease (PD). PD is characterized by the progressive degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNc), leading to motor impairments such as bradykinesia, tremor, and rigidity. Increasing evidence indicates that mitochondrial dysfunction and impaired mitochondrial quality control are central mechanisms underlying dopaminergic neuronal loss. In particular, abnormalities in mitophagy and mitochondrial fission-fusion balance contribute substantially to oxidative stress, energy metabolic failure, and neuronal injury. At present, most clinical treatments for PD mainly alleviate symptoms but do not effectively halt disease progression. Therefore, exploring new interventions targeting the core pathological mechanisms is of considerable significance. This study aims to investigate whether TMAS can improve neural damage and motor dysfunction in PD mice by regulating mitophagy and the fission/fusion dynamic balance, thereby providing theoretical and experimental support for its application in PD treatment. MethodsMale C57BL/6 mice were used in this study. A PD model was established by intraperitoneal injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) for 7 consecutive days. After model induction, mice in the intervention group received TMAS once daily for 14 consecutive days, whereas the corresponding control group received sham stimulation. The stimulation target was positioned over the primary motor cortex (M1). Motor performance was evaluated using the pole test and the open-field test. To verify the activation effect of TMAS on the target cortical region, c-Fos immunohistochemistry was performed in the M1. To assess nigral dopaminergic neuronal injury, tyrosine hydroxylase (TH) immunohistochemistry was used to quantify TH-positive neurons in the SNc. Mitochondrial function was evaluated by measuring reactive oxygen species (ROS) levels and adenosine triphosphate (ATP) content in the SNc. Western blot was further performed to determine the expression of mitophagy-related proteins, including PINK1, Parkin, LC3-II, and p62, as well as mitochondrial dynamics-related proteins, including Drp1 and Opa1. ResultsTMAS significantly increased the number of c-Fos-positive cells in M1 (P<0.000 1), indicating effective activation of neurons in the targeted cortical region. Compared with the control group, MPTP-treated mice exhibited marked motor dysfunction, including a significant reduction in total distance traveled in the open-field test (P<0.000 1) and mean speed (P=0.000 1), as well as significant prolongation of turn time and total climbing time in the pole test (P<0.000 1). These behavioral impairments were accompanied by a substantial loss of TH-positive dopaminergic neurons in the SNc, whereas TMAS significantly increased TH-positive neuron survival (P<0.000 1). In parallel, MPTP induced a pronounced increase in ROS levels and a significant reduction in ATP content, indicating severe mitochondrial dysfunction and energy metabolism impairment (P<0.01). TMAS treatment significantly improved motor performance, as reflected by the reversal of MPTP-induced impairment in the open-field and pole tests, and significantly reduced ROS accumulation (P<0.01) while restoring ATP production (P<0.001). At the molecular level, MPTP markedly downregulated PINK1 and Parkin, decreased p62 expression, increased LC3-II accumulation, elevated Drp1 expression, and reduced Opa1 expression, whereas TMAS significantly reversed these abnormalities, suggesting restoration of mitophagy-related mitochondrial quality control and re-establishment of mitochondrial fission-fusion balance. Collectively, these findings indicate that TMAS ameliorates MPTP-induced neurotoxicity and restores mitochondrial homeostasis and energy metabolism. ConclusionTMAS effectively attenuates neural damage and improves motor dysfunction in MPTP-induced PD mice. Its neuroprotective effects are closely associated with multidimensional regulation of the mitochondrial quality control system, including restoration of PINK1/Parkin-mediated mitophagy and rebalancing of Drp1/Opa1-related mitochondrial dynamics. Rather than acting only as a symptomatic neuromodulatory intervention, TMAS may influence a key pathological axis of PD by improving mitochondrial homeostasis in SNc and protecting nigral dopaminergic neurons. These findings provide experimental evidence supporting TMAS as a promising non-invasive physical intervention for PD.

ObjectiveTo evaluate the effect of neuromuscular electrical stimulation (NMES) on pain, quadriceps strength and motor function of patients after total knee arthroplasty (TKA). MethodsThe databases of CNKI, Wanfang data, VIP, PubMed, Embase, Cochrane, Web of Science and Scopus were retrieved from inception to April, 2025. Randomized controlled trials (RCT) related to the intervention of NMES after TKA were collected. The quality of the included literature was evaluated using the Cochrane Risk of Bias Assessment Tool and the Physical Therapy Evidence Database (PEDro) scale. Meta-analysis was performed with RevMan 5.4. ResultsA total of twelve RCT were included, involving 772 subjects. The PEDro scale score ranged from four to seven. NMES improved postoperative quadriceps muscle strength (SMD = 0.61, 95%CI 0.34 to 0.88, P < 0.001) and knee flexion range of motion (SMD = 1.35, 95%CI 0.30 to 2.41, P = 0.010), and reduced the Timed Up and Go Test (TUGT) time (SMD = -0.86, 95%CI -1.45 to -0.26, P = 0.005). Compared with the control group, the intervention group achieved better outcomes in the 2-Minute Walk Test (2MWT) (SMD = 19.44, 95%CI 10.44 to 30.43, P < 0.001), 3-Minute Walk Test (SMD = 23.57, 95%CI 14.77 to 32.36, P < 0.001), 6-Minute Walk Test (SMD = 42.29, 95%CI 9.71 to 74.86, P = 0.010), Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) (SMD = -0.52, 95%CI -1.00 to -0.04, P = 0.040), as well as the Physical Component Summary (PCS) (SMD = 2.90, 95%CI 0.73 to 5.06, P = 0.009) and Mental Component Summary (MCS) (SMD = 2.84, 95%CI 1.40 to 4.28, P = 0.040) of the 36-Item Short Form Health Survey (SF-36). Subgroup analysis demonstrated that two to four weeks after surgery, NMES enhanced patients' quadriceps muscle strength (SMD = 0.90, 95%CI 0.58 to 1.21, P < 0.001), shortened TUGT time (SMD = -1.28, 95%CI -2.57 to -0.02, P < 0.05) and increased walking distance in 2MWT (SMD = 20.43, 95%CI 10.44 to 30.43, P < 0.001). For patients followed up for two to three months, NMES yielded improvements in WOMAC scores (SMD = -0.44, 95%CI -0.79 to -0.09, P = 0.010) and SF-36 MCS scores (SMD = 4.17, 95%CI 2.43 to 5.91, P < 0.001). ConclusionNMES can significantly improve the quadriceps strength and walking ability of the TKA patients two to four weeks after surgery, and enhance the quality of life of patients two to three months after surgery.

ObjectiveTo investigate the protective effects of Zuogui Wan （ZGW） decoction on nephrotic syndrome （NS） through the regulation of gut microbiota. MethodsThirty male Sprague-Dawley （SD） rats were randomly divided into five groups， with 6 rats in each group： The control group， model group， low-dose group， medium-dose group， and high-dose group. The NS rat model was induced by tail vein injection of 6.5 mg·kg^-1 doxorubicin. After successful modeling， the control and model groups were gavaged with normal saline （10 mL·kg^-1） twice daily， while the low- （50 mg·kg^-1）， medium- （100 mg·kg^-1）， and high-dose （200 mg·kg^-1） groups were gavaged with ZGW （10 mL·kg^-1） twice daily. All rats were administered at fixed intervals daily for 8 consecutive weeks. The therapeutic effects of ZGW on NS in rats were observed， and the optimal dose was screened. Renal and intestinal pathological changes in rats were examined. Fecal samples were collected， and 16S rDNA sequencing technology was used to detect the diversity and abundance of gut microbiota in each group. ResultsCompared with the control group， 24-hour urinary protein， serum creatinine， urea nitrogen， and cholesterol levels significantly increased in the model group （P<0.01）， while serum albumin levels decreased （P<0.01）. These changes were ameliorated in the treatment groups （P<0.05， P<0.01）. Renal pathology revealed intact and orderly arranged glomeruli and renal tubules in the control group. In the model group， glomerular atrophy， widened mesangial areas， podocyte swelling， disordered renal tubular arrangement， and numerous casts were observed. Varying degrees of glomerular atrophy and disordered renal tubular arrangement were seen in the treatment groups. Specific protein assays revealed increased serum levels of kidney injury molecule-1（KIM-1） and α1-microglobulin （P<0.01）， and significantly decreased levels of E-cadherin， Podocin， and Nephrin in renal tissues （P<0.01）， along with a significant increase in transforming growth factor-β（TGF-β） （P<0.01） in the model group. In the treatment groups， serum KIM-1 and α1-microglobulin levels decreased， E-cadherin levels significantly increased （P<0.01）， and TGF-β levels significantly decreased （P<0.01）. Podocin and Nephrin levels increased in the high-dose group （P<0.05）. Additionally， intestinal mucosal atrophy， epithelial cell edema， decreased goblet cells， and multiple inflammatory infiltrations were observed in the model group. The sequencing results of gut microbiota demonstrate that ZGW can significantly ameliorate intestinal dysbiosis in rats， restore the abundance of beneficial bacteria， and exert a profound influence on the compositional profile of gut microbiota. ConclusionZGW can alleviate renal injury in rats with nephrotic syndrome by improving gut microbiota and protecting the intestinal barrier.

ObjectiveTo construct and validate a risk assessment model for post-transplant diabetes mellitus （PTDM） using multiple machine learning algorithms， and to realize the early identification of PTDM. MethodsA retrospective analysis was performed for the clinical data of the patients who underwent allogeneic liver transplantation in The First Hospital of Shanxi Medical University from April 1， 2020 to December 31， 2024， and they were randomly divided into a training set and a validation set at a ratio of 7∶3. The LASSO regression analysis combined with 5-fold cross-validation was used for feature selection. Seven machine learning models were developed in the training set， i.e.， logistic regression （LR）， decision tree （DT）， Naive Bayes （NB）， random forest （RF）， K-nearest neighbor （KNN）， extreme gradient boosting （XGBoost）， and adaptive boosting （AdaBoost）. In the validation set， various methods were used to assess the predictive performance of each model， such as accuracy， precision， recall rate， specificity， F1 score， area under the receiver operating characteristic curve （AUROC）， and area under the precision-recall curve （AUPRC）. The Brier score and decision curve analysis were used to assess the calibration and clinical practicability of the models， and the SHAP method was used to analyze feature importance. The independent-samples t test or the Wilcoxon rank-sum test was used for comparison of continuous data between two groups， and the chi-square test or the Fisher’s exact test was used for comparison of categorical data between two groups. ResultsA total of 135 liver transplant recipients were enrolled， among whom 26 developed PTDM， and there were 94 patients in the training set and 41 in the validation set. Feature extraction and screening identified 7 key features of sex， overweight or obesity， anhepatic phase， time of operation， length of hospital stay， early postoperative hypomagnesemia， and impaired fasting glucose （IFG）. In the validation set， the XGBoost model showed the best predictive performance， with an AUROC of 0.907 （95% confidence interval ［CI］： 0.807 — 0.989）， an AUPRC of 0.649 （95%CI： 0.339 — 0.955）， an accuracy of 0.878， a precision of 0.667， a recall rate of 0.750， an F1-score of 0.706， a specificity of 0.909， and a Brier score of 0.104. The decision curve analysis showed that when the threshold probability was below 0.667， application of the XGBoost model in clinical decision-making provided relatively high net benefit. The SHAP analysis showed that the length of hospital stay ranked first in terms of feature importance， followed by time of operation， overweight or obesity， sex， IFG， anhepatic phase， and early postoperative hypomagnesemia. ConclusionThe risk assessment model for PTDM in liver transplant recipients based on XGBoost algorithm has excellent performance and can effectively identify high-risk individuals； however， multicenter large-sample data are needed for further validation.

ObjectiveFrozen shoulder (FS) is a debilitating musculoskeletal disorder characterized by persistent inflammation and progressive fibrosis of the glenohumeral joint capsule, leading to pain and severely restricted range of motion. Given the limited efficacy of current pharmacotherapies, there is an urgent need for novel anti-fibrotic agents. Guyanxiao Tincture (GYX), a traditional Chinese herbal formula, has shown clinical benefits in alleviating FS symptoms. However, its bioactive constituents and the molecular mechanisms underlying its therapeutic effects remain poorly defined. This study aimed to systematically evaluate the therapeutic efficacy of GYX against FS and to elucidate the mechanisms by which GYX attenuates capsular fibrosis. MethodsA Sprague-Dawley (SD) rat model of FS was established by immobilizing the unilateral shoulder with a plaster cast for 21 d. Following model induction, animals were administered with GYX or its serum-identified bioactive component, icariside F2. The absorbed prototype compounds of GYX in FS rat serum were profiled using ultraperformance liquid chromatography-quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF-MS). Therapeutic effects were assessed by measuring shoulder range of motion (ROM), histopathological evaluation of the capsule via hematoxylin-eosin staining, and quantification of transforming growth factor‑β1 (TGF-β1) content by ELISA. To explore the underlying mechanisms, transcriptomic profiling of the shoulder capsule was performed using RNA sequencing, and differentially expressed genes were validated by real-time quantitative PCR. Protein expression and localization were examined through immunohistochemistry, immunofluorescence, and Western blot. Protein-protein interaction networks were constructed to identify key regulatory hubs. In vitro, primary shoulder capsule fibroblasts were stimulated with TGF‑β1 to induce a fibrotic phenotype and then treated with icariside F2. The expression of alpha cardiac muscle 1 (ACTC1), α‑smooth muscle actin, and collagen I was subsequently measured. ResultsSerum pharmacochemistry analysis identified icariside F2 as the predominant circulating bioactive component of GYX in FS rats. Both GYX and icariside F2 treatment significantly improved the ROM and ameliorated histopathological lesions, including the attenuation of synovial hyperplasia, inflammatory infiltration, and excessive collagen deposition in the shoulder capsule. Consistently, elevated TGF‑β1 levels in the model group were markedly reduced after the interventions. RNA sequencing revealed that actin ACTC1 was dramatically upregulated in the fibrotic capsule, accompanied by the enrichment of fibrosis-associated pathways such as TGF‑β signaling, focal adhesion, and ECM-receptor interaction. Protein-protein interaction network analysis demonstrated that ACTC1 directly interacts with core fibrotic genes, including Col1a1, Col1a2, Thbs2, and Fn1. Critically, icariside F2 administration significantly reversed the aberrant overexpression of ACTC1 and suppressed the activation of the aforementioned fibrosis-related pathways in vivo. In TGF‑β1-stimulated fibroblasts, icariside F2 dose-dependently downregulated ACTC1 at both the mRNA and protein levels and concurrently decreased the expression of the fibrotic markers α‑smooth muscle actin and collagen I. Immunofluorescence and Western blot further confirmed that icariside F2 attenuated stress fiber formation and collagen production in vitro. ConclusionGYX and its bioactive component icariside F2 effectively alleviate the progression of frozen shoulder by inhibiting capsular fibrosis. Mechanistically, the therapeutic action is functionally linked to the suppression of ACTC1 and its downstream profibrotic signaling cascade, highlighting ACTC1 as a promising therapeutic target for the management of frozen shoulder.

Objective To evaluate the advantages of powder-liquid double-chamber bag products compared with traditional powder injection. Methods The systematic review method was used to collect the literature on powder-liquid double-chamber bag, extract common evaluation indicators, evaluate the use value of powder-liquid double-chamber bag products, and conduct a comprehensive comparison with traditional powder injection products. Results A total of 23 articles were included in the literature. The effectiveness indicators used for evaluation were the stability of the liquid medicine, the accuracy of the preparation concentration, and the residual amount of the liquid medicine; the safety indicators were the incidence of insoluble particles and the incidence of punctures and scratches. The economic indicators were preparation cost, occupied volume of preparation supplies, waste weight, hospitalization cost and incidence of blood infection. The applicability indicators were preparation time, average occupation of medical staff, packaging weight and storage and transportation volume, environmental adaptability, and ease of waste disposal. Accessibility indicators are the number of manufacturers, raw material supply capacity, and patient affordability. Through the evaluation of literature evidence, it was found that the stability and concentration accuracy of the powder-liquid double-chamber bag were higher than those of the traditional powder injection, and the domestic supply had been achieved. The double-chamber bag method can reduce the infusion reaction and shorten the preparation time of the liquid medicine. Conclusion Compared with traditional powder injectabler products, powder-liquid double-chamber bags have advantages in the dimensions of effectiveness, safety, economy, suitability and innovation, and the accessibility dimension meets the requirements.

With reference to the Information and Documentation-Resource Description (GB/T 3792-2021) and Bibliographical Description for Ancient Chinese Books (GB/T 3792.7-2008) and other cataloging standards and rules, drawing on the practical experience of cataloging ancient TCM books, Bibliographical Cataloging for Ancient TCM Books was formulated. This standard specifies the entry items and their order of ancient TCM books, cataloging identifier, cataloging text, cataloging information source, and cataloging item details. The standard can provide standardized and unified guiding principles and methods for the work of ancient TCM books, and promote the sharing and utilization of ancient TCM books.

Objective This research was performed to identify rodent-borne pathogens in Hekou Port,Yunnan Province.Methods Rodents were captured using cages and dissected to collect their lungs,liver,spleen,and other viscera.Eight pathogens,including Yersinia pestis,Leptospira,Bartonella,and Anaplasmataceae,were identified using polymerase chain reaction amplification.Amplified pathogen sequences from positive samples were sequenced,and BLAST homology searches were conducted using GenBank to confirm pathogen identities.A phylogenetic tree of the identified pathogens was constructed using the neighbor joining method.Results The total of 31 rodents,identified as Rattus tanezumi,R.norvegicus,and Mus musculus,were captured.Among these,R.tanezumi was the dominant species,accounting for 64.52％of the total.Two pathogens,Leptospira interrogans and Neoehrlichia mikurensis,were detected,with positivity rates of 9.68％and 29.03％,respectively.No other pathogens were detected.The overall positivity rate for rodent-borne pathogens was 35.48％.Conclusions The single 16S rRNA gene fragment is insufficient for the molecular identification of all Neoehrlichia species.Accurate species identification should be based on a combined analysis of multiple genes.The prevalence of rodent-borne pathogens in Hekou Port indicates the necessity for enhanced surveillance of rodent-borne diseases and implementation of additional prevention and control measures in border ports.