Irritable bowel syndrome （IBS） is a functional bowel disorder characterized primarily by abdominal pain and altered defecation habits. In recent years， traditional Chinese medicine （TCM） has made progress in multiple aspects of IBS research and treatment， including syndrome distribution， development of TCM formulas， clinical efficacy evaluation， external therapies， and psychosocial regulation. However， it still faces challenges such as over-reliance on symptomatic manifestations rather than biomarkers for diagnostic criteria， and the lack of high-quality evidence-based data supporting the efficacy of TCM formulas in treating IBS. This paper proposed that TCM diagnosis and treatment of IBS should adhere to the strategy of integrating the holistic concept with syndrome differentiation and treatment， combining TCM external therapies such as acupuncture， moxibustion and acupoint application）， and emphasizing individualized diagnosis and treatment for psychosomatic abnormalities. Future research should integrate multi-omics technologies， artificial intelligence and other methods to deepen the understanding of the pathogenesis of IBS and the mechanisms of TCM formulas， so as to promote the standardization and internationalization of TCM in the diagnosis and treatment of IBS.

ObjectiveTo describe the disposal process of the first imported case of Zika virus disease in Shanghai, and to provide a reference for the prevention and control of imported infectious diseases in the future. MethodsA retrospective review was conducted of the process by which epidemiological investigation, etiological testing, and case management were performed by the Shanghai municipal-and district-level Centers for Disease Control and Prevention (CDC) after one imported case of Zika virus disease was identified by Shanghai Customs. ResultsOn April 8th, 2025, customs authority at a certain airport in Shanghai identified a febrile inbound case (case A, female, 40 years old). An antecubital venous blood specimen was obtained and analyzed by nucleic acid testing for various vector-borne pathogens, by which Zika virus nucleic acid was found to be positive. On 9 April, the district CDC collected antecubital venous blood specimens again from Case A and her three accompanying travelers (B, C, and D), and nucleic acid testing was conducted for multiple mosquito-borne infectious diseases. Case A again tested positive for Zika virus nucleic acid, while Traveler D (male, aged 6 years) tested positive for dengue virus nucleic acid. The other two travelers tested negative. Case A and Traveler D were subsequently transferred to a designated district hospital for isolation and treatment. After discharge, both cases left China and returned to their overseas residence. ConclusionCase A was the first imported case of Zika virus disease in Shanghai. For cases with a history of living in endemic areas of multiple infectious diseases such as dengue virus, Zika virus and chikungunya virus, it is necessary to carry out rapid testing of multiple pathogens simultaneously to prevent missed diagnosis or misdiagnosis.

Intestinal permeability plays a pivotal role in the gut-liver axis and has emerged as a critical target for the prevention and treatment of liver diseases. Based on recent studies in China and globally， this article reviews the definitions and interrelationship of intestinal barrier function and intestinal permeability， the methods for assessing intestinal permeability， and the mechanism of action and clinical significance of intestinal permeability in the development and progression of various liver diseases. Studies have shown that increased intestinal permeability is a significant hallmark and an important driving factor for multiple liver diseases， and this state leads to the translocation of bacteria and harmful substances， trigger a systemic inflammatory response， and thus exacerbates liver injury， fibrosis， and metabolic dysregulation. Therefore， it is closely associated with the development and progression of metabolic associated fatty liver disease， alcoholic liver disease， autoimmune liver diseases， and their end-stage events， including liver cirrhosis， liver failure， and hepatocellular carcinoma. Future research should focus on the standardization of assessment methods， the exploration of underlying mechanisms， and the clinical translation of these findings.

Chronic gastritis is a chronic inflammation of the gastric mucosa caused by various etiologies and can be categorized into chronic non-atrophic gastritis and chronic atrophic gastritis.Chronic atrophic gastritis is a common disorder of the digestive system characterized by gastric mucosal gland atrophy,mucosal thinning,and basal layer thickening.The development of intestinal metaplasia and atypical hyperplasia on this basis is recognized as a precancerous lesion of gastric cancer and represents a key stage in the"inflammation-cancer transformation"of chronic gastritis.However,universally recognized and effective treatment strategies for this"inflammation-cancer transformation"process are lacking in clinical practice.This study integrates Correa′s cascade reaction with clinical practice,summarizing the pathogenesis of the"inflammation-cancer transformation"of chronic gastritis as weakness of the middle jiao and blood stasis.It suggests that the"inflammation-cancer transformation"process involves the pathological development of spleen and stomach deficiency,transportation and transformation dysfunction,turbid phlegm,blood stasis,and the gradual formation of cancerous toxins,with spleen and stomach weakness as the core mechanism and phlegm and blood stasis as the crucial pathological link.Based on an in-depth exploration of the deficiency of the middle jiao and blood stasis,supported by pharmacological research and clinical experience,this paper proposes the therapeutic approach of strengthening the spleen and replenishing qi,expelling phlegm and activating blood.It discusses the related prescriptions in preventing and treating the"inflammation-cancer transformation"of chronic gastritis.This study aims to provide new perspectives and insights for the prevention and treatment of chronic gastritis with traditional Chinese medicine,offering a novel framework for clinical treatment.

Objective:To investigate the relationship between CXCL6 expression and prostate cancer,as well as its effects on the malignant progression of PC-3 cells and the underlying mechanisms.Methods:Multiple databases were used to analyze CXCL6 expression in prostate cancer.And survival analysis,GO,and KEGG enrichment analysis were conducted.According to the concentration of CXCL6,PC-3 cells were divided into 0,100 and 200 ng/ml CXCL6 groups.The effects of up-regulated CXCL6 expression on PC-3 cell proliferation,migration,apoptosis,cycle,and related genes were investigated using CCK-8,EdU assay,scratch test,flow cytometry,and prostate cancer-targeted PCR array.Results:Database analysis revealed that CXCL6 was significantly down-regulated in prostate cancer(P＜0.05),and patients with low CXCL6 expression had a worse prognosis(P＜0.05).In prostate cancer,proteins associated with CXCL6 expression included CXCL1 and CXCL2,and related genes included MIR325 and RASSF6.GO analysis indicated that differentially expressed genes(DEGs)of CXCL6 were primarily enriched in processes such as response to chemokines and the tubular endoplasmic reticulum network(P＜0.05).KEGG analysis showed that DEGs were mainly enriched in signaling pathways such as the Hippo signaling pathway(P＜0.05).CCK-8,EdU assay,scratch test,and flow cytometry results demonstrated that compared with the 0 ng/ml CXCL6 group,the 100 and 200 ng/ml CXCL6 groups exhibited significantly reduced proliferation and migration rates(P＜0.05),significantly increased apoptosis rate(P＜0.05).And the proportion of S-phase cells in the 200 ng/ml CXCL6 group was lower compared to the 0 ng/ml CXCL6 group(P＜0.05).PCR array results showed that compared with the 0 ng/ml CXCL6 group,the expression of genes such as CDH1 and HAL was increased in the 200 ng/ml CXCL6 group,while the expression of genes such as CD5L and EDNRB was decreased.Conclusion:CXCL6 plays a significant role in the malignant progression of PC-3 cells,and its mechanism may be associated with the methylation of promoters of genes such as RASSF1,RARB,and CDH1.

BACKGROUND:D1-3-n-butylphthalide has antioxidant and anti-inflammatory effects and has been explored to have protective role in Parkinson's disease,but the underlying mechanisms are unknown.OBJECTIVE:To investigate the protective effect of D1-3-n-butylphthalide by the approach of network pharmacology,molecular docking,and cellular experimental validation.METHODS:(1)Network pharmacology and molecular docking:The database was used to screen the targets of D1-3-n-butylphthalide and Parkinson's disease.The intersection was taken from the construction of the target protein interaction network,and then screen the core targets.The GO and KEGG pathway enrichment was used to further analyze the core targets.The interaction between the target proteins and D1-3-n-butylphthalide was verified by molecular docking.(2)Cell validation:The passage 6 PC12 cells were divided into six groups for culture.The control group was cultured with conventional culture medium.The model group was cultured with N-methyl-4-phenylpyridinium iodide to induce Parkinson's disease model.The ML385 inhibitor group was added with nuclear factor E2-related factor 2 inhibitor ML385 on the basis of inducing Parkinson's disease model.The D1-3-n-butylphthalide treatment group was added with butylphthalide on the basis of inducing Parkinson's disease model.The D1-3-n-butylphthalide combined with ML385 treatment group was added with D1-3-n-butylphthalide and ML385 on the basis of inducing Parkinson's disease model.The D1-3-n-butylphthalide group was cultured with conventional culture medium containing butylphthalide alone.Cell proliferation,intracellular reduced glutathione and malondialdehyde levels,and protein expression of protein kinase B/glycogen synthase kinase 3β/nuclear factor E2-related factor 2(AKT/GSK-3β/Nrf2)signaling pathway were detected.RESULTS AND CONCLUSION:(1)A total of 52 targets were screened for the intersection of drugs and disease targets,and the core targets including the matrix metalloproteinase 9 and GSK-3β were involved the phosphatidylinositol 3-kinase(PI3K)/AKT and oxidative stress-related signaling pathways.The molecular docking binding energy of D1-3-n-butylphthalide and GSK-3β was-18.27 kJ/mol,which indicated that D1-3-n-butylphthalide had a good binding ability with GSK-3β.(2)Compared with the model group,the PC12 cell activity and reduced glutathione level in the D1-3-n-butylphthalide treatment group were increased(P＜0.05),the malondialdehyde level was decreased(P＜0.05),and the expression of p-AKT,p-GSK-3β,Nu-Nrf2,and T-Nrf2 proteins was increased(P＜0.05).Compared with the D1-3-n-butylphthalide group,the PC12 cell activity and reduced glutathione level in the D1-3-n-butylphthalide combined with ML385 treatment group were decreased(P＜0.05),the malondialdehyde level was increased(P＜0.05),and the expression of Nu-Nrf2 and T-Nrf2 proteins was decreased(P＜0.05).(3)These results demonstrate that D1-3-n-butylphthalide can inhibit oxidative stress and improve cell activity through the AKT/GSK-3β/Nrf2 signaling pathway,and has a protective effect on the Parkinson's cell model induced by N-methyl-4-phenylpyridinium iodide.

Objective:To investigate the relationship between CXCL6 expression and prostate cancer,as well as its effects on the malignant progression of PC-3 cells and the underlying mechanisms.Methods:Multiple databases were used to analyze CXCL6 expression in prostate cancer.And survival analysis,GO,and KEGG enrichment analysis were conducted.According to the concentration of CXCL6,PC-3 cells were divided into 0,100 and 200 ng/ml CXCL6 groups.The effects of up-regulated CXCL6 expression on PC-3 cell proliferation,migration,apoptosis,cycle,and related genes were investigated using CCK-8,EdU assay,scratch test,flow cytometry,and prostate cancer-targeted PCR array.Results:Database analysis revealed that CXCL6 was significantly down-regulated in prostate cancer(P＜0.05),and patients with low CXCL6 expression had a worse prognosis(P＜0.05).In prostate cancer,proteins associated with CXCL6 expression included CXCL1 and CXCL2,and related genes included MIR325 and RASSF6.GO analysis indicated that differentially expressed genes(DEGs)of CXCL6 were primarily enriched in processes such as response to chemokines and the tubular endoplasmic reticulum network(P＜0.05).KEGG analysis showed that DEGs were mainly enriched in signaling pathways such as the Hippo signaling pathway(P＜0.05).CCK-8,EdU assay,scratch test,and flow cytometry results demonstrated that compared with the 0 ng/ml CXCL6 group,the 100 and 200 ng/ml CXCL6 groups exhibited significantly reduced proliferation and migration rates(P＜0.05),significantly increased apoptosis rate(P＜0.05).And the proportion of S-phase cells in the 200 ng/ml CXCL6 group was lower compared to the 0 ng/ml CXCL6 group(P＜0.05).PCR array results showed that compared with the 0 ng/ml CXCL6 group,the expression of genes such as CDH1 and HAL was increased in the 200 ng/ml CXCL6 group,while the expression of genes such as CD5L and EDNRB was decreased.Conclusion:CXCL6 plays a significant role in the malignant progression of PC-3 cells,and its mechanism may be associated with the methylation of promoters of genes such as RASSF1,RARB,and CDH1.

Objective By exploring changes of six degrees of freedom(6DOF)kinematics of the knee joint during extra weight bearing of the body trunk,the influence of extra weight on knee joint movement patterns was studied.Methods A total of 24 healthy subjects were recruited to walk/run on a treadmill at four speeds under two states:self-weight and wearing a 16 kg vest,and gait analysis was conducted.A three-dimensional(3D)portable knee kinematics analysis system based on infrared stereophotography was used to capture 6DOF movement trajectory data of the tibia relative to the femur.Results Compared to the self-weight state,when additional trunk weight was added,the knee external rotation angle was reduced at 3.6 km/h speed(1.4°-2.1°)and 5.4 km/h speed(2.2°-2.7°);the knee internal rotation angle was reduced at 10.8 km/h speed(2.1°-4.2°);the knee flexion angles was increased significantly at the speed of 3.6 km/h(1.5°-1.8°),9 km/h(1.6°-3.3°)和 10.8 km/h(1.9°-3.1°);the knee adduction angle increased at 5.4 km/h speed(0.5°-0.6°),and decreased at 10.8 km/h speed(0.9°-1.3°).At 10.8 km/h speed,the distal knee displacement(0.2-0.4 mm)was increased,and the lateral knee displacement(0.1-0.2 mm),and anterior knee displacement(0.2-0.3 mm)were significantly reduced.Conclusions The 6DOF kinematics of human knee is significantly affected by the extra trunk weight.Performance is also different at lower and higher speeds.It is suggested that there may exist a hidden injury in military training,and this study provides a kinematic basis for the occurrence of sports injury.

BACKGROUND:D1-3-n-butylphthalide has antioxidant and anti-inflammatory effects and has been explored to have protective role in Parkinson's disease,but the underlying mechanisms are unknown.OBJECTIVE:To investigate the protective effect of D1-3-n-butylphthalide by the approach of network pharmacology,molecular docking,and cellular experimental validation.METHODS:(1)Network pharmacology and molecular docking:The database was used to screen the targets of D1-3-n-butylphthalide and Parkinson's disease.The intersection was taken from the construction of the target protein interaction network,and then screen the core targets.The GO and KEGG pathway enrichment was used to further analyze the core targets.The interaction between the target proteins and D1-3-n-butylphthalide was verified by molecular docking.(2)Cell validation:The passage 6 PC12 cells were divided into six groups for culture.The control group was cultured with conventional culture medium.The model group was cultured with N-methyl-4-phenylpyridinium iodide to induce Parkinson's disease model.The ML385 inhibitor group was added with nuclear factor E2-related factor 2 inhibitor ML385 on the basis of inducing Parkinson's disease model.The D1-3-n-butylphthalide treatment group was added with butylphthalide on the basis of inducing Parkinson's disease model.The D1-3-n-butylphthalide combined with ML385 treatment group was added with D1-3-n-butylphthalide and ML385 on the basis of inducing Parkinson's disease model.The D1-3-n-butylphthalide group was cultured with conventional culture medium containing butylphthalide alone.Cell proliferation,intracellular reduced glutathione and malondialdehyde levels,and protein expression of protein kinase B/glycogen synthase kinase 3β/nuclear factor E2-related factor 2(AKT/GSK-3β/Nrf2)signaling pathway were detected.RESULTS AND CONCLUSION:(1)A total of 52 targets were screened for the intersection of drugs and disease targets,and the core targets including the matrix metalloproteinase 9 and GSK-3β were involved the phosphatidylinositol 3-kinase(PI3K)/AKT and oxidative stress-related signaling pathways.The molecular docking binding energy of D1-3-n-butylphthalide and GSK-3β was-18.27 kJ/mol,which indicated that D1-3-n-butylphthalide had a good binding ability with GSK-3β.(2)Compared with the model group,the PC12 cell activity and reduced glutathione level in the D1-3-n-butylphthalide treatment group were increased(P＜0.05),the malondialdehyde level was decreased(P＜0.05),and the expression of p-AKT,p-GSK-3β,Nu-Nrf2,and T-Nrf2 proteins was increased(P＜0.05).Compared with the D1-3-n-butylphthalide group,the PC12 cell activity and reduced glutathione level in the D1-3-n-butylphthalide combined with ML385 treatment group were decreased(P＜0.05),the malondialdehyde level was increased(P＜0.05),and the expression of Nu-Nrf2 and T-Nrf2 proteins was decreased(P＜0.05).(3)These results demonstrate that D1-3-n-butylphthalide can inhibit oxidative stress and improve cell activity through the AKT/GSK-3β/Nrf2 signaling pathway,and has a protective effect on the Parkinson's cell model induced by N-methyl-4-phenylpyridinium iodide.

Mesoporous carbon nanoparticles (MCNs) have received considerable attention for biomedical applications due to their unique structural features, including high specific surface area, adjustable pore size, and remarkable biocompatibility. These properties have addressed key challenges such as inefficiencies in drug loading and release, minimizing the side effects associated with conventional treatments. In this review, the classification and the research progress of MCNs are summarized firstly, the preparation and modification techniques to enhance their functionality and properties are further reviewed, the main physicochemical properties are introduced as well, highlighting their contributions to MCNs in applications. In addition, the biomedical applications of MCNs are emphasized, including tumor therapy, tumor theranostics, antibacterial, delivery of active molecules and biological detection. Finally, the prospects and challenges of clinical application based on MCNs are analyzed to provide an effective reference and lay the foundation for further research.