Zoonosis prevention and control is a complex public health concern, which requires the collaboration of multiple regions, disciplines, and departments to enhance the effectiveness. The One Health concept aims to achieve the joint health security of humans, animals and environments through cross-disciplinary, cross-sector and cross-field collaborations. This review summarizes the development of One Health and the successful practices in the prevention and control of echinococcosis, rabies, COVID-19 and schistosomiasis, as well as explores the challenges faced in applying this concept to the prevention and control of zoonoses, so as to provide insights into formulation of the integrated zoonoses control strategy and implementation of zoonoses control interventions at the human-animal-environment interface.

Objective: To explore the potential application of PAK4-PROTAC targeted degradation drug (PpD) in renal cancer immunotherapy. Methods: TIMER 2.0 and TISIDB databases were used to analyze the relationship among PAK4 expression, tumor purity and abundance of immune cell infiltration in renal tumor microenvironment (TEM).Renal cancer cell lines OS-RC-2, 786-O and ACHN were treated with 0, 125 and 250 nmol/L PpD, and the effects of Jurkat cell co-culture on the results were investigated.The cell apoptosis was detected with flow cytometry, and the expression of programmed cell death 1 ligand 1 (PD-L1) in renal cancer cells was detected with immunoblotting. Results: The high expression of PAK4 was positively related to immune purity, and inhibited the abundance of immune killer cells in TEM, such as CD8 T cells, CD4 T cells, natural killer cells and dendritic cells.With 250 nmol/L PpD treatment, there were 21.02% apoptotic cells in OS-RC-2, 29.67% apoptotic cells in 786-O, and 15.39% apoptotic cells in ACHN, respectively.However, with the same concentration of 250 nmol/L PpD treatment, cell apoptotic rate was sharply increased to 70.13% in OS-RC-2/Jurkat, 70.68% in 780-O/Jurkat, and 60.27% in ACHN/Jurkat co-culture models, respectively. Conclusion: PpD can promote apoptosis of renal cancer cells by reducing the expression of PAK4 protein, and enhance the killing effects of immune cells on tumor cells.

Education is a crucial element in the development of acupuncture as a discipline, providing essential talent support for its future advancement. A structured interview was conducted with renowned acupuncture expert Professor ZHAO Jiping, focusing on key topics such as the core of acupuncture education, the connotation and development of acupuncture textbooks, and acupuncture teaching models. Through in-depth discussion, the current problems in acupuncture education were analyzed, and possible solutions were explored, aiming to offer ideas for the innovative development of acupuncture education.
Acupuncture/trends* ; Humans ; Acupuncture Therapy ; China

OBJECTIVE: To investigate the effects of acupuncture on the neurotransmitter levels and gut microbiota in a mouse model of Tourette syndrome (TS). METHODS: Thirty-six male C57/BL6 mice were randomly divided into 4 groups using a random number table method: 3,3'-iminodipropionitrile (IDPN) group, control group, acupuncture group, and tiapride group, with 9 mice in each group. In the IDPN group, acupuncture group, and tiapride group, mice received daily intraperitoneal injections of IDPN (300 mg/kg body weight) for 7 consecutive days to induce stereotyped behaviors. Subsequently, in the acupuncture intervention group, standardized acupuncture treatment was administered for 14 consecutive days to IDPN-induced TS model mice. The selected acupoints included Baihui (DU 20), Yintang (DU 29), Waiguan (SJ 5), and Zulinqi (GB 41). In the tiapride group, mice were administered tiapride (50 mg/kg body weight) via oral gavage daily for 14 consecutive days. The control group, IDPN group, and acupuncture group received the same volume of saline orally for 14 consecutive days. Stereotypic behaviors were quantified through behavioral assessments. Neurotransmitter levels, including dopamine (DA), glutamate (Glu), and aspartate (ASP) in striatal tissue were measured using enzyme-linked immunosorbent assay. Dopamine transporter (DAT) expression levels were additionally quantified through quantitative polymerase chain reaction (qPCR). Gut microbial composition was analyzed through 16S ribosomal RNA gene sequencing, while metabolic profiling was conducted using liquid chromatography-mass spectrometry (LC-MS). RESULTS: Acupuncture administration significantly attenuated stereotypic behaviors, concurrently reducing striatal levels of DA, Glu and ASP concentrations while upregulating DAT expression compared with untreated TS controls (P<0.05 or P<0.01). Comparative analysis identified significant differences in Muribaculaceae (P=0.001), Oscillospiraceae (P=0.049), Desulfovibrionaceae (P=0.001), and Marinifilaceae (P=0.014) following acupuncture intervention. Metabolomic profiling revealed alterations in 7 metabolites and 18 metabolic pathways when compared to the TS mice, which involved various amino acid metabolisms associated with DA, Glu, and ASP. CONCLUSIONS Acupuncture demonstrates significant modulatory effects on both central neurotransmitter systems and gut microbial ecology, thereby highlighting its dual therapeutic potential for TS management through gut-brain axis regulation.
Animals ; Tourette Syndrome/metabolism* ; Gastrointestinal Microbiome ; Neurotransmitter Agents/metabolism* ; Acupuncture Therapy ; Male ; Mice, Inbred C57BL ; Mice

Microbial denitrification is a major pathway for nitrogen removal from water bodies. However, denitrification is often difficult to continue when there is a lack of microbially available organic matter in the water body to serve as electron donors. In recent years, studies have shown that some denitrifying bacteria can directly utilize photoelectrons generated by sunlight-excited semiconductor minerals or natural organic matter for denitrification without the need for bioavailable organic matter as electron donors. This process is defined as microbial photoelectrotrophic denitrification. The discovery of microbial photoelectrotrophic denitrification phenomenon reshapes the previous knowledge about the chemoheterotrophic mode of denitrifying bacteria and broadens the pathway of nitrogen removal by the new photoelectrotrophic metabolism, which is of great significance to our understanding and exploration of sunlight-driven nitrogen cycling process. In this paper, we comprehensively sort out the existing research reports in the field of microbial photoelectrotrophic denitrification, systematically summarize the principle and the current research progress of microbial photoelectrotrophic denitrification, deeply analyze the problems and challenges faced by this technology, and make an outlook on the future research directions and application prospects of this technology, providing a reference for the further research and application of this technology.
Denitrification/physiology* ; Nitrogen/isolation & purification* ; Bacteria/metabolism* ; Sunlight ; Phototrophic Processes

Objective To investigate the mechanism of metformin for regulating tumor-stromal cell cross-talk in breast cancer.Methods Tumor associated fibroblasts(CAFs)co-cultured with breast cancer cells were treated with metformin,and the changes in expressions of hypoxia-inducible factor-1α(HIF-1α),p-AMPK,stroma-derived factor-1(SDF-1)and interleukin-8(IL-8)in the CAFs were detected using ELISA,RT-qPCR or Western blotting;Transwell assay was used to evaluate the invasiveness of the tumor cells and its changes following treatment with exogenous SDF-1,IL-8 and TGF-β1.The effects of HIF-1α shRNA or overexpression plasmid,AMPK shRNA,and treatment with OG(a proline hydroxylase inhibitor)or 2-OXO(a proline hydroxylase activator)were examined on p-AMPK,HIF-1α,SDF-1 and IL-8 expressions and invasiveness of the CAFs.Results Metformin treatment significantly increased the expression levels of p-AMPK,SDF-1 and IL-8(P<0.05)and decreased HIF-1α expression(P<0.05)without affecting AMPK expression level(P>0.05)in the CAFs.The invasion ability of metformin-treated breast cancer cells was significantly decreased(P<0.05).Exogenous SDF-1 and IL-8,HIF-1α overexpression,and OG-induced upregulation of HIF-1α all significantly attenuated the inhibitory effects of metformin on breast cancer cell invasion(P<0.05)and HIF-1α,SDF-1 and IL-8 expressions in CAFs(P<0.05).Transfection with HIF-1α shRNA or treatment with 2-OXO significantly decreased the invasiveness of breast cancer cells(P<0.05).P-AMPK knockdown significantly suppressed the inhibitory effect of metformin on HIF-1α expression in CAFs and on invasion of breast cancer cells(P<0.05).Treatment with TGF-β1 partially decreased the inhibitory effect of metformin on HIF-1α expression in CAFs and invasiveness of the breast cancer cells(P<0.05).Conclusion Metformin suppresses HIF-1α expression in CAFs to block tumor-stromal cross talk in breast cancer.

Objective To investigate the mechanism of metformin for regulating tumor-stromal cell cross-talk in breast cancer.Methods Tumor associated fibroblasts(CAFs)co-cultured with breast cancer cells were treated with metformin,and the changes in expressions of hypoxia-inducible factor-1α(HIF-1α),p-AMPK,stroma-derived factor-1(SDF-1)and interleukin-8(IL-8)in the CAFs were detected using ELISA,RT-qPCR or Western blotting;Transwell assay was used to evaluate the invasiveness of the tumor cells and its changes following treatment with exogenous SDF-1,IL-8 and TGF-β1.The effects of HIF-1α shRNA or overexpression plasmid,AMPK shRNA,and treatment with OG(a proline hydroxylase inhibitor)or 2-OXO(a proline hydroxylase activator)were examined on p-AMPK,HIF-1α,SDF-1 and IL-8 expressions and invasiveness of the CAFs.Results Metformin treatment significantly increased the expression levels of p-AMPK,SDF-1 and IL-8(P<0.05)and decreased HIF-1α expression(P<0.05)without affecting AMPK expression level(P>0.05)in the CAFs.The invasion ability of metformin-treated breast cancer cells was significantly decreased(P<0.05).Exogenous SDF-1 and IL-8,HIF-1α overexpression,and OG-induced upregulation of HIF-1α all significantly attenuated the inhibitory effects of metformin on breast cancer cell invasion(P<0.05)and HIF-1α,SDF-1 and IL-8 expressions in CAFs(P<0.05).Transfection with HIF-1α shRNA or treatment with 2-OXO significantly decreased the invasiveness of breast cancer cells(P<0.05).P-AMPK knockdown significantly suppressed the inhibitory effect of metformin on HIF-1α expression in CAFs and on invasion of breast cancer cells(P<0.05).Treatment with TGF-β1 partially decreased the inhibitory effect of metformin on HIF-1α expression in CAFs and invasiveness of the breast cancer cells(P<0.05).Conclusion Metformin suppresses HIF-1α expression in CAFs to block tumor-stromal cross talk in breast cancer.

Objective:To preliminarily predict the potential pathways and targets of Xiaoban Tongmai Formula in anti-atherosclerosis(AS)by network pharmacology analysis,and to verify its possible mechanism combined with in vitro cell experiment.Method:The databases including Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform(TCMSP),GeneCards,Swiss Target Prediction,and Uniprot were used to collect the information on active compounds and corresponding targets of Xiaoban Tongmai Formula to construct the"compound-target-disease"network.The potential targets and pathways were predicted by protein-protein interaction(PPI)network,and the intersection targets were subjected to Gene Ontology(GO)functional enrichment analysis and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathway enrichment analysis.The human aortic vascular smooth muscle cells(HA-VSMCs)were cultured and identified in vitro,and the abnormal proliferation of HA-VSMCs were induced by oxidized low-density lipoprotein(ox-LDL)and identified;MTT method was used to detect the proliferation activities of the HA-VSMCs in various groups after treated with different concentrations of Xiaoban Tongmai Formula;the safety of Xiaoban Tongmai Fang was confirmed.The HA-VSMCs were divided into blank group,model group(the abnormal proliferation of HA-VSMCs was induced),rosuvastatin group(treated with 4 μmol·L-1 rosuvastatin after inducing the abnormal proliferation of HA-VSMCs),and low,medium,and high doses of Xiaoban Tongmai Formula groups(treated with 0.025,0.050,and 0.100 mng·L-1 Xiaoban Tongmai Formula after inducing the abnormal proliferation of HA-VSMCs);enzyme-linked immunosorbent assay(ELISA)was used to detect the levels of monocyte chemotactic protein-1(MCP-1),interleukin-6(IL-6),and interleukin-8(IL-8)in supernatant of the HA-VSMCs in various groups;real-time fluorescence quantitative PCR(RT-qPCR)method was used to detect the expression levels of nuclear factor kappa-B(NF-κB)p65 mRNA and fibroblast growth factors 2(FGF2)mRNA in the HA-VSMCs in various groups;Western blotting method was used to detect the expression levels of NF-κB p65 and FGF2 proteins in the HA-VSMCs in various groups.Results:Xiaoban Tongmai Formula contained 103 active ingredients that exert anti-AS effect by acting on 189 target genes.The potential targets included IL-6,IL-8,vascular endothelial growth factor A(VEGFA),nuclear factor kappa B1(NF-κB1),and RELA(NF-κB p65).The GO functional analysis and KEGG pathway enrichment analysis results showed that Xiaoban Tongmai Formula exerted anti-AS effects by regulating lipid metabolism,hypoxia-inducible factor-1(HIF-1),epidermal growth factor(EGF),phosphatidylinositol 3-kinase(PI3K)/protein kinase B(Akt),and NF-κB signaling pathways.The cell morphology and immunofluorescence staining results confirmed that the cells were HA-VSMCs.The oil red O staining results showed numerous red lipid droplets,indicating successful modeling.The MTT assay results showed that Xiaoban Tongmai Formula had no significant effect on the proliferation rate of HA-VSMCs within a certain dose range,indicating good safety.The ELISA results showed that compared with model group,the levels of MCP-1 and IL-6 in supernatant of the HA-VSMCs in rosuvastatin group and different doses of Xiaoban Tongmai Formula groups were decreased(P＜0.05 or P＜0.01),and the levels of IL-8 in supernatant of the HA-VSMCs in 0.050 and 0.100 mg·L-1 Xiaoban Tongmai Formula groups were decreased(P＜0.01);compared with rosuvastatin group,the levels of MCP-1 in supernatant of the HA-VSMCs in different doses of Xiaoban Tongmai Formula groups were decreased(P＜0.01),and the levels of IL-8 in supernatant of the HA-VSMCs in 0.050 and 0.100 mg·L-1 Xiaoban Tongmai Formula groups were decreased(P＜0.01).Compared with model group,the expression levels of NF-κB p65 mRNA in the HA-VSMCs in rosuvastatin group and different doses of Xiaoban Tongmai Formula groups were decreased(P＜0.01),and the expression levels of FGF2 mRNA in the HA-VSMCs in rosuvastatin group and 0.050 and 0.100 mg·L-1 Xiaoban Tongmai Formula groups were decreased(P＜0.01);compared with rosuvastatin group,the expression levels of NF-κB p65 and FGF2 mRNA in the HA-VSMCs in 0.050 and 0.100 mg·L-1 Xiaoban Tongmai Formula groups were decreased(P＜0.05 or P＜0.01).Compared with model group,the expression levels of NF-κB p65 and FGF2 proteins in the HA-VSMCs in rosuvastatin group and different doses of Xiaoban Tongmai Formula groups were decreased(P＜0.01);compared with rosuvastatin group,the expression levels of NF-κB p65 protein in the HA-VSMCs in 0.050 and 0.100 mg·L-1 Xiaoban Tongmai Formula groups were decreased(P＜0.01),and the expression level of FGF2 protein in the HA-VSMCs in 0.100 mg·L-1 Xiaoban Tongmai Formula group was decreased(P＜0.01).Conclusion:Xiaoban Tongmai Formula has anti-inflammatory effect,inhibitory effect on the proliferation of HA-VSMCs,and anti-AS effect,and its mechanism may be related to the inactivation of NF-κB/FGF2 pathway.

Objective To investigate the expression of long non-coding RNA(lncRNA),surfactant associated 1 pseudogene(SFTA1P)in lung squamous carcinoma and its effect on the biological functions of SFTA1P in lung squamous carcinoma cell lines.Methods Based on the cancer genome atlas(TCGA)database,the differential expression of SFTA1P in tumor and normal tissues were compared in patients diagnosed with lung squamous cell carcinoma.Then,the expression of SFTA1P was detected in human normal lung epithelial cell line BEAS-2B and lung squamous cell lines SK-MES-1 and H520 with real-time quantitative polymerase chain reaction(RT-qPCR).SK-MES-1 and H520 cells with overexpression and/or knockdown of SFTA1P were constructed by transfecting the overexpression plasmids(pcDNA3.1-SFTA1P)and small interfering RNAs(si-SFTA1P-1 and si-SFTA1P-2).CCK-8 assay and Transwell assay were used to investigate the effect of SFTA1P on biological functions in lung squamous carcinoma cells.Differential gene expression analysis,correlation analysis and functional enrichment analysis were employed to explore the potential mechanism that SFTA1P may affect biological functions of lung squamous cells.Results Analysis of TCGA showed that the expression of SFTA1P was significantly lower in lung squamous cell carcinoma tissue than adjacent normal tissue(P＜0.05).RT-PCR results showed that the expression of SFTA1P was obviously lower in lung squamous carcinoma cells than the human normal lung epithelial cells(P＜0.05).And the expression level of SFTA1P was relatively lower in the SK-MES-1 cells than the H520 cells(P＜0.05).Overexpression of SFTA1P suppressed the proliferation,migration and invasion of lung squamous carcinoma cells(P＜0.05),while its knockdown promoted these abilities(P＜0.05).Differential gene expression analysis,correlation analysis and functional enrichment analysis indicated that SFTA1P may inhibit MYC,G2m checkpoints and E2f signaling pathways in lung squamous cell carcinoma.Conclusion SFTA1P shows anti-cancer function in lung squamous cell carcinoma,and it may affect the biological functions of lung squamous cell carcinoma cells through down-regulating MYC,G2m checkpoints and E2f signaling pathways.