Objective By observing and measuring the relevant data of the buccal branch of the facial nerve,the parotid duct and the facial artery,the positional relationship among the three was analyzed to avoid accidental injury to the buccal branch of the facial nerve and the parotid duct when ligaturing the facial artery during the operation.Methods Forty adult head and neck specimens were dissected to observe the relationship between the buccal branch of the facial nerve and the parotid duct,the course and positional relationship of the facial artery,and the relationship between the buccal branch of the facial nerve and the peripheral vascular network.The relevant diameters were measured with a vernier caliper.Results The buccal branch of the facial nerve was divided into the superior buccal branch and the inferior buccal branch,and there was no direct anastomosis or connecting fiber between the buccal branch of the facial nerve and the parotid duct.The superior buccal branch was relatively thick,and it has a relatively constant position,which was parallel to the parotid duct.The position of the inferior buccal branch was not constant and it ran on or slightly above the plane of angulus oris.The superior buccal branch was located(10.76±5.54)mm from the parotid duct,while the inferior buccal branch was positioned(6.84±4.06)mm away from the parotid duct.The course of the main trunk of the facial artery was relatively fixed.Moreover,if the branch of the facial artery was missing,other branches of the facial artery would extend to replace the missing branch artery.The main trunk of the facial artery had a diameter of(2.34±0.83)mm,and its branches formed anastomoses with the buccal branch of the maxillary artery,creating a vascular network in the parotid and buccal regions.There was a vascular network around the buccal branch of the facial nerve,which was mostly small branches of the facial artery and the superficial temporal artery.Conclusion The buccal branch of the facial nerve exhibits a consistent anatomic relationship with the parotid duct and the facial artery.During the ligation of the facial artery,the parotid duct can serve as a landmark to accurately locate the buccal branch of the facial nerve,thereby significantly reducing the risk of inadvertent injury to the buccal branch of the facial nerve and the parotid duct.

Analyzing the spatial distribution pattern and formation factors of medicinal plant resources can provide a scientific basis for the protection and development of traditional Chinese medicine(TCM) resources. This study is based on the survey data of medicinal plant resources in 104 county-level administrative regions of Anhui province in the Fourth National Survey of TCM Resources. The global spatial autocorrelation analysis, trend surface analysis, local spatial autocorrelation analysis, hotspot analysis, and a geodetector were employed to analyze the spatial distribution pattern of medicinal plant richness, and its relationship with natural factors was explored. The results can provide a basis for the formulation of development strategies such as the protection and utilization of TCM resources, as well as offer a scientific foundation for the establishment of regional planning schemes for TCM resources in Anhui province. The results indicated that the richness of medicinal plant resources in Anhui province had significant spatial heterogeneity, exhibiting highly clustered distribution characteristics. Cold spots and hot spots presented clustered distribution patterns, with cold spots mostly located north of the Huaihe River and hot spots south of the Yangtze River. Overall, the distribution of medicinal plant resources in Anhui province showed an overall trend of high in the south and low in the north, which was consistent with the overall geomorphic trend of this province. In addition, natural factors such as altitude, precipitation, and vegetation type played an important role in the diversity and spatial distribution pattern formation of medicinal plant resources. The extraction and analysis of the spatial distribution characteristics of natural factors in cold and hot spot regions discovered that the heterogeneity of eco-environments constituted a fundamental condition for the formation of species diversity.
Plants, Medicinal/classification* ; China ; Spatial Analysis ; Conservation of Natural Resources ; Biodiversity

Objective To develop predictive models based on decision tree and logistic regression algo-rithms for pulmonary multidrug-resistant organism(MDRO)infection risk in intensive care unit(ICU)pa-tients,and compare their predictive performance to provide references for pulmonary MDRO infection preven-tion.Methods A total of 350 ICU patients admitted to the hospital from January 2021 to December 2023 were enrolled and divided into an infection group(n=52)and a non-infection group(n=298)based on the pres-ence of pulmonary MDRO infection.Clinical data from both groups were collected and analyzed to identify risk factors for pulmonary MDRO infection in ICU patients.Using the risk of pulmonary MDRO infection in ICU patients as the dependent variable and the indicators with statistically significant differences in univariate anal-ysis as the independent variables,predictive models for pulmonary MDRO infection risk were developed by u-sing decision tree algorithms and logistic regression analysis.The predictive performance of these two models was compared.Results There were statistically significant differences(P＜0.05)between the infection and non-infection groups in terms of age,history of diabetes,hospital stay≥2 weeks,indwelling urinary catheter,chlorine dioxide disinfection,prolonged bedridden status,and disturbance of consciousness.Logistic regression analysis with pulmonary MDRO infection risk in ICU patients as the dependent variable showed that age ≥60 years,indwelling catheter,hypoproteinemia,and disturbance of consciousness were risk factors for pulmonary MDRO infection in ICU patients,while chlorine dioxide disinfection was a protective factor.Based on these risk factors and regression coefficients,the original warning model was established as:logit(P 1)=0.856 × age+0.928 × indwelling catheter+0.916 × chlorine dioxide disinfection+0.866× hypoproteinemia+0.986 × disturbance of consciousness-4.371.The Hosmer-Lemeshow test indicated good model fit(coefficient of de-termination R2=0.579,P=0.531).The decision tree model for pulmonary MDRO infection risk in ICU pa-tients constructed using decision tree algorithm comprised 4 layers and 9 nodes,selecting four clinical features as nodes:presence of consciousness disturbance,indwelling catheter,hypoproteinemia,and age≥60 years,with consciousness disturbance being the most significant predictor.The decision tree model showed an area under the curve(AUC)of 0.892(95％CI:0.835-0.949)on receiver operating characteristic(ROC)analy-sis,compared to 0.862(95％CI:0.812-0.912)for the logistic regression model.Delong test revealed no sig-nificant difference in predictive performance between the two models(Z=1.148,P=0.095).Conclusion Both the decision tree model and logistic regression model established for predicting the risk of pulmonary MDRO infection in ICU patients demonstrate high predictive performance with comparable efficacy.

Objective By observing and measuring the relevant data of the buccal branch of the facial nerve,the parotid duct and the facial artery,the positional relationship among the three was analyzed to avoid accidental injury to the buccal branch of the facial nerve and the parotid duct when ligaturing the facial artery during the operation.Methods Forty adult head and neck specimens were dissected to observe the relationship between the buccal branch of the facial nerve and the parotid duct,the course and positional relationship of the facial artery,and the relationship between the buccal branch of the facial nerve and the peripheral vascular network.The relevant diameters were measured with a vernier caliper.Results The buccal branch of the facial nerve was divided into the superior buccal branch and the inferior buccal branch,and there was no direct anastomosis or connecting fiber between the buccal branch of the facial nerve and the parotid duct.The superior buccal branch was relatively thick,and it has a relatively constant position,which was parallel to the parotid duct.The position of the inferior buccal branch was not constant and it ran on or slightly above the plane of angulus oris.The superior buccal branch was located(10.76±5.54)mm from the parotid duct,while the inferior buccal branch was positioned(6.84±4.06)mm away from the parotid duct.The course of the main trunk of the facial artery was relatively fixed.Moreover,if the branch of the facial artery was missing,other branches of the facial artery would extend to replace the missing branch artery.The main trunk of the facial artery had a diameter of(2.34±0.83)mm,and its branches formed anastomoses with the buccal branch of the maxillary artery,creating a vascular network in the parotid and buccal regions.There was a vascular network around the buccal branch of the facial nerve,which was mostly small branches of the facial artery and the superficial temporal artery.Conclusion The buccal branch of the facial nerve exhibits a consistent anatomic relationship with the parotid duct and the facial artery.During the ligation of the facial artery,the parotid duct can serve as a landmark to accurately locate the buccal branch of the facial nerve,thereby significantly reducing the risk of inadvertent injury to the buccal branch of the facial nerve and the parotid duct.

OBJECTIVE: Huachansu injection (HCSI), a promising anti-cancer Chinese medicine injection, has been reported to have the potential for reducing the toxicity of chemotherapy and improving the quality of life for colorectal cancer (CRC) patients. The objective of this study is to explore the synergistic and detoxifying effects of HCSI when used in combination with irinotecan (CPT-11). METHODS: To investigate the effect of HCSI on anti-CRC efficacy and intestinal toxicity of CPT-11, we measured changes in the biological behavior of LoVo cells in vitro, and anti-tumor effects in LoVo cell xenograft nude mice models in vivo. Meanwhile, the effect of HCSI on intestinal toxicity and the uridine diphosphate-glucuronosyltransferase 1A1 (UGT1A1) expression was investigated in the CPT-11-induced colitis mouse model. Subsequently, we measured the effect of HCSI and its 13 constituent bufadienolides on the expression of UGT1A1 and organic anion transporting polypeptides 1B3 (OATP1B3) in HepG2 cells. RESULTS: The combination index (CI) results showed that the combination of HCSI and CPT-11 exhibited a synergistic effect (CI < 1), which significantly suppressing the LoVo cell migration, enhancing G2/M and S phase arrest, and inhibiting tumor growth in vivo. Additionally, the damage to intestinal tissues was attenuated by HCSI in CPT-11-induced colitis model, while the increased expression of UGT1A1 in HepG2 cells and in mouse was observed. CONCLUSION The co-therapy with HCSI alleviated the intestinal toxicity induced by CPT-11 and exerted an enhanced anti-CRC effect. The detoxifying mechanism may be related to the increased expression of UGT1A1 and OATP1B3 by HCSI and its bufadienolides components. The findings of this study may serve as a theoretical insights and strategies to improve CRC patient outcomes. Please cite this article as: Jiang B, Meng ZY, Hu YJ, Chen JJ, Zong L, Xu LY, Zhang XQ, Zhang JX, Han YL. Huachansu injection enhances anti-colorectal cancer efficacy of irinotecan and alleviates its induced intestinal toxicity through upregulating UGT1A1-OATP1B3 expression in vitro and in vivo. J Integr Med. 2025; 23(5):576-590.
Irinotecan/therapeutic use* ; Animals ; Glucuronosyltransferase/genetics* ; Humans ; Colorectal Neoplasms/metabolism* ; Drugs, Chinese Herbal/therapeutic use* ; Mice, Nude ; Mice ; Up-Regulation/drug effects* ; Male ; Xenograft Model Antitumor Assays ; Mice, Inbred BALB C ; Hep G2 Cells ; Cell Line, Tumor ; Intestines/drug effects* ; Amphibian Venoms

ObjectiveTo investigate the protective effect and mechanism of verbenalin on mouse mononuclear macrophage leukemia cells （RAW264.7） damaged by human coronavirus （HCoV）-229E infection， thereby providing experimental evidence for its development and application. MethodsRAW264.7 macrophages were infected with different concentrations of HCoV-229E to establish a coronavirus-induced macrophage injury model using the cell counting kit-8 （CCK-8） assay for assessing cell proliferation and viability. Cells were randomly divided into four groups： normal control， verbenalin group （125 μmol·L^-1）， model group （HCoV-229E）， and HCoV-229E + verbenalin group （HCoV-229E + 125 μmol·L^-1 verbenalin）. Cell viability was measured using the CCK-8 assay， and the maximum non-toxic concentration （CC₀）， half-maximal cytotoxic concentration （CC₅₀）， half-maximal effective concentration （EC₅₀）， and selectivity index （SI） of verbenalin were calculated. Calcein/PI double staining was used to assess cell viability and cytotoxicity， and JC-1 staining was applied to evaluate changes in mitochondrial membrane potential （MMP）. mito-Keima adenovirus labeling was used to assess mitophagy levels in each group. ResultsA macrophage infection model was successfully established by infecting RAW264.7 cells with the original concentration of HCoV-229E for 36 h. The CC₀ of verbenalin was 125 μmol·L^-1. The CC₅₀ was 448.25 μmol·L^-1. The EC₅₀ against HCoV-229E-infected cells was 46.28 μmol·L^-1， and the SI was 9.68. Compared with the normal group， the model group showed significantly reduced cell survival rate （P<0.01）， increased cell death rate （P<0.01）， decreased MMP （P<0.01）， and suppressed mitophagy （P<0.01）. In contrast， verbenalin treatment significantly improved cell survival rate （P<0.01）， reduced cell death rate （P<0.01）， alleviated MMP loss （P<0.01）， and enhanced mitophagy levels （P<0.01） compared with the model group. ConclusionVerbenalin can enhance the survival rate of macrophages following HCoV-229E infection. The underlying mechanism may be associated with the activation of mitophagy， maintenance of MMP stability， and alleviation of mitochondrial damage.

ObjectiveTo investigate the protective effect and mechanism of verbenalin on mouse mononuclear macrophage leukemia cells （RAW264.7） damaged by human coronavirus （HCoV）-229E infection， thereby providing experimental evidence for its development and application. MethodsRAW264.7 macrophages were infected with different concentrations of HCoV-229E to establish a coronavirus-induced macrophage injury model using the cell counting kit-8 （CCK-8） assay for assessing cell proliferation and viability. Cells were randomly divided into four groups： normal control， verbenalin group （125 μmol·L^-1）， model group （HCoV-229E）， and HCoV-229E + verbenalin group （HCoV-229E + 125 μmol·L^-1 verbenalin）. Cell viability was measured using the CCK-8 assay， and the maximum non-toxic concentration （CC₀）， half-maximal cytotoxic concentration （CC₅₀）， half-maximal effective concentration （EC₅₀）， and selectivity index （SI） of verbenalin were calculated. Calcein/PI double staining was used to assess cell viability and cytotoxicity， and JC-1 staining was applied to evaluate changes in mitochondrial membrane potential （MMP）. mito-Keima adenovirus labeling was used to assess mitophagy levels in each group. ResultsA macrophage infection model was successfully established by infecting RAW264.7 cells with the original concentration of HCoV-229E for 36 h. The CC₀ of verbenalin was 125 μmol·L^-1. The CC₅₀ was 448.25 μmol·L^-1. The EC₅₀ against HCoV-229E-infected cells was 46.28 μmol·L^-1， and the SI was 9.68. Compared with the normal group， the model group showed significantly reduced cell survival rate （P<0.01）， increased cell death rate （P<0.01）， decreased MMP （P<0.01）， and suppressed mitophagy （P<0.01）. In contrast， verbenalin treatment significantly improved cell survival rate （P<0.01）， reduced cell death rate （P<0.01）， alleviated MMP loss （P<0.01）， and enhanced mitophagy levels （P<0.01） compared with the model group. ConclusionVerbenalin can enhance the survival rate of macrophages following HCoV-229E infection. The underlying mechanism may be associated with the activation of mitophagy， maintenance of MMP stability， and alleviation of mitochondrial damage.

AIM: To investigate the genetic association and potential causal relationship between diabetic nephropathy(DN)and diabetic retinopathy(DR), and to elucidate their shared molecular mechanisms through differential gene expression analysis and Mendelian randomization(MR).METHODS: Transcriptomic data of DN and DR were obtained from the Gene Expression Omnibus(GEO)database and analyzed for differentially expressed genes(DEGs). Genes meeting the significance threshold(log2FC>1, P<0.05)were identified, followed by Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathway enrichment analysis to explore shared biological pathways. Using genome-wide association study(GWAS)summary statistics for DN and DR, two-sample MR analysis was performed, with DN as the exposure and DR as the outcome. The causal effect was primarily estimated with the inverse-variance weighted(IVW)method, and sensitivity analyses were conducted to assess robustness.RESULTS: MR analysis revealed that DN significantly increased the risk of DR. IVW estimates indicated that the odds ratio(OR)for non-proliferative DR(NPDR)was 3.23(95% CI: 2.12-4.95, P<0.001), and the OR for proliferative DR(PDR)was 1.10(95% CI: 1.06-1.15, P<0.001). DEG analysis identified several key genes, including FN1, COL1A2, and THBS2. FN1 and COL1A2 are involved in extracellular matrix remodeling and fibrosis, contributing to vascular permeability alterations and microvascular damage in diabetic complications. THBS2 is closely associated with angiogenesis and vascular homeostasis, suggesting its potential role in DR. KEGG enrichment analysis showed that these DEGs were mainly enriched in advanced glycation end products(AGEs)-RAGE signaling, extracellular matrix degradation, and oxidative stress pathways, all of which are highly relevant to the pathogenesis of DN and DR.CONCLUSION: This study demonstrates the genetic association between DN and DR using MR and DEGs analyses. The shared mechanisms, particularly involving extracellular matrix remodeling, inflammatory response, and angiogenesis, may serve as novel therapeutic targets and provide a theoretical basis for the early diagnosis and targeted treatment of diabetic complications.

ObjectiveTo evaluate the pharmacological effects of verbenalin on both in vitro and in vivo infection models of human coronavirus 229E （HCoV-229E） and to preliminarily explore the antiviral mechanism of verbenalin through proteomic analysis. MethodsIn vitro， the cell counting kit-8 （CCK-8） for cell proliferation and viability assessment was used to establish a model of HCoV-229E-induced injury in human lung adenocarcinoma cells（A549）. A549 cells were divided into five groups： normal group， model group， and three verbenalin treatment groups （125， 62.5， and 31.25 μmol·L^-1）. The cell protective activity of verbenalin was evaluated through cell viability assay and immunofluorescence staining. In vivo， 30 BALB/c mice were randomly divided into normal group， model group， chloroquine group， and high-dose， low-dose verbenalin groups （40 and 20 mg·kg^-1）， with six mice per group. An HCoV-229E-induced mouse lung injury model was established to evaluate the therapeutic effects of verbenalin. Lung injury was assessed by detecting the lung index and lung inhibition rate. The severity of pulmonary inflammation cytokines was measured by enzyme-linked immunosorbent assay （ELISA）， while the lung morphology and structure were analyzed by micro-computed tomography （Micro-CT）. Hematoxylin and eosin （HE） staining was used to assess histopathological changes in lung tissue. Additionally， four-dimensional data-independent acquisition （4D-DIA） proteomics was employed to preliminarily explore the potential mechanisms of verbenalin in treating HCoV-229E-induced lung injury in mice， through differential protein expression screening， functional annotation， enrichment analysis， and protein-protein interaction network analysis. ResultsThe A549 cells were infected with HCoV-229E at the original viral titer for 36 hours to establish an in vitro infection model. The maximum non-toxic concentration of verbenalin was 125 μmol·L^-1， and the half-maximal cytotoxic concentration （CC₅₀） was 288.8 μmol·L^-1. Compared with the normal group， the model group showed a significant decrease in cell viability （P<0.01）， a significant increase in the proportion of dead cells （P<0.01）， mitochondrial damage， and a significant reduction in mitochondrial membrane potential （P<0.01）. After treatment with different concentrations of verbenalin （125， 62.5， and 31.25 μmol·L^-1）， cell viability was significantly increased （P<0.01）， and the proportion of dead cells was reduced （P<0.01）， with mitochondrial membrane potential restored （P<0.01）. In vivo experiments further confirmed the therapeutic effect of verbenalin on HCoV-229E-infected mice. Compared to the normal group， the model group showed a significant increase in the lung index （P<0.01）， severe lung tissue injury， lung volume enlargement， and a significant increase in the expression of inflammatory cytokines， including interleukin-6 （IL-6） and tumor necrosis factor-α （TNF-α） （P<0.01）. In contrast， in the verbenalin treatment groups， these pathological changes were significantly improved， with a reduction in the lung index （P<0.01）， alleviation of lung tissue injury， reduced lung volume enlargement， and a significant decrease in inflammatory cytokine expression （P<0.01）. Proteomics analysis revealed that， compared to the normal group， the model group showed enrichment in several antiviral immune-related signaling pathways， including the nuclear factor-κB （NF-κB） signaling pathway （P<0.05）. Compared to the model group， the verbenalin treatment group showed enrichment in several signaling pathways related to inflammatory response and autophagy （P<0.05）， suggesting that verbenalin may exert its antiviral and anti-inflammatory effects by regulating these pathways. ConclusionVerbenalin demonstrates significant therapeutic effects in both in vitro and in vivo HCoV-229E infection models， with its mechanism likely related to the NOD-like receptor protein 3 （NLRP3） inflammasome pathway and mitochondrial autophagy.

At present, the cause of traditional Chinese medicine(TCM) in China has entered a new period of high-quality development. How to strengthen the foundation for the TCM industry from the source is an important issue that deserves the attention of the authorities, industry, and academia. This study systematically analyzed the regulatory system of TCM raw materials and preparations. The study took the TCM industry chain and the product life cycle as a clue and focused on the dimensions of TCM resource protection and plant cultivation(farming), production and quality supervision of TCM raw materials and preparations, and their market access and distribution. It analyzed the current situation of the regulation of TCM raw materials and preparations under the regulatory system of drugs, discussed the main problems, and put forward corresponding suggestions. The results can provide an important reference value for the subsequent improvement of the regulatory system of drugs and the construction of a prominent regulatory system of drugs in accordance with TCM characteristics.
Drugs, Chinese Herbal/economics* ; Medicine, Chinese Traditional/standards* ; China ; Quality Control ; Humans ; Plants, Medicinal/chemistry*