ObjectiveThis paper aims to investigate the material basis of the anti-inflammatory efficacy and mechanism of action of Bushen Tongdu prescription （BSTDP）. MethodsThe chemical components of BSTDP and its blood-absorbed components in vivo were systematically identified by using ultra-performance liquid chromatography-linear ion trap-electrostatic field orbitrap high-resolution mass spectrometry （UPLC-LIT-Orbitrap-MS）. Network pharmacology was employed to screen blood-absorbed bioactive components and potential targets of this formula. A protein-protein interaction （PPI） network of core targets was constructed to conduct enrichment analysis. Molecular docking was further utilized to verify the binding affinity between key components and targets. The inflammatory model was established and verified in vivo by using a transgenic zebrafish Tg （mpx： GFP）. At three days post-fertilization （3 dpf）， larvae of zebrafish were randomly assigned to blank group， model group， positive drug dexamethasone acetate group （75 μmol·L^-1）， and BSTDP groups with low， medium， and high doses （500， 1 000， and 2 000 mg·L^-1）. The distribution and quantity of neutrophils in the yolk sac region were observed under a fluorescence microscope. The mRNA expression levels of key genes in the toll-like receptor 4 （TLR4）/myeloid differentiation factor 88 （MyD88）/nuclear factor kappa-B （NF-κB） signaling pathway and inflammatory factors including interleukin （IL）-1β， IL-6， and tumor necrosis factor-α （TNF-α） were detected by Real-time quantitative polymerase chain reaction （Real-time PCR）. ResultsA total of 120 chemical components were identified in BSTDP， among which 26 original components were confirmed by using serum pharmacochemical methods. A total of 227 common targets linking rheumatoid arthritis （RA） and the blood-absorbed components were screened by network pharmacology. It is suggested that pseudobrucine， vomicine， sinapine， rehmannioside， cinnamyl alcohol glycoside， and methylephedrine exert anti-inflammatory effects by acting on core targets including protein kinase B1 （Akt1）， signal transducer and activator of transcription 3 （STAT3）， tumor necrosis factor （TNF）， TLR4， mitogen-activated protein kinase 14 （MAPK14）， and phosphatidylinositol-4，5-bisphosphate 3-kinase catalytic subunit α （PIK3CA）， thereby modulating multiple signaling pathways such as TLR4 and NF-κB. In vivo verification in zebrafish demonstrates that the maximum tolerable concentration of Bushen Tongdu Formula is 2 000 mg·L^-1. Compared to those in the blank group， zebrafish in the model group showed a significantly higher number of neutrophils in the yolk sac region （P<0.01） and rising mRNA levels of TLR4， MyD88， NF-κB， TNF-α， IL-6， and IL-1β （P<0.01）. Compared to that in the model group， the number of neutrophils was significantly reduced in BSTDP groups with medium and high doses， as well as the dexamethasone acetate group （P<0.05， P<0.01）. There was no statistically significant difference in the low dose group. The mRNA expression levels of TLR4， MyD88， NF-κB， TNF-α， IL-6， and IL-1β were significantly down-regulated （P<0.05， P<0.01）. ConclusionThis paper identifies the material basis of the efficacy of BSTDP， demonstrating that the formula can exert an anti-inflammatory effect through the TLR4/MyD88/NF-κB signaling pathway. The results provide scientific experimental evidence for its further clinical application.

ObjectiveThis paper aims to investigate the material basis of the anti-inflammatory efficacy and mechanism of action of Bushen Tongdu prescription （BSTDP）. MethodsThe chemical components of BSTDP and its blood-absorbed components in vivo were systematically identified by using ultra-performance liquid chromatography-linear ion trap-electrostatic field orbitrap high-resolution mass spectrometry （UPLC-LIT-Orbitrap-MS）. Network pharmacology was employed to screen blood-absorbed bioactive components and potential targets of this formula. A protein-protein interaction （PPI） network of core targets was constructed to conduct enrichment analysis. Molecular docking was further utilized to verify the binding affinity between key components and targets. The inflammatory model was established and verified in vivo by using a transgenic zebrafish Tg （mpx： GFP）. At three days post-fertilization （3 dpf）， larvae of zebrafish were randomly assigned to blank group， model group， positive drug dexamethasone acetate group （75 μmol·L^-1）， and BSTDP groups with low， medium， and high doses （500， 1 000， and 2 000 mg·L^-1）. The distribution and quantity of neutrophils in the yolk sac region were observed under a fluorescence microscope. The mRNA expression levels of key genes in the toll-like receptor 4 （TLR4）/myeloid differentiation factor 88 （MyD88）/nuclear factor kappa-B （NF-κB） signaling pathway and inflammatory factors including interleukin （IL）-1β， IL-6， and tumor necrosis factor-α （TNF-α） were detected by Real-time quantitative polymerase chain reaction （Real-time PCR）. ResultsA total of 120 chemical components were identified in BSTDP， among which 26 original components were confirmed by using serum pharmacochemical methods. A total of 227 common targets linking rheumatoid arthritis （RA） and the blood-absorbed components were screened by network pharmacology. It is suggested that pseudobrucine， vomicine， sinapine， rehmannioside， cinnamyl alcohol glycoside， and methylephedrine exert anti-inflammatory effects by acting on core targets including protein kinase B1 （Akt1）， signal transducer and activator of transcription 3 （STAT3）， tumor necrosis factor （TNF）， TLR4， mitogen-activated protein kinase 14 （MAPK14）， and phosphatidylinositol-4，5-bisphosphate 3-kinase catalytic subunit α （PIK3CA）， thereby modulating multiple signaling pathways such as TLR4 and NF-κB. In vivo verification in zebrafish demonstrates that the maximum tolerable concentration of Bushen Tongdu Formula is 2 000 mg·L^-1. Compared to those in the blank group， zebrafish in the model group showed a significantly higher number of neutrophils in the yolk sac region （P<0.01） and rising mRNA levels of TLR4， MyD88， NF-κB， TNF-α， IL-6， and IL-1β （P<0.01）. Compared to that in the model group， the number of neutrophils was significantly reduced in BSTDP groups with medium and high doses， as well as the dexamethasone acetate group （P<0.05， P<0.01）. There was no statistically significant difference in the low dose group. The mRNA expression levels of TLR4， MyD88， NF-κB， TNF-α， IL-6， and IL-1β were significantly down-regulated （P<0.05， P<0.01）. ConclusionThis paper identifies the material basis of the efficacy of BSTDP， demonstrating that the formula can exert an anti-inflammatory effect through the TLR4/MyD88/NF-κB signaling pathway. The results provide scientific experimental evidence for its further clinical application.

ObjectiveTo construct a standardized diagnostic scale for Qi-Yin deficiency with blood stasis syndrome in diabetic macrovascular disease. MethodsLiterature related to Qi-Yin deficiency with blood stasis syndrome in diabetic macrovascular disease was retrieved from CNKI， VIP， and Wanfang databases. Diagnostic information from four diagnostic methods was extracted and standardized， with items having a frequency of ≥15 included in the item pool. A three-round Delphi expert consultation was conducted， screening items using support degree， mean score， rank sum， and coefficient of variation. Item weights were determined using analytic hierarchy process （AHP）， gactor analysis （FA）， and combined weighting method （CWM）. The optimal weighting method was selected by comparing the area under the receiver operating characteristic （ROC） curve （AUC）. The Youden index was calculated to establish the diagnostic cutoff value， which was proportionally scaled. ResultsA total of 102 studies were included. Thirty-five items were incorporated into the item pool. The authority coefficients for the three Delphi rounds were 0.82， 0.85， and 0.86， with coordination coefficients of 0.648， 0.538， and 0.506， respectively. Fifteen items were retained after screening. ROC curve analysis showed the AUC ranking as FA > CWM > AHP. The maximum Youden index was 0.814， corresponding to a diagnostic cutoff of 8.361 （scaled to 40 points）. The final scale adopted a structured diagnostic framework： the symptom dimension requires at least 2 items， and the tongue or pulse dimension requires at least 1 category. ConclusionThis study developed a standardized diagnostic scale for Qi-Yin deficiency with blood stasis syndrome in diabetic macrovascular disease. Core items were screened via the Delphi method， with factor analysis identified as the optimal weighting method through AUC comparison. The diagnostic threshold （40 points） and structured diagnostic framework provide a quantitatively clear， clinically practical tool.

According to traditional Chinese medicine （TCM） theory， impaired spleen transportation function disrupts nutrient distribution， causing metabolic accumulation of lipids that transform into pathogenic phlegm-dampness. These pathological factors disseminate through the San Jiao and obstruct meridian pathways， ultimately forming the pathogenesis described as "all disorders involve phlegm". Phlegm and dampness share common pathogenic origins but manifest distinct clinical manifestations. Dampness， as the precursor， may congeal into phlegm， while existing phlegm accumulation can further exacerbate dampness stagnation， thereby establishing a self-perpetuating pathological cycle. Modern medical research has confirmed that the essence of "phlegm-dampness" syndrome is closely associated with energy metabolism disorders， serving as a common pathological basis for metabolic syndrome， type 2 diabetes mellitus， atherosclerosis， and other major chronic diseases. As a crucial vehicle for medical experimental research， disease-syndrome combination animal models serve as an indispensable means to advance the modernization of TCM. Currently， based on classical theories such as "rich and greasy foods produce phlegm" and "physical coldness combined with cold consumption causes external pathogens to invade the skin and hair， thereby generating internal dampness"， researchers primarily employ two paradigms to construct animal models of phlegm-turbidity， dampness obstruction， and phlegm-dampness syndromes： the first involves simulating TCM etiological factors （through methods like dietary irregularities， imblanace between work and rest， and combined internal-external dampness exposure）， while the second combines disease with syndrome differentiation （inducing pathological changes through physical， chemical， or biological interventions）. Through comprehensive evaluation incorporating macroscopic observation and microscopic index detection， model animals undergo systematic biological and pathological assessment， with further syndrome type verification achieved via the "prescription-based syndrome detection" approach. However， existing models still exhibit significant deficiencies in both the standardization of modeling methodologies and the systematization of evaluation criteria. This paper reviews the strategies for constructing "phlegm-dampness" syndrome animal models and their corresponding evaluation indices， focusing on the pathological correlations among different modeling approaches. The aim is to provide methodological guidance for research on TCM syndromes related to "phlegm-dampness" syndrome and to support the development of TCM therapies for resolving phlegm and eliminating dampness. This study not only contributes to advancing the standardization of TCM syndrome research but also provides crucial technical support for the modernization of TCM.

OBJECTIVE To investigate the mechanism by which Shenfukang capsule （SFK） ameliorates renal interstitial fibrosis （RIF） by regulating macrophage-fibroblast crosstalk via the signal transducer and activator of transcription 3 （STAT3）/Yes-associated protein （YAP） pathway. METHODS RAW264.7 macrophages were induced to polarize with transforming growth factor-β 1 （TGF-β 1 ）. Subsequently， a non-contact co-culture system of macrophages with renal fibroblasts NRK-49F， as well as a non-contact co-culture system of macrophages with YAP-knockdown renal fibroblasts， were established. Cells were treated with low， medium， and high concentrations （4， 8， 16 μg/mL） of SFK， as well as a STAT3 inhibitor （STAT3-I，1.64 μg/mL） and losartan potassium tablets （positive control， 0.28 μg/mL）， for 48 h. After intervention， the protein and mRNA expression levels of CD86， CD163， and STAT3 in macrophages， as well as CD86， F4/80， and STAT3 mRNA， were detected. In co-cultured renal fibroblasts， the protein and mRNA expression levels of α -smooth muscle actin （ α -SMA）， Vimentin， collagen type Ⅰ （Col-Ⅰ）， matrix metalloproteinase-1 （MMP-1）， and YAP were detected. In co-cultured YAP-knockdown renal fibroblasts， the protein and mRNA expression levels of α -SMA， Vimentin， and MMP-1 were also detected. RESULTS Following TGF-β 1 induction， the protein expression levels of CD86， CD163， and STAT3， as well as the mRNA expression levels of CD86， F4/80， and STAT3 in macrophages were significantly increased （ P ＜0.05）. The conditioned medium from polarized macrophages activated renal fibroblasts， as evidenced by significantly increased protein and mRNA expression levels of α -SMA， Vimentin， Col-Ⅰ， and YAP， and significantly decreased protein and mRNA expression levels of MMP-1 in renal fibroblasts （ P ＜0.05）. Treatment with SFK and STAT3-I reversed the changes in the above indicators， with the medium concentration SFK group showing stronge r effects on some indicators than the low and high concentration groups. In the non-contact co-culture experiment of macrophages and YAP-knockdown renal fibroblasts， there were no statistically significant differences in the protein and mRNA expression of α-SMA， Vimentin， and MMP-1 among the groups. CONCLUSIONS SFK can inhibit macrophage-renal fibroblast crosstalk by blocking the STAT3/YAP pathway， thereby delaying the progression of RIF.

OBJECTIVE To explore the influencing factors of Shenfukang capsule in the treatment of chronic kidney disease （CKD） and construct a nomogram prediction model for evaluating its therapeutic efficacy. METHODS CKD patients who were hospitalized from July 2019 to August 2022 in the First Affiliated Hospital of Guangxi Medical University and treated with Shenfukang capsule were selected as study subjects. Clinical data of the patients were collected from the hospital’s electronic medical record system， and they were divided into an effective group and an ineffective group based on treatment outcomes. Lasso-Logistic multivariate regression analysis was used to screen the influencing factors of the efficacy of Shenfukang capsule. Using the effectiveness of Shenfukang capsule treatment as the prediction outcome and the screened influencing factors as predictor variables， a nomogram prediction model was constructed using R software. All patients were randomly divided into a training cohort and a validation cohort. The discriminative ability， calibration， and clinical net benefit of the model were evaluated using the receiver operating characteristic （ROC） curve， calibration curve， and decision curve analysis， respectively. RESULTS Lasso-Logistic regression analysis revealed that concurrent diabetes mellitus， decreased levels of blood urea nitrogen， triglycerides， and serum phosphorus， as well as prolonged prothrombin time and elevated apolipoprotein AⅠ levels， were influencing factors for reduced efficacy of Shenfukang capsule in CKD treatment. The evaluation results of the nomogram prediction model showed that the area under curve values were 0.745 and 0.797 in the training and validation cohorts， respectively， which were close and both exceeded 0.70， indicating stable predictive performance. The calibration curves demonstrated good agreement in both datasets， suggesting satisfactory calibration performance. The clinical decision curves were positioned above the two extreme reference lines， indicating high clinical benefit of the model. CONCLUSIONS Diabetes mellitus， blood urea nitrogen， triglycerides， apolipoprotein AⅠ， serum phosphorus， and prothrombin time were factors associated with the efficacy of Shenfukang capsule in CKD patients. The nomogram prediction model established in this study may provide a basis for rational clinical application of Shenfukang capsule and for improving its therapeutic efficacy in CKD.

OBJECTIVE To explore the influencing factors of Shenfukang capsule in the treatment of chronic kidney disease （CKD） and construct a nomogram prediction model for evaluating its therapeutic efficacy. METHODS CKD patients who were hospitalized from July 2019 to August 2022 in the First Affiliated Hospital of Guangxi Medical University and treated with Shenfukang capsule were selected as study subjects. Clinical data of the patients were collected from the hospital’s electronic medical record system， and they were divided into an effective group and an ineffective group based on treatment outcomes. Lasso-Logistic multivariate regression analysis was used to screen the influencing factors of the efficacy of Shenfukang capsule. Using the effectiveness of Shenfukang capsule treatment as the prediction outcome and the screened influencing factors as predictor variables， a nomogram prediction model was constructed using R software. All patients were randomly divided into a training cohort and a validation cohort. The discriminative ability， calibration， and clinical net benefit of the model were evaluated using the receiver operating characteristic （ROC） curve， calibration curve， and decision curve analysis， respectively. RESULTS Lasso-Logistic regression analysis revealed that concurrent diabetes mellitus， decreased levels of blood urea nitrogen， triglycerides， and serum phosphorus， as well as prolonged prothrombin time and elevated apolipoprotein AⅠ levels， were influencing factors for reduced efficacy of Shenfukang capsule in CKD treatment. The evaluation results of the nomogram prediction model showed that the area under curve values were 0.745 and 0.797 in the training and validation cohorts， respectively， which were close and both exceeded 0.70， indicating stable predictive performance. The calibration curves demonstrated good agreement in both datasets， suggesting satisfactory calibration performance. The clinical decision curves were positioned above the two extreme reference lines， indicating high clinical benefit of the model. CONCLUSIONS Diabetes mellitus， blood urea nitrogen， triglycerides， apolipoprotein AⅠ， serum phosphorus， and prothrombin time were factors associated with the efficacy of Shenfukang capsule in CKD patients. The nomogram prediction model established in this study may provide a basis for rational clinical application of Shenfukang capsule and for improving its therapeutic efficacy in CKD.

This paper summarizes the perioperative nursing experience of a premature infant with congenital gastroschisis accompanied by malaria and heart disease during a medical aid mission in Africa.Nursing key points include:preoperative observation and protection of the protruding intestines to prevent intestinal injury and infection,timely identification and management of arrhythmias and acute hypoxic episodes;intraoperative close monitoring of vital signs and assisting the surgeon in creating an"artificial abdominal cavity";postoperative intensification of condition monitoring and intra-abdominal pressure surveillance,standardized medication administration and rational blood transfusion to prevent complications related to gastroschisis repair,and to control malaria-related symptoms,while providing nutritional support and reinforcing health education.Through collaborative diagnosis and treatment by a multidisciplinary team along with meticulous nursing care,the infant showed improvement and was discharged after 2 weeks.A follow-up visit 2 months postoperatively revealed normal feeding,good surgical wound healing,no recurrence of acute hypoxic episodes,and a persistent systolic murmur auscultated over the precordium.

BACKGROUND:The imbalance between proliferation and apoptosis of chondrocytes plays an important role in the occurrence and development of osteoarthritis. Previous studies have found that hsa-miR-3202 is involved in regulating the proliferation and apoptosis of various cells. However,no studies have explored the correlation between hsa-miR-3202 and osteoarthritis.OBJECTIVE:To investigate the expression of hsa-miR-3202 in osteoarthritic chondrocytes and its effect on the proliferation and apoptosis of chondrocytes. METHODS:(1) MicroRNAs differentially expressed in osteoarthritic chondrocytes were screened by biogenic analysis. Based on the current research situation at home and abroad,hsa-miR-3202 was selected for follow-up studies,and its target genes were predicted by gene ontology (GO) functional enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment. (2) Human normal chondrocyte cell lines C28/I2 in logarithmic growth phase were selected and randomly divided into four groups for culture:in normal group,cells were cultured in normal medium for 24 hours,the medium was then changed to normal medium for another 6 hours of culture,and changed to normal medium for subsequent culture;in lipopolysaccharide group,cells were cultured in lipopolysaccharide-containing medium for 24 hours,the medium was then changed to normal medium for another 6 hours,and changed to normal medium for subsequent culture;in lipopolysaccharide+NC group,cells were cultured in lipopolysaccharide-containing medium for 24 hours,and then transfected with has-miR-3202 mimics control for 6 hours,and the medium was change to normal medium for subsequent culture;in lipopolysaccharide+hsa-miR-3202 mimics group,cells were cultured in lipopolysaccharide-containing medium for 24 hours and then transfected with has-miR-3202 mimics for 6 hours,and the medium was changed to normal medium for subsequent culture. After further 48 hours of culture,the expression level of hsa-miR-3202 was detected by fluorescence quantitative PCR and cell apoptosis was detected by flow cytometry. After further culture of 0-72 hours,cell proliferation activity was detected by cell counting kit-8. RESULTS AND CONCLUSION:Bioinformatics analysis results indicated that hsa-miR-3202 was significantly down-regulated in osteoarthritic chondrocytes. GO functional enrichment and KEGG pathway enrichment showed that the function of hsa-miR-3202 target gene was closely related to cell growth and apoptosis. The results of in vitro cell experiments showed that compared with the normal group,the expression level of hsa-miR-3202 and proliferation ability of chondrocytes were significantly decreased in the lipopolysaccharide group (P<0.05),while the apoptotic rate was significantly increased (P<0.05). Compared with the lipopolysaccharide group,the expression level of hsa-miR-3202 and proliferation ability of chondrocytes were significantly increased in the lipopolysaccharide+hsa-miR-3202 mimics group (P<0.05),while the apoptotic rate was significantly decreased (P<0.05). To conclude,the expression of hsa-miR-3202 is down-regulated in osteoarthritic chondrocytes to inhibit cell proliferation and promote cell apoptosis,thus affecting the occurrence and development of osteoarthritis.

This paper summarizes the perioperative nursing experience of a premature infant with congenital gastroschisis accompanied by malaria and heart disease during a medical aid mission in Africa.Nursing key points include:preoperative observation and protection of the protruding intestines to prevent intestinal injury and infection,timely identification and management of arrhythmias and acute hypoxic episodes;intraoperative close monitoring of vital signs and assisting the surgeon in creating an"artificial abdominal cavity";postoperative intensification of condition monitoring and intra-abdominal pressure surveillance,standardized medication administration and rational blood transfusion to prevent complications related to gastroschisis repair,and to control malaria-related symptoms,while providing nutritional support and reinforcing health education.Through collaborative diagnosis and treatment by a multidisciplinary team along with meticulous nursing care,the infant showed improvement and was discharged after 2 weeks.A follow-up visit 2 months postoperatively revealed normal feeding,good surgical wound healing,no recurrence of acute hypoxic episodes,and a persistent systolic murmur auscultated over the precordium.