Objective: To prepare the erythrocyte-liposome drug delivery system to enhance the therapeutic effect of drugs on tumors and inhibit tumor metastasis. Methods: This study prepared and characterized paclitaxel (PTX)-plerixafor (AMD3100) liposomes (Lips), developed the erythrocyte-liposome drug delivery system, and evaluated its targeting efficiency and therapeutic efficacy through a series of in vitro cellular and in vivo animal experiments. Results: The particle size of PTX-AMD-Lips was (186.4±0.83) nm. Drug encapsulation efficiency of PTX-AMD-Lips was (75.50±5.27)% for PTX and (88.31±2.45)% for AMD. The Binding efficiency between RBC and liposomes in the drug delivery system was (69.93±2.55)%. Vitro cellular experiments revealed that PTX-AMD-Lips significantly inhibited tumor cell migration. In vivo animal experiments, the erythrocyte-liposome drug delivery system significantly increased drug accumulation in the lungs. At the experimental endpoint, the quantitative fluorescence signal of tumor size measured (4.04±0.44)×10 for the PTX-Lips group, and (5.14±3.40)×10 for the RBC-PTX-AMD-Lips group. Conclusion: The erythrocyte-liposome drug delivery system could enhance the lung-specific targeting capability of liposomes, kill tumor cells and suppress further metastasis effectively.

Objective: To construct a risk prediction model for pediatric metabolic dysfunction associated steatotic liver disease (MASLD), so as to provide practical tool for the early identification of high risk children. Methods: A healthy cohort of children in Southwest China was established from January 2021 to April 2025. A nested case-control study design was used to include 507 cases MASLD group and 507 cases in non MASLD group. Data on physical measurements, blood biochemical parameters, and liver ultrasound indicators were collected. Conditional Logistic regression was used to analyze the relationship between individual variables and MASLD, Lasso regression was applied for multivariable screening, and a high risk prediction model was constructed and presented in the form of a nomogram. Internal validation was performed using 10 repeated ten fold cross validations to assess model discrimination, accuracy, sensitivity, and specificity. Results: Logistic regression analysis showed that MASLD was associated with central obesity ( OR=22.11, 95%CI =15.62-31.29), apolipoprotein B ( OR=30.24, 95%CI =12.42-73.63), increased hepatorenal echo ( OR=326.00, 95%CI =183.87-578.01), hepatomegaly ( OR=24.98, 95%CI =16.66-37.46) (all P <0.05). The Lasso regression jointly selected 6 key variables, including hepatorenal echo, central obesity, hepatomegaly, right liver lobe inclination, body mass index, and alanine amino transferase. The results of cross validation showed that the average area under the curve (AUC) was 0.999 5, the average accuracy was 98.74%, and the sensitivity and specificity were 98.21% and 99.22% respectively, indicating a good predictive effect of the model. Conclusion The risk prediction model for high risk MASLD among children based on ultrasound and clinical indicators has good prediction effect, which is helpful for the early identification and risk stratification of pediatric MASLD.

Objective To enhance the gamma spectrometry analysis and detection capabilities of personnel in measuring radionuclides in bio-ash, and ensure the accuracy and precision of gamma spectrometer in our laboratory for the analysis of radionuclides in bio-ash. Methods The laboratory participated in the 2024 national interlaboratory comparison for radionuclide measurement in bio-ash. Radionuclides ²⁴¹Am, ¹³⁷Cs, and ⁴⁰K in four different bio-ash samples were measured. Based on the measurement methods specified in GB/T 16145—2022, sample measurement, result calculation, and uncertainty evaluation were performed using spectrometry analysis software and sourceless efficiency calibration software. The measurement results and performance evaluation of the laboratory in the comparison were analyzed, and factors affecting gamma-spectrometry measurement and result interpretation were discussed. Results The relative deviation (D) of the measurement results for radionuclides ²⁴¹Am and ¹³⁷Cs in the four bio-ash samples ranged from −10.2% to 2.0% and −1.7% to 0.3%, respectively. The P statistic ranged from 7.0% to 12.5% and 5.0% to 10.8%, respectively. These results met the criteria of |D| ≤ 20% (MARB), |D| ≤ 2.58P, and P ≤ 20% (MARB). The ζ-scores for the measurement of ⁴⁰K in the four bio-ash samples ranged from 0.8 to 1.3, satisfying the criterion of |ζ| < 2. All measurement results in this laboratory in the comparison were satisfactory. Conclusion The laboratory uses a high-purity germanium gamma spectrometer to measure radionuclides in bio-ash. The self-absorption correction method, analysis method, and uncertainty evaluation are appropriate, which can ensure the accuracy and precision of the measurement results. The measurement results are accurate and reliable.

ObjectiveTo investigate the expression patterns of key steroidogenic enzymes （CYP11A1， HSD3B1， and CYP19A1） in placental tissues from preeclampsia （PE） patients and evaluate​ their potential as biomarkers for PE. MethodsA case-control study was conducted using placental tissues from PE patients （PE group， n=3） and normotensive pregnant women （control group， n=3）. RNA sequencing was performed to identify differentially expressed genes （DEGs）， followed by validation of target gene expression using Western blot， qRT-PCR， and immunohistochemistry. Steroid hormone levels in placental tissues and serum were measured by ELISA. Spearman correlation analysis was used to assess associations between protein expression and clinical parameters， and receiver operating characteristic （ROC） curve analysis was performed to evaluate the predictive value of target genes for PE. ResultsThe results showed that 501 DEGs （P<0.05 and |Log₂Fold Change| >1） were identified in PE placental tissues， with KEGG enrichment analysis revealing significant involvement in steroid hormone biosynthesis pathways. Compared with the control group， PE placental tissues exhibited significantly decreased protein and mRNA expression of HSD3B1 and CYP19A1 （P<0.01）， while CYP11A1 expression was upregulated （P<0.05）. Serum estradiol （E2） and progesterone （P4） levels were significantly reduced in the PE group （P<0.01）， whereas testosterone （T） levels were elevated （P<0.05）. Correlation analysis demonstrated that CYP11A1 expression was positively associated with systolic blood pressure （SBP）， diastolic blood pressure （DBP）， and soluble fms-like tyrosine kinase-1 （sFlt-1） （P<0.01）， but negatively correlated with placental growth factor （PLGF） （P<0.01）. Conversely， HSD3B1 and CYP19A1 expression showed inverse correlations with these clinical parameters （P<0.01）. ROC analysis revealed that CYP11A1， HSD3B1， and CYP19A1 each had an area under the curve （AUC） of 0.778 for predicting PE， with 95%CI ranging from 0.614 to 0.942 （P=0.004）. The sensitivity was 94.4%， and the specificity was 66.7%. ConclusionThese findings suggest that dysregulated expression of steroidogenic enzymes in PE placental tissues contributes to hormonal imbalance， thereby playing a role in PE pathogenesis. Furthermore， CYP11A1， HSD3B1， and CYP19A1 may serve as potential diagnostic biomarkers for PE.

ObjectiveTo investigate the mechanism by which Luoshi Neiyi prescription treats endometriosis （EMs） through the Toll-like receptor 4 （TLR4）/nuclear factor-κB （NF-κB） signaling pathway. MethodsAnimal experiments were conducted with 50 female SD rats， which were randomized into a sham operation group （10 rats） and a modeling group （40 rats）. An autologous endometrial transplantation method was used for the modeling of EMs. The 36 successfully modeled rats were randomly allocated into four groups （n=9 each）： The model group， the low-dose （7.87 g·kg^-1） Luoshi Neiyi prescription group， the high-dose （15.74 g·kg^-1） Luoshi Neiyi prescription group， and the dienogest （0.20 mg·kg^-1） group. The physiological status and ectopic lesion volumes of rats in each group were observed. Hematoxylin-eosin （HE） staining was used to observe the morphology of the eutopic endometrial tissue. Enzyme-linked immunosorbent assay （ELISA） was employed to measure the levels of inflammatory factors including interleukin-1β （IL-1β） and prostaglandin E₂ （PGE₂） in the serum of EMs rats. Immunohistochemistry was used to detect the expression of matrix metalloproteinase-9 （MMP-9） and vascular endothelial growth factor A （VEGFA） in the eutopic endometrial tissue. Western blot was adopted to determine the protein levels of TLR4， myeloid differentiation factor 88 （MyD88）， phosphorylated nuclear factor-κB （p-NF-κB）/NF-κB， MMP-9， and VEGFA in the eutopic endometrial tissue. In the cell experiments， the cell-counting kit-8 （CCK-8） assay was employed to screen the optimal concentration of Luoshi Neiyi prescription-containing serum， and a scratch assay was performed to assess the migration ability of iheESCs cells. Interventions with Luoshi Neiyi prescription-containing serum， resatorvid （TAK-242， a TLR4 inhibitor）， and lipopolysaccharides （LPS， a TLR4 agonist） were conducted， and Western blot was used to detect the expression of proteins related to the TLR4/NF-κB signaling pathway. ResultsThis experiment successfully replicated 36 EMs rat models. Compared with the sham operation group， the model group exhibited visible ectopic lesions on the abdominal wall and an increase in the writhing response score （P<0.01）. Furthermore， HE staining revealed the model group exhibited a thickened eutopic epithelium， stromal cell disarrangement， and evident infiltration of inflammatory cells. In addition， the model group showed elevated serum levels of IL-1β and PGE₂ （P<0.05， P<0.01）， increased positive expression of MMP-9 and VEGFA in the ectopic endometrial tissue （P<0.01）， and up-regulated protein levels of TLR4， MyD88， p-NF-κB/NF-κB， MMP-9， and VEGFA in the ectopic endometrial tissue （P<0.05， P<0.01）. Compared with the model group， all treatment groups exhibited a reduction in the ectopic lesion volume （P<0.01）. Furthermore， the writhing response scores were decreased in the high-dose Luoshi Neiyi prescription group and the dienogest group （P<0.05， P<0.01）. The pathological state of the ectopic endometrial tissue was alleviated to varying degrees in the treatment groups. Low-dose Luoshi Neiyi prescription reduced serum PGE₂ levels， and high-dose Luoshi Neiyi prescription and dienogest decreased serum IL-1β and PGE₂ levels in EMs rats （P<0.05， P<0.01）. The treatment groups showed decreased positive expression of MMP-9 and VEGFA in the ectopic endometrial tissue （P<0.05， P<0.01） and down-regulated protein levels of TLR4， MyD88， p-NF-κB/NF-κB， MMP-9， and VEGFA in the ectopic endometrial tissue （P<0.05， P<0.01）. The cell experiments showed that 5%， 10%， and 20% Luoshi Neiyi prescription-containing sera significantly reduced the viability and inhibited the migration of iheESCs. Compared with the control group， 5%， 10%， and 20% Luoshi Neiyi prescription-containing serum groups and the TAK-242 group showed reduced protein levels of TLR4， MyD88， p-NF-κB/NF-κB， MMP-9， and VEGFA （P<0.01）. Compared with the control group， the LPS group showed increased expression of the above proteins （P<0.01）. Compared with the LPS group， the LPS+5%， 10%， and 20% Luoshi Neiyi prescription-containing serum groups showed reduced expression of the above proteins （P<0.05， P<0.01）. ConclusionLuoshi Neiyi prescription may modulate the TLR4/NF-κB signaling pathway to reduce the inflammatory response and histopathological damage in the eutopic endometrium and suppress the adhesive， invasive， and angiogenic biological processes in the ectopic endometrial tissue， thereby exerting its therapeutic effect on EMs.

ObjectiveTo investigate the effects and potential mechanisms of Babaodan （BBD） against acetaminophen （APAP）-induced acute liver injury （ALI） based on transcriptomics. MethodsA total of 36 male C57BL/6 mice were randomly divided into 6 groups （n=6 per group）： normal group， model group， N-acetylcysteine group （NAC， 120 mg·kg^-1）， and BBD low-， medium-， and high-dose groups （BBD-L， BBD-M， BBD-H groups， 75， 150， 300 mg·kg^-1， respectively）. Except for the normal group， all other groups were subjected to APAP-induced ALI. The serum levels of aspartate aminotransferase （AST）， alanine aminotransferase （ALT）， total cholesterol （TC）， triglyceride （TG）， and low-density lipoprotein cholesterol （LDL-C） were measured in each group. Hepatic levels or activities of malondialdehyde （MDA） and glutathione peroxidase （GSH-Px） were detected using commercial kits. Hematoxylin-eosin （HE） staining was performed to evaluate the degree of liver histopathological damage. Transcriptomic analysis was employed to screen differentially expressed genes （DEGs）， and Kyoto Encyclopedia of Genes and Genomes （KEGG） pathway enrichment analysis was performed to identify differential pathways involved in BBD intervention against ALI. Real-time quantitative polymerase chain reaction （Real-time PCR） and Western blot were applied to validate the expression of differential genes and related pathway proteins. Additionally， glucose （GLU） consumption， as well as lactate （LD） and adenosine triphosphate （ATP） content were assessed across all mouse groups. ResultsPharmacodynamic evaluation showed that， compared with the normal group， the model group exhibited significantly elevated serum levels of ALT， AST， TC， TG， and LDL-C （P<0.01）， significantly increased MDA level （P<0.01）， and significantly decreased GSH-Px level （P<0.05）. Compared with the model group， BBD intervention at different doses significantly reduced the serum levels of ALT， AST， TC， TG， and LDL-C （P<0.05， P<0.01）， increased GSH-Px level （P<0.05， P<0.01）， significantly decreased MDA level （P<0.01）， and ameliorated hepatic histopathological injury. Liver transcriptomic analysis revealed that， following high-dose BBD intervention， the core genes were mainly enriched in pathways related to inflammatory responses and energy metabolic reprogramming， including the interleukin-17 （IL-17） signaling pathway， the phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt） signaling pathway， fructose and mannose metabolism， and glycolysis. Real-time PCR validation demonstrated that， compared with the normal group， the mRNA expression levels of glycolysis-related genes ［hexokinase 1 （HK1）， hexokinase 2 （HK2）， 6-phosphofructo-2-kinase/fructose-2，6-bisphosphatase 3 （PFKFB3）， 6-phosphofructo-2-kinase/fructose-2，6-bisphosphatase 4 （PFKFB4）， pyruvate kinase M （PKM）， and lactate dehydrogenase A （LDHA）］， as well as inflammatory cytokines ［tumor necrosis factor-α （TNF-α）， interleukin-6 （IL-6）， and interleukin-1β （IL-1β）］ were significantly upregulated in the model group （P<0.05， P<0.01）. Compared with the model group， the BBD-H group showed significantly decreased mRNA expression of HK1， HK2， PFKFB3， PFKFB4， PKM， LDHA， TNF-α， IL-6， and IL-1β （P<0.05， P<0.01）. Western blot results indicated that， compared with the normal group， the model group had significantly increased expression of glycolysis-related proteins ［glucose transporter 1 （GLUT1）， HK1， PFKFB3， and PKM］， inflammatory proteins ［interleukin-18 （IL-18）， TNF-α， and IL-1β］， and phosphorylated （p）-PI3K and p-Akt proteins （P<0.05， P<0.01）. Compared with the model group， the BBD-H group exhibited significantly decreased expression of GLUT1， HK1， PFKFB3， PKM， IL-18， TNF-α， IL-1β， p-PI3K， and p-Akt （P<0.05， P<0.01）. Metabolic indicator measurements showed that， compared with the model group， the BBD-H group showed significantly reduced GLU consumption， LD and ATP content （P<0.05， P<0.01）. ConclusionBBD may alleviate APAP-induced ALI through dual regulation of metabolic reprogramming and inflammatory responses， potentially via inhibition of the PI3K/Akt signaling pathway.

ObjectiveTo investigate the effects and potential mechanisms of Babaodan （BBD） against acetaminophen （APAP）-induced acute liver injury （ALI） based on transcriptomics. MethodsA total of 36 male C57BL/6 mice were randomly divided into 6 groups （n=6 per group）： normal group， model group， N-acetylcysteine group （NAC， 120 mg·kg^-1）， and BBD low-， medium-， and high-dose groups （BBD-L， BBD-M， BBD-H groups， 75， 150， 300 mg·kg^-1， respectively）. Except for the normal group， all other groups were subjected to APAP-induced ALI. The serum levels of aspartate aminotransferase （AST）， alanine aminotransferase （ALT）， total cholesterol （TC）， triglyceride （TG）， and low-density lipoprotein cholesterol （LDL-C） were measured in each group. Hepatic levels or activities of malondialdehyde （MDA） and glutathione peroxidase （GSH-Px） were detected using commercial kits. Hematoxylin-eosin （HE） staining was performed to evaluate the degree of liver histopathological damage. Transcriptomic analysis was employed to screen differentially expressed genes （DEGs）， and Kyoto Encyclopedia of Genes and Genomes （KEGG） pathway enrichment analysis was performed to identify differential pathways involved in BBD intervention against ALI. Real-time quantitative polymerase chain reaction （Real-time PCR） and Western blot were applied to validate the expression of differential genes and related pathway proteins. Additionally， glucose （GLU） consumption， as well as lactate （LD） and adenosine triphosphate （ATP） content were assessed across all mouse groups. ResultsPharmacodynamic evaluation showed that， compared with the normal group， the model group exhibited significantly elevated serum levels of ALT， AST， TC， TG， and LDL-C （P<0.01）， significantly increased MDA level （P<0.01）， and significantly decreased GSH-Px level （P<0.05）. Compared with the model group， BBD intervention at different doses significantly reduced the serum levels of ALT， AST， TC， TG， and LDL-C （P<0.05， P<0.01）， increased GSH-Px level （P<0.05， P<0.01）， significantly decreased MDA level （P<0.01）， and ameliorated hepatic histopathological injury. Liver transcriptomic analysis revealed that， following high-dose BBD intervention， the core genes were mainly enriched in pathways related to inflammatory responses and energy metabolic reprogramming， including the interleukin-17 （IL-17） signaling pathway， the phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt） signaling pathway， fructose and mannose metabolism， and glycolysis. Real-time PCR validation demonstrated that， compared with the normal group， the mRNA expression levels of glycolysis-related genes ［hexokinase 1 （HK1）， hexokinase 2 （HK2）， 6-phosphofructo-2-kinase/fructose-2，6-bisphosphatase 3 （PFKFB3）， 6-phosphofructo-2-kinase/fructose-2，6-bisphosphatase 4 （PFKFB4）， pyruvate kinase M （PKM）， and lactate dehydrogenase A （LDHA）］， as well as inflammatory cytokines ［tumor necrosis factor-α （TNF-α）， interleukin-6 （IL-6）， and interleukin-1β （IL-1β）］ were significantly upregulated in the model group （P<0.05， P<0.01）. Compared with the model group， the BBD-H group showed significantly decreased mRNA expression of HK1， HK2， PFKFB3， PFKFB4， PKM， LDHA， TNF-α， IL-6， and IL-1β （P<0.05， P<0.01）. Western blot results indicated that， compared with the normal group， the model group had significantly increased expression of glycolysis-related proteins ［glucose transporter 1 （GLUT1）， HK1， PFKFB3， and PKM］， inflammatory proteins ［interleukin-18 （IL-18）， TNF-α， and IL-1β］， and phosphorylated （p）-PI3K and p-Akt proteins （P<0.05， P<0.01）. Compared with the model group， the BBD-H group exhibited significantly decreased expression of GLUT1， HK1， PFKFB3， PKM， IL-18， TNF-α， IL-1β， p-PI3K， and p-Akt （P<0.05， P<0.01）. Metabolic indicator measurements showed that， compared with the model group， the BBD-H group showed significantly reduced GLU consumption， LD and ATP content （P<0.05， P<0.01）. ConclusionBBD may alleviate APAP-induced ALI through dual regulation of metabolic reprogramming and inflammatory responses， potentially via inhibition of the PI3K/Akt signaling pathway.

ObjectivePhotoacoustic pump-probe imaging can effectively eliminate the interference of blood background signal in traditional photoacoustic imaging, and realize the imaging of weak phosphorescence molecules and their triplet lifetimes in deep tissues. However, background differential noise in photoacoustic pump-probe imaging often leads to large fitting results of phosphorescent molecule concentration and triplet lifetime. Therefore, this paper proposes a novel triplet lifetime fitting method for photoacoustic pump-probe imaging. By extracting the phase of the triplet differential signal and the background noise, the fitting bias caused by the background noise can be effectively corrected. MethodsThe advantages and feasibility of the proposed algorithm are verified by numerical simulation, phantom and in vivo experiments, respectively. ResultsIn the numerical simulation, under the condition of noise intensity being 10% of the signal amplitude, the new method can optimize the fitting deviation from 48.5% to about 5%, and has a higher exclusion coefficient (0.88>0.79), which greatly improves the fitting accuracy. The high specificity imaging ability of photoacoustic pump imaging for phosphorescent molecules has been demonstrated by phantom experiments. In vivo experiments have verified the feasibility of the new fitting method proposed in this paper for fitting phosphoometric lifetime to monitor oxygen partial pressure content during photodynamic therapy of tumors in nude mice. ConclusionThis work will play an important role in promoting the application of photoacoustic pump-probe imaging in biomedicine.

Objective:To investigate the mechanism of ursolic acid (UA) in inhibiting the growth and metastasis of breast cancer MDA-MB-231 (“231”) cells by downregulating ANXA6.Methods:This study conducted relevant in vitro cytology and molecular biology experiments in the Department of Clinical Laboratory and Central Laboratory of Putuo Hospital, Shanghai University of Traditional Chinese Medicine from February 2023 to August 2024. Human breast cancer 231 cells were cultured in vitro, and the effects of different concentrations of UA on the proliferation and invasion and metastasis of 231 cells were detected by CCK-8 and Transwell assays. Western Blot was used to detect the effect of UA on the expression of ANXA6 and invasion and metastasis-related proteins MMP9, β-catenin and N-cadherin in 231 cells. The 231 cells that interfered with and overexpressed ANXA6 were constructed by lentivirus transfection to generate stable ANXA6 interfering and overexpressing 231 cells, which were divided into 231/KD-ANXA6 group, 231/KD-NC group, 231/OE-ANXA6 group, and 231/OE-NC group. CCK-8 assay and Transwell assay were used to detect the proliferation activity, invasion and metastasis ability of 231 cells after interference and overexpression of ANXA6 and the effect of UA on the proliferation ability of 231 cells after interference and overexpression of ANXA6. Western Blot and RT-PCR assays were used to detect the expression of invasion and migration biomarkers such as MMP9, β-catenin, and N-cadherin in 231 cells after interference and overexpression of ANXA6. Immunohistochemistry was used to detect the expression level of ANXA6 in breast cancer tissues, and the relationship between ANXA6 expression and clinicopathological features and prognosis of breast cancer was analyzed.Results:The CCK-8 assay results showed that compared with the control group (0 μmol/L UA, 100.00%±7.37%), the proliferative activity of 231 cells at UA concentrations of 2.5, 5, 10, 20 and 40 μmol/L (90.23%±1.76%, t=2.24, P<0.05; 85.19%±4.23%, t=3.02, P<0.05; 65.45%±0.35%, t=8.11, P<0.01; 37.79%±0.98%, t=14.50, P<0.001; 18.18%±0.15%, t=19.23, P<0.001) were significantly decreased. Furthermore, UA (10, 15, 20 μmol/L) inhibited the invasion and metastasis ability of 231 cells; Western Blot assay showed that compared with the control group (0 μmol/L UA), the protein expressions of MMP9 (1.07±0.03 vs 0.99±0.11, t=1.27, P>0.05), β-catenin (1.21±0.01 vs 0.99±0.07, t=5.47, P<0.05), N-cadherin (1.05±0.09 vs 0.90±0.03, t=2.65, P>0.05) at UA of 10 μmol/L; MMP9 (1.07±0.03 vs 0.79±0.09, t=5.26, P<0.001), β-catenin (1.21±0.01 vs 0.89±0.05, t=10.55, P<0.001), and N-cadherin (1.04±0.09 vs 0.68±0.10, t=4.59, P<0.05) at UA of 15 μmol/L; MMP9 (1.07±0.03 vs 0.52±0.07, t=12.50, P<0.001), β-catenin (1.21±0.01 vs 0.83±0.02, t=24.01, P<0.000 1) and N-cadherin (1.04±0.09 vs 0.49±0.11, t=6.70, P<0.01) at UA of 20 μmol/L. Interfering with ANXA6 inhibits the proliferation, invasion and migration of 231 cells, and overexpression of ANXA6 promotes the proliferation, invasion and migration of 231 cells. Western Blot assay showed that compared with the control group (KD-NC group), the protein expressions of MMP9 (1.07±0.01 vs 0.62±0.16, t=4.86, P<0.01), β-catenin (1.02±0.14 vs 0.64±0.15, t=3.20, P<0.05), N-cadherin (0.98±0.14 vs 0.67±0.12, t=2.85, P<0.05) were decreased expression; Compared with the control group (OE-NC group), the protein expressions of MMP9 (0.54±0.22 vs 1.06±0.08, t=3.90, P<0.05), β-catenin (0.92±0.07 vs 1.06±0.04, t=3.06, P<0.05) and N-cadherin (0.90±0.07 vs 1.06±0.01, t=3.75, P<0.05) were significantly increased. Interference with ANXA6 promoted the inhibitory effect of UA on the proliferation ability of 231 cells ( P<0.05). Overexpression of ANXA6 weakened the inhibitory effect of UA on the proliferation of 231 cells ( P<0.05).The results of immunohistochemistry assay showed that the expression level of ANXA6 in breast cancer tissue was significantly increased, and the expression of ANXA6 was related to tumor size ( P<0.05), but not to age, T stage, N stage, pathological grade, AJCC stage, ER, PR and E-cad. Conclusion:The expression level of ANXA6 in breast cancer tissues is increased, and UA can inhibit the growth, invasion and metastasis of 231 cells by down-regulating the expression of ANXA6.

Objective:To explore the effect of recombinant human brain natriuretic peptide(rhBNP)combined with dopamine on cystatin C(CysC),homocysteine(Hcy)and cardiac function in patients with severe heart failure(HF).Methods:This randomized controlled study enrolled 110 severe HF patients admitted in Aerospace Center Hospital between December 2021 and December 2022.They were divided into control group(n=55,nitroglycerin combined dopamine)and combined treatment group(n=55,rhBNP combined dopamine).Each group received corresponding therapy based on basic treatment for one week.Therapeutic effect,levels of CysC,Hcy,left ventric-ular end-systolic diameter(LVESd),left ventricular end-diastolic diameter(LVEDd),left ventricular ejection fraction(LVEF),and incidence of adverse reactions were compared between two groups.Results:Compared with patients in control group,those in combined treatment group had significant higher total effective rate(81.82％vs.58.18％)and LVEF[(54.68±4.59)％vs.(44.79±4.37)％],and significant lower CysC[(1.02±0.19)mg/L vs.(1.40±0.21)mg/L],Hcy[(15.98±2.17)μmol/L vs.(21.05±2.82)μmol/L],LVESd[(35.13±3.51)mm vs.(41.71±3.28)mm]and LVEDd[(41.33±4.26)mm vs.(50.51±4.37)mm](P＜0.01 all).There was no significant difference in total incidence of adverse reactions between two groups(16.36％vs.7.27％,P=0.180).Conclusion:rhBNP combined with dopamine could significantly improve the clinical therapeutic effect,im-prove levels of CysC,Hcy and cardiac function with good safety in the treatment of severe HF.