Objective To develop a CT radiomics-based prediction model for prognosis of pancreatic ductal adenocarcinoma(PDAC)in order to provide evidence for individualized treatment decisions.Methods A retrospective study was carried on 118 PDAC patients admitted in the First Affiliated Hospital of Army Medical University between January 2020 and December 2023.They were assigned into a training group(n=83)and a validation group(n=35)at a 7∶3 ratio.ITK-SNAP software was used to perform 3-D segmentation on the preoperatively enhanced arterial phase CT images,and radiomic features were extracted using pyradiomics.High-reproducibility features were selected through ICC analysis(>0.85),and core features were determined using LASSO regression to construct the Rad-score.Cox regression analysis was employed to develop both a radiomics model and a model integrating radiomic and clinical features for predicting overall survival in PDAC patients.Receiver operating characteristic(ROC)curves and calibration curves were plotted to evaluate the prognostic models for survival prediction.Results From 1 453 extracted radiomic features,7 core features were finally selected to construct the Rad-score.The radiomics prediction model based on the Rad-score achieved an AUC value of 0.796(95%CI:0.702～0.890)and 0.744(95%CI:0.589～0.899)for 1-year survival prediction in the training and validation groups,respectively.The integrated model combining 2 types of features together demonstrated improved performance with an AUC value of 0.906(95%CI:0.842～0.970)and 0.872(95%CI:0.753～0.992)in the 2 groups.Calibration curve analysis indicated good prediction accuracy for both models.Conclusion Both the CT radiomics-based model and the integrated model incorporating clinical features demonstrate good predictive performance for survival outcomes.

Objective:To investigate the regulatory effect of leptin via the JAK2/STAT3 pathway on the core-binding factor β-subunit (CBFβ) and its molecular mechanism in promoting chondrocyte apoptosis.Methods:A total of five patients undergoing total knee arthroplasty due to knee osteoarthritis (OA group) and five patients undergoing amputation due to trauma (amputation group) were enrolled, and knee cartilage samples were obtained intraoperatively. Western blotting was used to detect the protein expression levels of leptin, CBFβ, matrix metalloproteinase-1 (MMP1), and MMP13. Flow cytometry was performed to determine the optimal treatment duration and concentration of leptin. Chondrocytes were divided into the following groups based on treatment conditions: control group (untreated chondrocytes), leptin group (chondrocytes treated with 50 ng/ml leptin), negative leptin group (chondrocytes transfected with a non-targeting sequence as a control), and leptin+shCBFβ group (chondrocytes transfected with shCBFβ to inhibit CBFβ expression). Apoptosis and the expression levels of MMP1 and MMP13 were analyzed in the four groups. Additionally, chondrocytes were categorized into the following groups for further analysis: control group (untreated cells), leptin group (cells stimulated with 50 ng/ml leptin for 48 h), AG490 group (cells treated with the JAK2/STAT3 inhibitor AG490), and leptin+AG490 group (cells pretreated with AG490 for 2 h followed by 50 ng/ml leptin stimulation for 48 h). The protein expression levels of CBFβ, MMP1, and MMP13, as well as the apoptosis rate, were examined in the four groups.Results:The relative expression levels of leptin, CBFβ, MMP1, and MMP13 in the amputation group were 0.66±0.06, 0.69±0.06, 0.74±0.05, and 0.41±0.03, respectively, which were significantly lower than those in the OA group (1.04±0.10, 1.06±0.09, 0.95±0.04, and 0.99±0.09, respectively) ( P<0.05). The optimal treatment duration and concentration of leptin were determined to be 48 h and 50 ng/ml, respectively. The expression levels of MMP1 and MMP13 significantly differed among the control, leptin, negative leptin, and leptin+shCBFβ groups ( P<0.05). Specifically, the leptin group showed higher expression levels compared to the control group, while the leptin+shCBFβ group exhibited lower expression levels than the leptin group ( P<0.05). The apoptosis rates of chondrocytes in the four groups were 4.55%±1.30%, 22.52%±2.03%, 22.03%±2.01%, and 5.15%±0.91%, respectively, with significant differences ( F=114.066, P<0.001). The apoptosis rate in the leptin group was significantly higher than that in the control group, while the leptin+shCBFβ group exhibited a significantly lower apoptosis rate than the leptin group ( P<0.05). Similarly, significant differences were observed in the expression levels of CBFβ, MMP1, and MMP13 among the control, leptin, AG490, and leptin+AG490 groups ( P<0.05). The expression levels in the leptin group were higher than those in the control group, while the leptin+AG490 group exhibited lower expression levels compared to the leptin group ( P<0.05). The apoptosis rates of chondrocytes in the control, leptin, AG490, and leptin+AG490 groups were 5.19±0.94%, 31.52±2.63%, 5.51±1.41%, and 10.47±0.85%, respectively, with significant differences ( F=117.104, P<0.001). The apoptosis rate in the leptin group was significantly higher than that in the control group, while the leptin+AG490 group exhibited a significantly lower apoptosis rate than the leptin group ( P<0.05). Conclusion:Leptin promotes CBFβ expression via the JAK2/STAT3 pathway, leading to chondrocyte apoptosis and extracellular matrix degradation.

Objective:To investigate the effect of β-Ecdysterone (β-Ecd), an active ingredient in cow′s knee, on hormonal femoral head necrosis in young rabbits and explore the mechanism involved.Methods:An animal study.Sixty New Zealand young rabbits were divided into control, model and intervention groups by random number table method, with 20 rabbits in each group.Prednisolone acetate (7.5 mg/kg) was injected bilaterally into the gluteal muscle of rabbits in both model and intervention groups twice a week.β-Ecd (0.5 mg/kg) was injected subcutaneously at the time of the first injection of Prednisolone acetate in the intervention group for 5 times a week.An equal amount of saline was injected into rabbits in control and model groups.Eight weeks after modelling, animals were put to death, and femoral heads were taken from both sides for gross observation.Micro computed tomography(Micro-CT) was used to analyze the microstructure of bone trabeculae and to measure bone microstructural parameters.Histological staining was used to detect changes in the morphology of bone tissues.Immunohistochemistry and Western blot were used to examine the expression of osteogenic and lipogenic factors and proteins in the femoral head tissue.Rabbit bone marrow mesenchymal stem cells (BMSCs) were divided into a blank control group, a Dexamethasone group and a β-Ecd intervention group.Cell damage was induced by Dexamethasone in Dexamethasone group and β-Ecd intervention group, and the β-Ecd intervention group was given the optimal concentration of β-Ecd.Western blot was used to detect the expression of osteogenic and lipogenic proteins in the cells of each group.Real-time quantitative polymerase chain reaction (RT-qPCR) was used to determine the mRNA expression of osteogenic and lipogenic marker genes.Results:After excluding 9 rabbits that died during the experimental period, 51 rabbits were finally included in the study, with 19 in the control group, 15 in the model group and 17 in the intervention group.Gross observation and Micro-CT showed that compared with that of the control group, the femoral head of the model group was obscure and greyish, with dark red necrotic areas.The bone trabeculae of the model group were sparse, thinned, disordered, and partially fractured, compared with those of the control group.The changes in the femoral head and bone trabeculae of the intervention group were between those of control and model groups.The bone mineral density, the number, thickness and relative volume of bone trabeculae significantly decreased and trabecular separation significantly increased in both model and intervention groups, compared with those in the control group ( F=12.78, 45.52, 32.74, 64.08, 8.83, all P<0.05).However, these symptoms in the intervention group were better than those in the model group.Pathological histology showed that in the control group, bone trabeculae were neatly arranged, robust and full, with a high number of osteoclasts and occasional empty bone sockets.In the model group, bone trabeculae were sparsely arranged and broken, with fewer osteoclasts, and the number of empty bone sockets increased and enlarged.In the intervention group, bone trabeculae had a more complete morphology, with fewer necrotic osteoclasts and reduced empty bone sockets, compared with the model group.Immunohistochemistry results showed that compared with the control group, the model group and intervention group had increased content of fatty acid binding proteins (FABP) and CCAAT/enhancer binding proteins α (CEBP) in the femoral head bone tissue, and decreased content of osteopontin (OPN) and Runt-related transcription factor 2 (RUNX2) .The changes in each index were greater in the model group than those in the intervention group ( F=21.07, 24.06, 17.92, 21.36, all P<0.05). Western blot detection showed that compared with the control group, the CEBP protein expression content of the femoral head in the model group and the intervention group was increased and the RUNX2 protein expression content was decreased. The changes of CEBP and RUNX2 were greater in the model group than those in the intervention group( F=73.43, 197.87, all P<0.05).Western blot detection of BMSCs showed that compared with the blank control group, the Dexamethasone group and β-Ecd intervention group had decreased expression of OPN and RUNX2 proteins and increased expression of FABP and CEBP proteins ( F=161.61, 358.01, 91.18, 69.04, all P<0.05).The changes in each index in the β-Ecd intervention group were smaller than those in the Dexamethasone group.RT-qPCR detection of BMSCs showed that in the Dexamethasone group had lower expression of OPN and RUNX2 and higher expression of CEBP and FABP than the blank control group ( F=19.71, 45.08, 61.46, 15.12, all P<0.05).The changes in each index in the β-Ecd intervention group were smaller than those in the Dexamethasone group. Conclusions:β-Ecd can attenuate the pathological changes of hormonal femoral head necrosis in young rabbits by promoting osteogenic differentiation of BMSCs, inhibiting lipogenic differentiation of BMSCs, and improving bone microstructure.

Objective:To investigate the effect of β-Ecdysterone (β-Ecd), an active ingredient in cow′s knee, on hormonal femoral head necrosis in young rabbits and explore the mechanism involved.Methods:An animal study.Sixty New Zealand young rabbits were divided into control, model and intervention groups by random number table method, with 20 rabbits in each group.Prednisolone acetate (7.5 mg/kg) was injected bilaterally into the gluteal muscle of rabbits in both model and intervention groups twice a week.β-Ecd (0.5 mg/kg) was injected subcutaneously at the time of the first injection of Prednisolone acetate in the intervention group for 5 times a week.An equal amount of saline was injected into rabbits in control and model groups.Eight weeks after modelling, animals were put to death, and femoral heads were taken from both sides for gross observation.Micro computed tomography(Micro-CT) was used to analyze the microstructure of bone trabeculae and to measure bone microstructural parameters.Histological staining was used to detect changes in the morphology of bone tissues.Immunohistochemistry and Western blot were used to examine the expression of osteogenic and lipogenic factors and proteins in the femoral head tissue.Rabbit bone marrow mesenchymal stem cells (BMSCs) were divided into a blank control group, a Dexamethasone group and a β-Ecd intervention group.Cell damage was induced by Dexamethasone in Dexamethasone group and β-Ecd intervention group, and the β-Ecd intervention group was given the optimal concentration of β-Ecd.Western blot was used to detect the expression of osteogenic and lipogenic proteins in the cells of each group.Real-time quantitative polymerase chain reaction (RT-qPCR) was used to determine the mRNA expression of osteogenic and lipogenic marker genes.Results:After excluding 9 rabbits that died during the experimental period, 51 rabbits were finally included in the study, with 19 in the control group, 15 in the model group and 17 in the intervention group.Gross observation and Micro-CT showed that compared with that of the control group, the femoral head of the model group was obscure and greyish, with dark red necrotic areas.The bone trabeculae of the model group were sparse, thinned, disordered, and partially fractured, compared with those of the control group.The changes in the femoral head and bone trabeculae of the intervention group were between those of control and model groups.The bone mineral density, the number, thickness and relative volume of bone trabeculae significantly decreased and trabecular separation significantly increased in both model and intervention groups, compared with those in the control group ( F=12.78, 45.52, 32.74, 64.08, 8.83, all P<0.05).However, these symptoms in the intervention group were better than those in the model group.Pathological histology showed that in the control group, bone trabeculae were neatly arranged, robust and full, with a high number of osteoclasts and occasional empty bone sockets.In the model group, bone trabeculae were sparsely arranged and broken, with fewer osteoclasts, and the number of empty bone sockets increased and enlarged.In the intervention group, bone trabeculae had a more complete morphology, with fewer necrotic osteoclasts and reduced empty bone sockets, compared with the model group.Immunohistochemistry results showed that compared with the control group, the model group and intervention group had increased content of fatty acid binding proteins (FABP) and CCAAT/enhancer binding proteins α (CEBP) in the femoral head bone tissue, and decreased content of osteopontin (OPN) and Runt-related transcription factor 2 (RUNX2) .The changes in each index were greater in the model group than those in the intervention group ( F=21.07, 24.06, 17.92, 21.36, all P<0.05). Western blot detection showed that compared with the control group, the CEBP protein expression content of the femoral head in the model group and the intervention group was increased and the RUNX2 protein expression content was decreased. The changes of CEBP and RUNX2 were greater in the model group than those in the intervention group( F=73.43, 197.87, all P<0.05).Western blot detection of BMSCs showed that compared with the blank control group, the Dexamethasone group and β-Ecd intervention group had decreased expression of OPN and RUNX2 proteins and increased expression of FABP and CEBP proteins ( F=161.61, 358.01, 91.18, 69.04, all P<0.05).The changes in each index in the β-Ecd intervention group were smaller than those in the Dexamethasone group.RT-qPCR detection of BMSCs showed that in the Dexamethasone group had lower expression of OPN and RUNX2 and higher expression of CEBP and FABP than the blank control group ( F=19.71, 45.08, 61.46, 15.12, all P<0.05).The changes in each index in the β-Ecd intervention group were smaller than those in the Dexamethasone group. Conclusions:β-Ecd can attenuate the pathological changes of hormonal femoral head necrosis in young rabbits by promoting osteogenic differentiation of BMSCs, inhibiting lipogenic differentiation of BMSCs, and improving bone microstructure.

Objective:To investigate the regulatory effect of leptin via the JAK2/STAT3 pathway on the core-binding factor β-subunit (CBFβ) and its molecular mechanism in promoting chondrocyte apoptosis.Methods:A total of five patients undergoing total knee arthroplasty due to knee osteoarthritis (OA group) and five patients undergoing amputation due to trauma (amputation group) were enrolled, and knee cartilage samples were obtained intraoperatively. Western blotting was used to detect the protein expression levels of leptin, CBFβ, matrix metalloproteinase-1 (MMP1), and MMP13. Flow cytometry was performed to determine the optimal treatment duration and concentration of leptin. Chondrocytes were divided into the following groups based on treatment conditions: control group (untreated chondrocytes), leptin group (chondrocytes treated with 50 ng/ml leptin), negative leptin group (chondrocytes transfected with a non-targeting sequence as a control), and leptin+shCBFβ group (chondrocytes transfected with shCBFβ to inhibit CBFβ expression). Apoptosis and the expression levels of MMP1 and MMP13 were analyzed in the four groups. Additionally, chondrocytes were categorized into the following groups for further analysis: control group (untreated cells), leptin group (cells stimulated with 50 ng/ml leptin for 48 h), AG490 group (cells treated with the JAK2/STAT3 inhibitor AG490), and leptin+AG490 group (cells pretreated with AG490 for 2 h followed by 50 ng/ml leptin stimulation for 48 h). The protein expression levels of CBFβ, MMP1, and MMP13, as well as the apoptosis rate, were examined in the four groups.Results:The relative expression levels of leptin, CBFβ, MMP1, and MMP13 in the amputation group were 0.66±0.06, 0.69±0.06, 0.74±0.05, and 0.41±0.03, respectively, which were significantly lower than those in the OA group (1.04±0.10, 1.06±0.09, 0.95±0.04, and 0.99±0.09, respectively) ( P<0.05). The optimal treatment duration and concentration of leptin were determined to be 48 h and 50 ng/ml, respectively. The expression levels of MMP1 and MMP13 significantly differed among the control, leptin, negative leptin, and leptin+shCBFβ groups ( P<0.05). Specifically, the leptin group showed higher expression levels compared to the control group, while the leptin+shCBFβ group exhibited lower expression levels than the leptin group ( P<0.05). The apoptosis rates of chondrocytes in the four groups were 4.55%±1.30%, 22.52%±2.03%, 22.03%±2.01%, and 5.15%±0.91%, respectively, with significant differences ( F=114.066, P<0.001). The apoptosis rate in the leptin group was significantly higher than that in the control group, while the leptin+shCBFβ group exhibited a significantly lower apoptosis rate than the leptin group ( P<0.05). Similarly, significant differences were observed in the expression levels of CBFβ, MMP1, and MMP13 among the control, leptin, AG490, and leptin+AG490 groups ( P<0.05). The expression levels in the leptin group were higher than those in the control group, while the leptin+AG490 group exhibited lower expression levels compared to the leptin group ( P<0.05). The apoptosis rates of chondrocytes in the control, leptin, AG490, and leptin+AG490 groups were 5.19±0.94%, 31.52±2.63%, 5.51±1.41%, and 10.47±0.85%, respectively, with significant differences ( F=117.104, P<0.001). The apoptosis rate in the leptin group was significantly higher than that in the control group, while the leptin+AG490 group exhibited a significantly lower apoptosis rate than the leptin group ( P<0.05). Conclusion:Leptin promotes CBFβ expression via the JAK2/STAT3 pathway, leading to chondrocyte apoptosis and extracellular matrix degradation.

Objective:This study aimed to investigate the regulatory role and mechanism of myosin heavy chain 9 (MYH9) in the invasion of Zika virus (ZIKV) into human glioma cells (U251).Methods:Utilizing CRISPR/Cas9 technology, MYH9-knockout U251 cells (U251-MYH9 KD) were constructed. Following ZIKV infection, the protein expression levels, RNA load, and viral titer of ZIKV were detected through western blot (WB), Real-time fluorescence quantitative polymerase chain reaction (qPCR), and plaque formation assays, respectively. The infection efficiency of ZIKV in U251 cells treated with the MYH9 inhibitor blebbistatin was assessed. The binding and internalization efficiency of ZIKV were measured in U251-MYH9 KD cells. The interaction between MYH9 and the ZIKV envelope protein (E) was studied using co-immunoprecipitation (Co-IP). The effects of soluble MYH9 recombinant protein and anti-human MYH9 antibodies on ZIKV infection were evaluated by qPCR and plaque formation assays. Results:It was found that knockout or inhibition of MYH9 significantly suppressed ZIKV infection in U251 cells. MYH9 knockout notably inhibited the binding and internalization of ZIKV in U251 cells. MYH9 interacted with the ZIKV E protein, and both MYH9 recombinant protein and anti-human MYH9 antibodies, by blocking the binding of ZIKV E protein to cell surface MYH9, inhibited ZIKV infection in U251 cells in a dose-dependent manner.Conclusions:MYH9 facilitates ZIKV invasion into U251 cells through interaction with the ZIKV E protein.

Objective:This study aimed to investigate the regulatory role and mechanism of myosin heavy chain 9 (MYH9) in the invasion of Zika virus (ZIKV) into human glioma cells (U251).Methods:Utilizing CRISPR/Cas9 technology, MYH9-knockout U251 cells (U251-MYH9 KD) were constructed. Following ZIKV infection, the protein expression levels, RNA load, and viral titer of ZIKV were detected through western blot (WB), Real-time fluorescence quantitative polymerase chain reaction (qPCR), and plaque formation assays, respectively. The infection efficiency of ZIKV in U251 cells treated with the MYH9 inhibitor blebbistatin was assessed. The binding and internalization efficiency of ZIKV were measured in U251-MYH9 KD cells. The interaction between MYH9 and the ZIKV envelope protein (E) was studied using co-immunoprecipitation (Co-IP). The effects of soluble MYH9 recombinant protein and anti-human MYH9 antibodies on ZIKV infection were evaluated by qPCR and plaque formation assays. Results:It was found that knockout or inhibition of MYH9 significantly suppressed ZIKV infection in U251 cells. MYH9 knockout notably inhibited the binding and internalization of ZIKV in U251 cells. MYH9 interacted with the ZIKV E protein, and both MYH9 recombinant protein and anti-human MYH9 antibodies, by blocking the binding of ZIKV E protein to cell surface MYH9, inhibited ZIKV infection in U251 cells in a dose-dependent manner.Conclusions:MYH9 facilitates ZIKV invasion into U251 cells through interaction with the ZIKV E protein.

Objective:To study the effects and the related molecular mechanisms of miR-148a-3p on the proliferation,invasion and migration of salivary adenoid cystic carcinoma SACC-LM cells.Methods:miR-148a-3p mimics and inhibitors,siRNA targeting EG-FR and their corresponding controls were transfected into SACC-LM cells.Bioinformatics was used to predict the potential target genes of miR-148a-3p.EGFR and miR-148a-3p mRNA expression levels were examined by qRT-PCR and the protein levels of EG-FR were detected by Western blotting.CCK-8,scratch,and Transwell assays were used to study the proliferation,migration,and invasion of SACC-LM cells,respectively.The direct targeting relationship between miR-148a-3p and EGFR was examined by using the double luciferase reporter gene assay.Statistical analysis of the data was performed by SPSS 22.0 software.Results:Overexpres-sion or inhibition of miR-148a-3p significantly inhibited or promoted the proliferation,invasion and metastasis of SACC-LM cells re-spectively(P＜0.05).Bioinformatics and double luciferase assay showed that miR-148a-3p directly targeted and regulated the expres-sion of EGFR(P＜0.001).Downregulation of EGFR inhibited the proliferation,migration and invasion of SACC-LM cells(P＜0.05)and partially reversed the promoting effect of miR-148a-3p inhibition(P＜0.05).Conclusion:The downregulation of miR-148a-3p leads to the abnormally high expression of its target gene EGFR,and promotes the proliferation,invasion,and migration of salivary adenoid cystic carcinoma cells.

Objective To investigate the clinical value of fiber nasopharyngoscope applied in adenoid hypertrophy(AH)combined with allergic rhinitis(AR)in children.Methods Clinical data of 174 pediatric patients from January 2021 to March 2024 was collected and analyzed.Among them,129 cases were diagnosed with AH via fiber nasopharyngoscope examination(79 cases with AR were assigned to the AH with AR group,the remaining 50 cases of simple AH without AR were assigned to the AH group),and 45 cases of simple AR without AH through fiber nasopharyngoscope examination were assigned to the AR group.And 25 healthy children who came to our pediatric health department for health examinations during the same period were selected as the healthy control(HC)group.On the day of admission,all subjects underwent lateral X-ray examination of the nasopharynx,and the ratio of the maximum thickness of adenoids to the anterior posterior diameter of the nasopharynx cavity(A/N ratio)was calculated.Meanwhile their of peripheral blood eosinophil(EOS)percentage,serum interleukin-17(IL-17),and tumor necrosis factor-α(TNF-α)levels were tested.The A/N ratio,peripheral blood EOS percentage,serum IL-17 and TNF-α levels were compared among the AH with AR group,AH group,AR group,and HC group.The A/N ratio,peripheral blood EOS percentage,serum IL-17 and TNF-α levels of children with different degrees of adenoid obstruction under fiber nasopharyngoscope were compared in AH and AR group.Spearman correlation coefficient was used to analyze the correlation between the degree of adenoid obstruction under fiber nasopharyngoscope and the levels of peripheral blood EOS percentage,serum IL-17 and TNF-α in children from AH and AR group.Result A/N ratio:the value in AH with AR group was higher than that in AH group(P＜0.05),the value in AH group was higher than that in AR group(P＜0.05),and the value in AR group was higher than that in HC group(P＜0.05).Peripheral blood EOS percentage,serum IL-17 and TNF-α levels:AH with AR group had higher levels than those in AR group(P＜0.05),AR group had higher levels than those in AH group(P＜0.05),and AH group had higher levels than those in HC group(P＜0.05).The A/N ratio,peripheral blood EOS percentage,serum IL-17 and TNF-α levels in children with adenoid obstruction degree Ⅲ～Ⅳ under fiber nasopharyngoscope in the AH group were significantly higher than those in children with degree Ⅰ～Ⅱ(P＜0.05).Spearman correlation analysis showed that the degree of adenoid obstruction under fiber nasopharyngoscope in children with AH accompanied by AR significantly positively correlated with peripheral blood EOS percentage,serum IL-17 and TNF-α levels(r values were 0.527,0.451,and 0.402 respectively,P＜0.05).Conclusion Fiber nasopharyngoscope can be used for the diagnosis of AH with AR in children,and can be positive in determining severity of the patient's condition when combined with peripheral blood EOS percentage,serum IL-17 and TNF-α levels.

Objective:To evaluate the safety and effectiveness of a new Chinese-made surgical biopatch for atrial septum under the establishment of atrial septal defect animal model in miniature pigs.Methods:From June 2018 to April 2019, 26 pigs were divided into experimental group (15 pigs) and the control group (11 pigs). Animal models of atrial septal defect were established by traditional surgical methods. The to-be-evaluated and listed surgical biological patches (with a diameter of 10 mm) were implanted in the experimental group and the control group to repair the atrial septal defect. Cardiac ultrasound and blood examination of all animals were performed before and at 7, 30, 90, 180 days after operation, the results were analyzed with repetitive measurement and analysis of variance. At 90 days and 180 days after the operation, tissue samples were taken from animals after euthanasia. Pathological examination of heart and major organs were conducted. The independent sample t test and rank sum test were used to compare the data between the two groups, and the nonparametric was used to compare the patch calcification score between the two groups. Results:In total of 26 animals, 14 animals in the experimental group(6 at 90 days, 8 at 180 days) and 9 animals in the control group(4 at 90 days, 5 at 180 days) reached the end of the experiment. The other 3 animals (1 in the experimental group and 2 in the control group) died of arrhythmia, whole heart failure and right heart failure, the results of pathological examination showed that the causes of death were unrelated to the experimental materials. Cardiac ultrasound showed no patch leakage in all animals. There was no statistically significant difference in cardiac ultrasound and blood examination between the two groups at different time points after operation (all P>0.05). The pathological results showed that all the implants were intact and had good biocompatibility. There was no significant difference in the mean endothelialization rate between the experimental group and the control group at 90 and 180 days after operation ((80.8±29.1)% vs. (82.5±23.6)%, t=0.095, P=0.927; (78.8±36.4)% vs. (82.0±19.2)%, t=0.182, P=0.859) on 90 and 180 days, there was no significant difference in the patch calcification score between the two groups (1.00(1.25) vs. 2.00(0.75), Z=6.500, P=0.214; 0(0.75) vs. 1.00(2.00), Z=12.000, P=0.139). Conclusion:The new Chinese-made surgical biopatch for atrial septum has comparable safety and efficacy to that of the marketable patch in miniature pig atrial septal defect animal model.