Objective To explore the effect of job satisfaction on job burnout among administrative staff in public hospitals and to examine the mediating effect of career growth in this relationship. Methods A total of 384 administrative staff from 20 public hospitals in Tianjin City were recruited as participants using the convenience sampling method. Their job burnout, job satisfaction, and career growth were measured with the Maslach Burnout Inventory, Job Satisfaction Scale, and Career Growth Scale, respectively. A structural equation model was constructed using AMOS 23.0, and the mediating effect was examined with the Bootstrap method. Results The mean scores of job burnout, job satisfaction, and career growth among participants were (43.1±15.4), (14.4±5.7), and (8.3±4.2), respectively. The results of the mediating effect analysis showed that career growth played a significant mediating role between job satisfaction and job burnout among the public hospital administrative staff, with the mediating effect accounting for approximately 22.2% to 52.2% of the total effect. Conclusion Job satisfaction of public hospital administrative staff can directly affect their job burnout, and it can also influence job burnout through the mediating effect of career growth. Effective measures to improve job satisfaction and promote career growth may help alleviate job burnout among administrative staff in public hospitals.

ObjectiveMethylthioadenosine phosphorylase (MTAP) is found to be frequently deleted in malignant cancers, but the role of MTAP underlying metastasis and stemness of liver cancer remains far from clear. 5-fluorouracil (5-Fu) is clinically used in treating advanced liver cancer, however, chemoresistance is one of the major barriers impeding its efficacy. Liver cancer stem cells are considered to be the reservoir for tumor progression and chemoresistance. This study aims to explore the role of MTAP in regulating stemness and chemoresistance of 5-Fu in liver cancer. It is designed to elucidate the molecular mechanisms underlying MTAP-manipulated stemness. How MTAP influences metastasis and chemoresistance against 5-Fu in liver cancer is also elaborated. MethodsThe correlation of MTAP expression with stemness marker CD133 was evaluated by flow cytometry. Colony formation assays were conducted to analyze the tumorigenic ability. Western blot assays were applied to delineate the molecular mechanisms underlying MTAP-regulated stemness. Trans-well assays were conducted to analyze the metastatic potential of liver cancer cells.In vivo experiments were performed using subcutaneous xenograft and lung metastasis model on nude mice. Tumor size and weight were analyzed upon 5-Fu treatment. Metastatic nodules on lungs were evaluated. Immunohistochemical and TUNNEL assays were performed on slides obtained from tumor tissues. ResultsMTAP overexpression inhibited expression of CD133 and colony formation, which is further ablated by MTAP inhibitor. MTAP deprivation augmented stemness and colony formation, which is reversed by protein arginine methyltransferase 5 (PRMT5) overexpression but not its catalytically inactive counterparts. Critically, SRY-box transcription factor 2 (SOX2) was found to be a downstream regulator of MTAP/PRMT5, leading to stemness of liver cancer cells. MTAP overexpression suppressed SOX2 expression, while MTAP inhibition augmented expression of SOX2. Critically, MTAP overexpression inhibited migration and invasion of liver cancer cells. In vivo experiments in animal model found that MTAP deprivation promotes tumor growth and metastatic nodules of liver cancer. Additionally, MTAP overexpression inhibits tumor growth. Moreover, MTAP deprivation contributes to chemoresistance shown by increased tumor size and weight treated by 5-Fu. In contrast, MTAP overexpression led to further decline in tumor size and weight elicited by 5-Fu treatment. Accordingly, SOX2 was inhibited in tumor tissues after MTAP overexpression. Marker of proliferation Ki67 (Ki67) expression was dampened while apoptosis was found in MTAP-overexpressed tumor tissues. ConclusionIn this study, plethora of experimental studies collectively demonstrated that MTAP deprivation enhances stemness of liver cancer by regulating SOX2, exerting anti-cancer and chemoresistant role against 5-Fu in liver cancer. It is also worth noting that MTAP inhibition promoted metastasis of liver cancer. MTAP overexpression augmented tumor shrinking elicited by 5-Fu and SOX2 was involved in this process. These results concluded that MTAP/PRMT5/SOX2 signaling axis was involved in regulating stemness and chemoresistance of liver cancer. These findings help to exploit novel therapies by targeting stemness in MTAP-depleted liver cancer. It shed novel light on unveiling MTAP-regulated stemness in antagonizing 5-Fu treatment in liver cancer. It also adds mounting evidence to the theoretical basis for accomplishing personalized chemotherapy of liver cancer patients by targeting MTAP or its downstream PRMT5/SOX2.

Objective To explore the relationship between PANoptosis and hepatic ischemia-reperfusion injury (HIRI), and to screen the key genes of PANoptosis in HIRI. Methods PANoptosis-related differentially expressed genes (PDG) were obtained through the Gene Expression Omnibus database and GeneCards database. Gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and Gene Set Enrichment Analysis (GSEA) were used to explore the biological pathways related to PDG. A protein-protein interaction network was constructed. Key genes were selected, and their diagnostic value was assessed and validated in the HIRI mice. Immune cell infiltration analysis was performed based on the cell-type identification by estimating relative subsets of RNA transcripts. Results A total of 16 PDG were identified. GO analysis showed that PDG were closely related to cellular metabolism. KEGG analysis indicated that PDG were mainly enriched in cellular death pathways such as apoptosis and immune-related signaling pathways such as the tumor necrosis factor signaling pathway. GSEA results showed that key genes were mainly enriched in immune-related signaling pathways such as the mitogen-activated protein kinase (MAPK) signaling pathway. Two key genes, DFFB and TNFSF10, were identified with high accuracy in diagnosing HIRI, with areas under the curve of 0.964 and 1.000, respectively. Immune infiltration analysis showed that the control group had more infiltration of resting natural killer cells, M2 macrophages, etc., while the HIRI group had more infiltration of M0 macrophages, neutrophils, and naive B cells. Real-time quantitative polymerase chain reaction results showed that compared with the Sham group, the relative expression of DFFB messenger RNA in liver tissue of HIRI group mice increased, and the relative expression of TNFSF10 messenger RNA decreased. Cibersort analysis showed that the infiltration abundance of naive B cells was positively correlated with DFFB expression (r=0.70, P=0.035), and the infiltration abundance of M2 macrophages was positively correlated with TNFSF10 expression (r=0.68, P=0.045). Conclusions PANoptosis-related genes DFFB and TNFSF10 may be potential biomarkers and therapeutic targets for HIRI.

Objective:To evaluate the clinical efficacy of returning, squeezing, patting and pulling orthopaedic manipulation combined with pelvic fabric tape fixation for the treatment of postpartum pubic symphysis separation.Methods:The clinical data of 80 patients with postpartum pubic symphysis separation from June 2015 to March 2019 were retrospectively analyzed, and all of them were given orthopaedic manipulative therapy using return squeezing and patting and pulling, once a week, for a total of 3 times. After the manipulative treatment, the patients were instructed to brake the pelvic fixation straps for not less than 8 h per day, and digital X-ray (DR) pelvic radiographs or ultrasound tests were performed before and after the treatment to measure the distance between the pubic symphysis. VAS scale was used to assess the degree of pain, and the Oswestry dysfunction index (ODI) was used to assess the degree of dysfunction. The clinical efficacy was evaluated.Results:After treatment of 80 patients, 6 showed significant improvement, 69 showed improvement, and 5 showed no improvement, with a total effective rate of 93.8%. Compared with before group, the inter-pubic symphysis distance [(15.09±3.10) mm, (12.01±4.36) mm, (9.64±0.30) mm, (8.18±1.56) mm vs. (19.35±1.08) mm, F=254.64] were significantly smaller at 1 week, 2 weeks, 3 weeks, and 1 month ( P<0.001); VAS scores (2.90±1.24, 1.29±0.88, 0.84±0.43, 0.56±0.32 vs. 6.11±2.93, F=122.60) were significantly lower than before treatment ( P<0.001); ODI (28.09±4.30, 22.01±4.95, 20.64±0.41, 14.18±1.36 vs. 45.43±4.01, F=734.17) were significantly reduced ( P<0.001). Conclusion:Returning, squeezing, patting and pulling orthopaedic manipulation combined with pelvic fabric tape fixation can quickly restore the separation distance of the pubic symphysis, reduce local pain and improve lumbosacral function.

Decidual natural killer(dNK)cells are the most abundant immune cells in the decidua.The functional acquisition during dNK cell development depends on NK cell education,a process in which the highly polymorphic killer cell immunoglobulin-like receptors(KIRs)and CD94/NKG2s expressed on dNK cells bind to major histocompatibility complex(MHC)class Ⅰmolecules expressed by extravillous trophoblast(EVT)cells.This interaction regulates the effector functions of NK cells.dNK cells participate in the establishment and maintenance of pregnancy by modulating immune tolerance at the maternal-fetal interface.Defects in dNK cell education leading to dNK dysfunction are potential pathological mechanisms underlying adverse pregnancy outcomes such as recurrent pregnancy loss(RPL).This review summarizes the characteristics of dNK cells,dNK cell education and its key associated molecules,and the pathological mechanisms by which poorly educated dNK cells contribute to RPL,aiming to offer insights for predicting and improving pregnancy outcomes in RPL patients associated with dNK cell abnormalities.

Objective To propose a high-precision deep learning-based image assessment method of osteosarcoma chemotherapy efficacy for clinical treatment,as existing methos have low accuracy of osteosarcoma assessment.Methods The low incidence of osteosarcoma led to the small scale of its imaging data and the problem of imbalance in data categories.This study combined deep learning with clinical medical information,combined the bone sarcoma generation module of BoneGAN and the scale lesion information capture module,and proposed OMLA-Net,a deep learning assessment network for chemotherapy effect of bone sarcoma based on multi-scale lesion attention network,which achieved computer-aided bone tumor assessment with integrated data augmentation and focused lesion information through pre-training and generalized loss training.Results In this study,40 cases of osteosarcoma MRI data were used as the basis for the comparison test on the generated dataset,and the OMLA-Net assessment outperformed the SOTA method Conv-LSTM-GAN in terms of the assessment effects such as accuracy and F1 scores,and the difference was statistically significant(Bootstrap statistical method P＜0.05);the subsequent K-fold cross-validation ablation experiments further demonstrated the effectiveness of each module proposed by OMLA-Net.Conclusion OMLA-Net can effectively perform the impact assessment of chemotherapy effect on osteosarcoma,which provides a new idea for subsequent clinical application.

Objective To analyze the levels and functions of CD4+T cell subsets in mouse spleen and lung tissues after Streptococcus pneumoniae(S.P.)infection,and to explore the immune regulatory mechanisms S.P.infection.Methods Flow cytometry was used to detect the proportions of CD4+T cell subsets(Th1,Th2,Th17,and Treg cells)in mouse spleen tissues from control group(n=4),S.P.infection at 12 h(n=4),and 24 h(n=4).H&E staining was used to examine lung tissue pathological characteristics.Differential gene sets and functional changes in lung tissues were analyzed after S.P.infection for 2 and 5 days,and immune cell abundance was predicted.Results Significant inflammatory pathological features were observed in the lung tissues of mice after S.P.infection.The proportions of Th1 and Treg cells in the spleen tissues gradually increased after S.P.infection,with Th1 and Treg cell proportions significantly higher than the control group at 24 h post-infection(P<0.05).At 5 d post-infection,only Treg cell proportion was significantly higher than the control group(P<0.05).Functional analysis revealed abnormal activation of IL6,IL10,and IL4/IL13 signaling pathways 2 days after infection,and abnormal enrichment of IL-2 and IL-6/TGF-β pathways 5 days after infection.Conclusion Treg and Th1 cells are key immune regulatory cells in mice following S.P.infection.Modulating Treg cell function mediated by IL-10 and Th1 cell function mediated by IL-2 can improve immune responses after S.P.infection.

Objective: To explore the therapeutic mechanism of puerarin in treating rheumatoid arthritis (RA) rats based on the serine/tyrosine protein kinase B (AKT)-phosphorylated forkhead box protein O1 (FOXO1)-interleukin-9 (AKT-FOXO1-IL-9) signaling pathway. Methods : 36 rats were randomly divided into a blank group , a model group , a positive control group , and low , medium , and high dose groups of puerarin. Except for the blank group , the other groups were induced with type Ⅱ collagen to establish a RA rat model. After successful modeling , different doses of puerarin and methotrexate were given to treat the rats. The body mass and toe thickness of the rats were measured , and biochemical indicators of rat blood rheology were detected. X-ray was used to observe changes in rat joint morphology. Safranin green staining were used to observe the pathology of rat joint tissue. ELISA was used to detect the levels of IL-9 and rheumatoid factors in rat serum , and Western blot was used to detect changes in levels of AKT and FOXO1 . 36 rats were randomly divided into a blank group , a model group , a positive control group , and low , medium , and high dose groups of puerarin. Except for the blank group , the other groups were induced with type Ⅱ collagen to establish a RA rat model. After successful modeling , different doses of puerarin and methotrexate were given to treat the rats. The body mass and toe thickness of the rats were measured , and biochemical indicators of rat blood rheology were detected. X-ray was used to observe changes in rat joint morphology. Safranin green staining were used to observe the pathology of rat joint tissue. ELISA was used to detect the levels of IL-9 and rheumatoid factors in rat serum , and Western blot was used to detect changes in levels of AKT and FOXO1 . Results: Compared with the blank group , the model group had the lowest toe thickness , and X-ray images showed more obvious segmental stenosis and more severe marginal bone invasion ; scaly like changes appeared at the edges of joints stained with safranin green , accompanied by the exudation of inflammatory cells and increased proliferation and secretion of chondrocytes ; the expression levels of inflammatory factors IL-9 and rheumatoid factors were the highest , and the expression levels of AKT and FOXO1 proteins were the highest (P < 0. 05) . Compared with the model group , the toe thickness of rats treated with different doses of puerarin decreased ; X-ray images showed that the puerarin treatment group of rats showed improvement in plantar joint stenosis and marginal bone invasion ; the results of safranin green staining showed that after treatment with different doses of puerarin , the infiltration of inflammatory cells decreased , and the expression levels of inflammatory factor IL-9 , rheumatoid factors , AKT , and FOXO1 proteins decreased significantly ( P < 0. 05 ) , with the high-dose puerarin group showing the most significant difference. Compared with the high-dose puerarin group , the positive control group showed a significant decrease in the above results and statistical differences (P < 0. 05) . Conclusion Puerarin has a good therapeutic effect on rats with RA by inhibiting the AKT-FOXO1-IL-9 pathway. The high-dose puerarin group (60 mg/kg) has the best therapeutic effect and the results show a dose-response relationship.

Objective To investigate the perioperative management of antithrombotic drugs in patients undergoing non-cardiac surgery.Methods Patients on long-term antithrombotic drugs who underwent non-cardiac surgery in our hospital were included.Through interviews with patients and physicians,perioperative antithrombotic medication regimens were reviewed and compared with the"Multidisciplinary Expert Consensus on Perioperative Management of Antithrombotic Therapy"to evaluate compliance with consensus and analyze influencing factors.Results A total of 372 patients were included in the analysis.Among them,355 patients were on long-term antiplatelet therapy alone,and 17 were on long-term oral anticoagulantion.364(97.8％)discontinued antithrombotic medications prior to surgery.109 patients(29.3％)received low molecular weight heparin(LMWH)bridging therapy.Among the 355 patients on antiplatelet therapy,108(30.4％)had discontinuation durations consistent with the consensus recommendations,while 186(52.4％)discontinued medications for longer periods.Postoperatively,the average hospital stay for antiplatelet therapy patients was 6.64 days,with only 37(10.4％)resuming therapy during hospitalization.The average hospital stay for patients on anticoagulants was 9.94 days,with only 2(11.8％)resuming therapy during hospitalization.Regarding perioperative risk assessment,only 40(10.8％)of patients underwent additional internal medical evaluation for thromboembolic risk after medication discontinuation,with the remainder assessed soly by surgeons.Coronary heart disease was an independent risk factor associated with internal medical evaluation(OR 2.851,95％CI 1.160-7.011,P=0.022).For bleeding risk assessment,surgeons evaluations aligned with the consensus in 68.0％of cases,but surgeons tended to underestimate risk compared to the consensus.Conclusions In this single-center study,perioperative antithrombotic management showed low compliance with expert consensus,characterized by prolonged preoperative medication discontinuation,high rates of LMWH bridging,and low postoperative in-hospital resumption of therapy.A robust multidisciplinary collaboration system should be established to enhance comprehensive patient assessment.

AIM To study the chemical constituents from Radix Puerariae Lobatae from Anhui province and their in vitro lipid-lowering activity.METHODS D101 macroporous resin,silica gel,MCI,and semi-preparative HPLC were used for isolation and purification,then the structures of obtained compounds were identified by physicochemical properties and spectral data.The lipid accumulation model was established by palmitic acid-induced hepatocyte AML12,and the in vitro lipid-lowering activity was evaluated.RESULTS Twenty-one compounds were isolated and identified as carboxymethyl isoferulate(1),methyl(E)feruloylglycolate(2),ariscucurbin-A(3),trans-p-coumaroygly colic acid(4),indole-3-carboxaldehyde(5),β-sitosterol(6),puerol A(7),pueroside C(8),cumoestrol(9),dihydrofurocoumarin(10),decuroside V(11),psoralen dimer(12),bergapten dimer(13),isoliquiritigenin(14),neoliquiritin(15),calycosin(16),daidzein(17),3,4,7-trihydroxyisoflavone(18),ononin(19),genistein(20),genistin(21).Compounds 1-4、7-10、13 and 17-19 significantly inhibited lipid accumulation in AML12 cells,and compound 9 inhibited PPAR-γ expression.CONCLUSION Compounds 1-6,10-13 are isolated from Pueraria genus for the first time.Compounds 1-4,7-10,13 and 17-19 have good lipid-lowering activity.