The gut microbiota is regarded as the "eighth organ" of the human body and plays a critical regulatory role in the occurrence and progression of various diseases. Ulcerative colitis （UC） is a chronic inflammatory bowel disease with a complex etiology and a tendency toward recurrent episodes. In recent years， studies have shown that gut microbiota dysbiosis plays a key role in its pathological processes. Meanwhile， an increasing number of studies have demonstrated that imbalances in the gut microbiota and abnormalities in its metabolites are closely associated with the development of atrial fibrillation （AF）. Although UC and AF belong to diseases of the digestive system and cardiovascular system， respectively， both exhibit systemic inflammatory characteristics and are often accompanied by gut microbiota dysregulation and abnormal metabolic products. However， systematic investigations into the mechanisms by which gut microbiota-derived metabolites act in these two diseases remain limited. Based on this， the present study adopts literature review and theoretical analysis methods， taking the "gut microbiota-gut-heart" axis as the entry point， to systematically summarize the signaling networks of three key classes of metabolites， i.e.， short-chain fatty acids （SCFAs）， bile acids （BAs）， and trimethylamine N-oxide （TMAO）， in the comorbidity mechanism of UC and AF. The findings indicate that these metabolites may activate key inflammatory pathways， such as NF-κB and NLRP3， thereby synergistically mediating intestinal barrier dysfunction and systemic inflammation and constructing a potential comorbidity network. On this basis， potential intervention strategies for the treatment of UC-AF comorbidity， including probiotic intervention and fecal microbiota transplantation， are further discussed. This study aims to provide new theoretical evidence and research perspectives for prevention and treatment strategies of cross-system diseases.

Objective:To evaluate the effects of chlorinated organophosphate flame retardants (Cl-OPFRs) via respiratory and digestive tract exposure on multiple organs in mice.Methods:A short-term repeated exposure model of tris(2-chloroethyl) phosphate (TCEP), tris(1-chloro-2-propyl) phosphate (TCIPP) and tris(1, 3-dichloro-2-propyl) phosphate (TDCIPP) in mice was established through intratracheal instillation and oral gavage administration. The exposure doses were 0.7, 1 and 2 mg·kg -1·day -1, respectively, with continuous administration for 14 days. The organs of the heart, liver, spleen, lung, kidney, stomach, large intestine, small intestine, bladder and testis were collected and weighed to calculate the organ coefficients. The pathological and histological changes were observed by hematoxylin-eosin staining to quantitatively assess the effects of the three Cl-OPFRs on the various organs by using the pathology score. Results:Analysis of organ coefficients in tracheal drip-treated mice showed that the organ coefficients in the testes of the TCEP, TCIPP and TDCIPP groups were lower than those in the control group ( PTCEP-testis=0.045, PTCIPP-testis=0.012 and PTDCIPP-testis<0.001). The organ coefficients were lower in the lungs and small intestines of the TCEP group ( PTCEP-lung=0.006, PTCEP-small intestine=0.042). The organ coefficients for the stomach and large intestine were higher in the TDCIPP group ( PTDCIPP-stomach=0.014, PTDCIPP-large intestine=0.049). Analyses of gavage-contaminated mice showed that the organ coefficients for liver, stomach and small intestine in the TCEP and TDCIPP groups were higher than those in the control group ( PTCEP-liver=0.007, PTCEP-stomach=0.003, PTCEP-small intestine<0.001, PTDCIPP-liver=0.001, PTDCIPP-stomach=0.004, and PTDCIPP-small intestine<0.001). Histopathological analyses of the organs of tracheal drip dyed mice showed significant pathological damage in the lung tissue of the TCIPP group, mainly in the form of thickening of the interstitium, infiltration of inflammatory cells and alveolar collapse. The results of the analysis of gavage poisoned mice showed that TCIPP exposure could lead to blurring of the red and white medullary boundaries of spleen tissues, destruction of white medullary structures, etc., and induce small intestinal cryptitis. TDCIPP induced significant pathological damage to the liver tissues of mice, which mainly included cytoplasmic washout, infiltration of inflammatory cells, acute inflammation, and other injurious effects. Significant pathological damage to the intestinal tissues of mice was also observed. Conclusions:This study demonstrates that the toxic effects of Cl-OPFRs are significantly associated with exposure routes and compound specificity. Respiratory exposure predominantly induces TCIPP-mediated pulmonary injury, while digestive exposure causes TDCIPP-driven hepatointestinal toxicity. These findings provide preliminary evidence for the toxicity screening of Cl-OPFRs.

This paper summarizes Professor WANG Xiuxia's clinical experience in treating hyperprolactinemia using the liver soothing therapy. Professor WANG identifies liver qi stagnation and rebellious chong qi （冲气） as the core pathomechanisms of hyperprolactinemia. Furthermore， liver qi stagnation may transform into fire or lead to pathological changes such as spleen deficiency with phlegm obstruction or kidney deficiency with essence depletion. The treatment strategy centers on soothing the liver， with a modified version of Qinggan Jieyu Decoction （清肝解郁汤） as the base formula. Depending on different syndrome patterns such as liver stagnation transforming into fire， liver stagnation with spleen deficiency， or liver stagnation with kidney deficiency， heat clearing， spleen strengthening， or kidney tonifying herbs are added accordingly. In addition， three paired herb combinations are commonly used for symptom specific treatment， Danggui （Angelica sinensis） with Chuanxiong （Ligusticum chuanxiong）， Zelan （Lycopus lucidus） with Yimucao （Leonurus japonicus） ， and Jiegeng （Platycodon grandiflorus） with Zisu （Perilla frutescens）.

Endometrial cancer is one of the most common malignant tumors in the female reproductive system.Previous studies have shown that the myometrial invasion depth for endometrial cancer affects the treatment choice.MRI is currently the preferred imaging method to assess the myometrial invasion.In recent years,some studies have shown that MRI radiomics has potential value in comprehensively assessing the depth of myometrial invasion in stage I endometrial cancer.This article summarizes the progress of MRI radiomics for myometrial invasion in stage I endometrial cancer.

Objective To explore the relationship between epstein-barr viral(EBV)load and T lymphocyte subsets distribution in peripheral blood of children with systemic lupus erythematosus(SLE)and its synergistic effect on liver injury.Methods A total of 212 children with SLE admitted to the Xinjiang Uygur Autonomous Region Children's Hospital from October 2021 to September 2023 were selected as the study subjects.The SLE disease activity index(SLEDAI)score was divided into active group(n=58)and inactive group(n=154).The clinical data and laboratory indexes of the two groups were compared.The curve relationship between EBV load and T lymphocytes was analyzed by local weighted scatterplot smoothing(LOWESS)method.According to the occurrence of liver injury,212 children with SLE were divided into two groups(n=166)without liver injury and(n=46)with liver injury.The clinical data of the two groups were compared.Multifactor Logistics regression analysis was used to screen the influencing factors of liver injury in SLE children.Restricted cubic spline(RCS)model was used to analyze the relationship between EBV load,T lymphocytes and liver injury.The unconditioned Logistic regression model was used to analyze the interaction between EBV load and T lymphocytes on liver injury.Results Compared with the inactive group,the active group had younger age(t=9.265),higher hormone dosage(t=2.369),decreased ALB,CD4+,CD4+/CD8+levels(t=4.870,3.463,5.820),and increased EBV load,CD3+,CD8+levels(t=40.830,12.719,5.048),and the differences were statistically significant(all P<0.05).LOWESS analysis showed that EBV load had a nonlinear relationship with CD3+,CD4+,CD8+and CD4+/CD8+.The proportion of children with liver injury who had a disease course of≤3 months,EBV load,CD3+and CD8+levels,and the proportion of active children were lower than those without liver injury(t/χ2=10.749～30.378);the levels of ALB,CD4+and CD4+/CD8+indexes were higher than those without live injury(t=13.561,3.117,13.204),and the differences were statistically significantly(all P<0.05).Multivariate Logistic regression analysis showed that disease duration≤3 months,EBV load,CD3+,ALB,CD4+/CD8+and active SLE were influential factors for liver injury in SLE children(Wald χ2=1.020～1.932,all P<0.05).The results of RCS model analysis showed that EBV load,CD3+and CD8+were positively correlated with liver injury in SLE children,and CD4+,CD4+/CD8+were negatively correlated with liver injury in SLE children.Interaction analysis results showed that EBV load≥450 IU/ml had a multiplicative and additive interaction with CD3+≥60%,CD4+<30%,CD8+≥37%and CD4+/CD8+<0.94,and the risk of liver injury in SLE children was higher when the two factors co-existed.Conclusion There is a nonlinear relationship between EBV load in peripheral blood of SLE children and CD3+,CD4+,CD8+and CD4+/CD8+.Peripheral blood EBV load and abnormal expression of CD3+,CD4+,CD8+and CD4+/CD8+are all factors affecting liver injury in children with SLE,and there is a multiplicative and additive interaction between the above factors.

Objective:To describe the positive rates of high-risk human papillomavirus (HR-HPV) DNA and serum-neutralizing antibody in cervical intraepithelial neoplasia (CIN) tissues of rural women in Xiangyuan County, Shanxi Province, and evaluate the association of HR-HPV DNA and neutralizing antibody positive status with the occurrence of CIN.Methods:In a cohort of 1 897 women aged 35-45 years established by the Shanxi Province Cervical Cancer Screening StudyⅠ, DNA typing (SPF10 PCR-DEIA-LiPA25) was performed by using tissue samples of women with positive HR-HPV test results [Hybrid CaptureⅡ(HC2)] or abnormal cytological or pathological results. Serum HR-HPV neutralizing antibody detection was conducted with multicolor pseudovirion-based neutralization assay. Cochran-Armitage trend test was used to analyze the changing trend of the positive rate of HR-HPV DNA and neutralizing antibody with the progression of CIN. Multivariate logistic regression models were used to evaluate the influence and multiplicative interaction of HR-HPV DNA and neutralizing antibody positive status on the occurrence of CIN. The relative excess risk ( RERI), attributable proportion of interaction ( AP), and the synergy index ( SI) of the interaction were calculated to evaluate the additive interaction of HR-HPV DNA and neutralizing antibody on the occurrence of CIN. Results:The positive rate of any type of HR-HPV DNA (HPV16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 68) in 479 women who were HC2 positive or had abnormal cytological or pathological detection results was 37.16%. In normal, CIN1, CIN2, and CIN3+ groups, the HR-HPV DNA positive rates were 18.03%, 49.53%, 90.24% and 94.59%, respectively. The positive rate of any type of HR-HPV neutralizing antibody was 63.88%. In normal, CIN1, CIN2, and CIN3+ groups, the positive rates of HR-HPV neutralizing antibody were 63.95%, 57.94%, 70.73%, and 72.97%, respectively. The positive rate of any type of HR-HPV neutralizing antibody was 53.31% in 1 418 women who were HC2 negative and had normal cytopathology, and the most common types were HPV51 (27.36%) and HPV39 (24.96%). Multivariate logistic regression analysis showed that any type of HR-HPV DNA positive status ( OR=9.15, 95% CI: 5.99-14.20, P<0.001) was the independent factor for the occurrence of CIN, HR-HPV neutralizing antibody positive status was not associated with the occurrence of CIN ( OR=0.95, 95% CI: 0.61-1.48, P=0.815). The OR value of the multiplication of HR-HPV DNA and neutralizing antibody positive status of the occurrence of CIN was 1.63 (95% CI: 0.67-3.95), P=0.283. Quantitative analysis of interaction showed that RERI was 1.65 (95% CI:-3.56-6.86), SI was 1.28 (95% CI: 0.58-2.82), and AP was 0.19 (95% CI:-0.36-0.75). Conclusions:HR-HPV DNA positive status was a risk factor for the occurrence of CIN, but neutralizing antibody positive status was not associated with the occurrence of CIN. They had no significant multiplicative or additive interaction with the occurrence of CIN.

Objective To investigate the effects of bis(acetylacetonato)oxovanadium(IV)[VO(acac)?]on human adrenocortical carcinoma cell lines SW-13 and NCI-H295R in vitro,aiming to determine whether VO(acac)?promotes or inhibits the proliferation,migration,and invasion of these cells.Methods SW-13 and NCI-H295R cells in logarithmic growth phase were exposed to VO(acac)? at concentrations of 6.25,12.5,25,50,75,100,and 200 μmol/L for 24 and 48 hours,respectively.Mitotane served as the positive control.Cell viability was assessed using the CCK-8 assay to evaluate the effects of VO(acac)? on SW-13 and NCI-H295R cells.Subsequently,cells were treated with VO(acac)? at concentrations of 0,6.25,12.5,and 25 μmol/L for 48 hours,and flow cytometry was employed to investigate the impact of VO(acac)? on apoptosis.The migratory ability of the cells was evaluated using a wound healing assay,while their invasive capacity was assessed via a Transwell assay.Additionally,the clonogenic assay was used to determine the proliferative potential of SW-13 and NCI-H295R cells following VO(acac)?treatment.Results The CCK-8 results demonstrated that VO(acac)2 inhibited the viability of SW-13 and NCI-H295R cells in a time-and concentration-dependent manner.Specifically,the half-maximal inhibitory concentra-tions(IC50)for VO(acac)2 against SW-13 cells were 62.98±6.67 μmol/L after 24 hours and(14.61±1.66)μmol/L after 48 hours of treatment,while the corresponding IC50 values for NCI-H295R cells were 46.78±7.89 μmol/L and 12.61±2.98 μmol/L,respectively.Flow cytometry analysis revealed that VO(acac)2 induced apoptosis in both SW-13 and NCI-H295R cells in a concentration-dependent manner(P<0.05).The wound healing assay indicated a significant reduction in the migratory rate of SW-13 and NCI-H295R cells with increasing concentrations of VO(acac)2(P<0.05).Transwell assay results showed that VO(acac)2 significantly inhibited the invasive ability of SW-13 and NCI-H295R cells in a concentration-dependent fashion.Finally,the clonogenic assay confirmed that VO(acac)2 suppressed the proliferative capacity of SW-13 and NCI-H295R cells in a concentration-dependent manner.Conclusion VO(acac)2 inhibits the proliferation,migration,and invasion of human adrenocortical carcinoma cells(SW-13 and NCI-H295R),while inducing apoptosis in these cell lines.

Objective:To establish and validate a multimodal model based on radiomics and deep learning for predicting acute pancreatitis (AP) complicated with acute respiratory distress syndrome (ARDS).Methods:Patients diagnosed with AP from The First Affiliated Hospital of Soochow University, Donghai County People's Hospital and Jintan Affiliated Hospital of Jiangsu University between January 2017 and December 2023 were enrolled. Based on the diagnosis of ARDS within 1 week after admission, the patients were classified into the ARDS group and the non-ARDS group. Patients in the First Affiliated Hospital of Soochow University ( n=406) was used as the training set (non-ARDS group n=212 vs ARDS group n=194), while Donghai and Jintan hospitals served as the test set ( n=175; non-ARDS group n=104 vs ARDS group n=71). Clinical data, laboratory tests and the occurrence of systemic inflammatory response syndrome (SIRS) within 24 hours after admission were collected. Scoring systems such as bedside index for severity in acute pancreatitis (BISAP), Ranson score and modified CT severity index (MCTSI) were calculated. Radiomics features were extracted from three-dimensional CT images to develop a radiomics model based on XGBoost algorithm. At the same time, a deep learning model was constructed using deep convolutional networks to extract deep features. Finally, clinical features and the predictions from the aforementioned models were integrated to establish a multimodal model based on XGBoost algorithm. To enhance model visualization, variable importance ranking and local interpretable visualization were used. The receiver operating characteristic (ROC) curves of the three models and the three scores including BISAP, Ranson and MCTSI were plotted and the area under the curves (AUCs) were calculated to evaluate the prediction performance for ARDS in AP patients, as well as sensitivity and specificity. Results:In the multimodal model for predicting ARDS in AP patients, predictions of the deep learning model and the radiomics model were the most important variables, followed by SIRS, C-reactive protein, procalcitonin, albumin, glucose, creatinine, neutrophil, and Ca 2+. In the training set, the multimodal model achieved an AUC of 0.933 for predicting ARDS in AP patients, higher than the radiomics model (0.727), the deep learning model (0.877), MCTSI (0.870), Ranson (0.620) and BISAP (0.898). In the test set, the model's AUC was 0.916 for predicting ARDS in AP patients, higher than the radiomics model (0.660), the deep learning model (0.864), MCTSI (0.851), Ranson (0.609), and BISAP (0.860). Conclusions:Based on clinical structured data, radiomics and deep learning features, the multimodal model could predict the risk of ARDS in AP patients at an early stage, whose performance is better than the single-modal models and the traditional scoring systems.

Objective:To describe the positive rates of high-risk human papillomavirus (HR-HPV) DNA and serum-neutralizing antibody in cervical intraepithelial neoplasia (CIN) tissues of rural women in Xiangyuan County, Shanxi Province, and evaluate the association of HR-HPV DNA and neutralizing antibody positive status with the occurrence of CIN.Methods:In a cohort of 1 897 women aged 35-45 years established by the Shanxi Province Cervical Cancer Screening StudyⅠ, DNA typing (SPF10 PCR-DEIA-LiPA25) was performed by using tissue samples of women with positive HR-HPV test results [Hybrid CaptureⅡ(HC2)] or abnormal cytological or pathological results. Serum HR-HPV neutralizing antibody detection was conducted with multicolor pseudovirion-based neutralization assay. Cochran-Armitage trend test was used to analyze the changing trend of the positive rate of HR-HPV DNA and neutralizing antibody with the progression of CIN. Multivariate logistic regression models were used to evaluate the influence and multiplicative interaction of HR-HPV DNA and neutralizing antibody positive status on the occurrence of CIN. The relative excess risk ( RERI), attributable proportion of interaction ( AP), and the synergy index ( SI) of the interaction were calculated to evaluate the additive interaction of HR-HPV DNA and neutralizing antibody on the occurrence of CIN. Results:The positive rate of any type of HR-HPV DNA (HPV16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 68) in 479 women who were HC2 positive or had abnormal cytological or pathological detection results was 37.16%. In normal, CIN1, CIN2, and CIN3+ groups, the HR-HPV DNA positive rates were 18.03%, 49.53%, 90.24% and 94.59%, respectively. The positive rate of any type of HR-HPV neutralizing antibody was 63.88%. In normal, CIN1, CIN2, and CIN3+ groups, the positive rates of HR-HPV neutralizing antibody were 63.95%, 57.94%, 70.73%, and 72.97%, respectively. The positive rate of any type of HR-HPV neutralizing antibody was 53.31% in 1 418 women who were HC2 negative and had normal cytopathology, and the most common types were HPV51 (27.36%) and HPV39 (24.96%). Multivariate logistic regression analysis showed that any type of HR-HPV DNA positive status ( OR=9.15, 95% CI: 5.99-14.20, P<0.001) was the independent factor for the occurrence of CIN, HR-HPV neutralizing antibody positive status was not associated with the occurrence of CIN ( OR=0.95, 95% CI: 0.61-1.48, P=0.815). The OR value of the multiplication of HR-HPV DNA and neutralizing antibody positive status of the occurrence of CIN was 1.63 (95% CI: 0.67-3.95), P=0.283. Quantitative analysis of interaction showed that RERI was 1.65 (95% CI:-3.56-6.86), SI was 1.28 (95% CI: 0.58-2.82), and AP was 0.19 (95% CI:-0.36-0.75). Conclusions:HR-HPV DNA positive status was a risk factor for the occurrence of CIN, but neutralizing antibody positive status was not associated with the occurrence of CIN. They had no significant multiplicative or additive interaction with the occurrence of CIN.

Objective To investigate the effects of bis(acetylacetonato)oxovanadium(IV)[VO(acac)?]on human adrenocortical carcinoma cell lines SW-13 and NCI-H295R in vitro,aiming to determine whether VO(acac)?promotes or inhibits the proliferation,migration,and invasion of these cells.Methods SW-13 and NCI-H295R cells in logarithmic growth phase were exposed to VO(acac)? at concentrations of 6.25,12.5,25,50,75,100,and 200 μmol/L for 24 and 48 hours,respectively.Mitotane served as the positive control.Cell viability was assessed using the CCK-8 assay to evaluate the effects of VO(acac)? on SW-13 and NCI-H295R cells.Subsequently,cells were treated with VO(acac)? at concentrations of 0,6.25,12.5,and 25 μmol/L for 48 hours,and flow cytometry was employed to investigate the impact of VO(acac)? on apoptosis.The migratory ability of the cells was evaluated using a wound healing assay,while their invasive capacity was assessed via a Transwell assay.Additionally,the clonogenic assay was used to determine the proliferative potential of SW-13 and NCI-H295R cells following VO(acac)?treatment.Results The CCK-8 results demonstrated that VO(acac)2 inhibited the viability of SW-13 and NCI-H295R cells in a time-and concentration-dependent manner.Specifically,the half-maximal inhibitory concentra-tions(IC50)for VO(acac)2 against SW-13 cells were 62.98±6.67 μmol/L after 24 hours and(14.61±1.66)μmol/L after 48 hours of treatment,while the corresponding IC50 values for NCI-H295R cells were 46.78±7.89 μmol/L and 12.61±2.98 μmol/L,respectively.Flow cytometry analysis revealed that VO(acac)2 induced apoptosis in both SW-13 and NCI-H295R cells in a concentration-dependent manner(P<0.05).The wound healing assay indicated a significant reduction in the migratory rate of SW-13 and NCI-H295R cells with increasing concentrations of VO(acac)2(P<0.05).Transwell assay results showed that VO(acac)2 significantly inhibited the invasive ability of SW-13 and NCI-H295R cells in a concentration-dependent fashion.Finally,the clonogenic assay confirmed that VO(acac)2 suppressed the proliferative capacity of SW-13 and NCI-H295R cells in a concentration-dependent manner.Conclusion VO(acac)2 inhibits the proliferation,migration,and invasion of human adrenocortical carcinoma cells(SW-13 and NCI-H295R),while inducing apoptosis in these cell lines.