Objective To investigate the differences in demographic characteristics,reproductive health status,and the distribution of pregnancy-related diseases between couples conceived via assisted reproductive technology(ART)and naturally conceived couples,and to analyze the impact of ART treatment on the incidence of preterm birth(PTB)in singleton and twin and multiple pregnancies.Methods We conducted a retrospective analysis of the maternal and infant cohort data of Jing'an District from 2013 to 2020.Based on the conception method,the subjects were categorized into two groups:the ART group and the natural conception group.Chi-square test was applied to compare baseline characteristics and disease distributions differences between the two groups,and logistic regression models were used to evaluate the association between ART and the PTB risks.A causal mediation model was used to evaluate the mediating effect of twin and multiple pregnancy in the relationship between ART and PTB.Results A total of 117 717 parturients were included,6 265 in the ART group and 111 452 in the natural conception group.Compared with the natural conception group,couples in the ART group were significantly older and had a higher prevalence of reproductive system diseases.The incidences of diabetes and hypertensive disorders during pregnancy in ART parturient were 13.76%and 9.99%,respectively,which were significantly higher than 7.88%and 4.75%in the natural conception group(both P<0.001).The overall PTB rate in the ART group was 14.81%,higher than 5.35%in the natural conceptions group(P<0.001).The PTB rate in ART for singleton pregnancies in the ART group was 6.40%,higher than 4.83%in the natural conception group(P<0.001),while the PTB rate in ART for twin and multiple pregnancies in the ART group was 53.97%,lower than 60.42%in the natural conception group(P<0.05).Mediation analysis showed that 97.99%of the effect of ART on PTB was mediated by twin and multiple pregnancy,with ART increasing the PTB risk by 3.44 times through multiple pregnancy.Conclusion The overall PTB rate of ART recipients is higher than that of natural recipients,but ART does not increase the PTB risk in singleton and twin and multiple pregnancies.Twin and multiple pregnancy is the key mediating factor contributing to PTB in ART-conceived recipients.Compared with naturally conceived couples,ART conception couples own more advanced maternal age,and have higher risks of suffering gestational diabetes,gestational hypertension,and PTB.

[Objective]To investigate the expression of scaffold protein PDLIM5 in multiple sclerosis(MS)patients and the mouse microglial cell line BV2,and to explore its effects on the phagocytosis of microglial cells.[Methods]Peripheral blood samples were collected from 24 MS patients and 6 healthy volunteers as controls.The expression levels of PDLIM5 were detected by real-time quantitative PCR.A neuroinflammation cell model was established by treating the mouse microglial cell line BV2 with lipopolysaccharide(LPS,1 μg/mL).The expression levels of PDLIM5 were measured by Western Blot.The effect of PDLIM5 expression on phagocytosis was analyzed by transfecting BV2 cells with PDLIM5 shRNA plasmids or PDLIM5 overexpression plasmids.[Results]Real-time quantitative PCR results showed that compared with the healthy control group,the expression level of PDLIM5 from the MS patients was significantly increased in monocytes[2.78(0.70-6.86)vs.0.54(0.39-1.51),P=0.036]and lymphocytes[1.62(0.90-2.26)vs.0.11(0.05-0.21),P<0.001].Western Blot results indicated that PDLIM5 expression was significantly upregulated in BV2 cells following LPS stimulation(P<0.05).Plasmid transfection experiments demonstrated that knockdown of PDLIM5 inhibited the phagocytic capacity of BV2 cells as measured by trypan blue uptake(P<0.05),while overexpression of PDLIM5 enhanced the phagocytic ability of BV2 cells(P<0.001).[Conclusion]Under neuroinflammatory conditions,PDLIM5 expression is elevated,and this upregulation promotes the phagocytosis of microglial cell.

Objective:To compare the effects of propofol and dexmedetomidine for sedation on the outcome in mechanically ventilated patients with severe pulmonary infection.Methods:Patients with severe pulmonary infection (Clinical Pulmonary Infection Score >7) requiring mechanical ventilation from the Medical Information Mart for Intensive Care Ⅳ database between 2008 and 2020 were selected and divided into propofol group and dexmedetomidine group based on the sedative agent used. The primary outcome was all-cause in-hospital mortality, and secondary outcomes included 90-day all-cause mortality and duration of mechanical ventilation. Inverse probability of treatment weighting (IPTW) was used to adjust for baseline confounders, and logistic regression and linear regression were applied to analyze the effects of the two sedative drugs on the outcomes of mechanically ventilated patients with pulmonary infection. Kaplan-Meier survival curves were used to analyze survival outcomes.Results:A total of 6 204 critically ill patients with pulmonary infection requiring mechanical ventilation were included, with 3 439 cases in propofol group and 2 765 cases in dexmedetomidine group. The baseline characteristics between the two groups were well balanced (standardized mean difference < 0.1) after IPTW adjustment. In the IPTW-adjusted cohort, the in-hospital all-cause mortality and 90-day all-cause mortality were significantly lower in dexmedetomidine group than in propofol group (439.2[18.7%] vs 563.6[24.1%], 618.0[26.3%] vs 733.6[31.3%], P<0.001), the results of Further Kaplan-Meier survival curve analysis showed that the 90-day all-cause mortality was significantly lower in dexmedetomidine group than in propofol group ( P<0.01). Conclusions:Compared with propofol, dexmedetomidine can decrease the mortality rate and improve the prognosis in mechanically ventilated patients with severe pulmonary infection when used for sedation.

AIM To investigate the effects of Yiqi Juanbi Formula on chondrocyte pyroptosis in rat models of collagen-induced arthritis(CIA).METHODS Fifty rats were subcutaneously injected at the tail base with an emulsion containing equal volumes of bovine type Ⅱ collagen and incomplete Freund's adjuvant(IFA)to establish the CIA models.These rats were then randomly assigned to the model group,the methotrexate group(0.35 mg/kg),and the low-dose,medium-dose,and high-dose Yiqi Juanbi Formula groups(9.4,18.7,37.4 g/kg),in contrast to the ten intact rats serving in the normal control group.Following four weeks of intragastric administration,the rats had their general conditions observed;their joint swelling and arthritis indices measured;their ankle joint pathology assessed by HE staining;their serum levels of IL-1β,IL-18 and TNF-ɑ detected by ELISA;their mRNA expressions of NLRP3,Caspase-1,GSDMD,IL-1β,IL-18 and TNF-ɑ in ankle cartilage quantified by RT-qPCR;their protein expressions of NF-κB,NLRP3 and Caspase-1 in ankle cartilage analyzed by Western blot;and their NLRP3 and GSDMD positive expressions in ankle cartilage examined by immunohistochemistry.RESULTS Compared to the control group,the model group showed significantly increased joint swelling and arthritis indices(P＜0.01);elevated serum levels of IL-1 β,IL-18 and TNF-ɑ(P＜0.01);pathological changes including cartilage surface defects,reduced cell count,altered cellular morphology,irregular cell arrangement,and significant inflammatory cell infiltration in synovial tissue;upregulated mRNA expressions of NF-κB,NLRP3,Caspase-1,GSDMD,IL-1β,IL-18 and TNF-ɑ(P＜0.01)and increased protein expressions of NF-κB,NLRP3 and Caspase-1(P＜0.01)in ankle cartilage;enhanced positive expressions of NLRP3 and GSDMD in ankle cartilage(P＜0.01).Compared to the model group,the groups intervened with methotrexate or medium-or high-dose Yiqi Juanbi Formula exhibited reduced joint swelling and arthritis indices(P＜0.01);alleviated pathological damage in ankle joints;decreased serum levels of IL-1β,IL-18 and TNF-ɑ(P＜0.01);downregulated mRNA expressions of NF-κB,NLRP3,Caspase-1,GSDMD,IL-1β,IL-18 and TNF-ɑ(P＜0.05,P＜0.01),and reduced protein expressions of NF-κB,NLRP3 and Caspase-1(P＜0.05,P＜0.01)in ankle cartilage;and diminished positive expressions of NLRP3 and GSDMD in ankle cartilage(P＜0.01).CONCLUSION Yiqi Juanbi Formula alleviates inflammation in CIA rats,potentially by inhibiting the activation of the NF-κB/NLRP3/Caspase-1 signaling pathway,thereby suppressing chondrocyte pyroptosis.

Objective To investigate the correlation between myocardial fibrosis(MF)and left ventricular ejection fraction(LVEF)and myocardial injury markers in heart failure patients via cardiac magnetic resonance(CMR).Methods Seventy-six patients with heart failure were selected,including 32 cases of heart failure with preserved ejection fraction(HFpEF)(HFpEF group),15 cases of heart failure with mid-range ejection fraction(HFmEF)(HFmEF group),and 29 patients of heart failure with reduced ejection fraction(HFrEF)(HFrEF group).Additionally,7 healthy individuals undergoing physical examinations were included(control group).CMR parameters and biological markers for the heart failure groups were collected for all subjects.The differences in native T1 value and extracellular volume fraction(ECV)between the heart failure group and the control group were compared,respectively.The differences in native T1 value,ECV,late gadolinium enhancement(LGE)score,serum creatine kinase-MB(CK-MB),cardiac troponin Ⅰ knockdown(cTnI-KD),and N-terminal pro-brain natriuretic peptide(NT-proBNP)among heart failure subgroups were also compared,respectively.Spearman correlation analysis was used to examine the relationships between MF imaging indicators and LVEF,as well as NT-proBNP levels.Results The differences in native T1 value,ECV,LGE score,and NT-proBNP between the heart failure group and the control group,as well as between the heart failure subgroups were statistically significant(P＜0.05).The native T1 value,ECV,and LGE score in the heart failure group were positively correlated with NT-proBNP,and negatively correlated with LVEF.Conclusion The native T1 value,ECV value and LGE score are correlated with heart failure severity.CMR can detect myocardial injury early in patients with HFpEF and provide valuable information for risk stratification of MF.

Objective:To investigate the effect of COX6C on the proliferation of multiple myeloma(MM)cells and its mechanism of action.Methods:The expression of COX6C in MM cell lines were detected by RT-PCR.siRNA technology was used to knockdown COX6C expression in OPM2 cells.MTT assay and flow cytometry were employed to assess the effect of COX6C knockdown by siRNA on cell proliferation,mitochondrial membrane potential(Δ Ψm),and intracellular adenosine triphosphate(ATP)levels.The mitochondrial morphological changes in OPM2 cells pre-and post-siRNA-mediated COX6C knockdown were observed by transmission electron microscopy(TEM).Results:The relative expression level of COX6C was significantly increased in MM cell lines(P＜0.01).Following siRNA-mediated COX6C knockdown,OPM2 cell proliferation was inhibited,with viable cells accounting for 62.32％±3.43％and 47.01％±5.12％after 48 and 72 hours of culture,respectively.siRNA-mediated COX6C knockdown also caused significant reductions in mitochondrial membrane potential and intracellular ATP levels(P＜0.05),accompanied by mitochondrial shortening,swelling,and incomplete cristae structures.Conclusion:COX6C may promote the proliferation of MM cells by altering the mitochondrial structure and elevating intracellular ATP levels.

Primary sclerosing cholangitis(PSC)is an autoimmune disease characterized by chronic inflamma-tion and progressive fibrosis that affects both intrahepatic and extrahepatic bile ducts.Despite ongoing research,the under-lying mechanisms of PSC pathogenesis remain incompletely understood.The ductular reaction is not only a key pathologi-cal feature of PSC but also serves as a driving force in its progression.This review examines the promoting effects of the ductular reaction on PSC advancement from multiple perspectives,including the proliferation of biliary epithelial cells,in-flammation,and fibrosis.By providing theoretical insights into the pathogenesis of PSC,this review aims to facilitate the identification of novel therapeutic strategies.

Objective:To analyze the surveillance results of brucellosis in Shanxi Province, to gain a understanding of the epidemic characteristics and changing trend of brucellosis in Shanxi Province, and to provide scientific basis for formulating prevention and control strategies and measures for brucellosis.Methods:The surveillance data of brucellosis in Shanxi Province from Infectious Disease Reporting Information Management System of China Disease Prevention and Control Information System, and the active surveillance results of 5 national brucellosis surveillance sites from 2018 to 2023 were collected for descriptive analysis.Results:From 2018 to 2023, a total of 24 041 cases of human brucellosis were reported in Shanxi Province, with the number of cases increased from 2 800 in 2018 to 5 131 in 2023. The annual reported incidence was 11.22/100 000, ranging from 7.56/100 000 to 14.74/100 000, showing an overall upward trend (χ 2trend = 1 377.43, P < 0.001). The epidemic had affected all counties (cities and districts) in the province, mainly concentrated in Linfen City, Jinzhong City, Datong City, and Shuozhou City, with a total of 13 489 cases of human brucellosis reported, accounting for 56.11%. The population distribution was mainly composed of individuals aged 40 - 69 (17 682 cases), males (18 513 cases), farmers (20 295 cases), and household and unemployed individuals (1 017 cases). The onset of the disease showed obvious seasonality, with the peak time from March to August, accounting for 66.39% (15 961/24 041). A total of 14 130 occupational individuals were investigated at the surveillance sites, and 11 141 underwent serological tests, with a positive rate of 5.25% (585/11 141), including 299 new cases. The positive rate of serological tests was relatively high in Qinyuan County, at 8.51% (241/2 832). Etiological culture was conducted on 338 human blood samples, and 43 strains of Brucella were isolated, with a detection rate of 12.72%. All strains were Brucella melitensis, including 42 strains of Brucella melitensis biovar 3. Conclusions:The overall trend of human brucellosis epidemic in Shanxi Province from 2018 to 2023 is on the rise, and it is still at a high level. It is suggested to continue strengthening monitoring, study the epidemic situation in a timely manner, take comprehensive prevention and control measures, and effectively control the spread of brucellosis.

Objective To analyze the effects of irbesartan(IBN)regulating the stromal cell-derived factor-1(SDF-1)/CXC chemokine receptor 4(CXCR4)pathway on proliferation,migration,and radiosensitivity of lung cancer cells.Methods Human lung cancer A549 cells were randomly divided into the A549 group(without treatment),radiation group(4 Gy X-ray radiation),IBN group(1 μmol/L IBN treatment for 24 hours),IBN+radiation group(1 μmol/L IBN treatment for 24 hours+4 Gy X-ray radiation),pcDNA3.1 group(transfected with pcDNA3.1+1 μmol/L IBN treatment for 24 hours+4 Gy X-ray radiation),and SDF-1 group(transfected with pcDNA3.1 SDF-1+1 μmol/L IBN treatment for 24 hours+4 Gy X-ray radiation).The cell viability,colony formation,apoptosis,and migration of each group were observed.The leakage rate of lactate dehydrogenase(LDH)and Ang Ⅱ levels in cells were detected.Immunofluorescence method was applied to analyze the number of γH2AX focal points of cells in each group.Western blot was applied to detect the expression of proliferation and apoptosis related proteins and SDF-1/CXCR4 pathway related proteins.Results Both radiation and IBN treatment inhibited the proliferation and migration of A549 cells,promoted cell apoptosis,upregulated the number of γH2AX focal points and LDH leakage rate,upregulated the expression of Caspase-3,Bax,and Caspase-7,and downregulated the level of Ang Ⅱand expression of SDF-1,CXCR4,Bcl-2 and PCNA(P<0.05).The combined treatment of radiation and IBN further enhanced the changes of the above indicators(P<0.05).And SDF-1 treat-ment effectively reversed the effects of radiation and IBN treatment on the changes of the above indicators(P<0.05).Conclusion IBN can limit proliferation and migration of lung cancer cells,and increase radiosensitivity by inhibiting the SDF-1/CXCR4 pathway.

Objective To analyze the effects of irbesartan(IBN)regulating the stromal cell-derived factor-1(SDF-1)/CXC chemokine receptor 4(CXCR4)pathway on proliferation,migration,and radiosensitivity of lung cancer cells.Methods Human lung cancer A549 cells were randomly divided into the A549 group(without treatment),radiation group(4 Gy X-ray radiation),IBN group(1 μmol/L IBN treatment for 24 hours),IBN+radiation group(1 μmol/L IBN treatment for 24 hours+4 Gy X-ray radiation),pcDNA3.1 group(transfected with pcDNA3.1+1 μmol/L IBN treatment for 24 hours+4 Gy X-ray radiation),and SDF-1 group(transfected with pcDNA3.1 SDF-1+1 μmol/L IBN treatment for 24 hours+4 Gy X-ray radiation).The cell viability,colony formation,apoptosis,and migration of each group were observed.The leakage rate of lactate dehydrogenase(LDH)and Ang Ⅱ levels in cells were detected.Immunofluorescence method was applied to analyze the number of γH2AX focal points of cells in each group.Western blot was applied to detect the expression of proliferation and apoptosis related proteins and SDF-1/CXCR4 pathway related proteins.Results Both radiation and IBN treatment inhibited the proliferation and migration of A549 cells,promoted cell apoptosis,upregulated the number of γH2AX focal points and LDH leakage rate,upregulated the expression of Caspase-3,Bax,and Caspase-7,and downregulated the level of Ang Ⅱand expression of SDF-1,CXCR4,Bcl-2 and PCNA(P<0.05).The combined treatment of radiation and IBN further enhanced the changes of the above indicators(P<0.05).And SDF-1 treat-ment effectively reversed the effects of radiation and IBN treatment on the changes of the above indicators(P<0.05).Conclusion IBN can limit proliferation and migration of lung cancer cells,and increase radiosensitivity by inhibiting the SDF-1/CXCR4 pathway.