Objective To analyze the clinical characteristics and prognostic risk factors of patients with atrial fibrillation(AF)related to septic shock admitted to the intensive care unit(ICU).Methods This retrospective cohort study included 152 patients with septic shock who were admitted to the ICU between January 2020 and December 2023.Patients were categorized into AF(n=48)and non-AF(n=104)groups based on the occurrence of AF.Clinical parameters were compared between the two groups,and variables with statistically significant differences(P<0.05)were entered into a multivariate logistic regression analysis to identify clinical features associated with AF.Patients were also stratified into survival(n=103)and death(n=49)groups based on 28-day outcomes.Variables showing signifi-cant intergroup differences(P<0.05)were further included in a multivariate model to identify independent risk factors for mortality.Kaplan-Meier survival analysis was performed using AF as a binary variable,and log-rank tests were applied to compare survival curves.Results The incidence of AF was 31.58%among patients with septic shock.Compared with the non-AF group,the AF group was older,received higher cumulative doses of vasoactive agents,and had elevated levels of lactate(Lac),N-terminal brain natriuretic peptide precursor(NT-proBNP),troponin I(cTnI),tumor necrosis factorα(TNF-α),and C-reactive protein(CRP).The AF group also had higher E/e'ratios,left ventricular ejection fraction(LVEF),Acute Physiology and Chronic Health Evaluation-Ⅱ(APACHEⅡ)scores,Sequen-tial Organ Failure Assessment(SOFA)scores,and 28-day mortality rates(all P<0.05).Multivariate logistic regression identified age(odds ratio[OR]=1.060,P=0.015),SOFA score(OR=1.525,P=0.001),TNF-α(OR=1.009,P=0.026),CRP(OR=1.008,P=0.002),and E/e'(OR=1.363,P=0.023)as independent risk factors for AF.The 28-day mortality rate was 32.24%.Compared with survivors,non-survivors had significantly higher Lac,cTnI,E/e',LVEF,and TNF-α levels,higher APACHEⅡand SOFA scores,longer ICU stays,and a higher incidence of AF(all P<0.05).Multivariate analysis identified SOFA score,cTnI,E/e',and AF as independent predictors of 28-day mortality.Kaplan-Meier analysis revealed significantly poorer survival in patients with AF(χ2=6.747,P=0.009).Conclusion AF is common in ICU patients with septic shock.Advanced age,greater organ dysfunction,elevated inflammatory markers,and diastolic dysfunction are associated with AF occurrence.Organ dysfunction,myocardial injury,diastolic dysfunction,and AF are inde-pendent predictors of mortality in this population.Greater clinical attention is warranted in patients with AF and septic shock due to their elevated risk of poor outcomes.

Objective To investigate the effects of leflunomide combined with belimumab on the activity index and renal function of patients with lupus nephritis(LN).Methods A total of 82 patients with LN admitted to Tangshan Gongren Hospital from January 2022 to January 2024 were selected as study subjects and randomly divided into two groups:the combination group(belimumab+leflunomide treatment)and the control group(leflunomide treatment),with 41 patients in each group.Renal function indicators(blood urea nitrogen(BUN),serum creatinine(sCr),uric acid(UA),and 24-hour urine protein),disease activity[Systemic Lupus Erythematosus Disease Activity Index(SLEDAI)score],laboratory indicators(anti-double-stranded DNA antibody,anti-ds-DNA;C-reactive protein,CRP;tumor necrosis factor α,TNF-α),efficacy,and safety were compared before and after treatment between the two groups.Results After treatment,the levels of BUN,sCr,UA,and 24-hour urine protein in the combination group were significantly lower than those in the con-trol group(P<0.05).Furthermore,the SLEDAI score,anti-ds-DNA,CRP,and TNF-α levels in the combination group were also lower than those in the control group(P<0.05).The total effective rate in the combination group(97.56%)was higher than that in the control group(85.37%,P=0.048),despite no statistically significant difference in the incidence of adverse reactions between the two groups(P>0.05).Conclusion Leflunomide combined with belimumab treatment for LN can effectively improve clinical efficacy,reduce disease activity,alleviate inflammation,enhance immune function,and improve renal function,with a certain level of safety,thus making the regimen highly valuable for clinical application and promotion.

Objective To investigate the effect of PTGS2 knockdown on tumor-associated macrophage(TAM)M2 polarization in the treatment of nasopharyngeal carcinoma(NPC).Methods Adenovirus-mediated knockdown of PTGS2 was performed in primary NPC cells.A co-culture system of primary NPC cells and TAMs and a mixed three-dimensional(3D)co-culture of primary NPC cells,TAMs,and human CD8+T cells were established in vitro.The control,Adv-PTGS2 shRNA,and Adv-shRNA NT groups were subjected to in vitro and in vivo experiments.In the co-culture system of primary NPC cells and TAMs,IL-12,IL-10,and TGF-βlevels in the culture superna-tants were determined using the ELISA.MMP-2 and MMP-9 expression levels in primary NPC were determined using Western blotting.In the mixed culture system of the three types of cells,cell viability was measured using the CCK-8 method.IFN-γand GZMBmRNA levels were determined using qPCR.The three types of cell-mixed cultures were injected subcutaneously into xenografts,and tumor growth was monitored for 21 d.Results Compared with control group,IL-12 levels increased and IL-10 and TGF-βlevels decreased in the culture supernatant of Adv-PTGS2 shRNA cells(P<0.05).MMP-2 and MMP-9 expression levels in primary NPC decreased(P<0.05).Com-pared with the control group,CD8+T cell proliferation ability and relative IFN-γand GZMBmRNA expression levels increased(P<0.05 for both experiments)in the Adv-PTGS2 shRNA cells.Compared with the control group,the Adv-PTGS2 shRNA group showed slower tumor growth(P<0.05)and lower tumor mass(P<0.05)in in vivo xenografts.Conclusion PTGS2knockdown inhibited TAM M2 pola-rization,regulated the immune-hot state in the tumor microenvironment,and inhibited NPC growth.

Objective To investigate the impact of minocycline(MC)on myocardial cell damage in rats with chronic heart failure(CHF)by regulating the hypoxia-inducible factor 1α(HIF-1α)/B-cell lymphoma-2/adenovirus E1B 19-kDa interacting protein(BNIP3).Methods All rats were randomly divided into Sham,CHF,positive drug(LP),low dose MC,high dose MC(HMC),and HMC+HIF-1α activator(DMOG)groups.Cardiac function was detected using echocardiography.HE staining,transmission electron microscopy,and TUNEL assay were used to evaluate myocardial pathology and apoptosis.Enzyme-linked immunosorbent assay was applied to quantify tumor necrosis factor α(TNF-α),interleukin-1β,superoxide dismutase(SOD),and malondialdehyde(MDA).Quantitative real-time PCR was used to detect the mRNA levels of Bcl-2 and Bcl-2-related X protein(Bax),while Western blotting was applied to detect the expres-sion of HIF-1α,BNIP3,Beclin-1,and microtubule-associated protein 1 light chain 3(LC3)proteins.Results Compared to rats in the sham group,rats from the CHF group exhibited increased left ventricular end-diastolic diameter(LVEDD),left ventricular end-systolic diameter(LVESD),cell apoptosis rate,TNF-α,IL-1β,MDA,Bax,HIF-1α,BNIP3,Beclin-1,and LC3Ⅱ/Ⅰwith decreased left ventricular ejection fraction(LVEF),left ventricular shortening fraction(LVFS),SOD,and Bcl-2 levels(P<0.05).Compared with CHF group,rats from LP group,LMC group and HMC group exhibited decreased levels of LVEDD,LVESD,apoptosis rate,TNF-α,IL-1β,MDA,Bax,HIF-1α,BNIP3,Beclin-1,LC3Ⅱ/Ⅰ,and increased levels of LVEF,LVFS,SOD and Bcl-2(P<0.05).DMOG attenuated the protective effect of high-dose MC on myocardial cell damage in rats of the CHF group(P<0.05).Conclusion MC improves myocardial cell damage in rats of CHF group by inhibiting the HIF-1α/BNIP3 signaling pathway.

Objective To compare the effects of single antiplatelet therapy(SAPT)versus dual antiplatelet therapy(DAPT)on bleeding and ischemic events in patients undergoing transcatheter aortic valve replacement(TAVR)without long-term anticoagulation indications.Methods This randomized controlled trial included 90 post-TAVR patients without anticoagulation indications,who were allocated to the SAPT group(n=46,aspirin 100 mg/d)or DAPT group(n=44,aspirin 100 mg/d+clopidogrel 75 mg/d for 3 months,followed by aspirin monotherapy).Maximum aggregation rates of platelets induced by arachidonic acid(MARAA)and adenosine diphosphate(MARADP)were measured 1,3,6,and 12 months postoperatively.Bleeding and ischemic events were recorded during the follow-up visits.Results The SAPT group exhibited significantly higher MARAA and MARADP scores at 1 and 3 months,and higher MARAA scores at 6 months compared to the DAPT group(P<0.05).At the 12-month follow-up,the SAPT group had a significantly lower inci-dence of bleeding events compared to the DAPT group(13.0%vs.31.8%,P=0.043).No statistically significant difference was observed in ischemic events between the groups(15.2%vs.11.4%,P=0.759).Conclusion For TAVR patients without anticoagulation indica-tions,SAPT significantly reduced the 1-year bleeding risk compared to DAPT,without increasing ischemic events.These findings support the safety and efficacy of SAPT after TAVR.

Objective To investigate the role of PTGDR2 in the progression of lung adenocarcinoma(LUAD)and its potential as a thera-peutic target in regard to regulating tumor stemness via autophagy.Methods In vitro experiments were conducted by silencing PTGDR2 with siRNA and treating LUAD A549 cells with PGD2 in order to evaluate its effects on cell proliferation,invasion,and stem cell marker expression.Autophagy regulation was further verified by rapamycin treatment.Results Activation of PTGDR2 signaling inhibited A549 cell proliferation and invasion,induced the upregulation of autophagy markers,and reduced the expression of stem cell markers.In con-trast,silencing PTGDR2blocked autophagy and enhanced tumor stemness.Conclusion PTGDR2 inhibits tumor stemness through the activation of autophagy,and therefore has potential as a therapeutic target to overcome drug resistance in LUAD.

Chronic kidney disease(CKD)is a major global health threat owing to its progressive nature and limited means of early diagnosis,with a significant majority of patients diagnosed in the mid-to-late stages of the disease and high mortality rates.With recent advancements in technology,the importance of disease prediction models in the management of CKD has increased.Disease incidence risk prediction models can identify high-risk groups at an early stage and provide support for timely intervention and management.These disease prognosis models can accurately assess the risk of future adverse events and optimize management strategies for patients.The aim of this review is to discuss the progress of disease prediction models in assessing the occurrence and prognosis of CKD and explore their potential for improving the early diagnosis of the disease,optimizing treatment,and improving patient prognosis.These advancements would assist in effectively preventing and treating CKD as well as improving treatment efficacy and quality of life of patients.

Cell ablation has recently emerged as a valuable technique for investigating cell lineage and function during the development of organisms.The nervous system contains diverse cellular populations,whose roles under physiological and pathological conditions are still not fully understood.Various cell ablation methods have been reported to specifically ablate different types of cell populations in the nervous system and have also been used to study cellular functions under physiological conditions as well as the pathogenesis of neurologi-cal system diseases.In this article,we have summarized common cell ablation techniques and focus on their applications in neurobio-logical and neurological system disease research.

Objective To investigate the effects of transcranial magnetic stimulation(TMS)combined with human umbilical cord mesen-chymal stem cells(hUC-MSCs)on ferroptosis following spinal cord injury(SCI)in rats.Methods Allen percussion was used to estab-lish the SCI model.A total of 60 SD rats were randomly divided into sham,SCI,TMS,hUC-MSC,and TMS+hUC-MSC groups,with 12 rats in each group.Motor function was evaluated using the Basso-Beattie-Bresnahan(BBB)score.Spinal cord tissues were sampled and stained with hematoxylin and eosin(HE)as well as Nissl to observe tissue damage as well as the changes in neurons and Nissl bodies,respectively.The colorimetric method was used to detect the contents of ferrous ions(Fe2+)and reduced glutathione(GSH).Transmission electron microscopy was applied to observe the ultrastructure of the mitochondria.Western blotting was performed to detect the expres-sion levels of SLC7A11,GPX4,and ACSL4.Results The SCI group had lower BBB scores,higher Fe2+and ACSL4 protein expression levels,and lower GSH,SLC7A11,and GPX4 protein expression levels than the sham group(P<0.05).The mitochondrial cristae reduced with membrane shrinkage,neuronal damage was severe,and Nissl bodies were absent in the SCI group.The TMS,hUC-MSC,and TMS+hUC-MSC groups had higher BBB scores,lower Fe2+and ACSL4 protein expression levels,and higher GSH,SLC7A11,and GPX4 protein expression levels than the SCI group(P<0.05).The mitochondrial cristae increased with an intact membrane structure,the pathological damage was attenuated,neuronal morphology was restored,and Nissl bodies were clearly visible in TMS,hUC-MSC,and TMS+hUC-MSC groups.Conclusion TMS combined with hUC-MSC inhibits ferroptosis through activating the SLC7A11/GSH/GPX4 pathway,alleviates secondary injury after SCI,and promotes functional recovery and neural remodeling in rats.

Objective To investigate the effect of loganin(Log)on glutamine metabolism in cervical cancer through the regula-tion of nuclear factor red blood cell 2 related factor 2(NFE2L2)-ferritin heavy chain 1(FTH1)-glutathione peroxidase 4(GPX4).Methods Bioinformatics analysis was conducted to identify common targets of Log,glutamine metabolism,and cervical cancer.Hela cells were divided into Blank,control(Ctrl),Log,cisplatin(DDP),NFE2L2 activator(TBHQ),NFE2L2 inhibitor(ML385),and TBHQ+Log groups to detect cell proliferation,invasion,apoptosis,glutamine metabolism,and the protein expression of NFE2L2,FTH1,and GPX4.A cervical cancer xenograft mouse model was established to investigate the in vivo effects of Log on the progression of cervical cancer.Results Bioinformatics analysis confirmed that NFE2L2 might be a target of Log in the treatment of cervical cancer.Both Log and DDP reduced the proliferation and invasion abilities of Hela cells,increased apoptosis,and decreased the levels of glutamine and glutamic acid,as well as the protein expression of glutaminase(GLS1)and glutamic dehydrogenase(GLUD1,P<0.05).The NFE2L2 activator TBHQ had opposite effects,whereas ML385 had a similar impact on the Log.Additionally,Log treatment inhibited the protein expression of NFE2L2,FTH1,and GPX4(P<0.05).Animal experiments showed that Log significantly inhibited cervical cancer progression(P<0.05).Conclusion Log affects cervical cancer progression via glutamine metabolism by inhibiting the NFE2L2-FTH1-GPX4 signaling pathway.