The onset of pregnancy is marked by the formation of a zygote, while the culmination of gestation is manifested by the delivery of a fetus. Meanwhile, a successful pregnancy entails a meticulously coordinated sequence of events from embryo implantation to sustained decidualization of the uterus to placental development and childbirth. The decidual reaction, a pivotal process occurring within the endometrium during pregnancy, is finely regulated by sex steroids and cytokines. Notably, fibroblast growth factors (FGFs), particularly FGF2, play a critical role in this physiological cascade. Dysregulated FGF expression may trigger inadequate decidualization, precipitating a spectrum of adverse pregnancy outcomes, including preeclampsia, recurrent implantation failure, and miscarriage. Furthermore, the human decidua, distinct from most mammalian species and similar to great apes, undergoes regular cycles of formation and shedding, independent of the presence of the embryo in the endometrium. This process is also tightly controlled by various FGFs. In this review, we comprehensively compare diverse research decidualization models, delineate the trend of endometrial FGFs during the menstrual cycle, and provide a synopsis of endometrial diseases triggered by FGF dysregulation.
Humans ; Female ; Pregnancy ; Decidua/physiology* ; Animals ; Endometrium/physiology* ; Fibroblast Growth Factors/metabolism* ; Embryo Implantation ; Menstrual Cycle/physiology*

Intestinal aging is central to systemic aging, characterized by a progressive decline in intestinal structure and function. The core mechanisms involve dysregulation of epithelial cell renewal and gut microbiota dysbiosis. In addition to previous results in model organisms like Drosophila melanogaster, recent studies have shown that in mammalian models, aging causes increased intestinal permeability and intestinal-derived systemic inflammation, thereby affecting longevity. Therefore, anti-intestinal aging can be an important strategy for reducing frailty and promoting longevity. There are three key gaps remaining in the study of intestinal aging: (1) overemphasis on aging-related diseases rather than the primary aging mechanisms; (2) lack of specific drugs or treatments to prevent or treat intestinal aging; (3) limited aging-specific dysbiosis research. In this review, the basic structures and renewal mechanisms of intestinal epithelium, and mechanisms and potential therapies for intestinal aging are discussed to advance understanding of the causes, consequences, and treatments of age-related intestinal dysfunction.

Invasive fungal infections (IFIs) have become prominent global health threats, escalating the burden on public health systems. The increasing occurrence of invasive fungal infections is due primarily to the extensive application of chemotherapy, immunosuppressive therapies, and broad-spectrum antifungal agents. At present, therapeutic practices utilize multiple categories of antifungal agents, such as azoles, polyenes, echinocandins, and pyrimidine analogs. Nevertheless, the clinical effectiveness of these treatments is progressively weakened by the emergence of drug resistance, thereby substantially restricting their therapeutic utility. Consequently, there is an imperative need to expedite the discovery of novel antifungal agents. This review seeks to present an exhaustive synthesis of novel antifungal drugs and candidate agents that are either under current clinical investigation or anticipated to progress into clinical evaluation. These emerging compounds exhibit unique benefits concerning their modes of action, antimicrobial spectra, and pharmacokinetic characteristics, potentially leading to improved therapeutic outcomes relative to conventional antifungal regimens. It is anticipated that these novel therapeutic agents will furnish innovative treatment modalities and enhance clinical outcomes in managing invasive fungal infections.

Objective The aim of this study is to analyze the expression level of cell-free DNA(cf-DNA),a biomarker of neutrophil extracellular traps(NETs),in children with Mycoplasma pneumoniae pneumonia(MPP),and to explore the predictive efficacy of cf-DNA(as a marker of NETs)for the severity of MPP in these children.Methods A total of 115 children with MPP were prospectively selected as the MPP group.Based on the disease severity,the MPP group was categorized into the mild group(n=75)and the severe group(n=40).During the same period,50 healthy children undergoing physical examinations were selected as the control group.The levels of serum cf-DNA in the MPP group and the control group,as well as the levels of C-reactive protein(CRP),D-dimer,lactate dehydrogenase(LDH),interleukin-6(IL-6),interferon-γ(IFN-γ),and tumor necrosis factor-α(TNF-α)in the MPP group were detected.The differences in the levels of serum cf-DNA and related inflammatory factors among the groups were compared,and the role of serum cf-DNA in evaluating the severity of MPP was analyzed.Results The level of serum cf-DNA in children of the MPP group was notably higher than that in the control group,with a more significant elevation observed in the severe group(P<0.05).The levels of CRP,D-dimer,LDH,IL-6,IFN-γ,and TNF-α were all higher in the severe group than in the mild group(P<0.05).Multivariate logistic regression analysis showed that the increased levels of serum cf-DNA,CRP,and IL-6 were closely related to the severity of MPP(P<0.05).The results of receiver operating characteristic(ROC)curve analysis showed that the area under the curve(AUC)of the combination of serum cf-DNA,CRP,and IL-6 for predicting severe MPP was 0.981,which was higher than that of each index alone(P<0.05).Conclusions Serum cf-DNA(as a marker of NETs)is closely related to the severity of MPP in children.The combined detection of cf-DNA,CRP,and IL-6 is more beneficial for assessing the severity of MPP in children.

BACKGROUND:Studies have shown that immune cells are involved in all processes of ischemic stroke,in which cuproptosis also plays a key role.OBJECTIVE:To screen diagnostic biomarkers related to the progression of ischemic stroke through bioinformatics,and analyze and validate cuproptosis-related genes closely related to the occurrence and development of ischemic stroke.METHODS:The GSE16561 microarray was obtained from the GEO database,containing data from 39 cases of ischemic stroke(ischemic stroke group)and 24 controls(control group).Differentially expressed genes from the ischemic stroke microarray data were analyzed.Gene ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses were performed.By using LASSO and Random Forest methods,key genes affecting the occurrence and development of ischemic stroke were screened,and a diagnostic model was established and validated.Differential gene analysis was performed through immune cell infiltration and weighted gene co expression network.The differentially expressed immune-related genes were intersected with cuproptosis genes to obtain the hub genes related to cuproptosis immunity.In vitro cell experiments were conducted to divide rat hippocampal neurons into a normal group and an ischemic stroke group,and qPCR experiments were performed to verify the results.RESULTS AND CONCLUSION:(1)573 differentially expressed genes were obtained by differential analysis.Differentially expressed genes were mainly enriched in biological processes,such as positive regulation of immune response,and signaling pathways such as lipid and atherosclerosis.(2)Machine learning methods were used to screen diagnostic genes such as MFN2,PKM2,CREG1,and FOXO3A,which may have some diagnostic value for ischemic stroke.(3)Immune infiltration analysis revealed resting plasma cells,NK cells,macrophages,etc.,indicating that immune cells play a certain role in the pathogenesis of ischemic stroke.(4)Weighted gene co-expression network analysis combined with immune infiltration analysis obtained 118 key module genes,which were intersected with cuproptosis genes to obtain 2 cuproptosis and immune characteristic genes.The correlation analysis between four diagnostic genes and Hub genes showed that the expression of FOXO3A and MFN2,PKM2 and BCL2L1,MTF1 and MFN2,ATP7B and BCL2L1 were correlated.(5)The qPCR results showed significant differences in the genes MTF1 and ATP7B between the ischemic stroke group and the blank group.To conclude,ATP7B and MTF1 can serve as characteristic genes for cuproptosis in ischemic stroke.It is possible to improve ischemic stroke by intervening in ATP7B and MTF1 to regulate cuproptosis.

Objective:To explore the relationship between impulsivity traits,anxiety,and symptoms of eating disorders,with a focus on the mediating effect of anxiety between impulsivity and eating disorder symptoms.Me-thods:A total of 244 patients with eating disorders meeting the DSM-5 diagnostic criteria for anorexia nervosa(AN)and bulimia nervosa(BN)were enrolled,and the Eating Disorder Inventory-1(EDI-1),Barratt Impulsive-ness Scale(BIS-11),and the State Anxiety Inventory(SAI)were assessed.Mediation role analysis was performed by SPSS macro PROCESS program.Results:There was a significant positive correlation between the total score of BIS-11,SAI and EDI-1 in AN and BN patients(AN,r=0.56,0.63,0.72;P＜0.001.BN,r=0.51,0.31,0.56;P＜0.001 or P＜0.01).The total score of SAI played a mediating effect between the total score of BIS-11 and the total score of EDI-1,but the total score of SAI played a partial mediating effect(effect ratio was 46.9％)in patients with AN,and the total score of SAI played a full mediating effect in patients with BN.Conclusion:Impulsive trait and anxiety may be positive predictors of eating disorder symptoms.Anxiety mediates the relationship between impul-sivity trait and eating disorder symptoms,with a partial mediating effect in patients with AN and a full mediating effect in patients with BN.

Objective:To explore the relationship between impulsivity traits,anxiety,and symptoms of eating disorders,with a focus on the mediating effect of anxiety between impulsivity and eating disorder symptoms.Me-thods:A total of 244 patients with eating disorders meeting the DSM-5 diagnostic criteria for anorexia nervosa(AN)and bulimia nervosa(BN)were enrolled,and the Eating Disorder Inventory-1(EDI-1),Barratt Impulsive-ness Scale(BIS-11),and the State Anxiety Inventory(SAI)were assessed.Mediation role analysis was performed by SPSS macro PROCESS program.Results:There was a significant positive correlation between the total score of BIS-11,SAI and EDI-1 in AN and BN patients(AN,r=0.56,0.63,0.72;P＜0.001.BN,r=0.51,0.31,0.56;P＜0.001 or P＜0.01).The total score of SAI played a mediating effect between the total score of BIS-11 and the total score of EDI-1,but the total score of SAI played a partial mediating effect(effect ratio was 46.9％)in patients with AN,and the total score of SAI played a full mediating effect in patients with BN.Conclusion:Impulsive trait and anxiety may be positive predictors of eating disorder symptoms.Anxiety mediates the relationship between impul-sivity trait and eating disorder symptoms,with a partial mediating effect in patients with AN and a full mediating effect in patients with BN.

Objective The aim of this study is to analyze the expression level of cell-free DNA(cf-DNA),a biomarker of neutrophil extracellular traps(NETs),in children with Mycoplasma pneumoniae pneumonia(MPP),and to explore the predictive efficacy of cf-DNA(as a marker of NETs)for the severity of MPP in these children.Methods A total of 115 children with MPP were prospectively selected as the MPP group.Based on the disease severity,the MPP group was categorized into the mild group(n=75)and the severe group(n=40).During the same period,50 healthy children undergoing physical examinations were selected as the control group.The levels of serum cf-DNA in the MPP group and the control group,as well as the levels of C-reactive protein(CRP),D-dimer,lactate dehydrogenase(LDH),interleukin-6(IL-6),interferon-γ(IFN-γ),and tumor necrosis factor-α(TNF-α)in the MPP group were detected.The differences in the levels of serum cf-DNA and related inflammatory factors among the groups were compared,and the role of serum cf-DNA in evaluating the severity of MPP was analyzed.Results The level of serum cf-DNA in children of the MPP group was notably higher than that in the control group,with a more significant elevation observed in the severe group(P<0.05).The levels of CRP,D-dimer,LDH,IL-6,IFN-γ,and TNF-α were all higher in the severe group than in the mild group(P<0.05).Multivariate logistic regression analysis showed that the increased levels of serum cf-DNA,CRP,and IL-6 were closely related to the severity of MPP(P<0.05).The results of receiver operating characteristic(ROC)curve analysis showed that the area under the curve(AUC)of the combination of serum cf-DNA,CRP,and IL-6 for predicting severe MPP was 0.981,which was higher than that of each index alone(P<0.05).Conclusions Serum cf-DNA(as a marker of NETs)is closely related to the severity of MPP in children.The combined detection of cf-DNA,CRP,and IL-6 is more beneficial for assessing the severity of MPP in children.

BACKGROUND:Studies have shown that immune cells are involved in all processes of ischemic stroke,in which cuproptosis also plays a key role.OBJECTIVE:To screen diagnostic biomarkers related to the progression of ischemic stroke through bioinformatics,and analyze and validate cuproptosis-related genes closely related to the occurrence and development of ischemic stroke.METHODS:The GSE16561 microarray was obtained from the GEO database,containing data from 39 cases of ischemic stroke(ischemic stroke group)and 24 controls(control group).Differentially expressed genes from the ischemic stroke microarray data were analyzed.Gene ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses were performed.By using LASSO and Random Forest methods,key genes affecting the occurrence and development of ischemic stroke were screened,and a diagnostic model was established and validated.Differential gene analysis was performed through immune cell infiltration and weighted gene co expression network.The differentially expressed immune-related genes were intersected with cuproptosis genes to obtain the hub genes related to cuproptosis immunity.In vitro cell experiments were conducted to divide rat hippocampal neurons into a normal group and an ischemic stroke group,and qPCR experiments were performed to verify the results.RESULTS AND CONCLUSION:(1)573 differentially expressed genes were obtained by differential analysis.Differentially expressed genes were mainly enriched in biological processes,such as positive regulation of immune response,and signaling pathways such as lipid and atherosclerosis.(2)Machine learning methods were used to screen diagnostic genes such as MFN2,PKM2,CREG1,and FOXO3A,which may have some diagnostic value for ischemic stroke.(3)Immune infiltration analysis revealed resting plasma cells,NK cells,macrophages,etc.,indicating that immune cells play a certain role in the pathogenesis of ischemic stroke.(4)Weighted gene co-expression network analysis combined with immune infiltration analysis obtained 118 key module genes,which were intersected with cuproptosis genes to obtain 2 cuproptosis and immune characteristic genes.The correlation analysis between four diagnostic genes and Hub genes showed that the expression of FOXO3A and MFN2,PKM2 and BCL2L1,MTF1 and MFN2,ATP7B and BCL2L1 were correlated.(5)The qPCR results showed significant differences in the genes MTF1 and ATP7B between the ischemic stroke group and the blank group.To conclude,ATP7B and MTF1 can serve as characteristic genes for cuproptosis in ischemic stroke.It is possible to improve ischemic stroke by intervening in ATP7B and MTF1 to regulate cuproptosis.

Non-small cell lung cancer is one of the cancers with the highest incidence and mortality rate in the world, and precise prognostic models can guide clinical treatment plans. With the continuous upgrading of computer technology, deep learning as a breakthrough technology of artificial intelligence has shown good performance and great potential in the application of non-small cell lung cancer prognosis model. The research on the application of deep learning in survival and recurrence prediction, efficacy prediction, distant metastasis prediction, and complication prediction of non-small cell lung cancer has made some progress, and it shows a trend of multi-omics and multi-modal joint, but there are still shortcomings, which should be further explored in the future to strengthen model verification and solve practical problems in clinical practice.