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Objective To study the effects and potential mechanisms of the aquaporin 1(AQP1) inhibitor acetazolamide(AZ) on the proliferation, apoptosis, and inflammatory response of rheumatoid arthritis(RA) fibroblast-like synoviocytes(FLS). Methods TNF-α-induced RA-FLS was served as in vitro RA model. MTT assay, IF staining, and EdU incorporation assay were applied to study AZ′s effects on RA-FLS proliferation. Hoechst staining, flow cytometry analysis of Annexin V-FITC/PI-stained cells, and mitochondrial membrane potential detection experiments were used to detect cell apoptosis. ELISA and quantitative real-time PCR methods were used to measure pro-inflammatory cytokine production. Cell autophagy was evaluated using IF staining and mCherry-GFP-LC3B puncta assay. Western blot was performed to detect the levels of autophagy, apoptosis, and proliferation-related proteins. Moreover, the role of autophagy inhibition in AZ′s effects on RA-FLS was examined by co-treating with the autophagy activator rapamycin(RAPA) or the autophagy inhibitor 3-methyladenine(3-MA). Results AZ dose-dependently inhibited cell proliferation, promoted apoptosis, and reduced the production of pro-inflammatory cytokines in RA-FLS. Furthermore, AZ suppressed cytoprotective autophagy in these cells, as evidenced by decreased LC3B levels(P

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Objective To explore the role and molecular mechanism of parthenolide(PTL) in regulating tumor-associated macrophage(TAM) polarization to inhibit the malignant progression of gallbladder cancer cells. Methods M0 macrophages were co-cultured with human gallbladder cancer cell line GBC-SD and treated with PTL, and the cells were divided into control group, TAM group, TAM+PTL group. Flow cytometry was used to determine the levels of CD86 and CD206 in macrophages. RT-qPCR and Western blot were used to determine the expressions of CD163, interleukin-10(IL-10) and arginase-1(Arg-1). ELISA and Western blot were used to determine the secretion of CC chemokine ligand 2(CCL2) in the supernatant of GBC-SD cells and the expression of CCL2 in the cells. GBC-SD cells were transfected with a CCL2 overexpression vector and divided into TAM, TAM+PTL, TAM+PTL+OE-NC, TAM+PTL+OE-CCL2 groups. Flow cytometry was used to assess CD86 and CD206 levels in macrophages, RT-qPCR and Western blot were used to assess CD163, IL-10 and Arg-1 expression. CCK-8 assay, plate-based colony formation assay and Transwell chamber assay were used to assess GBC-SD cell proliferation, migration and invasion, respectively. Results Compared with the TAM group, the TAM+PTL group showed increased CD86 expression and decreased CD206 expression in macrophages, the mRNA and protein expressions of CD163, IL-10 and Arg-1 were downregulated, the CCL2 content and protein expression in GBC-SD cells decreased, cell proliferation activity, colony formation, migration and invasion were all reduced(P

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Objective To investigate the effect and mechanism of long non-coding RNA RMRP(LncRNA RMRP) on oxygen-glucose deprivation/reperfusion(OGD/R)-induced ferroptosis in mouse HL-1 cardiomyocytes by regulating miR-766-5p. Methods HL-1 cells were cultured in vitro, and OGD/R models were established. The expression levels of LncRNA RMRP in HL-1 cells at various reperfusion time points were subsequently quantified using qRT-PCR. The LncRNA RMRP small RNA interference fragment(si-RMRP) and its corresponding negative control(si-NC), as well as the miR-766-5p inhibitor and its respective negative control(inhibitor-NC), were transfected into HL-1 cells. Subsequently, the cells were subjected to OGD/R treatment. CCK-8 assay was employed to evaluate cell viability. Assay kits were employed to measure the levels of lactate dehydrogenase(LDH) in the cell supernatant, as well as the intracellular levels of malondialdehyde(MDA), superoxide dismutase(SOD), glutathione(GSH), and ferrous ion(Fe2+). qRT-PCR analysis was conducted to assess the expression levels of LncRNA RMRP and miR-766-5p. Western blot analysis was conducted to assess the expression levels of proteins associated with ferroptosis including GPX4, SLC7A11, and FTH1. Dual-luciferase reporter assays were performed to investigate the sponge adsorption relationship between LncRNA RMRP and miR-766-5p. Results As reperfusion time extended, the expression level of LncRNA RMRP in cells progressively increased(P2+ levels within the cells, and decreased the activities of SOD and GSH in cells(P2+ levels within the cells, and promoting SOD and GSH activities in cells(P

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Objective To identify ferroptosis-related genes associated with gastric cancer prognosis and investigate their potential molecular functions. Methods Gene expression profiles and clinical information of gastric cancer tissues and adjacent normal tissues were obtained from TCGA database. Differential expression analysis of ferroptosis-related genes was performed using the "DESeq2" package in R software. Key genes were identified and a prognostic model for gastric cancer was constructed through Cox regression analysis based on the LASSO algorithm. Patients were stratified into high-risk and low-risk groups according to the median risk score. The accuracy of the model was evaluated using Kaplan-Meier survival analysis and ROC curve analysis. Immune cell infiltration in gastric cancer patients was assessed with the "CIBERSORT" package. The mRNA expression of differentially expressed genes(DEGs) with prognostic significance was examined in both gastric cancer and adjacent normal tissue samples. In vitro experiments were conducted to validate the impact of hydroxycarboxylic acid receptor 1(HCAR1) on the malignant biological behavior of gastric cancer. Results Based on ferroptosis-related genes from the TCGA database, a novel prognostic model was constructed. It demonstrated robust predictive power for survival in both training and validation cohorts. RT-qPCR analysis of 8 pairs of gastric cancer and normal tissues revealed that the expression patterns of 6 prognostic DEGs in cancer tissues were consistent with those predicted by the model. In vitro experiments confirmed that downregulation of the key gene HCAR1 could inhibit the proliferation, invasion, and metastasis of gastric cancer cells. Conclusion The ferroptosis-related gene based prognostic model exhibits robust predictive capability, allowing for accurate determination of prognosis and survival in individuals with gastric cancer.

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Objective To explore the active components, key targets, and mechanism of action of turnip in alleviating pulmonary fibrosis(PF) based on network pharmacology and animal experiments. Methods The active components and targets of Brassica rapa L. were screened using the traditional Chinese medicine systems pharmacology database and analysis platform database, and PF-related targets were obtained from disease databases such as online mendelian inheritance of man(OMIM) and DrugBank. The intersection targets were used to construct a protein-protein interaction(PPI) network to identify core targets, followed by gene oncology(GO)/Kyoto encyclopedia of genes and genomes(KEGG) pathway enrichment analysis. In the animal experiments, a bleomycin-induced PF mouse model was established. Pathological changes in lung tissue were evaluated using HE and Masson staining. qRT-PCR was used to detect the mRNA expression of tumor necrosis factor-α(TNF-α), phosphatidylinositol 3-kinase(PI3K), and akstrain transforming 1(AKT1), and immunofluorescence staining was used to measure the protein expression of TNF-α, PI3K, and AKT1. Results The 68 active components identified in Brassica rapa L. may regulate PI3K-Akt signaling pathway by acting on 89 potential targets such as TNF-α and AKT1. The results of animal experiments showed that polysaccharide of Brassica rapa L.(BRPs) could significantly reduce the degree of bleomycin induced pulmonary fibrosis in mice; HE and Masson staining of lung tissue showed that compared with the model group, the damage of alveolar structure, the infiltration of inflammatory cells and the deposition of collagen fibers in the BRPs treatment group were significantly reduced. Further mechanism studies showed that BRPs could significantly down-regulate the mRNA and protein expression levels of TNF-α, PI3K and AKT1 in lung tissue of pulmonary fibrosis mice. Conclusion Brassica rapa L. can synergistically alleviate pulmonary fibrosis through “multi-component, multi-target and multi-channel” approach; BRPs is one of the main active components, and plays an anti-fibrosis role by inhibiting TNF-α/PI3K Akt signaling pathway.

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Objective To determine the expression of melanoma-associated antigens D4(MAGED4) and SIRT7 in human glioma, and to analyze the potential effects of MAGED4 and SIRT7 on glioma cell proliferation. Methods The MAGED4 and SIRT7 expression levels and their correlation were compared by the China glioma genome atlas(CGGA), human protein atlas(HPA), and UALCAN databases. Survival analysis, ROC curve analysis, and Cox regression analysis were used to predict the outcome of MAGED4 and SIRT 7 in glioma patients. Gene ontology(GO) and Kyoto encyclopedia of genes and genomes(KEGG) signaling pathway enrichment analysis were used to explore the biological functions of MAGED4 and SIRT7 in glioma. Western blot experiment was used to investigate whether MAGED4 protein exerted its regulatory effects on the activity of the PI3K/AKT signaling pathway via SIRT7. The effect of MAGED4 on cell proliferation in glioma through SIRT7 was explored by CCK-8. Results The analysis results of CGGA, UALCAN, and HPA databases showed that the expression levels of MAGED4 and SIRT7 in glioma tissues were higher than those in normal brain tissue, and the expression were positively correlated. Results of survival, ROC, and Cox analysis showed that high expression of MAGED4 and SIRT7 mRNA were risk factors for poor prognosis in glioma. Results of KEGG enrichment analysis showed that MAGED4 and SIRT7 were associated with the PI3K/AKT signaling in glioma, and Western blot results showed that MAGED4 activated the PI3K/AKT signaling pathway by regulating SIRT7. The CCK-8 results showed that MAGED4 promotes the proliferation of glioma cells through SIRT7. Conclusion MAGED4 and SIRT7 are highly expressed in glioma and associated with poor prognosis, and MAGED4 promotes glioma cell proliferation through activation of the PI3K/AKT signaling pathway by SIRT7.

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Objective To investigate the role mechanism of doublecortin(DCX) in glioma and screen DCX overexpression-related differentially expressed genes, so as to provide new targets for glioma targeted therapy. Methods Using rat glioma C6 cells as the target cells, LV-DCX-EGFP, LV-Cas9-Puro, and LV-Ctrl-EGFP lentiviruses were constructed. DCX overexpressing and control C6 cell lines were established through Cas9 dual-vector system transfection and screening. Transcriptome sequencing was used to obtain the differentially expressed gene profiles. iDEP and DESeq2 were applied to screen differentially expressed genes with the threshold of |Log_2FC|>2 and P0.7, indicating good diagnostic value. RT-qPCR validation showed that the mRNA expression levels of some upregulated genes(POU2F3, LPAR6, SREBF1) significantly increased(P

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Objective To establish a mouse model of lung injury induced by self-antigens and explore its pathological mechanisms to provide a reliable animal model for studying the pathogenesis of rheumatoid arthritis-associated interstitial lung disease(RA-ILD). Methods The mice were injected intradermal with antigenemulsion made of complete freund′s adjuvant(CFA) and lung tissue protein, and the emulsion prepared with incomplete Freund′s adjuvant(IFA) was used to enhance immunity. HE staining was used to observe the histopathological changes in the mice. Masson staining was used to detect pulmonary fibrosis. The mRNA levels of rheumatoid factor(RF), krebs von den lungen-6(KL-6) and surfactant protein D(SP-D) were detected by qPCR. The levels of ACPA, IgG1, IgG2a and IgG3 antibodies were detected by ELISA. The changes of inflammatory cells and α-smooth muscle actin(α-SMA)expression in lung tissue were detected by immunofluorescence staining. The protein expression levels of Collagen I and α-SMA were detected by Western blot. The changes of immune cells were detected by flow cytometry. Results HE staining showed that inflammatory cell infiltration increased and tissue structure changed significantly in lung tissue after the model was established by self-lung tissue antigen. Masson staining showed increased collagen deposition in lung tissue of model mice. qPCR tests revealed elevated mRNA levels of RF, KL-6 and SP-D. ELISA tests revealed elevated levels of ACPA, IgG1 and IgG3 antibodies. Immunofluorescence results showed that monocytes and T cells increased, and α-SMA expression increased in the model group. Western blot results showed increased protein expressions of Collagen Ⅰ and α-SMA. The flow cytometry results showed an increase in T cells and monocytes in the lung tissue. Conclusion The mouse model of lung injury induced by self-antigens is successfully established, and T cells and monocytes may be involved in the occurrence and progression of the disease.

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Objective To explore the association between mammalian sterile 20-like kinase 2(MST2) gene polymorphism and haplotype and the risk of colorectal cancer, rectal cancer, and colon cancer in the Han population in Baotou area by case-control association study. Methods A total of 390 patients with colorectal cancer diagnosed by pathology and 413 normal physical examination pop-ulation were collected, and 2 mL of peripheral blood was taken for subsequent gene genotyping. Single nucleotide polymorphisms(SNPs) of MST2 gene were screened according to the genetic polymorphism data of Chinese Han population provided by the NCBI-Hapmap database. Gene genotyping was performed by Taqman method. Logistic regression was used to calculate the association between each SNP and the risk of colorectal cancer, colon cancer, and rectal cancer under codominant, dominant, overdominant, and recessive genetic models. Results Five SNPs of MST2 gene were screened, namely rs11783149, rs10955176, rs7827435, rs4075986, rs3019295. Among them, SNP rs4075986 was associated with the risk of colorectal cancer. Compared with the rs4075986 GG+AA genotype, carrying the AG genotype [OR(95%CI)=2.473(1.844-3.316) could increase the risk of colorectal cancer. Compared with the rs4075986 GG genotype, carrying the AG+AA genotype [OR(95%CI)=2.475(1.844-3.323) could increase the risk of colorectal cancer. SNP rs4075986 and rs3019295 were associated with the risk of rectal cancer. Compared with the rs4075986 GG+AA genotype, carrying the AG genotype [OR(95%CI)=3.411(2.387-4.874)] could increase the risk of rectal cancer. Compared with the rs3019295 GG+AA genotype, carrying the AG genotype [OR(95%CI)=0.706(0.501-0.996)] could reduce the risk of rectal cancer. SNP rs11783149 and rs4075986 were associated with the risk of colon cancer. Compared with the rs11783149 CC genotype, carrying the TT [OR(95%CI)=10.883(1.186-99.862)] and CT [OR(95%CI)=1.665(1.036-2.675)] genotype could increase the risk of colon cancer, respectively. Compared with the rs4075986 GG genotype, the AG+AA genotype [OR(95%CI)=1.824(1.262-2.638)] could increase the risk of colon cancer. Conclusion MST2 gene SNP rs3019295 AG genotype may be protective factor for rectal cancer. SNP rs11783149 CT and TT genotypes maybe risk factors for colon cancer. SNP rs4075986 AG and AG+AA genotypes may be a common risk factors for colorectal cancer, rectal cancer and colon cancer.

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Objective To analyze the bioinformatics of domestic Clostridium difficile toxin B(TcdB) and prepare it to provide data support for the development of effective vaccines. Methods Using bioinformatics software such as Snippy, Blast, Muscle, and the dist.alignment() and hclust() functions in R, 1 355 strains of Clostridium difficile from NCBI GenBank in China were compared and analyzed, and TcdB were grouped. The maximum likelihood tree and phylogenetic tree were beautified and displayed using iTOL. An online bioinformatics analysis website was used to predict and analyze the spatial structure and antigenic epitopes of the two largest subgroups, TcdB1 and TcdB2. The antigen protein TcdB was expressed and purified by prokaryotic system. Results According to the genotype of toxin B, the 1 355 prevalent strains of Clostridium difficile in China could be roughly divided into 12 subtypes, among which TcdB1 and TcdB2 were the main subtypes, accounting for more than 93.94% of all isolated strains, and about 17.20% of the strains were nontoxigenic or lack TcdB. The antigen epitope prediction of TcdB1 and TcdB2 showed that their antigen epitope distributions were basically the same, and many of them were distributed outside the C-terminal combined repetitive oligopeptides domains. Conclusion A specialized typing system for C. difficile TcdB in China has been established, and its main subtypes have been predicted for antigenic epitopes. The screened TcdB has been expressed for recombinant preparation.

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Objective To investigate the regulatory relationship between long non-coding RNA LINC01578 and c-Myc, and to explore the effect of LINC01578 on the metabolic process of oral squamous cell carcinoma(OSCC). Methods After c-Myc was knocked down in OSCC cell line CAL27, LINC01578, a long non-coding RNA that is positively regulated by c-Myc, was identified by high-throughput sequencing technology. qRT-PCR was employed to measure the expression levels of c-Myc and LINC01578 in OSCC tissues and adjacent normal tissues. Following overexpression or knockdown of c-Myc in CAL27 and HN6 cells, qRT-PCR was conducted to validate the consistency with sequencing results. The binding of c-Myc to the LINC01578 promoter was confirmed using a dual luciferase reporter assay. Seahorse, ATP production and lactate production assays were utilized to examine the impact of c-Myc on glucose metabolism in OSCC via LINC01578. Colony formation assays assessed the proliferative capacity of OSCC cell lines. Results qRT-PCR analysis revealed significantly higher expression levels of c-Myc and LINC01578 in OSCC tissues compared to adjacent tissues(P

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Objective To investigate the potential mechanisms of Xanthatin in inhibiting the proliferation of laryngeal squamous cell carcinoma(LSCC) cells by integrating network pharmacology and in vitro experiments. Methods The targets of Xanthatin were identified using databases such as PharmMapper, while disease-related targets for LSCC were obtained from databases such as DisGeNET. The overlapping targets between Xanthatin and LSCC were determined by intersecting these datasets. A protein-protein interaction(PPI) network was constructed based on the overlapping targets, and key targets were identified. Gene ontology(GO) and Kyoto encyclopedia of genes and genomes(KEGG) enrichment analyses of the overlapping targets were performed using R software. A "Xanthatin-target-pathway" network was visualized using Cytoscape 3.8.0 software. The preliminary validation of the aforementioned results was performed using molecular docking and transcriptomics. The effects of Xanthatin on the proliferation of TU177 cells were assessed using CCK-8 and colony formation assays. Additionally, Western blot analysis was employed to measure the expression levels of PI3K, p-PI3K, Akt, and p-Akt proteins. Results A total of 159 overlapping targets between Xanthatin and LSCC were identified, and seven key targets, including AKT1, were screened. GO enrichment analysis yielded 2 455 entries, and KEGG enrichment analysis identified 172 pathways, such as the PI3K-Akt signaling pathway. Xanthatin exhibited favorable binding activity with the core target proteins of LSCC in molecular docking experiments. The transcriptomics results showed high consistency with the predictions from network pharmacology. CCK-8 and colony formation assays demonstrated that Xanthatin at concentrations of 1, 2, and 4 μmol/L significantly inhibited the proliferation of TU177 cells in a dose-dependent manner. The expression levels of p-PI3K and p-Akt proteins decreased with increasing concentrations of Xanthatin. Conclusion Xanthatin may exert an inhibitory effect on the proliferation of LSCC cells by modulating the PI3K-Akt signaling pathway.

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Objective To construct a prognostic model for gastric cancer using NETosis-related long non-coding RNA(LncRNA) and to investigate their expression and functional roles in gastric cancer progression. Methods Data from gastric cancer patients were obtained from the TCGA database, and 85 NETosis-related genes were identified from the GeneCards database. NETosis-associated LncRNAs were screened using Pearson correlation analysis. A LncRNA-based prognostic model was constructed and evaluated through survival analysis, ROC curves, C-index, and nomogram analysis. Differences in gene set enrichment between high-and low-risk groups were further explored. Additionally, RT-qPCR was performed to validate LncRNA expression in gastric cancer patients, and the CCLE database was utilized to investigate LncRNA expression across various tumor cell lines. Results A risk prognostic model for gastric cancer was constructed using 12 LncRNAs. Based on risk scores, samples were stratified into high-and low-risk groups across multiple datasets. Validation results demonstrated significantly worse survival outcomes in the high-risk group compared to the low-risk group, with excellent predictive performance of the model(AUC=0.758, 95%CI: 0.688-0.828). Gene set enrichment analysis revealed that the high-risk group was enriched in gene sets strongly associated with inflammatory progression, whereas the low-risk group showed enrichment in gene sets related to normal DNA function. RT-qPCR confirmed differential expression of LncRNAs between tumor and paired normal gastric tissues(P

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Objective To explore the effect of transcription factor ZNF174 on the stemness of non-small cell lung cancer(NSCLC). Methods StemChecker online analysis was employed to assess the impact of ZNF174 on tumor stemness markers. The ZNF174 knockdown plasmid was constructed via restriction enzyme digestion and enzyme-linked assembly, while the ZNF174 overexpression plasmid was generated through homologous recombination. Lentiviral infection established stable cell lines with ZNF174 knockdown or overexpression. Tumor stem cell spheroid formation assays were conducted to evaluate stemness maintenance capacity. RNA-seq and quantitative real-time polymerase chain reaction(qPCR) were utilized to detect effects on key stemness gene expression. Results The transcription factor ZNF174 promoted cellular stemness in non-small cell lung cancer(NSCLC). It promoted the expression of key stemness genes: B-cell-specific moloney murine leukemia virus insertion site 1(BMI1), acetaldehyde dehydrogenase 2(ALDH2), SRY-box transcription factor 2(SOX2), recombinant high mobility group AT hook protein 2(HMGA2), and snail family transcriptional repressor 1(Snail1) and enhanced tumor spheroid formation in NSCLC stem cells. Conclusion ZNF174 promotes the expression of tumor stemness genes in NSCLC and may become a novel therapeutic and prognostic target for NSCLC.

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Objective To investigate the role of murine double minute 2(MDM2) in dihydroartemisinin′s(DHA) inhibition of lung adenocarcinoma cell proliferation and migration. Methods CCK8 assay was used to detect the inhibitory effect of gradient concentrations of DHA(0, 5, 10, 25, 50 and 100 μmol/L) and time gradients(0, 24, 48, and 72 h) on the proliferation of lung adenocarcinoma A549 and PC9 cells, and the half maximal inhibitory concentrate(IC50) were calculated respectively. Colony formation and scratch assays were used to detect the inhibitory effects of DHA on colony formation and migration of A549 and PC9 cells. Western blot was used to detect the inhibitory effects of DHA on MDM2 expression and epithelial-mesenchymal transition(EMT)-related proteins E-cadherin and N-cadherin. The promoting effects of MDM2 on proliferation, migration and EMT of lung adenocarcinoma cells were verified by small interfering RNA-mediated knockdown of MDM2(si-MDM2). The reversal effects of MDM2 overexpression on DHA′s inhibition on the proliferation and migration of A549 and PC9 cells were observed. Results DHA inhibited the proliferation of A549 and PC9 cells in a dose-and time-dependent manner, with IC50 values of 30.57 and 78.61 μmol/L, respectively. Compared with the Control group, A549 and PC9 cells had significantly decreased colony formation(both P

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Objective To explore the role of tumour necrosis factor-α(TNF-α) in splenic infection of mice by Leishmania major. Methods To establish an infection model, promastigotes of Leishmania were injected intradermally into the right hind foot of mice. The thickness of the footpad and body weight were measured to monitor the infection. Histological changes in the spleen after infection were observed by HE staining. Changes in lymphocytes and monocytes in the spleen were detected by flow cytometry. The expression level of arginase-1(Arg-1) and inducible nitric oxide synthase(iNOS) in the spleen was determined by indirect immunofluorescence. The effect of TNF-α on macrophage infection with Leishmania was evaluated in vitro. Results Compared to B6.WT mice, the spleens of B6.TNF-/- mice showed significant enlargement 42 days post-infection, with structural disruption. Various cells infiltrated and were dispersed throughout the entire spleen. Flow cytometry results indicated that after infection with Leishmania, there was no significant change in the proportions of T cells and B cells in the spleens of the mice, while CD11b monocytic cells significantly increased. Immunofluorescence results revealed that the M2 macrophage/monocyte marker Arg-1 was highly expressed in the spleens of B6.TNF-/- mice(P-/- mice following subcutaneous inoculation of Leishmania in the hind footpad may be associated with the absence of TNF-α, which leads to M2-type differentiation of macrophages and reduced nitric oxide production.

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Objective To investigate the iodine nutrition status of children aged 8-10 in Guangming, Longhua and Yantian District of Shenzhen in 2023, and to explore the influencing factors of thyroid volume. To evaluate prevention strategies and to provide a scientific basis for the elimination of iodine deficiency disorders. Methods Urine and household salt samples were randomly collected from 580 non-boarding students aged 8-10 years foriodine content detection. Thyroid volume was measured using a fully digital ultrasound imaging system, and goiter prevalence was calculated. Results A total of 580 samples was tested. The median salt iodine concentration was 23.86 mg/kg, with 93.62% qualified iodized salt and 94.48% coverage rate. The median of urinary iodine was 265.00 μg/L, mainly distributed between 200--4, P

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Objective To analyze the temporal changes in lipid levels in patients following acute pancreatitis(AP) and explore the factors associated with post-AP serum triglyceride(TG) level changes. Methods Patients diagnosed with AP were included in this study. Clinical data were collected retrospectively, and lipid profile data from follow-up visits after discharge were tracked. Kaplan-Meier(K-M) curves were used to stratify follow-up duration, while Spearman correlation analysis assessed the relationship between lipid levels and follow-up time. A linear regression model was used to investigate factors influencing TG level changes post-AP. Results A total of 141 patients with 306 follow-up visits were included. Spearman correlation analysis showed a mild increase in lipid levels over time post-discharge: TG(r=0.159, P=0.005), total cholesterol(TC)(r=0.231, P

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Objective To investigate independent risk factors for lower extremity amputation(LEA) in hospitalized patients with diabetic foot ulcers(DFUs). Methods A multicenter retrospective analysis was conducted on the clinical data of 329 DFUs hospitalized patients with diabetic foot ulcers from four general hospitals across the nation. A multivariate Logistic regression model was constructed, and prediction analysis was performed using R 4.2.1. The discriminative ability of the model was assessed using receiver operating characteristic curves, while calibration accuracy and clinical applicability were evaluated via calibration curves and decision curve analysis. Results The study revealed that patients with higher education backgrounds showed lower disease severity(Wagner grade)(Z=-4.331, P

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Objective To construct a deep learning model based on convolutional neural network(CNN)-long short term memory network(LSTM)-Attention to explore the correlation between meteorological and clinical factors and the incidence of ischemic stroke. Methods A fusion model CNN-LSTM-Attention based on CNN, LSTM, and Attention was constructed by incorporating clinical data and meteorological data of ischemic stroke inpatients. The predictive performance of the model was evaluated by maximum prediction error and root mean square error(RMSE). The impact of different lag days on prediction performance was investigated by selecting lag periods ranging from 1 to 7 days. Results In both short-term and long-term predictions, the CNN-LSTM-Attention fusion model(short-term: 1.5 and 0.6; long-term: 8.3 and 2.5) showed superior maximum prediction bias and RMSE compared to the LSTM model(short-term: 2.8 and 1.2; long-term: 19.5 and 5.5) and the CNN-LSTM model(short-term: 2.0 and 0.8; long-term: 11.2 and 3.3). After incorporating lag days, the maximum prediction deviation and RMSE for lags of 3 days(short-term: 0.7 and 0.4; long-term: 5.5 and 1.9) and 5 days(short-term: 0.8 and 0.3; long-term: 6.5 and 2.0) in both short-term and long-term forecasts were smaller than lags of 0 days(short-term: 1.5 and 0.6; long-term: 8.3 and 2.5). The maximum prediction deviation and RMSE in the short-term forecast were greater than lag 0 days for both lag 1 days(1.5 and 0.8) and lag 7 days(1.9 and 0.9). In the long-term forecast, the two indicators for lag 1 days(6.8 and 2.4) were lower than those for lag 0 days but higher than those for lag 3 days and 5 days. The maximum prediction deviation for lag 7 days(7.5) was lower than that for lag 0 days, but the RMSE(2.7) is higher than that for lag 0 days. Conclusion The established CNN-LSTM-Attention model demonstrates significant predictive value for the onset of ischemic stroke and can provide reference for the rational allocation of medical resources.

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Objective To explore the effect of tumor cell perineural invasion on the prognosis of cervical cancer and the early predictive factors of perineural invasion in patients with cervical cancer. Methods A retrospective analysis was conducted on the clinical, pathological, and survival data of 551 patients with cervical cancer. These patients were categorized into a survival group(n=477) and a death group(n=74). The baseline characteristics of the two groups were compared using independent samples t-tests, Wilcoxon rank-sum tests, and chi-square tests. Multivariate binary Logistic stepwise regression analysis was employed to identify independent risk factors associated with mortality. In addition, univariate Logistic regression analysis was performed to determine predictive factors for perineural invasion. A predictive model for perineural invasion in cervical cancer was subsequently developed based on the multivariate regression equation, and its predictive accuracy was assessed using the ROC curve. Results In the basic data of cervical cancer patients, the high level of perineural invasion, lymphatic metastasis and postopera-tive pathological stage in pathological data had an impact on the poor prognosis of patients(P

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Objective To predict and screen potential biomarkers of systemic lupus eythematosus(SLE) based on machine learning algorithms and structural biology, and to reveal their mechanisms of action and to provide new targets for disease diagnosis and treatment. Methods Four machine learning algorithms, random forest(RF), eXtreme gradient boosting(XGBoost), support vector machine(SVM), least absolute shrinkage and selection operator(LASSO), were used to analyze the gene expression data of SLE patients in GEO(datasets: GSE121239 and GSE11907) to analyze the gene expression data of SLE patients and screen key markers. Peripheral blood single nucleated cells(PBMCs) from SLE patients were collected and RT-qPCR was used to detect differential gene expression levels. Subsequently, GSEA enrichment analysis was used to identify biomarker-related pathways. CIBERSORT immune infiltration analysis and protein interactions network were applied to calculate the sample immune cell infiltration abundance. Single-cell data were analyzed for gene expression specificity in immune cells. Interaction relationships in combination with AlphaFold3(AF3) were predicted. Results Multiple algorithms were screened together to identify the unique marker gene HERC5, and expression analysis of multiple datasets showed that HERC5 was highly expressed in SLE compared to the normal group(P

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Migraine is a widespread neurovascular disorder, the pathogenesis of which is closely linked to the release of calcitonin gene-related peptide(CGRP), leading to a significant impairment in patients′ quality of life. CGRP receptor antagonists exert their therapeutic effect by inhibiting the interaction between CGRP and its receptors, thereby preventing migraine attacks. Currently, several agents, including Rimegepant and Ubrogepant, have either received approval from the U. S. Food and Drug Administration or are in advanced stages of clinical trials.These drugs offer multiple advantages, such as the absence of vasoconstrictive effects, a rapid onset of action, and minimal interference with the immune system. Nevertheless, further investigation is necessary to assess their longterm safety, the potential emergence of drug resistance, and the development of individualized treatment protocols.Moreover, the integration of these novel therapies with existing treatment strategies remains a critical area for future research. This review aims to summarize recent national and international scientific advancements to establish a theoretical basis for the application of precision medicine in migraine management.

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Inhibitor of DNA binding 1(ID1) is a crucial regulator of cell differentiation and plays a significant role in maintaining normal hematopoietic differentiation and development. Due to the lack of DNA-binding motif, ID1 functions as a dominant-negative inhibitor of basic helix-loop-helix factors to antagonize their abilities to bind to DNA and transcriptionally regulate target genes. Abnormal expression of ID1 is strongly associated with various hematologic disorders, including myeloid and lymphoblastic leukemia, multiple myeloma and myeloproliferative neoplasms. ID1 acts as a potential oncogene by participating in multiple signaling pathways that promote the malignant proliferation, invasion and therapy resistance in leukemic cells. Significant strides have yielded promising antileukemic effects of ID1 inhibitors, both alone and in combination with targeted therapies against oncogenic signaling pathways. Here, we review the relationship between ID1 expression and the initiation and progression of blood disorders, and summarize the clinical significance of ID1 as a novel therapeutic target and potential prognostic biomarker for hematologic malignancies.