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Objective To construct and validate a prognostic model for lung cancer based on acrolein-related genes using bioinformatics methods.Methods Lung cancer datasets GSE30219 and GSE68465 were obtained from the GEO database,and acrolein-related gene sets were retrieved from the CTD database.Differentially expressed genes(DEGs) between cancer and adjacent tissues were identified in the GSE30219 dataset.The intersection of these DEGs and acrolein-related genes was then used to identify candidate genes.Gene set variation analysis(GSVA)was performed to assess functional alterations based on the intersection genes.A protein-protein interaction(PPI)network was constructed based on the STRING database to identify core hub genes.Subsequently,support vector machine recursive feature elimination(SVM-RFE) and LASSO-Cox regression analyses were employed to develop a prognostic model based on acrolein-related genes,which was independently validated using the GSE68465 dataset.The CIBERSORT algorithm was applied to evaluate the immune cell infiltration characteristics between high-and low-risk groups,and functional enrichment analysis of DEGs between the two groups was conducted to further explore the potential molecular mechanisms underlying the prognostic model.Results A total of 361 acrolein-related DEGs were identified in lung cancer,and 7 key genes were selected for model construction.Kaplan-Meier survival analysis revealed that patients in the high-risk group had significantly lower survival rates compared to those in the low-risk group(P

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Objective To investigate the antibacterial properties and biocompatibility of a novel hydrogel fabricated by integrating plasma-activated water(PAW) and bletilla striata polysaccharide(BSP).Methods The experiments were carried out by dividing the hydrogels into four groups based on their compositions:the deionized water(DW)-carbomer 940(CBM940)-carboxymethyl chitosan(CMCS) hydrogel group(H group),the PAW-CBM940-CMCS hydrogel(PAH) group,the DW-BSP-CBM940-CMCS hydrogel(BSPH) group,and the PAW-BSP-CBM940-CMCS hydrogel(PA/BSPH) group.Physical properties of the hydrogels were evaluated by testing water loss rate and water vapor transmission rate.The content of active substances was determined using a microplate reader and an electron spin resonance spectrometer(ESR).The pH and ORP values were measured using a pH meter and an oxidation-reduction potential(ORP) electrode.The antibacterial mechanism was elucidated by analyzing the integrity of bacterial biofilms.Antibacterial activity was evaluated via the zone of inhibition assay.Cytotoxicity testing was performed using the cell counting kit-8(CCK-8) assay,and combined with the cell scratch assay,to collectively evaluate the effects of the hydrogel on cellular biocompatibility and migration ability.Results The water loss rate and water vapor transmission rate of PA/BSPH hydrogel were(32.3±2.3) % and(2 228.2±181.1) g/(m2·d).Compared with the H group hydrogel,the contents of hydrogen peroxide(H_2O2) and hydroxyl radicals(·OH) in PAH and PA/BSPH groups significantly increased(P 2 and·OH in PAW.The incorporation of BSP enhances the water retention and breathability of the wound dressing while significantly reducing the cytotoxicity of PAW.This modification endows the hydrogel with improved biocompatibility and promotes cell proliferation.The PA/BSPH hydrogel demonstrates clinical potential by offering a novel therapeutic strategy for chronic infected wound management.

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Objective To investigate the expression of triple motif protein 21(TRIM21) at different time points in Cisplatin induced acute kidney injury(Cis-AKI) mouse model and its correlation with pathological score.Methods Acute kidney injury(AKI) model was induced by intraperitoneal injection of cisplatin(20 mg/kg).Peripheral blood serum was collected at 12,24,48 and 72 h,respectively.Body weight and kidney mass were also recorded.The dynamic changes of serum creatinine(SCr) and urea nitrogen(BUN) were detected.The expressions of TRIM21 protein and endoplasmic reticulum stress(ERS) proteins GRP78,GRP94,P-elf2α and CHOP were detected by Western blot.HE staining was used to observe the pathology of renal tissue and analyze the correlation between the expression of TRIM21 protein at different time points.Results Compared with the control group,the renal body ratio of Cis-AKI mice significantly increased at 48 h and 72 h(P

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Objective To investigate the role and mechanism of IQ motif containing GTPase activating protein 1(IQGAP1) in oxygen-glucose deprivation/reoxygenation(OGD/R)-induced polarization of BV-2 microglia cells.Methods The IQ GAP1 overexpression plasmid(oe-IQGAP1) and its negative control plasmid(Vector) were transfected into BV-2 cells,and then the polarization of BV-2 cells was induced by OGD/R,and exogenous interferon-γ(IFN-γ) recombinant protein was used for intervention.Cell proliferation rate was detected by cell counting kit-8(CCK-8) assay.The level of lactate dehydrogenase(LDH) in the supernatant was detected using a test kit.The mRNA expression levels of IQGAP1,IFN-γ and microglial polarization markers inducible nitric oxide synthase(iNOS),CD86,CD206 and arginasel(Arg1) were detected by quantitative real-time polymerase chain reaction(RT-qPCR).The levels of IFN-γ,tumor necrosis factor-α(TNF-α),interleukin(IL)-1β,IL-4 and IL-10 in the cell supernatant were detected by enzyme-linked immunosorbent assay(ELISA).The protein expression levels of IQGAP1 and IFN-γ were detected by Western blot.Results Following OGD/R treatment,the proliferation rate of BV-2 cells,the levels of IL-4 and IL-10 in the supernatant,and the mRNA expression levels of CD206 and Argl were significantly reduced(all P

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Objective To investigate the ferroptosis induced by sesamin in triple-negative breast cancer(TNBC)4T1 cells and its underlying mechanism.Methods The binding energy of sesamin with glutathione peroxidase 4(GPX4),solute carrier family 7 member 11(SLC7A11),and P53 was analyzed by molecular docking.Mouse TNBC cell line 4T1 was used as a model.Different concentrations of sesamin were administered to 4T1 cells.The effect of sesamin on cell viability was assessed using the cell counting kit 8(CCK-8).Transwell assay was used to evaluate the effect of sesamin on cell migration and invasion.The contents of Fe2+,malondialdehyde(MDA),and reduced glutathione(GSH) in the cells were measured using kits.2',7'-dichlorofluorescein diacetate(DCFH-DA)probe was employed to detect the content of reactive oxygen species(ROS) in cells.Real-time quantitative reverse transcription polymerase chain reaction(RT-qPCR) and Western blot were performed to evaluate the expression of GPX4,SLC7A11,and P53 at mRNA and protein levels.Results The binding energies of sesamin with GPX4,SLC7A11 and P53 were-21.46,-21.67,and-27.03 kJ/mol,respectively.Compared with the control group,the viability of 4T1 cells in different concentrations of sesamin groups decreased gradually(P 2+,MDA,and ROS in 4T1 cells of 20,40,and 80 μmol/L sesamin groups increased,and the content of GSH decreased.Compared with the control group,the mRNA and protein expression of GPX4 and SLC7A11 in 4T1 cells in the sesamin treatment group decreased,and the mRNA and protein expression of P53 increased(all P

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Objective To investigate whether TYRO protein tyrosine kinase-binding protein(TYROBP) affects the progression of diabetic kidney disease(DKD) through the extracellular signal-regulated kinase(ERK) pathway.Methods Key genes in DKD were identified through bioinformatics analysis.Immunohistochemical staining and quantitative real-time PCR(qPCR) were used to validate the expression levels of TYROBP in a DKD mouse model and high glucose-stimulated NRK-52E cells.NRK-52E cell models with stable TYROBP overexpression/knockdown and their corresponding empty vector(ev)/scrambled sequence(ss) controls were established via lentiviral transfection.Cells were treated with 5.5 mmol/L or 30.0 mmol/L glucose for 72 hours to mimic normal glucose(NG)and high glucose(HG) conditions,respectively.High glucose medium containing 3.5 μmol/L FR180204 was used for ERK inhibitor intervention.The experiment included seven groups:ev+NG,ev+HG,oe-TYROBP+HG,ss+NG,ss+HG,sh-TYROBP+HG,and sh-TYROBP+HG+ERK inhibitor.Western blot was used to detect the expression levels of phosphorylated ERK/total ERK(p-ERK/ERK),apoptosis-related proteins B-cell lymphoma-2(Bcl-2) and Bcl-2-associated X protein(Bax),and epithelial-mesenchymal transition(EMT)-related proteins E-cadherin and α-smooth muscle actin(α-SMA).Tetramethylrhodamine ethyl ester(TMRE) staining and Annexin V-fluorescein isothiocyanate/propidium iodide(Annexin V-FITC/PI) flow cytometry were performed to assess mitochondrial membrane potential and apoptosis levels.Results Bioinformatics analysis identified TYROBP as a key gene in DKD.In vivo and in vitro validation showed increased TYROBP mRNA levels in DKD models.The results from the HG model indicated that,compared to the ev+NG/ss+NG group,the ev+HG/ss+HG group demonstrated increased p-ERK/ERK expression,reduced mitochondrial membrane potential,elevated apoptosis,and enhanced EMT.In TYRO BP-perturbed NRK-52E cells,compared to the ev+HG group,the oe-TYROBP+HG group showed decreased p-ERK/ERK expression(P

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Objective To investigate the protective effects and mechanisms of acellular nerve allografts(ANA) on motor neurons in the spinal cord anterior horn of sciatic nerve injury(SNI) rats. Methods SPF grade male SD rats were randomly divided into normal, model, ANA-bridged(bridge group), and autologous nerve transplantation groups(autograft group), with 6 rats in each group. The SNI rat model was established using the right sciatic nerve clamp method for 10 mm. In the bridge group, the ANA was bridged to the two severed ends of the injured sciatic nerve, and in the autograft group, the autologous nerves were flipped head to tail and then bridged to the two severed ends. A spectrophotometer was applied to determine the DNA content in normal nerves and ANA. The footprint test was used to determine the sciatic nerve function index(SFI) of the rats in each group, the wet weight ratio of the anterior tibialis muscle was calculated. The morphology and structure of the anterior horn motor neurons of the spinal cord of each group were observed by HE staining. The immunofluorescence and Western blot were used to detect Apaf-1, Caspase-3, Bcl-2, Bax, and Cyt-C proteins expression in the L4-6 segment of the spinal cord. Results The DNA content in the ANA prepared in this study was significantly lower than that in normal nerves(P

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Objective To investigate the expression of ribosomal protein L26(RPL26) in gastric cancer cells(GC) and its effect on cell apoptosis and proliferation.Methods The expression of RPL26 in GES-1 and GC cell lines was detected by Western blot.GC cell line HGC-27 was used to construct RPL26 overexpression cell line,and GC cell lines HGC-27 and AGS cells were used to construct RPL26 knockdown cell line.The overexpression and knockdown efficiency of RPL26 were detected by Western blot.Cell counting kit-8(CCK-8),colony formation assay and Trans well assay were used to detect the effects of the overexpression and knockdown of RPL26 on the proliferation and migration of GC cells.Western blot was used to detect the expression of Phosphatidylinositol-3-kinase(PI3K)/protein kinase B(AKT) signaling pathway related factors PI3K,AKT,phosphorylated phosphatidylinositol-3-kinase(p-PI3 K),phosphorylated protein kinase B(p-AKT) and downstream factors B-Cell lymphoma-2(Bcl-2),Bcl-2 associated X protein(Bax) and Cyclin A,G1/S-specific Cyclin D1(Cyclin D1),Cyclin-dependent kinases(CDK)4 and CDK2 in overexpression and knockdown of RPL26 stably transfected cell lines.Results Compared with GES-1,RPL26 was highly expressed in HGC-27 cells(tHGC-27=4.97;P HGC-27=11.50,tAGS=4.77;P HGC-27=9.63,tAGS=4.05;P p-PI3K/PI3K=3.86,tp-AKT/AKT=8.29;P 1/S phase by inhibiting the PI3K/AKT signaling pathway,thereby inhibiting cell proliferation and promoting apoptosis.

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Objective To investigate the molecular mechanism of NOD-like receptor(NLR) signaling pathway induced cellular focal death in mouse kidney tissues under plateau hypoxia based on transcriptomic sequencing technology.Methods Animal models were constructed in high-altitude kidney test group(HKT group) and plain kidney control group(PKC group),and C57/BL6 mice were bred at an altitude of 4 200 m and 400 m,respectively.Kidney tissues were aseptically taken out after 30 d and used for observation of renal histopathological changes and transcriptomics sequencing,respectively,and then differentially expressed genes(DEGs) were enriched by KEGG and GO analysis.Key gene and protein expression levels were verified by reverse transcription quantitative polymerase chain reaction(RT-qPCR) and Western blot analysis.Results Hematoxylin-eosin(HE) staining showed that the renal tubules of HKT mice were disorganized,and the tubular epithelial cells were edematous with inflammatory cell aggregation.Transcriptomics sequencing analysis revealed that a total of 3 007 DEGs were identified in the HKT group,and KEGG analysis showed that DEGs were significantly enriched in the NLR signaling pathway.The mRNA expression of the key differentially expressed genes,CASP1,CASP11,GSDMD,IFI16,NAIP5,IRF9,and the downstream inflammatory factors,IL-1β and IL-18,was upregulated,and protein expression of CASP1,CASP11,and GSDMD was up-regulated.Conclusion The plateau hypoxic environment induces cellular pyroptosis by regulating the expression of NLR signaling pathway and releases downstream inflammatory factors to cause inflammatory responses.

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Objective To investigate the mechanism of Anemoside B4(AB4) on glutamine metabolism in oral lichen planus(OLP) epithelial cells via the nitric oxide synthase 3(NOS3)-dihydrofolate reductase(DHFR) axis.Methods Bioinformatics analysis was performed to identify the intersection of molecular targets of OLP,AB4,and genes related to glutamine metabolism.A lipopolysaccharide(LPS)-induced HOK-16B model of OLP was established.HOK-16B were divided into Ctrl group,OLP group,AB4 group,OLP+oe-NOS3 group,OLP+sh-NOS3group,OLP+sh-NOS3+oe-DHFR group,and OLP+sh-NOS3+AB4 group.Cell proliferation was detected by cell counting kit-8(CCK-8);cell apoptosis was detected by TdT-mediated dUTP Nick-End Labeling(TUNEL);inflammatory factors ilnterleukin(IL)-1β,tumor necrosis factors-α(TNF-α) concentrations in cell supernatants were measured using enzyme-linked immunosorbent assay(ELISA) kits;glutamine uptake and glutamate production were determined using kits;and the protein expression of alanine-serine-cysteine transporter2(ASCT2) and glutamine synthase(GLS) was assessed by Western blot.Results Bioinformatics analysis of molecular targets of OLP,AB4,and genes related to glutamine metabolism revealed three intersection targets:NFE2L2,NOS1,and NOS3.Compared with the Ctrl group,the OLP group exhibited decreased HOK-16B cell viability(P

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Objective To analyze differences in the expression levels of lipid metabolism-related proteins in adipose tissue exosomes between obese mice and wild-type mice using proteomic techniques.Methods Wild-type(WT) and obese(ob/ob) model mice of the same age were selected,with 8 mice per group.Adipose tissue from both groups was minced and cultured for 48 hours.Conditioned media was collected,and exosomes were isolated using differential centrifugation.Liquid chromatography-tandem mass spectrometry(LC-MS/MS) was utilized for proteomic analysis to screen differentially expressed proteins(DEPs).Gene ontology(GO) enrichment analysis and kyoto encyclopedia of genes and genomes(KEGG) pathway enrichment analysis were performed on the DEPs.Heatmaps were generated to visualize DEPs expression patterns,and Western blot was employed to validate DEPs expression levels.Results Exosomes were successfully extracted from the culture supernatant of adipose tissues from mice in the WT group and the ob/ob group.Mass spectrometry analysis identified a total of 25 629 peptides and 3 376 proteins.Compared with the WT group,there were 699 proteins with high expression and 632 proteins with low expression in the exosomes derived from adipose tissues of ob/ob mice.Both GO and KEGG analyses showed that DEPs were mainly enriched in metabolic pathways.Heatmap analysis visualized the expression patterns of metabolism-related DEPs,and the expression levels of lipid metabolism-related proteins such as acyl-Co A synthetase long-chain family member 1(ACSL1),apolipoprotein E(ApoE),and albumin(Alb) changed significantly in the obese state(P

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Objective To investigate the extraction,purification,and identification methods of Polygonum cuspidatum(P.cuspidatum)-derived exosomes and to obtain high-purity exosomes,and thus providing a reliable material foundation for their functional studies.Methods Exosomes were isolated from fresh P.cuspidatum using ultracentrifugation combined with sucrose density gradient centrifugation.Morphological characteristics,size distribution,and surface charge properties were analyzed by transmission electron microscopy(TEM),nanoparticle tracking analysis(NTA),and Zeta potential measurements.Results The purified P.cuspidatum exosomes exhibited characteristic cup-shaped or spherical bilayer morphology with a predominant size distribution of 100-200 nm,consistent with established plant exosome characteristics.The surface of these exosomes exhibits a negative charge,with the Zeta potential absolute value of root-derived exosomes being slightly higher than that of stem/leaf-derived counterparts.Conclusion The study successfully isolates and characterizes P.cuspidatum exosomes,with comprehensive analysis confirming their distinctive structural and biophysical properties.It lays a good material foundation for further exploration of its active ingredients and biological functions.

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Objective To explore the alleviating effect of geniposide on ulcerative colitis(UC) and to investigate its potential mechanism.Methods A UC mouse model was induced using 5% dextran sulfate sodium(DSS).These mice were randomly divided into 6 groups(n=8):control group,model group,sulfasalazine group [100mg/(kg·d)],low-dose geniposide group[10 mg/(kg·d)],medium-dose geniposide group[20 mg/(kg·d)],and high-dose geniposide group[40 mg/(kg·d)].The mice were orally administered for consecutive 10 days.The colon length and mouse body mass were measured,and the colon mucosal damage index(CMDI) and disease activity index(DAI) were scored.The pathological changes in colon tissue were observed using hematoxylin-eosin(HE) staining.The reagent kits were used to measure the levels of malondialdehyde(MDA),myeloperoxidase(MPO),catalase(CAT),and glutathione(GSH) in colon tissue.The enzyme linked immunosorbent assay(ELISA) was used to analyze the expression levels of tumor necrosis factor-α(TNF-α),interleukin-6(IL-6),and IL-1 β in colon tissue.Western blot was used to detect the protein expression of mucin 1(MUC-1),occludin,IL-6,p-JAK2,and p-STAT3 in colon tissue.Results Compared with the normal control group,the body mass and colon length of the model group mice significantly reduced.The expression of MUC-1 and occludin proteins significantly reduced(P

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Objective To investigate the correlation of chemerin levels in the serum and intestinal mucosal with intestinal mucosal inflammation in IBS-D mice.Methods A total of 128 female C57BL/6J mice were randomly divided into IBS-D group and control group,with 64 mice in each group.Wire Restraint Stress method(WRS) was used to construct an animal model of IBS-D.Enzyme-linked immunosorbent assay was used to detect serum and colonic mucosal chemerin levels in mice.Hematoxylin-eosin(HE) staining was used to observe colonic mucosal inflammation.Geboes value was used to evaluate the severity of colonic mucosal inflammation.Results In the IBSD group,the concentration of serum chemerin increased and reached the peak in the first week of the experiment(t=6.538,P

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Objective To investigate the effects of paeoniflorin(Pae) on acute kidney injury(AKI) and mouse renal tubular epithelial cell(mRTEC) damage induced by lansoprazole(LPZ) and cisplatin(CIS) through in vivo and in vitro experiments.Methods The C57BL/6J mice or mRTECs were divided into four groups:normal control(NC) group,NC+LPZ group,CIS group,and CIS+LPZ group.Serum creatinine(CRE) and blood urea nitrogen(BUN) levels in mice were measured,and kidney pathology was observed with HE staining.Western blot,immunohistochemistry,and immunofluorescence were used to detect the expression levels of kidney injury molecule-1(KIM-1) and receptor-interacting protein kinase(RIPK) 1,RIPK3,and mixed lineage kinase domain-like protein(MLKL).Subsequently,C57BL/6J mice or mRTECs were divided into six groups:NC group,NC+Pae group,CIS+LPZ(M) group,and CIS+LPZ+Pae(M+Pae) group.Serum CRE and BUN levels in each group were measured,kidney pathology was observed with HE staining,and ultrastructural changes in the kidney were observed with transmission electron microscopy.The KIM-1 and necroptosis-related protein expression levels were detected by Western blot,immunohistochemistry,and immunofluorescence.Results Compared with the NC group,CRE and BUN levels were elevated in the CIS group,and these levels were further increased after LPZ intervention(all P

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Objective To construct a Family with sequence similarity 50 member A(FAM50A) gene knockout mouse insulinoma pancreatic β-cell line Beta-TC-6 using CRISPR/Cas9 gene editing technology and to prepare polyclonal antibodies specifically recognizing FAM50A.Methods Two guide RNAs(sgRNAs) targeting the FAM50A gene were designed,and a recombinant plasmid expressing blue fluorescent protein(BFP) was constructed for gene knockout.The successfully constructed plasmid was transfected into Beta-TC-6 cells,and BFP-positive single cells were isolated for clonal expansion.The expanded monoclonal cell lines were genotyped by Sanger sequencing,and FAM50A protein expression was assessed by Western blot.Purified human recombinant FAM50A protein was used to immunize New Zealand rabbits for the preparation of a polyclonal antibody.The specificity of the prepared antibody was then validated using the successfully established FAM50A knockout cell line.Results A monoclonal cell line with a successful knockout of the FAM50A gene was identified.Sanger sequencing confirmed base deletions at the target site.Western blot analysis showed a complete absence of FAM50A protein expression in this cell line.The prepared polyclonal antibody successfully recognized endogenous murine FAM50A protein in wild-type Beta-TC-6 cells and in hTERT-RPE1 cells overexpressing human FAM50A-GFP fusion protein,while no signal was detected in the FAM50A knockout cells.Conclusion This study successfully established a FAM50A gene knockout Beta-TC-6 cell model and generated a FAM50A polyclonal antibody,providing powerful tools for future research.

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Objective To investigate the aberrant alterations of microRNAs(miRNAs) in exosomes derived from bone marrow stromal cells(BMSCs) in the bone marrow supernatants of patients with acute myeloid leukemia(AML) and their impact on the prognosis of AML patients.Methods Bone marrow supernatant samples were collected from three AML patients and three healthy donors.Exosomes were isolated using a commercial kit,identifying the morphology and marker expression,and subjected to miRNA sequencing to determine differentially expressed miRNAs(DE-miRNAs).The DE-miRNAs were then intersected with the exosomal miRNA expression profiles of primary AML cells(GSE64029) to exclude AML cell-derived signals and to identify BMSC-derived DEmiRNAs.Subsequently,candidate miRNAs were identified through Cox regression and Lasso regression analyses based on data from The Cancer Genome Atlas(TCGA).A prognostic risk model for AML was constructed,and patients were stratified into high-risk and low-risk groups according to the median risk score.The prognostic value and clinical relevance of the model were further validated.Finally,the target genes of the candidate miRNAs were predicted,followed by pathway enrichment analysis,construction of key regulatory networks,and correlation analysis between the expression levels of key miRNAs and their corresponding target genes.Results Isolated exosomes exhibited a typical cup-shaped morphology with intact structures with particle size of 30-150 nm,and expressed exosomal markers CD63,ALIX,and TSG101.miRNA sequencing identified 103 DE-miRNAs in AML patients compared with healthy donors;after intersection with the GSE64029 dataset,83 BMSC-derived DE-miRNAs were retained.Among these,five candidate miRNAs(miR-25-3p,miR-532-5p,miR-194-5p,miR-10a-5p,and miR-20a-5p) were used to construct the prognostic model.Kaplan-Meier survival analysis demonstrated significantly longer overall survival in the low-risk group compared with the high-risk group(P

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Objective To explore the role of leukemia inhibitory factor(LIF) in dental pulp inflammation.Methods Human dental pulp stem cells(hDPSCs) were cultured in vitro as the target cells,the inflammatory response was induced by lipopolysaccharide(LPS),and high-throughput sequencing was used to detect relevant highly expressed genes in the inflammatory state.The expression of LIF under graded concentrations of LPS stimulation was detected by real-time fluorescence quantitative PCR(qPCR).The expression levels of interleukin-6(IL-6),interleukin-1β(IL-1β),and tumor necrosis factor-α(TNF-α) were detected after LIF knockdown and overexpression in hDPSCs by qPCR.Normal and inflammatory pulp tissues were collected,and the expression of LIF in both tissues was detected by qPCR and immunofluorescence(IF).Results The expression level of LIF increased in human dental pulp cells after LPS stimulation.The expression level of LIF was subsequently elevated in inflammatory pulp induced by graded concentrations of LPS.The expression of IL-6,IL-1β,and TNF-α was significantly downregulated in hDPSCs after LIF knockdown in response to LPS stimulation,while LIF overexpression upregulated the expression of these cytokines.qPCR and IF assays showed high expression of LIF in inflamed pulp tissue.Conclusion LIF is involved in dental pulp inflammation and promotes the development of pulpitis.

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Objective To explore the relationship between muscle fat deposition,muscle iron deposition,and glucose metabolism in elderly obese patients.Methods Elderly obese patients who visited the outpatient clinic were selected.Oral glucose tolerance tests were performed.Muscle fat and iron deposition in the abdominal wall and paraspinal muscles at the L3 vertebra level were quantified using the Dixon technique based on nuclear magnetic resonance.Results A total of 140 elderly obese patients were included,among which 46 were newly diagnosed with type 2 diabetes mellitus(T2DM),44 had impaired glucose tolerance(IGR),and 50 had normal glucose tolerance(NGT).Compared to NGT and IGR groups,patients with T2DM had significantly increased muscle fat deposition,iron deposition,and visceral fat,while subcutaneous fat was significantly reduced(P

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Objective To investigate hepatocellular carcinoma(HCC) risk factors in hepatitis B e antigen(HBeAg)-negative cirrhotics,and to develop and validate a predictive model using these indicators.Methods A total of 649 hospitalized patients with HBeAg-negative hepatitis B cirrhosis and HBeAg-negative primary HCC were enrolled.Patients were randomly divided into a modeling group(n=298) and a validation group(n=351) at a 7:3 ratio.Logistic regression analysis was used to screen for independent predictors of HCC occurrence.A predictive model was constructed and validated using receiver operating characteristic(ROC) curves.The clinical net benefit of the prediction model was assessed via decision curve analysis.Results Univariate analysis showed significant statistical differences between the modeling and validation groups in serum alanine aminotransferase(ALT),aspartate aminotransferase(AST),triglycerides(TG),gamma-glutamyl transferase(GGT),red blood cell count(RBC),hemoglobin(Hb),platelet count(PLT),international normalized ratio(INR),alpha-fetoprotein(AFP),serum calcium(Ca2+),serum cholinesterase(CHE),and HBV DNA levels.Multivariate logistic regression analysis identified AST,GGT,Hb,PLT,Ca2+,CHE,and HBV DNA as independent influencing factors for HCC occurrence(P

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Objective To investigate the effects of cranial electrotherapy stimulation(CES) with varying parameter configurations on sleep quality in patients diagnosed with chronic insomnia disorder.Methods Seventy-two participants meeting diagnostic criteria for chronic insomnia disorder were randomly allocated to a four-arm parallel study design.The intervention protocol comprised:Group 1(G1) received CES at 0.5 Hz,300 μA;Group 2(G2) underwent CES treatment at 1.5 Hz,300 μA;Group 3(G3) administered 100 Hz,300 μA stimulation;and Group4(G4) received sham stimulation with identical device placement but no current delivery.Primary outcomes were quantified through polysomnography(PSG) recordings conducted at baseline and post-intervention,whereas secondary outcomes were assessed via standardized sleep questionnaires including the Pittsburgh sleep quality index(PSQI) and Insomnia Severity Index(ISI).Results Following a 10-day intervention protocol,significant clinical improvements were observed across all active treatment groups(G1-G3) as evidenced by reductions in PSQI.Insomnia severity index(ISI) scores quantitative polysomnographic analysis revealed that both G2(1.5 Hz) and G3(100 Hz) cohorts demonstrated statistically significant enhancements in Flinders Fatigue Scale(FFS) scores,total sleep time(TST),and sleep efficiency(SE),accompanied by reduced sleep onset latency(SOL) compared to baseline measurements.However,no statistically significant differences were detected between the G2 and G3 intervention arms across all measured parameters.CES exerted no significant effect on sleep architecture.Conclusion CES can effectively improve the sleep of patients with chronic insomnia.Within a certain range,a higher frequency of CES leads to better sleep improvement effects.

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Objective To explore the brain-predicted age difference(Brain-PAD) in patients with type 2 diabetes mellitus(T2DM) by a machine learning prediction model based on structural magnetic resonance(sMRI) in the Southwest University Adult Lifespan Dataset(SALD),and to reveal the relationship between Brain-PAD and duration of T2DM and cognition.Methods Group comparisons about demographic variables and cognitive function were conducted respectively in local database of 104 T2DM patients and 83 healthy controls(HC).The prediction model via Gaussian process regression(GPR) was constructed by training sMRI data of 329 healthy volunteers in SALD,then its performance was validated and evaluated.Furthermore,Brain-PAD(predicted age-chronological age) in the local database was calculated.Group comparisons of Brain-PAD between T2DM patients and HCs were conducted by Mann-Whitney U test.Finally,Pearson correlation coefficient(r) was calculated between Brain-PAD and duration of disease and cognition.Results Poor performance in auditory verbal learning test(AVLT)-delayed recall,AVLT-recognition,symbol digital modalities test(SDMT)(P

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Objective To identify the risk factors for pulmonary arterial hypertension(PAH) in maintenance peritoneal dialysis(MPD) patients and to develop and validate a nomogram-based risk-prediction model.Methods A total of 168 hospitalized MPD patients from the Department of Nephrology were enrolled.Body-fluid composition was measured by bioelectrical impedance analysis,and pulmonary-artery systolic pressure(PASP) was assessed by echocardiography.Patients were randomly allocated into a training set and a validation set at 1:1 ratio.Variables with P< 0. 05 in multivariable Logistic regression in the training set were incorporated to construct a nomogram .The validation set was used to test the model ’s predictive performance . ROC curves , calibration curves , and deci-sion-curve analysis were applied to evaluate accuracy , consistency , and clinical usefulness of the model . Results Dialysis vintage ( OR : 1 . 038 , 95% CI: 1 . 008 - 1 . 069 , P = 0. 012) , hemoglobin level ( OR : 0. 961 , 95% CI: 0. 929 - 0. 994 , P = 0. 021) , and extracellular water/intracellular water ratio (E/I) (OR : 1 . 069 , 95% CI: 1 . 024- 1 . 115 , P = 0. 002) were independent risk factors for PAH . ROC analysis yielded area under curve as 0. 867 (95% CI: 0. 782 - 0. 953) and 0. 808 (95% CI: 0. 714 - 0. 902) in the training and validation sets , respectively .Calibration plots showed that the predicted curves for both the training and validation sets closely overlapped with the ideal reference line , indicating that the nomogram risk-prediction model had good predictive performance . Deci-sion-curve analysis demonstrated that , within threshold ranges of 0. 13 - 0. 76 ( training set ) and 0. 20 - 0. 76 (val- idation set ) , clinical net benefit was substantial when interventions were guided by the nomogram . Conclusion Dialysis vintage , hemoglobin level , and fluid-overload index (E/I) are independent risk factors for PAH in MPD patients . The nomogram based on these parameters reliably predicts PAH risk and may aid clinical decision-mak- ing.

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Objective To investigate the expression of TIPE3 in colorectal cancer(CRC) and its correlation with tumor immune infiltration and prognosis.Methods The expression of TIPE3 in tumor and adjacent normal tissues from 110 CRC patients was detected using real-time fluorescence quantitative enzyme chain reaction(qPCR),Western blot,immunohi stochemi stry(IHC),bioinformatics analysis,and single-cell RNA sequencing(scRNAseq).The association between TIPE3 expression and clinicopathological factors,prognosis,and immune cell infiltration was analyzed.Results Transcriptomic and proteomic analyses revealed that among the TIPE family,TIPE(P

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CCAAT/enhancer binding protein β(C/EBPβ) is a transcription factor that plays a vital role in diverse biological processes,including cell proliferation,cell apoptosis,inflammation,and immune regulation.It is expressed in female reproductive organs such as the ovary and uterus,and it serves as a critical regulator of both physiological functions and pathological conditions.This review comprehensively summarizes the significant contributions of C/EBPβ to physiological processes such as follicular development and decidualization,as well as its involvements and mechanisms in reproductive disorders including polycystic ovary syndrome,endometriosis,and ovarian tumors,aiming to provide a potential research target in the field of reproduction.

abstract:
Cachexia is one of the serious complications in patients with end-stage cancer.Progressive depletion of skeletal muscle is an important feature of cachexia.Previous studies have found that excessive activation of autophagy accelerates skeletal muscle wasting in cachexia,and glutamine released from excessive catabolism of muscle tissue can trigger the autophagy.Mammalian target of rapamycin complex 1(mTORC1) and AMP-activated protein kinase(AMPK) signaling regulate autophagy genesis;moreover,glutamine regulates the mTORC1 and AMPK signaling pathways.Therefore,it is deduced that higher level of glutamine may result in abnormal autophagy by regulating mTORC1 and AMPK in cancer cachexia,which contributes to the development of skeletal muscle wasting.Here,this review discusses the following three perspectives:firstly,autophagy hyperactivation is involved in skeletal muscle wasting in cancer cachexia.Secondly,how mTORC1 and AMPK signaling pathways regulate autophagy.Finally,glutamine is involved in skeletal muscle wasting in cancer cachexia by induced autophagy hyperactivation via regulating mTORC1/AMPK signaling.Our study will provide a scientific basis for the development of potential therapeutic strategies.