To reveal the molecular mechanism by which nuclear epidermal growth factor receptor (nEGFR) synergistically regulates the expression of cell migration-inducing protein (CEMIP) by forming a complex with the transcription factor Yin Yang 1 (YY1), and to investigate the biological functions of the nEGFR-YY1-CEMIP signaling axis in invasion of hepatocellular carcinoma (HCC).

After HCC cells were serum-starved for 24 h, the cells were treated with 100 ng/mL EGF. Thus, the cells were divided into a control group and EGF-treated groups at different time points. Nuclear expression and localization changes of EGFR were detected by Western blotting and immunofluorescence (IF). To investigate the interaction between nEGFR and YY1, their nuclear colocalization and interaction were examined by IF and co-immunoprecipitation (Co-IP), respectively. Transcriptional profiling was performed using RNA sequencing (RNA-seq) to identify differentially expressed genes at the genome-wide level. Combined with Gene Ontology (GO) functional enrichment analysis and transcription factor binding profiles via using the JASPAR database, CEMIP was identified as a candidate target gene. To validate the regulatory mechanism, the following experimental groups were established, Control, EGF, siYY1, and siYY1+EGF. The expression of CEMIP at protein and mRNA levels was detected by Western blotting and RT-qPCR. To elucidate the molecular mechanism of nEGFR/YY1 binding to the CEMIP promoter, the control and EGF-treated groups were established. Chromatin immunoprecipitation followed by quantitative PCR (ChIP-qPCR) was performed to assess the enrichment of nEGFR/YY1 at the CEMIP promoter region. Luciferase reporter assay was conducted following transfection with either wild-type EGFR (EGFR-WT), nuclear localization-deficient mutant (EGFR-dNLS), YY1 overexpression plasmid (YY1-OE), or dominant-negative YY1 mutant (YY1-DN) to evaluate changes in promoter activity. Subsequently, cell migration and invasion capabilities were evaluated using scratch wound healing assay and Transwell assay, while hyaluronic acid (HA) level was quantified by ELISA. The expression of matrix metalloproteinases (MMP2/9) was analyzed via Western blotting to assess the regulatory role of the nEGFR/YY1-CEMIP axis in the migration and invasion of HCC cells. By analyzing the CEMIP expression profiles in HCC patients from National Center for Biotechnology Information (NCBI) public databases, its potential association with tumor metastasis risk was validated.

Western blotting and IF demonstrated that EGF treatment significantly induced nuclear translocation of EGFR, peaking at 30 min (P<0.001). Co-IP and IF assays indicated both physical interaction and nuclear co-localization between nEGFR and YY1. RNA-seq analysis identified CEMIP as a significantly differentially expressed gene. GO enrichment analysis revealed that CEMIP was significantly enriched in biological processes related to cell invasion promotion. JASPAR prediction identified conserved YY1 potential binding region within the CEMIP promoter region. Western blot and RT-qPCR analyses confirmed that EGF treatment up-regulated CEMIP at both protein and mRNA levels (P<0.05). Notably, YY1 knockdown significantly suppressed CEMIP expression, while exogenous EGF supplementation restored CEMIP level in YY1-deficient cells (P<0.05). ChIP-qPCR analysis demonstrated specific enrichment of the nEGFR/YY1 complex at the CEMIP promoter region, with EGF stimulation significantly enhancing its binding affinity (P<0.001). Luciferase reporter assay confirmed that nEGFR/YY1 robustly enhanced CEMIP promoter activity (P<0.01), while either the EGFR-dNLS or the YY1-DN substantially attenuated this transcriptional activation. Functional phenotyping showed that the nEGFR/YY1-CEMIP axis significantly enhanced the migration and invasion of HCC cells by promoting HA catabolism and up-regulating MMP2/9 expression (P<0.05). Analysis of NCBI datasets revealed that CEMIP expression was significantly up-regulated in HCC tumor tissues than adjacent normal tissues (P<0.001). Moreover, HCC patients with elevated CEMIP expression exhibited higher risk of metastasis (P<0.001).

nEGFR promotes HCC invasion by forming a transcriptional complex with YY1 to cooperatively activate CEMIP expression.

Toreveal the mechanism by which the programmed death-ligand 1 （PD-L1）- protein tyrosine phosphatase 1B （PTP1B）-focal adhesion kinase （FAK） signaling axis promotes the progression of hepatocellular carcinoma （HCC） and elucidate its effector functions in HCC.

GEPIA database was used to plot a 10-year survival curve for PD-L1 and FAK expression levels in HCC patients. Immunohistochemical （IHC） staining was utilized to analyze the relative expression levels of PD-L1 and FAK phosphorylated at the Y397 site ［p-FAK（Y397）］ in HCC tissues，and the results were compared to those in the adjacent non-tumor tissues. Subsequently，endogenous PD-L1 expression was detected with Western blotting in HCC cell lines with low （SNU-387） and high （Hep3B） PD-L1 expression levels. After lentivirus-transduced SNU-387^PDL1+ and Hep3B^PDL1-cells were constructed，the effect of high and low expression of PD-L1 on the expression of p-FAK（Y397） with Western blotting. To elucidate the functional mechanism of FAK in HCC，functional rescue experiments were performed by administering a FAK inhibitor to SNU-387^PDL1+ cells and a FAK activator to Hep3B^PDL1- cells，combined with wound healing scratch assay，Transwell invasion assay，EdU proliferation assay，and colony formation assay to evaluate tumor malignant effects. The GENEMANIA database predicted functional interactions between protein tyrosine phosphatase 1B （PTP1B），PD-L1，and FAK. IHC staining was performed to analyze the correlation among PD-L1，PTP1B，and p-FAK（Y397） expression. Co-immunoprecipitation （Co-IP） and indirect immunofluorescence （IF） were applied to validate the interaction between PD-L1 and PTP1B. Western blotting was utilized to confirm the regulatory relationship between PD-L1 and PTP1B. In vitro PTP1B phosphatase activity assay measured the changes in PTP1B activity. Subsequently，Western blotting was used to screen cell lines with high endogenous PTP1B expression （SNU-387） and low endogenous PTP1B expression （Hep3B）. Furthermore，Hep3B^PTP1B+ and SNU-387^PTP1B- cell lines were generated，and then p-FAK（Y397） levels were then detected in these modified cell lines，and the aforementioned functional effect assays （migration，invasion，proliferation and colony formation） and rescue experiments were repeated. Furthermore，Western blotting was employed to detect changes in downstream signaling pathways following enhancement or attenuation of p-FAK（Y397） in SNU-387 and Hep3B cells.

IHC staining revealed a positive correlation between PD-L1 and p-FAK（Y397） expression in HCC tissues （95%CI：1.065~3.801，P<0.01）. In SNU-387^PDL1+ cells，PD-L1 overexpression significantly enhanced phosphorylation at the FAK Y397 site （P<0.01） and increased cell migration，invasion，proliferation，and colony formation capabilities （P<0.01），and these effects could be reversed by FAK inhibitor treatment （P<0.05）. Conversely，in Hep3B^PDL1- cells，PD-L1 knockdown significantly reduced FAK Y397 phosphorylation （P<0.01） and decreased cell migration，invasion，proliferation，and colony formation abilities （P<0.01），and these effects were restored by FAK activator treatment （P<0.05）. IHC staining further showed a negative correlation between PTP1B expression and both PD-L1 and p-FAK（Y397） in HCC tissues （95%CI：1.886~3.514，P<0.05）. Co-IP and IF assays confirmed a direct interaction between PD-L1 and PTP1B，with PD-L1 suppressing PTP1B expression level and reducing its activity （P<0.01）. In SNU-387^PTP1B- cells，PTP1B knockdown significantly increased FAK Y397 phosphorylation （P<0.01） and enhanced cell migration，invasion，proliferation，and colony formation （P<0.01），and these effects were reversed by FAK inhibitor （P<0.05）. While in Hep3B^PTP1B+ cells，PTP1B overexpression significantly decreased FAK Y397 phosphorylation （P<0.01） and reduced cell migration，invasion，proliferation，and colony formation （P<0.01），and those effects were restored by FAK activator treatment （P<0.05）. Furthermore，enhanced phosphorylation at the FAK Y397 site in SNU-387 cells activated downstream PI3K/AKT and MEK/ERK signaling pathways （P<0.01），whereas inhibition of FAK（Y397） phosphorylation in Hep3B cells attenuated the activation of these signaling pathways （P<0.01）.

PD-L1 activates FAK by suppressing PTP1B，thereby promoting migration，invasion，and proliferation in HCC.

To investigate the effects of glutathione peroxidase 7 (GPX7) on the proliferation and senescence of hepatocellular carcinoma (HCC) cells and its potential value as a therapeutic target.

Clinical and transcriptomic data from HCC patients in The Cancer Genome Atlas (TCGA) database were analyzed to evaluate the relationship between GPX7 expression and prognosis. Western blotting, qRT-PCR, CCK-8 assay, EdU staining, and SA-β-Gal staining were employed to compare the expression and function of GPX7 in HCC cell lines and normal liver cells. A stable GPX7-knockdown Hep3B cell line was established, and transcriptomic changes were analyzed using RNA-seq. The PI3K inhibitor LY294002 and its activator 740 Y-P were utilized to determine the role of GPX7 in regulating cell senescence via the PI3K-AKT pathway. An orthotopic xenograft model was constructed using 18 male nude mice (6 weeks old, 18~22 g) to observe tumor growth. Tumor and adjacent tissue samples from 56 HCC patients (obtained from the Eighth Medical Center of Chinese PLA General Hospital between January 2012 and December 2022) were analyzed to assess the relationship between GPX7 expression and clinicopathological features.

TCGA data analysis revealed that GPX7 was significantly highly expressed in HCC tumor tissues (P<0.01), and the patients with high GPX7 expression had obviously shorter overall survival (OS) (P=0.018). Western blotting and qRT-PCR showed that the expression level of GPX7 was notably higher in the HCC cell lines than the normal liver cells (P<0.01). After GPX7 knockdown, the CCK-8 absorbance values of HCC cells were significantly reduced (P<0.01), the proportion of EdU-positive cells was obviously decreased (P<0.01), and the proportion of SA-β-Gal positive cells was notably increased (P<0.01). RNA-seq analysis revealed that differentially expressed genes were significantly enriched in the PI3K-AKT signaling pathway (P<0.05). The PI3K inhibitor LY294002 significantly enhanced the GPX7 knockdown-induced cell senescence (P<0.01), while the activator 740 Y-P partially reversed this effect (P<0.05). In the xenograft model, GPX7 knockdown significantly inhibited tumor growth in nude mice (P<0.01), and the PI3K activator 740 Y-P partially reversed this effect (P<0.01). Clinical sample analysis displayed that high GPX7 expression was negatively correlated with tumor differentiation (P<0.05), and its high expression was associated with shortened OS (HR=2.61, 95%CI: 1.26~5.39, P=0.005).

GPX7 regulates cell proliferation and senescence through the PI3K-AKT pathway, and may serve as a potential therapeutic target for HCC treatment.

To investigate the mechanism by which INKA2-AS1 promotes hepatocellular carcinoma(HCC) migration, invasion, and macrophage-related immunosuppression.

Based on the Cancer Genome Atlas Program (TCGA)-HCC data and Genotype-Tissue Expression (GTEx) databases, differentially expressed genes were analyzed in 374 HCC tissues and 160 normal liver tissues. Survival analysis was used to investigate the relationship between INKA2-AS1 and the prognosis of HCC patients. Cox regression analysis was performed on INKA2-AS1. The relationship between INKA2-AS1 and immune infiltration in HCC tissues was analyzed using the Tumor Immune Estimation Resource Database. A total of 90 HCC patients were recruited from the Department of Hepatobiliary Surgery, Chongqing Hygeia Hospital from January 2019 to January 2021. The HCC tissues and adjacent normal tissues were collected. Hepa 1-6 liver cancer cells were grouped into: normal control (NC), INKA2-AS1, siNC and siINKA2-AS1. INKA2-AS1 was overexpressed and silenced by transfection. The proliferation, migration and invasion of cells in each group were detected by CCK-8, EdU, TUNEL, wound healing and Transwell assays. Each group of Hepa 1-6 cells were co-cultured with macrophages to analyze their effects on macrophages. Twenty nude mice (SPF grade, 4 weeks old, 15~19 g, half male and half female) were randomly divided into 4 groups (n=5): NC, INKA2-AS1, siNC and siINKA2-AS1. Tumor-bearing nude mouse models were established by subcutaneous injection of INKA2-AS1 silenced and overexpressed Hepa1-6 cells. The effect of INKA2-AS1 on tumor volume and mass were detected. Macrophage immunity was analyzed by Western blot analysis of IL-10 and FAP protein levels in tumor tissues.

The level of INKA2-AS1 in HCC tissues was significantly higher than that in normal tissues(P<0.05). INKA2-AS1 was associated with the histological grade, pathological stage of HCC (P<0.05). The survival rate (P=0.05), disease-specific survival (P=0.036) and progression-free interval (P=0.024) of HCC patients with high INKA2-AS1 expression were significantly lower than those of patients with low INKA2-AS1 expression. The level of INKA2-AS1 in HCC tissues was significantly higher than that in adjacent normal tissues (P<0.05). Cox regression analysis showed that INKA2-AS1 was an independent predictor of OS in HCC patients (P=0.005). INKA2-AS1 expression was associated with immune cells such as T cells and macrophages. The proliferation, migration, and invasion abilities of the siINKA2-AS1 group were lower than those of the siNC group (P<0.05), the apoptotic rate was higher than that of the siNC group (P<0.05), and inhibited the expression of IL-10 and FAP at mRNA and protein levels in co-cultured macrophages (P<0.05). The proliferation, migration and invasion abilities of the INKA2-AS1 group were higher than those of the NC group (P<0.05), the apoptotic rate was lower than that of the NC group (P<0.05), and promoted the expression of IL-10 and FAP at mRNA and protein levels in co-cultured macrophages (P<0.05). The tumor volume and mass of the siINKA2-AS1 group were lower than those of the siNC group (P<0.05), while the tumor volume and mass of the INKA2-AS1 group were higher than those of the NC group (P<0.01). The levels of IL-10 and FAP proteins in tumor tissues of the siINKA2-AS1 group were lower than those of the siNC group (P<0.05), while the levels of IL-10 and FAP proteins were increased (P<0.05).

INKA2-AS1 increment is related to poor prognosis of HCC patients, and the molecule promotes the proliferation and metastasis of HCC cells and induces the transformation of tumor-associated macrophages.

To investigate the value of enhanced MRI image features combined with apparent diffusion coefficient(ADC) in the differential diagnosis of primary hepatic mucosa-associated lymphoid tissue(MALT) lymphoma and hepatocellular carcinoma(HCC).

The clinical data of 10 patients with pathology-confirmed primary MALT lymphoma admitted in our hospital from January 1997 to May 2025 were retrospectively collected. Their enhanced MRI images were analyzed, mainly including the number of lesions, morphology, signal characteristics, enhancement methods, and presence or absence of vessel floating signs, and the ADC value was calculated in order to screen statistically significant variables. Firth regression analysis was used to screen independent predictors of primary MALT lymphoma in the liver. Receiver operating characteristic(ROC) curve was plotted, and the area under the curve(AUC) was calculated to evaluate the diagnostic efficacy.

Compared with the HCC group, the primary MALT lymphoma group had significantly higher incidence in the females(P=0.026), alpha-fetoprotein(AFP) <8 ng/mL(P<0.001), lower T2WI signal(P=0.001), lower ADC value(P<0.001), and mostly continuously enhanced lesions(P<0.001), and more vessel floating signs(P=0.008). Univariate Firth regression analysis showed that sex(95%CI: 1.36~52.10, P=0.020), T2 value(95%CI: 3.89~5 121.00, P<0.001), AFP(95%CI: 0~0.21, P<0.001), ADC value(95%CI: 0~0.21, P<0.001), and dynamic reinforcement(95%CI: 0~0.23, P<0.001), and vessel floating sign(95%CI: 0~0.40, P=0.004) were diagnostic predictors for primary MALT lymphoma of the liver. Multivariate Firth regression analysis indicated that ADC value(95%CI: 0~0.62, P=0.006), AFP(95%CI: 0~0.047, P=0.01), and dynamic reinforcement(95%CI: 0~0.39, P=0.005) were independent predictors for primary MALT in the liver. ROC curve analysis indicated that the AUC value of ADC value in diagnosing primary MALT lymphoma was 0.96, with a sensitivity of 0.8 and a specificity of 1.0, and the AUC value of AFP level in diagnosing primary MALT lymphoma was 0.85, with a sensitivity of 1.0 and a specificity of 0.7. The AUC value of dynamic reinforcement in diagnosing primary MALT lymphoma was 0.85, with a sensitivity of 0.8, and a specificity of 0.9.

Dynamic reinforcement and ADC value can be used as differential markers for primary MALT lymphoma and HCC, providing reliable reference for clinical preoperative evaluation.

To investigate the correlation between the combined assessment of preoperative 5-factor modified frailty index (mFI-5) and Naples prognostic score (NPS) with overall survival in patients with unresectable hepatocellular carcinoma (uHCC) following interventional therapy.

‍‍A retrospective cohort study enrolled 292 patients with uHCC who underwent interventional therapy at the Department of Hepatobiliary Pancreatic Surgery of the Second Affiliated Hospital in Army Medical University from October 2017 to December 2021. Patients were stratified into high-risk and low-risk groups based on mFI-5 (≥1), NPS (≥3), and CONUT (≥4) scores. Propensity score matching (PSM) was performed to balance baseline characteristics (post-matching n=186). The primary endpoint was overall survival (OS), analyzed using Kaplan-Meier curves with log-rank tests. The predictive performance of combined indicators was evaluated by receiver operating characteristic (ROC) curves, and prognostic factors were assessed via Cox regression analysis.

After PSM, baseline characteristics (including age, tumor markers, and treatment-related parameters) showed no significant differences between the two groups. Survival analysis demonstrated a 2.252-fold higher risk of death in the mFI-5 plus NPS high-risk group (95%CI:1.60~3.18,P<0.001). The combination of mFI-5 and NPS scores yielded an area under curve (AUC) of 0.718 for predicting 3-year overall survival, significantly outperforming either index alone (P=0.007). Multivariable Cox regression analysis identified that dual positivity for mFI-5 and NPS (HR=1.46; 95%CI: 1.01~2.11, P=0.044), portal vein tumor thrombosis (HR=1.49; 95%CI: 1.03~2.16, P=0.035), tumor diameter >5 cm (HR=2.01; 95%CI:1.27~3.17, P=0.003), Barcelona clinic liver cancer (BCLC) stage C disease (HR=2.05; 95%CI: 1.37~3.07, P<0.001) were independent predictors of poor prognosis. Postoperative combination targeted therapy and immunotherapy was associated with significantly reduced mortality risk (HR=0.57; 95%CI: 0.39~0.81, P=0.002).

The combination of mFI-5 and NPS scores is significantly associated with overall survival in patients with unresectable hepatocellular carcinoma (uHCC) undergoing locoregional therapy, providing a validated tool for clinical risk stratification and personalized treatment planning.

To compare the intestinal injury induced by different intensities of waveshock in rats exposed to extremely cold environment and to preliminarily explore the characteristics of the injury.

Sixty healthy male SD rats (2 months old, weighing 200~250 g) were randomly divided into 6 groups(n=10): blank control group, low-temperature control group, 5.0 MPa shock control group, and low-temperature+4.0, 4.5 and 5.0 MPa shock groups. The rats in the experimental groups were pre-treated in a -10 ℃ low-temperature environment for 30 min and then subjected to intestinal injury by using BST-I biological shock tube with different driving pressures. At 3, 8, and 24 h after injury, the serum levels of IL-6, TNF-α, intestinal fatty acid binding protein (I-FABP), and diamine oxidase (DAO) were detected, and the survival of rats within 24 h was recorded. At 24 h after injury, the rats were anesthetized and dissected, the characteristics of intestinal injury were observed, and pathological examination was performed. The differences of intestinal injury were compared among the 6 groups to explore the characteristics of intestinal injuries after different intensities of shockwave in rats after exposure to extremely cold environment.

Compared with the blank control group, the other 5 groups exhibited different severities of intestinal injury, and the rats in the low-temperature+ different shock groups were more prone to intestinal edema and trauma. The mortality rate was significantly increased in the low-temperature+5.0 MPa shock group (P<0.05). Pathological and serological studies found that dual effects of very cold environment and blast injury resulted in intestinal mucosal hemorrhage, edema, and disintegration of lamina propria in the experimental rats. The indicators of intestinal mucosal injury and intestinal inflammatory factors were also significantly increased when compared with the blank control group, and significant differences were among the groups with increment of shock intensity (P<0.05).

Exposure to very cold environment combined with abdominal blast injury increases mortality rate in rats, manifested by elevated serological indicators and intestinal inflammatory factors, as well as varying severities of intestinal wall edema and submucosal bleeding. Furthermore, the severity of the injury is positively related to the impact intensity, with worsened as the impact intensity increasing.

To investigate the alterations in skeletal muscle function and mass in an experimental mouse model of high-intensity exercise in a hot and humid environment.

Twenty-four male C57BL/6J mice (7~8 weeks old, weighing 21.30±0.67 g) were randomly assigned to a control group (CON group), a normal temperature and humidity exercise group (NE group), and a high temperature and humidity exercise group (HE group), with 8 mice in each group. The HE group was subjected to a high-temperature simulation chamber, maintaining a temperature of 37~39 ℃ and humidity of 70%~80%, for a 60-minute exercise intervention at a 10° incline and 80% of maximum velocity (12 min of exercise followed by 8 min of rest, for 3 cycles). The CON group did not exercise, while the NE group exercised in the same manner in a normal temperature and humidity environment. The overall condition of the mice was evaluated by monitoring their body weight and analyzing their body composition. Their serum creatinine and urea levels were detected using an automated biochemical analyzer. After exercise, skeletal muscle function in the mice of each group was assessed by measuring their grip strength and exhaustion time. The skeletal muscle contractility and resistance to fatigue were evaluated using an in situ/in vivo/ex vivo muscle testing system. HE staining was employed to observe the morphological and structural changes in the skeletal muscles, and the average cross-sectional area and diameter of the muscle fibers were analyzed. Genes related to protein synthesis (Eif4ebp1, p70S6k) and breakdown (Foxo3, Fbxo32, Trim63) and heat stress-related genes (Hsf-1, Hspa1a, Hsp90aa) were quantified using RT-qPCR.

① Compared with the CON and NE groups, the HE group exhibited significant decreases in body weight (P<0.01) and lean body mass (P<0.05), an upward trend of creatinine level (P<0.05), and increases in the urea content (P<0.01). ② The mice in the HE group had notably reduced grip strength (P<0.001), diminished skeletal muscle contraction, and weakened resistance to fatigue (P<0.05) than the CON and NE groups. ③ The HE group demonstrated a reduction in the average cross-sectional area of muscle fibers (P<0.05) and a decrease in average fiber diameter (P<0.05), with particular up-regulation of Fbxo32, Trim63 and Eif4ebp1 (P<0.01) and down-regulation of p70S6k (P<0.05) in comparison to the NE and CON groups. ④ The expression levels of heat stress-related genes were higher in the HE group than the CON and NE groups (P<0.05).

High-intensity exercise in a hot and humid environment can lead to a decline in skeletal muscle function and mass in mice, potentially due to the disturbance of skeletal muscle protein synthesis and degradation triggered by excessive heat stress.

To investigate the effects of meropenem and amikacin on gut microbiota diversity and composition in a neonatal rat model of necrotizing enterocolitis (NEC).

Neonatal SD rats (1~2 d, weighing 5~10 g, both sexes) were subjected to establish a NEC model through artificial formula feeding, hypoxic-cold stress, and lipopolysaccharide (LPS) gavage. The rats were randomly divided into normal control group (Group C, n=12), NEC group (Group N, n=20), meropenem intervention group (Group M, n=20), and amikacin intervention group (Group A, n=20). Following modeling, Group M and Group A received intraperitoneal injections of meropenem (125 mg/kg) or amikacin (468 mg/kg), twice daily for 3 consecutive days. Groups C and N were administered an equal volume of normal saline. At the end of the intervention, colonic contents or fecal samples were collected. The gut microbiota structure was analyzed using 16S rDNA high-throughput sequencing. Bioinformatics analysis was performed using the QIIME2 platform. Alpha diversity was evaluated using Chao1, Shannon, and Simpson indices. Beta diversity was assessed based on Bray-Curtis distance through principal coordinate analysis (PCoA) and non-metric multidimensional scaling (NMDS). Venn and UpSet plots were generated to visualize the composition and overlap of operational taxonomic units (OTUs). Linear discriminant analysis effect size (LEfSe) was applied to identify differentially abundant taxa across groups.

High-throughput 16S rDNA sequencing showed that the N group had significantly lower 3 indices of α diversity than the C group (P<0.01), that is, a Chao1 index from 230 to 40, a Shannon index from 1.65 to 0.85, and a Simpson index from 0.65 to 0.42. After antibiotic intervention, both the M group and A group obtained obvious increases in the Chao1 index than the N group (P<0.001), with a greater increase observed in the M group than in the A group (P<0.05). However, neither antibiotic group exhibited notable improvements in the Shannon index or Simpson index compared with the N group (P>0.05). Venn and UpSet analyses revealed that the M group had the highest number of unique OTUs (283), while the A group shared the most OTUs (63) with the C group. PCoA and NMDS analyses indicated that the microbial structure of the A group was closer to that of the C group, with better clustering. Taxonomic composition and LEfSe analysis demonstrated that the N group was enriched with potentially pathogenic taxa such as Escherichia coli B2 and Klebsiella under the phylum Proteobacteria, while beneficial bacteria including Lactobacillaceae and Bifidobacteriaceae (phylum Firmicutes) were significantly reduced, indicating severe dysbiosis. In contrast, the A group exhibited a significant increase in beneficial bacteria and a structural tendency toward ecological recovery. The M group, however, was enriched with various conditionally pathogenic and environmentally associated genera, displaying a microbial configuration notably deviating from a healthy state.

Meropenem and amikacin exhibit differential regulatory effects on the intestinal microbiota in the context of NEC. Amikacin demonstrates superior efficacy in restoring microbial stability and levels of beneficial bacteria, whereas meropenem, although effective for early infection control, warrants caution due to its potential long-term impact on the gut microbiome.

To investigate the impact of adequate lumen preparation on the 12-month primary patency rate of drug-eluting stents (DES) in patients with lower extremity arteriosclerosis obliterans （ASO） and to identify risk and protective factors for in-stent restenosis.

A retrospective cohort study was conducted on 141 patients who underwent DES implantation for ASO at the Department of Vascular Surgery of the First Affiliated Hospital of Chongqing Medical University between April 2022 and April 2024. According to post-percutaneous transluminal angioplasty (PTA) dissection grade [severe dissection is defined as type C or higher based on National Heart, Lung, and Blood Institute (NHLBI) criteria] and residual stenosis rate (severe stenosis is defined as ≥30%), the patients were categorized into an adequate preparation group (no severe dissection or severe residual stenosis; n=59) and an inadequate preparation group (n=82). DES primary patency at 12 months was assessed by color Doppler ultrasonography or angiography, defined as a peak systolic velocity ratio ≤2.4 on duplex ultrasound or angiographic stenosis <50%. Kaplan-Meier analysis was used to compare intergroup differences in DES patency rate and freedom from clinically driven target lesion revascularization (CD-TLR). Multivariate logistic regression analysis was employed to identify risk and protective factors for DES restenosis and to evaluate the risk contributions of post-PTA dissection and residual stenosis to DES restenosis.

Post-PTA, vascular dissection occurred in 94.3% (133/141) of treated limbs, among which 42.1% (56/133) were severe dissections, and severe residual stenosis was present in 44.0% (62/141) of limbs. Kaplan-Meier analysis revealed that the 12-month primary patency rate was significantly higher in the adequate preparation group than the inadequate group (HR=0.322, 95%CI: 0.132~0.789, P=0.013), while no significant difference was found in the rate of freedom from CD-TLR (HR=0.608, 95%CI: 0.187~1.937, P=0.407). Multivariate logistic regression analysis identified adequate lumen preparation (OR=0.228, 95%CI: 0.069~0.747, P=0.015) and Rutherford category 2~3 (OR=0.205, 95%CI: 0.058~0.725, P=0.014) as independent protective factors against DES restenosis. The patency rate in the subgroup with coexisting severe dissection and residual stenosis was significantly lower than that in the uncomplicated group (55.6% vs 89.8%, P<0.001), with a 7.067-fold increased risk of re-stenosis (95%CI: 2.424~20.602, P<0.001).

Adequate lumen preparation significantly improves the 12-month primary patency rate of DES. It, along with Rutherford category 2~3, serves as an independent protective factor against in-stent restenosis. Concurrent severe dissection and significant residual stenosis should be actively avoided during the procedure.

To explore the predictive value of fat attenuation index （FAI） and fibrous plaque index （FPI） for the prognosis of patients with acute coronary syndrome （ACS）.

‍A retrospective cohort study was conducted on 334 ACS patients undergoing percutaneous coronary intervention （PCI） in the First Affiliated Hospital of Army Military Medical University and Yongchuan Hospital of Chongqing Medical University from March 2021 to July 2023. All patients received coronary computed tomography angiography （CCTA） to measure FAI and FPI. According to the occurrence of major adverse cardiovascular events （MACE） with 1 year of follow-up，they were divided into MACE group （n=108） and non-MACE group （n=226）. The baseline data，CCTA data and results of laboratory tests were collected and compared between the 2 groups. Multivariate logistic regression analysis was used to analyze the relationship of FAI and FPI with the prognosis of ACS patients，and ROC curve was drawn to evaluate its predictive efficiency.

Among the 334 ACS patients，108 （32.34%） experienced MACE. When compared with the non-MACE group，the MACE group exhibited significantly larger proportions of diabetes （72.22% vs 31.86%） and left main coronary artery disease （18.52% vs 7.08%），but lower success rate of operation （79.63% vs 93.81%，P<0.05）. Radiologic results showed that the proportion of severe stenosis （20.37% vs 10.62%），FAI （-80.12±6.41 HU vs -72.34±7.09 HU） and FPI （0.58±0.41 vs 0.26±0.12） were obviously increased in the MACE group than the non-MACE group （P<0.05）. Laboratory tests indicated that there were statistical differences between the 2 groups in high-density lipoprotein-cholesterol （HDL-C，1.20±0.15 vs 1.09±0.16 mmol/L），miR-126 （0.91±0.12 vs 0.96±0.15） and SST2 （38.45±5.67 vs 34.30±4.89 ng/mL，P<0.05）. Multivariate Logistic regression analysis revealed that FAI （OR=1.200，95%CI：1.136~1.268），FPI （OR=63.157，95%CI：14.126~282.374），moderate stenosis （OR=1.332，95%CI：1.024~1.859），severe stenosis （OR=1.480，95%CI：1.074~2.039），miR-126 （OR=0.007，95%CI：0.001~0.077），and sST2 （OR=1.192，95%CI：1.113~1.277） were independent predictors of MACE （P<0.05）. ROC curve analysis displayed that stenosis degree （AUC=0.622，95%CI：0.561~0.683，P=0.001），FAI （AUC=0.790，95%CI：0.741~0.839，P=0.001） and FPI （AUC=0.700，95%CI：0.638~0.761，P=0.001），miR-126（AUC=0.646，95%CI：0.584~0.707，P=0.001），sST2 （AUC=0.700，95%CI：0.638~0.761，P=0.001） had certain predictive values for ACS prognosis.

Coronary FAI and FPI can be used as independent prognostic indicators of ACS patients，and their numerical changes are closely related to plaque stability and inflammatory state.

To evaluate the short-term efficacy of 3D-printed customized prostheses in limb-salvage surgery for pediatric distal femoral osteosarcoma.

A single-center retrospective study was conducted on the outcomes of 19 eligible children at the Affiliated Children's Hospital of Chongqing Medical University from May 2021 to February 2025. Among them, 9 cases were in the epiphysis-preserving group and received 3D-printed personalized epiphysis-preserving prosthesis implantation; 10 cases were in the hinge group and underwent 3D-printed individual hinge prosthesis implantation. Their basic clinical data, perioperative data, and follow-up information were collected and analyzed.

All the 19 subjected patients completed the surgeries as preoperatively planned. The knee joint function of the children recovered well after surgery. In the epiphysis-preserving group, there were 8 males and 1 female, at an average age of 11.05±2.75 years. During a follow-up time of 21.67±15.87 months, 8 cases obtained disease-free survival, with a mean Musculoskeletal Tumor Society (MSTS) score of 27.56±1.33, and the left 1 case deceased. The hinge group included 4 males and 6 females, at an age of 10.12±2.30 years, and they were followed up for 22.30±11.23 months. For the 7 cases with disease-free survival, their MSTS score was 25.30±2.21, and the other 3 cases dead.

In the limb salvage treatment of children with osteosarcoma in the distal femur, 3D-printed personalized prosthesis implantation achieves satisfactory short-term outcome.

To understand the latent profiles of kinesiophobia in kidney transplant recipients and explore the influencing factors of different profiles.

A cross-sectional study was conducted on 230 kidney transplant recipients subjected with convenient sampling from Department of Nephrology, the First Affiliated Hospital of Army Medical University from November 2024 to February 2025. General Information Questionnaire, Tampa Scale of Kinesiophobia-11 (TSK-11), Exercise Compliance Questionnaire, Fatigue Scale-14 (FS-14), Patient Health Questionnaire-9 (PHQ-9) and Chinese Version of the Self-Efficacy to Manage Chronic Disease Scale (C-SEMCD) were used for investigation and latent profile analysis. Univariate analysis and logistic regression analysis were applied to explore the influencing factors of different profiles.

Kinesiophobia in the participants was classified into 3 latent profiles: fearless movement type-low kinesiophobia group (54 cases, 23.48%), cautious movement type-moderate kinesiophobia group (98 cases, 42.61%), and resistant movement type-high kinesiophobia group (78 cases, 33.91%). Statistical differences were observed among the 3 groups in terms of age, education level, post-operative duration, depression score, fatigue score, and self-efficacy score of chronic disease management (P<0.05). Logistic regression analysis showed that age (OR=8.82, 95%CI: 1.27~61.10), education level [junior high school or below (OR=0.14, 95%CI: 0.04~0.50); technical secondary school or senior high school (OR=0.08, 95%CI: 0.02~0.27)], post-operative duration [<1 year (OR=11.39, 95%CI: 2.53~51.30); 1-5 years (OR=11.05, 95%CI: 2.48~49.22)], fatigue (OR=1.32, 95%CI: 1.10~1.59), and depression (OR=1.53, 95%CI: 1.19~1.98) were influencing factors for resistant movement type-high kinesiophobia in the kidney transplant recipients. Education level (technical secondary school or senior high school: OR=0.32, 95%CI: 0.12-0.86) and self-efficacy of chronic disease management (OR=0.95, 95%CI: 0.90-1.00) were influencing factors for cautious movement type-moderate kinesiophobia in the recipients.

Kinesiophobia in kidney transplant recipients can be classified into 3 latent profiles. Recipients’ age, education level, post-operative duration, fatigue, and depression are influencing factors for the resistant movement type-high kinesiophobia, and education level and chronic disease management self-efficacy are important influencing factors for the cautious movement type-moderate kinesiophobia.

To prepare glucose transporter 1 (Glut1) -targeted doxorubicin (DOX)-loaded liposomes (doxorubicin/polyphyllin H-liposomes, DOX/ppH-LPs) using polyphyllin H (ppH) instead of cholesterol as the liposomal membrane material, and to investigate their in vitro synergistic anti-tumor activity against non-small cell lung cancer (NSCLC).

DOX/ppH-LPs were prepared using thin-film hydration, and the formulation was optimized by single-factor investigation. The optimized DOX/ppH-LPs were characterized for morphology, particle size, polydispersity index (PDI), and zeta potential with transmission electron microscopy (TEM) and dynamic light scattering (DLS). Drug loading DL% was determined by high-performance liquid chromatography (HPLC). The storage stability was evaluated by observing in PBS at 4 ℃ for 7 d, and the serum stability was observed in DMEM containing 10% fetal bovine serum (FBS) at 37 ℃ for 48 h. In vitro drug release was studied in PBS at pH 7.4 and pH 5.0 values, respectively. Human NSCLC A549 cells were subjected as the model, MTT assay was performed to detect the proliferation inhibition by DOX/ppH-LPs at different concentrations (0.5, 5.0, 15.0 μg/mL) and the control group (ppH + DOX/LPs, a physical mixture of free ppH and DOX-loaded liposomes). Fluorescence microscopy was used to observe cellular uptake of DOX/ppH-LPs and DOX/LPs (containing 5 μg/mL DOX) at 15 min and 2 h. Live/dead cell staining was applied to assess apoptosis/necrosis induced by formulations (15 μg/mL DOX) after 48 h incubation. Transwell assay was conducted to evaluate inhibitory effect on cell migration and invasion, and the targeting property and in vitro synergistic anti-NSCLC activity of DOX/ppH-LPs were then comprehensively evaluated.

The optimal formulation of DOX/ppH-LPs was determined as hydration temperature at 50 ℃, 6 mg DOX, 2 mg ppH, and 24 mg lecithin. The prepared DOX/ppH-LPs were in spherical shape, uniform distribution, and at an average particle size of 145.13±22.14 nm, a PDI of 0.15±0.05, a zeta potential of -23.92±1.73 mV, and a DL of 10.13±0.71 % for DOX and (1.22±0.21)% for ppH. DOX/ppH-LPs maintained stable particle size, PDI, and exhibited significantly unchanged zeta potential after storage in PBS at 4 ℃ for 7 d or incubation in DMEM containing 10% FBS at 37 ℃ for 48 h, demonstrating excellent physical and serum stability. Both liposomes showed slow release at pH 7.4 value, while drug release was significantly accelerated at pH 5.0 value (P<0.05), indicating pH-sensitive release characteristics. MTT assay revealed that DOX/ppH-LPs exerted significantly stronger cytotoxicity against A549 cells than the ppH+DOX/LPs control group (P<0.05). Compared with ppH+DOX/LPs, DOX/ppH-LPs showed remarkably enhanced cellular uptake in A549 cells (P<0.05), with more DOX localized in the nucleus. Live/dead cell staining showed that at the same DOX concentration (15 μg/mL), the proportion of apoptotic/necrotic cells induced by DOX/ppH-LPs was significantly higher than that of the DOX/LPs control group. Transwell assay demonstrated that there were significantly less cells migrating and invading through the membrane in the DOX/ppH-LPs group than the ppH+DOX/LPs group.

Glut1-targeted doxorubicin-loaded liposomes (DOX/ppH-LPs) constructed by substituting cholesterol with ppH can target NSCLC cells, significantly enhance the in vitro synergistic anti-NSCLC activity of DOX and ppH.