To investigate the protective effects of Qiji Special Dietary Food on exercise-induced myocardial injury in mice.

An exercise-induced myocardial injury model was established using a treadmill running protocol, and at the same time, the modeled mice were administered Qiji Special Dietary Food via oral gavage, followed by a 4-week treadmill exhaustion test. Serum levels of cardiac troponin T (cTnT), creatine kinase (CK), and lactate dehydrogenase (LDH) were measured. Myocardial tissues were analyzed for superoxide dismutase (SOD) activity and malondialdehyde (MDA) content. Histopathological alterations and ultrastructural changes in myocardial tissue were evaluated using light microscopy and transmission electron microscopy (TEM).

After 4 weeks of exhaustive training, compared to the control group, the model group exhibited significantly elevated serum cTnT, CK, and myocardial MDA levels (P<0.01), along with reduced myocardial SOD activity (P<0.01). Compared to the model group, high-, medium-, and low-dose treatment significantly attenuated the exhaustive exercise-induced increases in serum cTnT level and myocardial MDA content (P<0.01), restoring these indicators to the levels comparable to those of the normal control group (P<0.05). Additionally, all treatment groups had markedly increased myocardial SOD activity, with no significant difference from the normal group. Histopathological and ultrastructural analyses revealed markedly alleviated myocardial damage in the treatment groups, with the medium-dose group exhibiting the most pronounced protective effects.

Qiji Special Dietary Food demonstrates significant protective effects against exercise-induced myocardial injury in mice, which maybe associated with its antioxidant activity and mitigation of oxidative stress.

To investigate whether olfactory mucosa mesenchymal stem cells (OM-MSCs) attenuate oxygen glucose deprivation and recovery (OGD/R)-induced ferroptosis in neurons through glutathione oxidase 4 (GPX4).

The middle nasal tissue were collected from a patient with nasal polyps admitted in our hospital, and then OM-MSCs were isolated from the tissue, which were confirmed by morphological observation under light microscopy and phenotypic characterization through flow cytometry for surface markers, including CD34, CD45, CD73, CD90, CD105, and CD146. Mouse hippocampal neuronal cell line HT22 was randomly divided into control, Control, OGD/R, OGD/R+OM-MSCs, OGD/R+sh-NC, OGD/R+sh-GPX4 and OGD/R+sh-GPX4+OM-MSCs groups. After the cells were subjected to OGD/R modeling, the cells were subsequently co-cultured with OM-MSCs and/or knockdown of GPX4. Neuronal apoptosis was quantified by flow cytometry, while cell viability was assessed using CCK-8 assay. Biochemical markers associated with ferroptosis, including MDA, ROS, GSH, and Fe²⁺ levels, were measured with corresponding reagent kits. The GPX4 expression at both mRNA and protein levels was determined through qPCR and Western blotting, respectively.

The isolated and primarily cultured OM-MSCs showed typical characteristics of OM-MSCs in cell surface markers (negative expression of CD34 and CD45 but positive expression of CD73, CD90, CD105, and CD146 on cell surface) and morphology (adherent cells in a spindle-like shape). Significant differences were observed among the control, OGD/R, and OGD/R+OM-MSCs groups in terms of cell viability, MDA, ROS, GSH, Fe²⁺ and GPX4 (P<0.05). The OGD/R group showed notable decreases in cell activity and GSH (P<0.05), increases in MDA, ROS, and Fe²⁺ (P<0.05), and down-regulation of GPX4 when compared with the control group (P<005). Co-culture with OM-MSCs enhanced cell activity and GSH (P<0.05), decreased MDA, ROS, and Fe²⁺ (P<0.05), and up-regulated GPX4 as compared to the conditions in the OGD/R group (P<0.05). While, OGD/R+sh-GPX4 treament developed the decreases in cell viability, GSH, and GPX4 and the increases in MDA, ROS, and Fe²⁺ as compared to the OGD/R+sh-NC group (P<0.05), however, all of these could be reversed by OM-MSCs.

OM-MSCs inhibit OGD/R-induced ferroptosis in HT22 cells by up-regulating GPX4.

To investigate the effects of open reading frame 1 protein (ORF1p), encoded by long interspersed nuclear element-1 (LINE-1), on the proliferation, migration, and invasion of esophageal squamous cell carcinoma (ESCC) cells, and explore the underlying molecular mechanism.

① Western blotting was performed to compare the expression of ORF1p between normal esophageal squamous epithelial cells and ESCC cells. ② Immunohistochemistry (IHC) assay was used to examine ORF1p expression in ESCC tissues and paired normal tissues adjacent to tumor. ③ The effects of ORF1p knockdown and overexpression on malignant behaviors in ESCC cells were determined through functional assays. ④ Xenograft tumor model in nude mice was established to evaluate the impact of ORF1p on tumor growth in vivo. ⑤ Transcriptome sequencing combined with cell functional rescue experiments were conducted to identify downstream targets regulated by ORF1p.

① Western blot analysis demonstrated the expression of ORF1p was significantly higher in the ESCC cell lines than the normal esophageal squamous epithelial cells (P<0.05). ② IHC confirmed remarkable up-regulation of ORF1p in ESCC tissues than paired adjacent normal tissues (P<0.000 1). ③ Functional assays and experiments on xenograft tumor models revealed that ORF1p substantially enhanced the proliferation, migration, and invasion of ESCC cells, as well as tumorigenic potential in vivo (P<0.05). ④ Functional rescue experiments showed that ORF1p facilitated the proliferation, migration, and invasion of ESCC cells by modulating AJUBA expression (P<0.05).

ORF1p is significantly up-regulated in ESCC and promotes the proliferation, migration, and invasion of ESCC cells by regulating AJUBA expression.

To investigate the role and primary mechanism of a novel fusion gene RELCH-RET in driving the malignant transformation of normal human bronchial epithelial (HBE) cells.

Based on retrospective clinical data from 456 non-small cell lung cancer (NSCLC) patients admitted in the Second Affiliated Hospital of Army Medical University from January 2019 to June 2022, a fusion gene, RELCH-RET,was identified as a research target. Three cell models were established: negative control (HBE VC, transfected with empty lentiviral vector), RET control (HBE RET, transfected withlentiviral overexpression vector of Flag-RET), and experimental group (HBE RELCH-RET, transfected with lentiviral overexpression vector of Flag-RELCH-RET). MTS assay and Transwell assay were used to detect cell proliferation and migratory and invasive abilities. In vivo tumorigenicity of the 3 cell models was assessed in 15 female non-obese diabetic/severe combined immunodeficiency (NOD/SCID) mice (SPF grade, 4 weeks old, weighing 15.1±0.4 g) via subcutaneous xenograft experiments, with 5 animals in each group. Western blotting was employed to detect the autophosphorylation of RET (Y905) and the phosphorylation of downstream signaling proteins ERK1/2, EGFR (Y845) and STAT3 (Y705). Dimerization and multimerization status of RELCH-RET were analyzed by chemical cross-linking (DTME treatment) in combination with Western blotting, with the reversibility being confirmed through de-cross-linking experiments.

There were 3 cases carrying RELCH-RET fusion gene screened out from the 469 NSCLC patients. Compared with the HBE VC and HBE RET groups, the HBE RELCH-RET group exhibited significantly enhanced cell proliferation (P<0.01), and acquired migratory and invasive abilities (P<0.01), while the control groups did not demonstrate the abilities. In the mouse xenograft tumor model, HBE cells stably expressing RELCH-RET developed significant tumor nodules (P<0.001), whereas the control groups (empty vector and wild-type RET) failed to exhibit detectable tumor growth. Western blotting revealed that RELCH-RET could induce the autophosphorylation of the RET tyrosine residue (Y905) and significantly up-regulate the phosphorylation levels of ERK1/2, EGFR (Y845), and STAT3 (Y705) proteins. Chemical cross-linking combined with Western blot analysis demonstrated that RELCH-RET formed a dimer (~170 kDa) in HBE cells, which is reversibly dissociated into monomers upon decross-linking treatment.

The novel fusion gene RELCH-RET, promotes ligand-independent dimerization/oligomerization, thereby mediating RET autophosphorylation, subsequently activates the downstream typical RET signaling pathway and ultimately drives the malignant transformation of normal HBE cells.

To investigate the effect of nutritional deficiency on autophagic flux in human hepatoblastoma HepG2 cells and the autophagy-dependent molecular pathway mediated by ATG5 against nutritional stress.

Lentiviral siRNA knockdown of ATG5 was performed to knock down the expression in HepG2 cells, and the transfection was verified by Western blotting and qRT-PCR. HBSS was used to treat HepG2 cells for 0, 1, 2, 3, 4, 5, 6 and 7 h for starvation-induced autophagy. Monodansylcadaverine (MDC) fluorescence staining was employed to detect the formation of intracellular autophagic vesicles. Western blotting was performed to measure the expression changes in microtubule-associated protein 1A/1B-light chain 3 (LC3), autophagy receptor protein (sequestosome 1, P62), autophagy-related gene 5 (ATG5) and nutrient stress pathway (AMPK/mTOR pathway) related proteins. CCK-8 assay was utilized to test cell proliferation.

Compared with the HepG2 cells under conventional culture medium, starvation induction resulted in more autophagic vacuoles (accumulation of autofluorescent marker, MDC), which peaked at 6 h of starvation (P<0.000 1), up-regulated protein levels ofLC3B-Ⅱ and ATG5 (P<0.05), decreased protein expression ofP62 (P<0.05), gradual activation of the AMPK/mTOR pathway with elapse of starvation time, and increase in the intensity of autophagic flux. However, in the HepG2 cells with ATG5 knockdown, starvation treatment led to decreased ATG5 expression, no significant difference in LC3B-II and P62 changes, inhibited autophagic flux, and suppressed cell proliferation (P<0.000 1).

Human hepatoblastoma HepG2 cells can regulate autophagic flux to against nutritional stress by inducing ATG5 expression.

To investigate the effect of endothelial cells in the perivascular niche on the stem cell-like characteristics of osteosarcoma cells and primarily explore the possible molecular mechanism.

A co-culture model was established in vitro using SV40T- human umbilical vein endothelial cells (HUVEC-T1) and osteosarcoma stem cells (OSCs) derived from the human osteosarcoma cell line 143B.Thus, there were 2 groups of cells, OSCs and co-cultured OSCs. The self-renewal capacity of OSCs between the 2 groups was assessed using a limiting dilution forming sphere assay. Flow cytometry and Western blotting were used to detect the expression of stem cell marker CD133 and stemness transcription factors SOX2 and NANOG. Fourteen female nude mice (4~6 weeks old, weighing 18~20 g) were randomly and equally divided into 2 groups of subcutaneous xenograft models: the control group (OSCs suspension) and the experimental group (OSCs+HUVEC-T1 mixed suspension). The tumor volume and mass were compared between the 2 xenograft groups. Immunofluorescence (IF) staining was used to verify the spatial proximity between endothelial cells and OSCs in vivo, while immunohistochemistry was employed to compare microvessel density (MVD) and CD133 expression level between the 2 groups. RNA-seq was performed to identify potential signaling pathways of endothelial cells affecting the stemness of OSCs. PCR and Western blotting were applied to confirm the RNA-seq findings. Exogenous protein treatment, IF staining, Western blotting and sphere formation assay were utilized to preliminarily validate the role of the identified pathway in regulating the stemness phenotype of OSCs.

The in vitro co-culture model of HUVEC-T1 and OSCs was successfully established. Compared with the control group, the co-culture group exhibited significantly enhanced self-renewal ability of OSCs, laeger proportion of the stemness marker CD133⁺ [(8.20±1.64)% vs (4.32±1.34)%, P<0.05], enhanced expression of CD117, SOX2 and NANOG (P<0.05), along with more sphere formation (P<0.05) and elevated SOX2/NANOG protein levels. The xenograft mice from the experimental group showed larger tumor volume (643.10±413.50 vs 247.90±93.66 mm³, P<0.05) and heavier tumor weight (0.52±0.27 vs 0.24±0.10 g, P<0.05) when compared the control group, correspondingly showing increased MVD (22.57±11.84 vs 11.43±5.38, P<0.05) and elevated CD133 expression (P<0.05). IF staining confirmed the adjacency of CD31-labeled endothelial cells and CD133-labeled OSCs in vivo. RNA-seq and functional experiments demonstrated that CXCR4 was highly expressed in co-cultured OSCs, CXCL12 was highly expressed in co-cultured endothelial cells, and exogenous CXCL12 promoted the sphere formation and expression levels of SOX2 and NANOG of OSCs (P<0.05).

Endothelial cells within the perivascular niche may promote the stemness phenotype of osteosarcoma cells via the CXCL12/CXCR4 pathway.

To investigate the effect and underlying mechanism of serine and arginine rich splicing factor 1 (SRSF1) on the replication of hepatitis B virus (HBV).

The effects of SRSF1 on HBV replication were investigated in different HBV replicating cell models by Southern blotting, Northern blotting and ELISA. Quantitative PCR , luciferase reporter assay and chromatin immunoprecipitation (ChIP) were applied to determine the effects of SRSF1 on the activities of HBV core promoter/enhancer in HepG2 cells. The relationship between SRSF1 and P53 was explored with Western blotting and ubiquitination assay. The effects of P53 on HBV replication were verified in different HBV replicating cell models, and the role of P53 in SRSF1 inhibition of HBV was clarified.

Overexpression of SRSF1 significantly inhibited HBV DNA and HBV RNA and reduced HBsAg and HBeAg secretion levels in a variety of HBV replicative cell models (P<0.0001). SRSF1 also inhibited the activity of HBV core promoter, although this inhibition was regulated by indirect mechanisms. In addition, SRSF1 enhanced P53 stability by protecting P53 from ubiquitination and subsequent proteasomal degradation. Meanwhile, the regulatory effect of overexpression or knockdown of P53 on HBV was validated in different cell models (P<0.0001).

Overexpression of splicing factor SRSF1 significantly inhibits HBV replication in a variety of cell models, and this inhibitory effect is mediated by its enhancement of P53 stability.

To investigate the clinical significance of the miR-543/syntrophin beta 1 (SNTB1) axis in colorectal cancer (CRC) and its influence on the tumor immune microenvironment.

The expression of SNTB1 in CRC tissues was analyzed using public data, such as, The Cancer Genome Atlas (TCGA), Genotype-Tissue Expression (GTEx), and Human Protein Atlas (HPA). Then Kaplan-Meier survival analysis, univariate Cox regression analysis and correlation analysis were performed to evaluate the prognostic value of SNTB1 and its relationship with immune microenvironment in CRC. The targeting relationship between miR-543 and SNTB1 was confirmed through online databases and fluorescence assays in HT-29 cells. For in vitro experiments, after transfecting si-SNTB1, miR-543 mimics and/or SNTB1 overexpression plasmids, HT-29 cells were co-cultured with CD8⁺ T cells, the expression of miR543 and SNTB1 and the viability and cytotoxicity of CD8⁺ T cells were assessed with qRT-PCR, Western blotting, flow cytometry, ELISA, and lactate dehydrogenase (LDH) release assay.

Analysis of public databases revealed significantly higher expression of SNTB1 in CRC tissues than normal tissues (P<0.001). The CRC patients with high SNTB1 expression exhibited poorer prognosis when compared with those with low expression level (P<0.05). Moreover, high SNTB1 expression was negatively correlated with immune scores in the tumor microenvironment and immune cell infiltration, especially CD8⁺ T cells (P<0.05). Furthermore, Knockdown of SNTB1 in HT-29 cells enhanced the cytotoxic activity of CD8⁺ T cells (P<0.01). Online database and in vitro experiments confirmed that miR-543 targets SNTB1, while the expression of miR-543 was decreased in colorectal cancer (P<0.001). Transfection with the miR-543 mimic inhibited the expression of SNTB1 in HT-29 cells (P<0.001), while overexpressing SNTB1 counteracted the promotion effect of miR-543 mimics on CD8⁺ T cell-mediated cytotoxicity (P<0.05).

MiR-543 activates CD8⁺ T cells and enhances their cytotoxicity against HT-29 cells by directly targeting SNTB1.

To investigate the perioperative outcomes and postoperative pregnancy outcomes of patients with intrauterine adhesions(IUA) treated by see-and-treat hysteroscopy and traditional hysteroscopy in transcervical resection of adhesions(TCRA).

A retrospective cohort study was performed on 485 patients with moderate-to-severe IUA who met the inclusion criteria and admitted in our hospital from January 2019 to December 2021. According to surgical approaches, the patients were assigned into a see-and-treat mode group and a traditional mode group. After clinical diagnosis(ultrasound and symptoms) of IUA, the patients from the former group received direct hysteroscopic adhesion separation surgery, and those of the latter group were diagnosed by outpatient hysteroscopy first and then hysteroscopic adhesion separation surgery. The perioperative indicators, postoperative three-dimensional transvaginal ultrasound(3D-TVUS) examination related characteristics, postoperative menstrual recovery, postoperative pregnancy outcomes, obstetric related complications, and neonatal outcomes were collected and compared between the 2 groups.

Among the enrolled 485 patients, there were 277 in the see-and-treat group and 208 in the traditional group. The success rate of surgical treatment was 89.89% in the see-and-treat group and 92.79% in the traditional group, but no statistical difference was seen between them(Chi-square=1.234, P=0.267). 3D-TVUS examination displayed that the see-and-treat mode group obtained better improvement of endometrial morphology, uterine morphology and menstruation after operation than the traditional group(P<0.001). The postoperative pregnancy rate was slightly higher in the see-and-treat group than the traditional mode group(58.84% vs 58.17%, P=0.882). However, the see-and-treat mode showed obvious advantage in the postoperative natural pregnancy rate, with a rate of 90.80%, obviously higher than that in the traditional mode group(81.82%, P=0.026). The live birth rate was 70.55% in the see-and-treat mode group, excluding 1 case with ongoing pregnancy in the second trimester and 1 case with ongoing pregnancy in the third trimester, and the rate was 74.38% in the traditional group, excluding 3 cases with ongoing pregnancy in the third trimester, but there was no statistical difference between the 2 groups(P=0.303). In terms of obstetric-related complications, there were 0 cases of blood transfusion during delivery hospitalization in the see-and-treat group, while there were 7 cases in the traditional group(P=0.003). In neonatal outcomes, the rate of transfer to the pediatric department was 10.43% in the see-and-treat mode group and 22.22% in the traditional mode group(P=0.021). For health economics, the see-and-treat hysteroscopy group demonstrated a significant advantage over the traditional hysteroscopy group(P<0.001). There was no significant difference in pain scores between the 2 groups.

The see-and-treat approach is a safe, feasible, and highly efficient strategy for integrating the diagnosis and treatment of IUA, enabling maximal minimization of surgical trauma while optimizing time and cost efficiency.

To compare the midterm outcomes of the Bentall procedure versus isolated aortic valve replacement (AVR) in patients with bicuspid aortic valve (BAV) complicated with severe stenosis and ascending aortic dilation in order to assess the therapeutic value of these surgical approaches for this complex cardiac condition.

A retrospective cohort study was conducted on 96 eligible patients who underwent surgical treatment in our institute between January 2018 and December 2022. According to surgical approaches, they were divided into an AVR group (65 cases) and a Bentall group (31 cases). Demographic features, comorbidities, preoperative status, and echocardiographic parameters were collected in all patients. Propensity score matching (PSM) was applied in a 1∶1 ratio to balance baseline characteristics. Perioperative indicators and follow-up data were compared and analyzed between matched cohorts after control of cofounding factors.

After PSM, 25 matched pairs were screened out and analyzed with comparable baseline data (all P>0.05). The Bentall group demonstrated significantly more superior intraoperative effective orifice area (EOA, 2.69±0.47 vs 2.35±0.47 cm², P=0.013) and EOA index (EOAI, 1.69±0.30 vs 1.47±0.29 cm²/m², P=0.010), and obviously longer cardiopulmonary bypass time [190.00 (147.00, 257.00) vs 101.00 (88.50, 124.50) min, P<0.01] and aortic cross-clamp time [141.00 (120.00, 166.00) vs 66.00 (55.00, 81.50) min, P<0.01] when compared with the AVR group. During a median follow-up of 28 months, the AVR group had notably larger aortic sinus diameter [32.00 (30.00, 34.00) vs 26.80 (26.00, 28.00) mm, P<0.01] and ascending aortic diameter [38.00 (34.50, 42.00) mm vs 26.00 (26.00, 28.00) mm, P<0.01], with ongoing dilation in the ascending aorta, while the Bentall group maintained stable dimensions. The Bentall group also showed statistically lower peak aortic valve pressure gradients [21.00 (15.50, 27.00) vs 25.00 (19.50, 31.00) mmHg, P=0.049].

Both Bentall procedure and AVR are effective in treatment of BAV complicated with severe stenosis and ascending aortic dilation. But, Bentall procedure offers advantages in hemodynamic optimization and aortic stability.

To evaluate the efficacy and safety of the combination of immunotherapy and targeted therapy and chemotherapy in third-line treatment of patients with microsatellite stable (MSS) metastatic colorectal cancer (mCRC).

A retrospective cohort trial was conducted on patients with MSS mCRC treated with third-line immunotherapy combined with targeted therapy and chemotherapy in our hospital from January 2020 to December 2023. The clinical data were collected. Kaplan-Meier survival analysis was employed to analyze progression-free survival (PFS) and overall survival (OS). Objective response rate (ORR), disease control rate (DCR) and other indicators were statistically analyzed to evaluate the clinical efficacy. The incidence and severity of adverse events during the treatment process were recorded to assess the safety.

A total of 80 patients were included in the analysis, 55 in the group of immunotherapy plus targeted therapy and 25 in the group of immunotherapy combined with targeted therapy and chemotherapy. The group of immunotherapy combined with targeted therapy and chemotherapy had significantly longer median PFS (6.3 vs 4.4 months; HR=0.58, 95%CI: 0.35~0.96; P=0.031) and OS (15.5 vs 10.1 months; HR=0.47, 95%CI: 0.27~0.81; P=0.006), and obviously higher ORR (32.0% vs 10.9%; OR=0.26, 95%CI: 0.07~0.79; P=0.021) and DCR (92.0% vs 78.2%; OR=0.31, 95%CI: 0.07~1.52; P=0.132) when compared to the group of immunotherapy plus targeted therapy. The incidence of adverse events at all grade and at grade 3 and above was 96.4% and 32.7% in the group of immunotherapy plus targeted therapy, and 100.0% and 36.0% in the group of immunotherapy combined with targeted therapy and chemotherapy, which mainly included bone marrow hematopoietic inhibition, hand-foot skin reaction, liver function impairment and thyroid function abnormality.

The triple therapy of immunotherapy plus targeted therapy and chemotherapy is a more effective and safer treatment than the double therapy of immunotherapy plus targeted therapy in treatment of MSS mCRC patients.

To explore the potential cuproptosis-related genes （CRGs） in patients with multiple myeloma （MM） and develop a prognostic model for improving prognosis and revealing features of the MM immune microenvironment.

① Transcriptome sequencing data and clinical information were retrieved from the GSE4581 dataset in the Gene Expression Omnibus （GEO） database and the Cancer Genome Atlas-Multiple Myeloma Research Foundation （TCGA-MMRF） database. The 859 patients from the TCGA-MMRF database were assigned into a training set，and the other 414 ones from the GSE4581 dataset into a validation set. LASSO-Cox and multivariate Cox regression analyses were used to construct prognostic models and calculate risk scores. Based on the median risk score，they were categorized into high- and low-risk cohorts. Time-dependent receiver operating characteristic （ROC） and calibration curves were plotted to assess the predictive performance and accuracy of the model. The differences between the high- and low-risk cohorts were explored using Kaplan-Meier survival curve analysis and immune microenvironment correlation analysis. ② RT-qPCR and Western blotting were used to verify the expression of prognostic model genes in MM cell lines and normal bone marrow single-nucleated cells，and CCK-8 assay，flow cytometry，and Western blotting were applied to verify the biological function of UBE2D1 in MM cells.

① LASSO-Cox and multivariate Cox regression analyses revealed that the model consisted of 4 genes，CDKN2A ［HR=1.60 （95%CI：1.24~2.05），P=2.5e-4］，PDE3B ［HR=1.33 （95%CI：1.09~1.62），P=4.2e-3］，UBE2D1 ［HR=1.65 （95%CI：1.20~2.26），P=2.1e-3］ and COA6 ［HR=1.35 （95%CI：1.07~1.71），P=0.01］. In the training set，the time-dependent ROC curves predicted that the area under curve （AUC） value of 1-，3-，and 5-year survival rate was 0.63，0.71，and 0.78，respectively，and in the validation set，the AUC value was 0.656，0.657，and 0.797，respectively. Calibration curve analysis showed excellent agreement in predicting 1-，3-，and 5-year prognosis. In the training set，Kaplan-Meier curves showed that patients in the high-risk cohort had a significantly shorter overall survival （OS） than the low-risk cohort ［HR=2.18 （95%CI：1.58~3.02），P<0.001］，and in the validation set，the high-risk cohort still had a shorter OS than the low-risk cohort ［HR=2.45 （95%CI：1.49~4.05），P<0.001］. Immune correlation analysis revealed that the ratios of immune cells，such as plasma cells and CD4⁺ T cells were significantly lower in the high-risk cohort （P<0.05），and the risk scores were positively correlated with the expression of immune checkpoint CTLA-4，tumor-targeted therapeutic sites TNFSF4 and ENTPD1，and microenvironmental chemokines CXCL16，CCL8，and CCL16 （P<0.05）. ② Remarkable differences were observed in the expression of all 4 prognostic model genes between the MM cell lines and normal bone marrow single-nucleated cells （P<0.05），and knockdown of UBE2D1 notably inhibited the proliferation of MM cells （P<0.05）.

Our prognostic models based on CDKN2A，PDE3B，UBE2D1，and COA6 genes can predict the prognosis of MM patients. The risk scores of the genes are significantly correlated with immune infiltration in the tumor microenvironment，which providing new molecular markers for individualized therapy.

To construct a prognostic model of centrosome amplification-related genes (CARGs) by machine learning and evaluate its prediction performance for the prognosis of esophageal squamous cell carcinoma (ESCC).

CARGs were obtained from Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) datasets. The RNA-sequencing (RNA-seq) transcriptome datasets of ESCC were retrieved from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO), and assigned into training and validation sets, respectively. Subsequently, single-sample gene set enrichment analysis (ssGSEA) and weighted gene co-expression network analysis (WGCNA) were employed to screen CARGs. A prognostic model of CARGs was constructed by incorporating 12 machine learning algorithms, and univariate and multivariate Cox regression analyses were applied to evaluate whether the 12 models as an independent prognostic factor or not. Eventually, 15 paired ESCC and adjacent non-tumor tissue samples were collected from the Department of Gastroenterology of the Second Affiliated Hospital of Army Medical University, and real-time quantitative PCR (RT-qPCR) and immunohistochemistry staining were performed to detect the expression of these genes ESCC samples.

Our 9-CARGs prediction model for ESCC prognosis was constructed. RT-qPCR confirmed that the mRNA expression levels of DENR, TRIP13,BRCA2, TTF2, TCFL5 and NUP188 were significantly higher in ESCC tissues than normal tissues (P<0.05), and the protein levels of DENR, TRIP13, TTF2 and TCFL5 were also elevated when compared to normal tissues.

DENR, TRIP13, TTF2 and TCFL5 are highly expressed and closely associated with poor prognosis of ESCC, suggesting their potential roles in the pathogenesis and progression of this malignancy.

To explore the network structural characteristics, core factors, and gender differences in the comprehensive assessment of mental health in military personnel.

A total of 4 105 officers and soldiers were subjected and surveyed using the Comprehensive Mental Health Assessment Questionnaire for Soldiers. Through network analysis, a network model for comprehensive mental health assessment of military personnel was constructed with the R qgraph Package. The core factors of their mental health were explored using the qgraph package, and the reliability of the network structure was evaluated using the bootnet package. Then a comparative analysis was conducted on the network characteristics of comprehensive mental health assessments between male and female participants using permutation tests with the NetworkComparisonTest package in R.

In the network of the comprehensive assessment of military personnel mental health, the strongest association was observed between institutional trust and interpersonal trust, followed by interpersonal trust and sense of meaning in life, adaptability and positive coping, as well as depression and negative emotions, with a regularized partial correlation coefficient of 0.49, 0.45, 0.44, and 0.42, respectively. The core factors were interpersonal trust, work engagement, and institutional trust, with an expected influence of 1.095, 1.060, and 1.039, respectively. The 95% confidence intervals (CIs) obtained from the edge weight accuracy assessment were relatively narrow, and the correlation stability coefficient of the network was 0.75, indicating a stable and reliable network structure. Furthermore, there were significant differences in the network structure of comprehensive mental health assessments between male and female participants (M=0.335, P<0.001), especially in the core factor, interpersonal trust, with particularly significant gender difference (P<0.01).

Interpersonal trust, work engagement, and institutional trust are the core factors in the comprehensive assessment of military personnel’s mental health. There are gender differences in the network structure of the comprehensive assessment of mental health for military personnel.