Table of Content

05 October 2026, Volume 46 Issue 10

Previous Issue   

Original Articles

The association between multimorbidity patterns, frailty transitions,and 2-year mortality in hospitalized older adults in China

LIU Junting, YU Miao, JIAO Jing, XU Tao

2026, 46(10):  1307-1315.  doi:10.16352/j.issn.1001-6325.2026.10.1307

Asbtract ( 34 )   PDF (1769KB) ( 8 )  

References | Related Articles | Metrics

Objective To examine the association between frailty transitions and distinct multimorbidity patterns in relation to mortality risk among hospitalized older adults. Methods This prospective cohort study enrolled 8 270 hospitalized elderly patients aged 65 years and above. Frailty status was assessed using the FRAIL scale,and patients were classified into five categories based on frailty trajectories at baseline and 3-month follow-up. Principal component analysis was used to identify five distinct multimorbidity patterns,and their impact on mortality risk was evaluated. Results A total of 56.77% of participants exhibited multimorbidity,and frailty trajectories were closely associated with mortality risk. The mortality risk for patients in the persistent frailty and worsening frailty groups was 14.27 times and 10.02 times higher,respectively, compared to the persistent non-frail group. Multimorbidity patterns,such as cardiometabolic disorders,sensory-psychiatric impairments,and cancer,significantly increased mortality risk. Conclusions Frailty trajectories and multimorbidity patterns significantly influence the mortality risk in hospitalized elderly patients. Early identification and intervention for the risk factors of frailty and multimorbidity are crucial for slowing disease progression and improving the health of the elderly population.

Ferroptosis is involved in spermatogenic dysfunction in mice under heat stress

XU Zixun, CHEN Xiangting, SUN Ao, JIA Mingdi, XIA Qing

2026, 46(10):  1316-1321.  doi:10.16352/j.issn.1001-6325.2026.10.1316

Asbtract ( 20 )   PDF (3924KB) ( 5 )  

References | Related Articles | Metrics

Objective To investigate the correlation between ferroptosis and spermatogenic dysfunction in mice under heat stress. Methods Adult male C57BL/6 mice were divided into the control group and the heat stress (HS) group. Spermatozoa were collected from the epididymal ducts, and indicators such as sperm motility were detected using a sperm motility analyzer. Mouse testes were collected, and RNA-Seq technology was used for differential gene analysis, as well as Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses. A rescue experiment was conducted using the ferroptosis inhibitor Ferrostatin-1 (Fer1), with an additional Fer1-HS group established. Hematoxylin-eosin (HE) staining and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) staining were used to detect changes in testicular tissue structure, respectively. Kits were used to detect changes in ferroptosis-related indicators (Fe²⁺ and glutathione, GSH) in testicular tissue. Results Heat stress (HS) tended to reduce sperm motility and concentration in mice, caused loosening of seminiferous tubules, thinning of the spermatogenic epithelium, and massive apoptosis of spermatogenic cells. Moreover, the level of Fe²⁺ in testicular tissue was significantly higher than that in the control group (P＜0.05), while the GSH level showed a downward trend. RNA-seq identified ferroptosis-related genes Miox, Prap1, and Mt3. GO analysis revealed that heat stress enhanced the activity of GO pathways related to iron ions and lipid peroxides in mouse testes(Intracellular sequestering of iron ion, cellular lipid catabolic process and negative regulation of oxidoreductase activity). After treatment with Fer1, the Fer1-HS group showed partial recovery in the loosening degree of testicular seminiferous tubules and the shedding of spermatogenic cells compared with the HS group. Additionally, the Fe²⁺ level in the testes of the Fer1-HS group was significantly lower than that in the HS group(P＜0.05), while the GSH level showed a tendency to increase compared with the HS group. Conclusions Ferroptosis is involved in inducing testicular spermatogenic dysfunction in mice under heat stress, mainly manifested by excessive iron levels.

Construction of a murine model of pathological cardiac remodeling and transcriptomic analysis

LIU Ruyi, DENG Hui, ZHANG Shu, YANG Xiaowen, DONG Daqian, LIU Tianlong, ZHENG Wei

2026, 46(10):  1322-1328.  doi:10.16352/j.issn.1001-6325.2026.10.1322

Asbtract ( 16 )   PDF (4015KB) ( 27 )  

References | Related Articles | Metrics

Objective Mouse myocardial transcriptome sequencing data were analyzed to identify transcription factors regulating pathological cardiac remodeling,and to elucidate its mechanism. Methods A mouse cardiac remodeling model was established via subcutaneous implantation of angiotensin Ⅱ(AngⅡ) micro-osmotic pump,and the mouse model was evaluated at anatomical and pathological levels.Transcriptomic sequencing of mouse myocardial tissue was performed to identify differentially expressed transcription factors between groups.Gene Set Enrichment Analysis(GSEA) was employed to delineate relevant signalling pathways.Pearson correlation analysis was used to establish correlations between transcription factors and signalling pathways,which were validated by western blot. Results After micro-osmosis pump implantation for 4 weeks,significant alterations in cardiac structure and function were observed. Compared with control mice,the mice in model group exhibited markedly reduced ejection fraction(EF) and shortening fraction(FS)(P＜0.05),while heart-to-tibia weight ratio and heart-to-leg ratio were significantly increased in the model group mice(P＜0.05).The myocardial WGA staining and Picro Sirius Red staining of myocardial tissue revealed that the mouse heart in model group exhibited significant increased in cardiac hypertrophy and fibrosis(P＜0.05).Transcriptomic sequencing data revealed a significantly increase in transcription factor Etv4 expression in mouse myocardial tissue from the model mice compared with vehicle mice. The extracellular matrix(ECM) receptor pathway was markedly activated,and Etv4 expression in myocardial tissue showed a significant positive correlation with gene expression involved in the ECM receptor pathway(P＜0.05),which was further validated at the protein level. Conclusions The transcription factors Etv4 may facilitate pathological cardiac remodeling, potentially via the ECM receptor pathway.

Role of ferroptosis-related gene Slc4a1 in age-related sarcopenic mice

HOU Jingwen, LIU Beibei, Nuerguli·ABULAITI, ZHU Xinhua

2026, 46(10):  1329-1335.  doi:10.16352/j.issn.1001-6325.2026.10.1329

Asbtract ( 16 )   PDF (3744KB) ( 28 )  

References | Related Articles | Metrics

Objective To systematically explore the key genes related to ferroptosis and their potential mechanisms in age-related sarcopenia through gene expression data analysis and animal model experiments. Methods The skeletal muscle gene expression data of age-related sarcopenia mice and healthy control mice were collected from public databases GSE226117 and GSE175562. Through differential expression analysis and weighted gene co-expression network analysis (WGCNA), key genes related to sarcopenia were screened, and their relationship with ferroptosis was further explored by functional enrichment analysis. An aged sarcopenia mouse model was established, and young mice were used as the control. Skeletal muscle tissues and serum samples were collected. HE staining was used to observe the histopathological changes, and immunohistochemistry was employed to detect the expression of the key gene Slc4a1. The levels of GSH, MDA and ROS were detected by ELISA. The expression levels of Slc4a1, Fth1, Gpx4, Slc7a11 and Tfrc were detected by RT-qPCR and Western blot. Results Differential expression analysis identified a total of 1 326 differentially expressed genes in the GSE226117 and GSE175562 datasets, and these genes were clustered into 5 co-expression modules through WGCNA. Among them, the brown module had the highest correlation with age(P＜0.05). Enrichment analysis revealed that Slc4a1, Slc39a8 and Tfrc in the brown module were significantly involved in the regulation of ferroptosis. Slc4a1 was significantly downregulated in both datasets and was further identified as a key gene for sarcopenia(P＜0.05). Compared with the young control group, in the aged sarcopenia mouse model, HE staining showed that the skeletal muscle tissue structure was sparse, and the expression of Slc4a1 was significantly decreased. The level of the antioxidant marker GSH was significantly reduced, while the levels of the lipid peroxidation product MDA and the oxidative stress marker ROS were significantly increased (P＜0.05). The expressions of ferroptosis-related genes including Slc4a1, Fth1, Gpx4, Slc7a11 and Tfrc were all significantly downregulated (P＜0.05). Conclusions Slc4a1 may play a role in the pathological mechanism of sarcopenia by participating in the regulation of ferroptosis, providing a potential target for the diagnosis and treatment of sarcopenia.

CX3CR1 aggravates cerebral ischemia/ reperfusion injury by regulating microglial polarization

MENG Qinghua, TIAN Wei, LI Lin, ZHANG Weizhi, PENG Shuangchun

2026, 46(10):  1336-1343.  doi:10.16352/j.issn.1001-6325.2026.10.1336

Asbtract ( 16 )   PDF (2731KB) ( 7 )  

References | Related Articles | Metrics

Objective To investigate the role and mechanism of CX3C chemokine receptor 1 (CX3CR1) in regulating microglial polarization via the MFGE8/Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signaling pathway in cerebral ischemia/reperfusion injury (CI/RI). Methods A transient middle cerebral artery occlusion (tMCAO) model was established in mice, which were randomly divided into the following groups: sham operation, tMCAO, shNC, shCX3CR1, and shCX3CR1+shMFGE8. Infarct volume was assessed by TTC staining; neurological deficits were evaluated using the Longa scoring system; and histopathological changes in brain tissue were observed via HE staining and Nissl staining. Western blot and RT-qPCR were used to detect the expression of proteins related to the MFGE8/JAK2/STAT3 pathway and marker genes of microglial polarization. The levels of inflammatory cytokines (TNF-α, IL-6, IL-1β, etc.) in brain tissue were measured by ELISA. Results Compared with the sham group, the tMCAO group showed significantly increased infarct volume and neurological scores, accompanied by increased neuronal necrosis, nuclear pyknosis, and structural disruption, as well as elevated pro-inflammatory cytokine levels. The mRNA and protein levels of Cx3cr1 were up-regulated, while those of Mfge8 were down-regulated (P＜0.05). Compared with the shNC group, the shCX3CR1 group exhibited reduced infarct volume and neurological scores, decreased neuronal necrosis, and lower pro-inflammatory cytokine levels. Additionally, the expression of M2-type microglial marker genes (Arg1, Cd206, YM1/2) was increased, whereas M1-type marker genes (Nos2, Tnf, Il1b) were decreased. MFGE8 protein levels were elevated, while total JAK2 and STAT3 protein levels remained unchanged, with reduced phosphorylation levels of p-JAK2 and p-STAT3 (P＜0.05). Compared with the shCX3CR1 group, the shCX3CR1+shMFGE8 group showed opposite trends in the above indicators (P＜0.05). Conclusions CX3CR1 may aggravate neuronal necrosis and CI/RI by inhibiting MFGE8 to activate the JAK2/STAT3 signaling pathway, thereby promoting M1-type microglial polarization.

Colchicine mitigates acute aortic dissection induced by β-aminopropionitrile combined with angiotensin-Ⅱ in mice

SONG Zhiping, YANG Xi, HOU Xingzhi, HUANG Bo, FENG Jian

2026, 46(10):  1344-1351.  doi:10.16352/j.issn.1001-6325.2026.10.1344

Asbtract ( 20 )   PDF (5604KB) ( 3 )  

References | Related Articles | Metrics

Objective To evaluate whether colchicine mitigates acute aortic dissection (AAD) in mice and to define its mechanistic basis. Methods Sixty 12-week-old male mice were randomized into control (n=20),model (n=20),and colchicine (Col,n=20) groups. AAD incidence,aortic diameter,and medial architecture were assessed by HE and Verhoeff-Van Gieson staining. Macrophage infiltration (CD68⁺ cells) was quantified by flow cytometry. Systemic and local inflammatory markers (IL-6, TNF-α) were measured by ELISA, qPCR, Western blot. Smooth muscle cell (SMC) phenotypic switching and apoptosis were evaluated by α-SMA immunohistochemistry and TUNEL staining,respectively. Apoptosis-related proteins (cleaved caspase-3,total caspase-3,Bax,Bcl-2) and NF-κB pathway components (phosphorylated NF-κB,total NF-κB,IκBα) were analyzed by Western blot. Results Colchicine reduced AAD incidence from 75% to 30% (P＜0.05),limited aortic expansion,and preserved medial thickness with intact elastic lamellae. Macrophage accumulation in the aortic wall was markedly suppressed in the Col group(P＜0.05). Both serum and tissue levels of IL-6 and TNF-α were downregulated by colchicine (P＜0.05). The model group displayed increased SMC apoptosis,loss of α-SMA positivity,an elevated cleaved/total caspase-3 ratio,Bax upregulation,and Bcl-2 downregulation—changes that were attenuated by colchicine (P＜0.05). Mechanistically,the Model group exhibited IκBα degradation and enhanced NF-κB phosphorylation,whereas colchicine stabilized IκBα and suppressed NF-κB activation (P＜0.05). Conclusions Colchicine confers protection against AAD in this murine model by interrupting NF-κB-mediated inflammatory reaction and SMC apoptosis.

Effects of disulfiram on proliferation, apoptosis and gefitinib resistance of lung cancer cell line H1975

YIN Jie, WANG Xue, DENG Shukai

2026, 46(10):  1352-1358.  doi:10.16352/j.issn.1001-6325.2026.10.1352

Asbtract ( 18 )   PDF (4017KB) ( 6 )  

References | Related Articles | Metrics

Objective To investigate the effects of disulfiram (DSF) on the proliferation, apoptosis and gefitinib sensitivity of non-small cell lung cancer H1975 cells. Methods H1975 cells were cultured in vitro and treated with different concentrations of disulfiram for 24, 48, and 72 hours. The CCK-8 assay was used to assess the impact of disulfiram on cell proliferation, and appropriate concentrations were selected for subsequent experiments. Cells were treated with varying concentrations of gefitinib alone or in combination with disulfiram for 48 hours, and the half-maximal inhibitory concentration (IC₅₀) was calculated to determine the reversal fold. Cells were treated with gefitinib, disulfiram and N-acetylcysteine alone or in combination for 48 hours. Apoptosis was detected by flow cytometry, intracellular reactive oxygen species levels were measured using the DCFH-DA method, and Western blotting was performed to assess the expression of stemness-related markers (ALDH1A1, SOX2), pathway-related markers (p-STAT3, STAT3), and apoptosis-related markers (Bax, Bcl-2). Results Disulfiram significantly inhibited H1975 cell proliferation in a concentration-dependent (0-10 μmol/L) and time-dependent (24-72 hours) manner (P＜0.05). The IC₅₀ of gefitinib alone was 11.13 μmol/L, which decreased to 4.148 μmol/L when combined with 1 μmol/L disulfiram, indicating that disulfiram effectively reversed gefitinib resistance by 2.68 times. Disulfiram significantly suppressed the upregulation of stem cell-related proteins SOX2 and ALDH1A1 induced by gefitinib (P＜0.05), and this effect was partially counteracted by the reactive oxygen species inhibitor N-acetylcysteine. Compared to gefitinib and disulfiram monotherapy groups, the combination therapy group exhibited significantly increased apoptosis rates, elevated reactive oxygen species levels and pro-apoptotic Bax expression, and reduced p-STAT3 and anti-apoptotic Bcl-2 expression (P＜0.05). Further clearance of reactive oxygen species with N-acetylcysteine reversed disulfiram′s inhibitory effect on the STAT3 pathway(P＜0.05). Conclusions Disulfiram may enhance gefitinib sensitivity by upregulating reactive oxygen species levels and inhibiting the STAT3 signaling pathway.

Correlation of thromboelastography parameters and thrombomodulin levels in patients with traumatic brain injury

TANG Ningjian, LIU Dan, WU Zhongjun, LIAO Bingrong

2026, 46(10):  1359-1365.  doi:10.16352/j.issn.1001-6325.2026.10.1359

Asbtract ( 17 )   PDF (2715KB) ( 8 )  

References | Related Articles | Metrics

Objective To explore the relationship between the changes in thromboelastography(TEG) parameters and the levels of thrombomodulin(TM) in patients with traumatic brain injury(TBI). Methods A total of 179 patients with TBI who were admitted from January 2020 to June 2024 were selected. The correlation between TM and TEG parameters was analyzed using the Local Weighted Regression Scatter Smoothing Method(LOWESS). Multivariate Logistic regression was used to analyze the factors associated with poor prognosis in TBI patients; Generalized Linear Model and Restricted Cubic Spline were used to analyze the relationship between TM and poor prognosis in patients with different severity of TBI. Results TM was positively correlated with the α angle and Ma, and negatively correlated with the K value and R value(P＜0.05). The increase in the α angle, Ma, TM, K value, and R value was an influencing factor for the poor prognosis of TBI patients(P＜0.05). The TM level showed a non-linear dose-response relationship in the prognosis of poor outcomes in patients with mild, moderate, and severe TBI(P_{non-linearity}＜0.05). When the K value was less than 1.05 min, the correlation between the TM level and the risk of poor prognosis in TBI patients was more significant(P_interaction＜0.01). Conclusions The increases in α angle, Ma, TM, K value, and R value are factors influencing the poor prognosis of TBI patients.

Spliceosome LSM4 inhibits the malignant progression of triple-negative breast cancer cell MDA-MB-231 through regulating DNA damage repair pathway

Zinati·NUERTAI, ROU Qian, ZHANG Meng, LIU Ying, CHENG Fang

2026, 46(10):  1366-1374.  doi:10.16352/j.issn.1001-6325.2026.10.1366

Asbtract ( 17 )   PDF (10189KB) ( 41 )  

References | Related Articles | Metrics

Objective To explore the biological functions and potential regulatory mechanisms of spliceosome LSM4 in triple-negative breast cancer (TNBC). Methods The mRNA and protein expression levels of LSM4 in TNBC were analyzed using The Cancer Genome Atlas (TCGA) and Clinical Proteomics Tumor Analysis Consortium (CPTAC) samples, and small interfering RNA (siRNA) was used to transiently knock down LSM4 in MDA-MB-231 cells. CCK-8 assay for cell proliferation, annexin V/PI double staining for apoptosis, Transwell to detect cell invasion and migration, and RNA-seq to analyze the differentially expressed genes and regulated alternative splicing events. Results LSM4 was abnormally expressed in TNBC patients, and knockdown of LSM4 in vitro significantly promoted the proliferation, invasion and migration of MDA-MB-231 cells and inhibited apoptosis. The alternative splicing genes regulated by LSM4 were mainly enriched in the signaling pathways related to DNA damage repair, especially involved in modulating the exon exclusion and skipping events of DNA polymerase β (POLB), possibly promoting the generation of transcript isoforms with non-coding or encoding for a shorter protein, thereby affecting the genomic stability of cancer cells. Conclusions LSM4 might affect the onset and progression of TNBC via activating and modulating alternative splicing events of genes involved in DNA damage repair pathway.

Effects of Xinshuai Heji on energy metabolism, autophagic flux and PYGM/Thbs1 expression in hypoxia-exposed cardiomyocytes

PENG Tianjie, ZHANG Zimeng, QIU Shenglei, YANG Dan, SHANG Juju, LI Sinai, ZHANG Zhenmin

2026, 46(10):  1375-1383.  doi:10.16352/j.issn.1001-6325.2026.10.1375

Asbtract ( 25 )   PDF (8447KB) ( 6 )  

References | Related Articles | Metrics

Objective To investigate the effects of Xinshuai Heji (XSHJ) on energy metabolism and autophagic flux disruption in hypoxia-exposed HL-1 cardiomyocytes, and to observe the concomitant changes in the expression of glycogen phosphorylase, muscle-associated(PYGM) and thrombospondin-1(Thbs1). Methods A hypoxia- induced injury model was established in HL-1 cells with interventions of XSHJ at various concentrations and empagliflozin as a positive control. Cell viability and apoptosis were assessed. Mitochondrial network morphology and membrane potential were observed by fluorescence staining. The oxygen consumption rate (OCR) was measured using a Seahorse analyzer, along with biochemical markers of energy and redox metabolism. Autophagic flux was evaluated utilizing a tandem fluorescent reporter assay. Furthermore, the protein expression levels of PYGM, Thbs1, and autophagy-related markers were determined via Western blot analysis. Results Compared with the model group, XSHJ dose-dependently increased cell viability, reduced apoptosis, and ameliorated the damaged mitochondrial network structure. XSHJ also elevated basal OCR and intracellular levels of ATP, NADPH, and GSH, while decreasing reactive oxygen species (ROS) accumulation. Concurrently, XSHJ reversed the hypoxia-induced reduction in the LC3-Ⅱ/Ⅰ ratio and the abnormal accumulation of p62 protein, accompanied by increased numbers of autophagosomes and autolysosomes. Protein expression profiling revealed that XSHJ upregulated PYGM and downregulated Thbs1 expression. These protective effects were comparable to those of empagliflozin. Conclusions XSHJ alleviated hypoxia-induced cardiomyocyte injury, improved energy metabolism, and promoted the restoration of autophagic flux. These protective effects may be associated with the involvement of PYGM and Thbs1, though the underlying mechanisms require further investigation.

Longitudinal study of multimodal quantitative EEG characterization in Kleine-Levin syndrome

ZHANG Le, HUANG Yan, CHEN Jianhua

2026, 46(10):  1384-1391.  doi:10.16352/j.issn.1001-6325.2026.10.1384

Asbtract ( 15 )   PDF (5912KB) ( 28 )  

References | Related Articles | Metrics

Objective To characterize longitudinal quantitative electroencephalography(qEEG) changes from the symptomatic to recovery phase of Kleine-Levin syndrome (KLS) and examine the temporal relationship between clinical and electrophysiological recovery. Methods Longitudinal changes in brain electrical dynamics during a KLS episode were investigated using quantitative EEG approaches. A 14-year-old boy underwent serial EEG recordings on illness Days 2, 3, 4, 5, 8 and 14. Twelve age-matched healthy participants provided reference distributions. Six-minute artifact-cleaned eyes-closed segments were analyzed by conventional EEG assessment, microstate analysis, power spectral density (PSD), and correlation-based Omega complexity. The six KLS sessions were treated as repeated observations from one individual, with healthy reference-based standardized scores and single-case methods used for exploratory comparison. Results Days 2-5 showed paroxysmal generalized theta-delta slowing, poor preservation of conventional NREM markers, and occasional posterior sharp-and-slow-wave activity. Low-frequency intermittent photic stimulation elicited a self-limited bilateral occipital photoparoxysmal response. Clinical hypersomnia resolved by Day 8, although mild residual slowing remained; the conventional EEG was overall normal by Day 14. Global microstate mean duration decreased from 122.44-139.07 ms on Days 2-5 to 89.47 ms on Day 8 and 80.28 ms on Day 14, while occurrence increased from 7.19-8.17/s to 11.18/s and 12.46/s, respectively. PSD showed marked symptomatic delta predominance with progressive alpha-beta recovery. Omega complexity showed frequency- and region-dependent spatial changes. Conclusions KLS is associated with reversible temporal, spectral and spatial EEG abnormalities. Clinical recovery is preceded complete electrophysiological normalization, supporting quantitative EEG as a candidate tool for tracking disease-state transitions.

Clinical Sciences

The assessment value of joint detection of serum FEIR, LAG-3, KLF5 for the prognosis of mycoplasmal pneumonia

LI Nike, ZHANG Xiangyan

2026, 46(10):  1392-1396.  doi:10.16352/j.issn.1001-6325.2026.10.1392

Asbtract ( 15 )   PDF (932KB) ( 2 )  

References | Related Articles | Metrics

Objective To assess the value of joint detection of serum immune adhesion inhibitory factor (FEIR), lymphocyte activation gene 3 (LAG-3), and Kruppel like factor 5 (KLF5) in assessing the prognosis of mycoplasmal pneumonia (MPP). Methods A total of 176 MPP patients in Guizhou Provincial People′s Hospital were included in MPP group. Complying with the severity of disease, they were assigned into the severe MPP group (74 cases) and the mild MPP group (102 cases). According to the prognosis, they were included into the good prognosis group(135 cases) and the poor prognosis group (41 cases). Another 176 healthy volunteers who underwent physical check-ups were considered as the control group. ELISA was used to detect serum FEIR, LAG-3, and KLF5. Multivariate logistic regression was performed to analyze the factors affecting the prognosis of MPP. ROC curve was performed to analyze the predictive value of joint detection of serum FEIR, LAG-3, KLF5 for prognosis of MPP. Results Compared with control group, the MPP group had significantly higher serum FEIR, LAG-3, and KLF5 (P＜0.05). Compared with the mild MPP group, the serum levels of FEIR, LAG-3, and KLF5 in the severe MPP group were significantly increased (P＜0.05). Compared with the good prognosis group, the poor prognosis group had significantly higher C-reactive protein (CRP), FEIR, LAG-3, and KLF5 (P＜0.05). High FEIR, LAG-3, and KLF5 were independent risk factors affecting the prognosis of MPP (P＜0.05). The AUC of serum FEIR, LAG-3, and KLF5 alone in predicting the prognosis of MPP was 0.825, 0.810, and 0.819, respectively. The AUC of the joint prediction of the three factors was 0.939, which was better than single prediction of the three factors (Z_FEIR-joint=3.023, Z_LAG-3-joint=3.180, Z_KLF5-joint=3.328, all P＜0.05). Conclusions The FEIR, LAG-3, and KLF5 are upregulated in serum of MPP. The three are closely related to the severity of MPP. Joint detection is of high value in assessing the prognosis of MPP.

Effect of early use of evolocumab in combination with statin on lipids, lipid ratio and cardiac function in patients with acute coronary syndromes

ZHU Enhui, CHEN Yujie, Aikedai·AIHEMAITIJIANG, FEI Shasha, YANG Rujia, WANG Juan

2026, 46(10):  1397-1401.  doi:10.16352/j.issn.1001-6325.2026.10.1397

Asbtract ( 27 )   PDF (748KB) ( 5 )  

References | Related Articles | Metrics

Objective To investigate the lipid-lowering efficacy and safety of early evolocumab administration in ACS patients. Methods A total of 311 ACS patients (Jan-Dec 2023) receiving atorvastatin (20 mg QN) were randomized: observation group (Obs, n=213) started evolocumab within 48 h of hospital admission; control group (Ctrl, n=98) started post-PCI. Lipid profile (LDL-C, TC, TG, ApoB, HDL-C, ApoA-Ⅰ), LDL-C goal rate (＜1.4 mmol/L),the lipid ratios (TC/HDL-C, TG/HDL-C, LDL-C/HDL-C, ApoB/ApoA-Ⅰ), lipid variability (SD, CV, cVIM),cardiac function (LVEDD, LVESD, LVMI, LVEF), and liver/kidney function were assessed at discharge and 1, 3, 6 months. Results At 1 month, lipids decreased significantly vs baseline in both groups (P＜0.05). Obs showed greater reductions in LDL-C, TC, TG, ApoB vs Ctrl (P＜0.05). LDL-C goal rate increased over time, consistently higher in Obs (P＜0.05). Lipid ratios decreased more in Obs (P＜0.05). In both groups, LVEDD, LVESD, and LVMI decreased, while LVEF increased; the Obs group showed significantly greater improvements(P＜0.05) and milder liver/kidney impairment(P＜0.05).Liver/kidney impairment was less in Obs(P＜0.05). Conclusions Early evolocumab+ statin significantly lowers lipids, increases LDL-C goal attainment, reduces lipid variability, improves cardiac function/remodeling, and demonstrates better safety (less liver/kidney impairment) in ACS patients.

Human neutrophil lipocalin and cytokines in the efficacy evaluation of DPMAS artificial liver therapy in liver failure

GUO Guifang, WANG Liang, CHENG Xiaoyu, LI Ming, CHEN Jiali, LI Xiaopeng

2026, 46(10):  1402-1406.  doi:10.16352/j.issn.1001-6325.2026.10.1402

Asbtract ( 22 )   PDF (986KB) ( 4 )  

References | Related Articles | Metrics

Objective To explore the dynamic changes of human neutrophil lipocalin (HNL) and cytokines (TNF-α,IL-6, IL-1β) in patients with liver failure undergoing double plasma molecular adsorption system (DPMAS)artificial liver therapy, as well as their value in evaluating treatment efficacy. Methods A total of 167 patients with liver failure admitted to the Department of Infectious Diseases at the First Affiliated Hospital of Nanchang University from January 2023 to December 2024 were selected. They were divided into an effective group (n=132) and an ineffective group (n=35) according to the therapeutic effect 4 weeks after treatment. The levels of HNL, TNF-α,IL-6, and IL-1β were detected in both groups before treatment and at 1 week, 2 weeks, and 4 weeks after treatment. Meanwhile, alanine transaminase (ALT), total bilirubin (TBIL), albumin (ALB), prothrombin activity (PTA), and international normalized ratio (INR) were measured synchronously. The correlation between HNL, cytokines and liver function indicators was analyzed, and the predictive value of HNL and cytokines for the efficacy of DPMAS was evaluated. Results In the effective group, the levels of HNL, IL-6, TNF-α, IL-1β, ALT, TBIL, and INR at 1 week, 2 weeks, and 4 weeks after treatment were significantly lower than those before treatment and in the ineffective group at the same period, while ALB and PTA were significantly higher than those before treatment and in the ineffective group at the same period (P＜0.05). HNL and cytokines were positively correlated with ALT, TBIL, and INR, and negatively correlated with ALB and PTA (P＜0.05). The AUC of HNL combined with cytokines in predicting the efficacy of DPMAS was 0.956, which was significantly higher than that of each index alone(P＜0.05). Conclusions HNL and cytokines can dynamically reflect the therapeutic effect of DPMAS, and their combined detection has important clinical value in evaluating the efficacy of liver failure treatment.

Correlation between oral frailty and severity of osteoporosis in elderly women

LI Xiaoxiao, BIAN Lili, DING Jing, DU Xueping

2026, 46(10):  1407-1413.  doi:10.16352/j.issn.1001-6325.2026.10.1407

Asbtract ( 22 )   PDF (909KB) ( 30 )  

References | Related Articles | Metrics

Objective To investigate the association between oral frailty and the severity of osteoporosis in elderly women, identify the risk threshold of oral frailty for osteoporosis, and provide evidence for joint assessment in patients seeking care at primary healthcare institutions. Methods A cross-sectional study was conducted using convenience sampling. A total of 215 women aged ≥60 years who visited the Yuetan Community health service centers were enrolled. Bone mineral density(BMD) was measured by dual-energy X-ray absorptiometry(DXA),and participants were classified into three groups according to T-scores: normal bone mass,osteopenia,and osteoporosis. Oral frailty was assessed using the Oral Frailty Index-8(OFI-8) and categorized into low-risk(0-2 points),moderate-risk (3 points),and high-risk(≥4 points) groups. Spearman correlation analysis,Mantel-Haenszel linear trend test,and ordinal logistic regression were performed to analyze the association,adjusting for age,BMI,and monthly income. The proportional odds assumption was verified by the parallel lines test prior to regression modeling. Results Oral frailty grouping was positively correlated with BMD diagnostic grouping(r=0.226,P=0.001),and a significant graded association trend was observed(χ²=9.682,P=0.002). After adjusting for confounders,the high-risk oral frailty group(OFI-8 ≥4) was independently associated with greater severity of osteoporosis(OR=2.126, P=0.018),whereas the moderate-risk group showed no significant association(OR=0.669, P=0.266),suggesting that ≥4 points may serve as a screening cutoff for functional impairment.BMI was independently and negatively associated with osteoporosis severity(OR=0.892, P=0.005).Age(OR=1.051, P=0.026) and low income(OR=3.857, P=0.038) were independently and positively associated with osteoporosis severity. The parallel lines test was nonsignificant(χ²=9.696, df=6, P=0.138),confirming that the proportional odds assumption was satisfied. Conclusions Among elderly women visiting primary healthcare institutions,oral frailty demonstrates a graded association trend with osteoporosis severity. An OFI-8 score of ≥4 may be used as a screening cutoff for identifying high-risk populations for osteoporosis.

Distribution characteristics and influencing factors of peripheral perfusion index in intensive care unit patients

FANG Ning, ZHAO Mingxi, YUE Wenjing, LIU Xinyi, JIANG Miao, FAN Liyi, LUO Hongbo

2026, 46(10):  1414-1418.  doi:10.16352/j.issn.1001-6325.2026.10.1414

Asbtract ( 18 )   PDF (879KB) ( 4 )  

References | Related Articles | Metrics

Objective To investigate the distribution characteristics and influencing factors of peripheral perfusion index (PPI) in intensive care unit (ICU) patients. Methods A retrospective study was conducted on 308 patients admitted to the ICU of Peking Union Medical College Hospital in Beijing from October 2023 to March 2024. Based on the stable mean PPI value measured within 1 hour of admission, patients were divided into a decreased perfusion group(PPI＜0.6) and a normal perfusion group(PPI≥0.6). Results The incidence of decreased PPI was 21.4%(66/308).Multivariate logistic regression analysis showed that circulatory system diseases,increased heart rate,elevated partial pressure of oxygen(PaO₂),mechanical ventilation,and blood purification therapy were independent risk factors for a decreased PPI,while higher dorsal hand temperature and higher arterial blood pH were protective factors(all P＜0.05). Conclusions Peripheral perfusion abnormality is relatively common in critically ill patients, and decreased PPI is associated with multiple clinical factors. Dynamic PPI monitoring and comprehensive assessment are recommended for high-risk patients to improve clinical outcomes.

Mini Reviews

Research progress of acupuncture combined with mesenchymal stem cell therapy for stroke

CAI Qian, JIANG Tianxiang, PAN Zixin, GAN Lin, MA Congcong, LIN Xianming

2026, 46(10):  1419-1423.  doi:10.16352/j.issn.1001-6325.2026.10.1419

Asbtract ( 26 )   PDF (750KB) ( 4 )  

References | Related Articles | Metrics

Stroke can lead to sequelae such as limb paralysis and speech impairment. Clinically, the delivery of relevant neurotropic drugs into the brain is hindered by the blood-brain barrier (BBB), which imposes significant limitations on patient treatment.Mesenchymal stem cells (MSCs) therapy is a new strategy for stroke treatment currently. Its pluripotent differentiation potential and paracrine capabilities can promote immune regulation, angiogenesis, and neural circuit reconstruction. However, many challenges still need to be overcome before its therapeutic application. Acupuncture can enhance the efficacy of MSCs in treating stroke by inhibiting inflammatory responses, activating cell signaling pathways, and promoting neural functional differentiation. This article explores the molecular mechanism of the synergistic effect between the two and discusses the innovative application of interdisciplinary technologies in clinical translation.

Research progress in targeting voltage-dependent anion channel-1 for cancer therapy

XU Jiaai, GUO Ying, ZHANG Chao, LI He, YANG Chunhua

2026, 46(10):  1424-1428.  doi:10.16352/j.issn.1001-6325.2026.10.1424

Asbtract ( 17 )   PDF (756KB) ( 6 )  

References | Related Articles | Metrics

Voltage-dependent anion channel-1 (VDAC1), a key regulator of mitochondrial function, is highly expressed in various cancers and is associated with poor prognosis. It participates in tumor progression through multiple mechanisms: by enhancing glycolysis upon channel closure, driving metabolic reprogramming to support tumor proliferation, and influencing the tumor microenvironment; upon oligomerization, it increases mitochondrial outer membrane permeability, inducing apoptosis and ferroptosis; and it can also activate PINK1/Parkin-dependent autophagy, promoting tumor cell survival. Current VDAC1-targeted therapeutic strategies primarily include miRNA/siRNA-based gene silencing to reduce VDAC1 expression, VDAC1-specific targeted agents to inhibit glycolysis/induce cell death, and other non-specific targeted drugs that exert effects through VDAC1.

Research progress on the organ- protective effects of esketamine in the perioperative period

LU Yapeng, WANG Yingbin, LU Wensheng

2026, 46(10):  1429-1434.  doi:10.16352/j.issn.1001-6325.2026.10.1429

Asbtract ( 18 )   PDF (888KB) ( 2 )  

References | Related Articles | Metrics

Esketamine, the dextro-isomer of ketamine, primarily acts as a noncompetitive antagonist of the N-methyl-D-aspartate (NMDA) receptor. Beyond its anesthetic properties, esketamine confers organ protection through multiple mechanisms, including the suppression of inflammatory responses and oxidative stress, regulation of calcium overload, modulation of gut microbiota, control of cellular autophagy, and inhibition of ferroptosis. Consequently, it emerges as a promising therapeutic strategy for mitigating perioperative organ injury.

Medical Education

Evaluation of ultrasound tomography applied in musculoskeletal ultrasound teaching

JIANG Jie, ZHAO Bo, LIN Zhuohua, JIANG Ling

2026, 46(10):  1435-1439.  doi:10.16352/j.issn.1001-6325.2026.10.1435

Asbtract ( 18 )   PDF (862KB) ( 4 )  

References | Related Articles | Metrics

Objective To investigate the effectiveness of ultrasound tomography (UT) as a teaching tool in musculoskeletal(MSK) ultrasound anatomy training. Methods Sixty-eight trainee physicians in MSK ultrasound were randomly assigned to a control group (n=34) or an experimental group (n=34). The control group received conventional teaching,while the experimental group received additional UT-based instruction. After four weeks,both groups were compared on anatomical structure recognition scores,spatial structure understanding test results,and standard plane acquisition ability. A 5-point Likert scale was used to evaluate teaching outcomes. Baseline characteristics between groups were compared,and intergroup differences were analyzed using the Mann-Whitney U test or chi-square test as appropriate. Results No significant differences in baseline characteristics were found between the two groups (all P＞0.05),confirming their comparability. The experimental group significantly outperformed the control group in all three objective assessments: anatomical structure recognition, spatial structure understanding,and standard plane acquisition (all P＜0.01). Trainees′ acceptance of UT teaching was high,with a mean total Likert scale score of 25.04±6.26 (out of 30) and mean item scores ranging from 4.15 to 4.19 (out of 5); the proportion of those who agreed or strongly agreed was ≥85.3% for all six items. The scale demonstrated excellent internal consistency (Cronbach′s α=0.993) and good test-retest reliability. Conclusions The integration of ultrasound tomography into MSK ultrasound training significantly improves trainees′ anatomical recognition,spatial understanding,and standard plane acquisition skills. UT is an effective teaching method with strong potential for broader application in clinical education.

Construction and application of a problem-based learning teaching model based on the DeepSeek-R1 model

LIU Yuxi, XU Xiaofei, WANG Mingjie, XIANG Meng, YANG Dawei, YOU Linya, LIU Qiong

2026, 46(10):  1440-1446.  doi:10.16352/j.issn.1001-6325.2026.10.1440

Asbtract ( 23 )   PDF (1337KB) ( 8 )  

References | Related Articles | Metrics

Objective To leverage the chain-of-reasoning capability of DeepSeek-R1 (DS) to construct an AI patient capable of demonstrating the clinical reasoning process,and integrate it into PBL teaching for respiratory diseases,evaluating its effectiveness in improving students′ clinical reasoning skills,pathophysiological understanding,and learning motivation. Methods The study participants were eight-year program medical students enrolled in this course at Fudan University. A total of 127 students,divided into five teaching groups,were participated in DS-PBL teaching practice. Post-class questionnaires were used to evaluate their feedbacks. A 5-point Likert scale and multiple-choice questions were employed to evaluate teaching effectiveness,and open-ended questions were analyzed thematically. Results Students reported a high overall satisfaction with the DS-PBL teaching model(79.5% selected “satisfied” or “very satisfied”). 92.1% of the students agreed that “AI intervention helped broaden my diagnostic thinking,” and 90.6% agreed that “by comparing the AI′s debriefing with that of the instructor,I gained a clearer understanding of the limitations of AI in clinical decision-making.” Regarding multidimensional competency improvement,students showed notable gains in understanding acute respiratory distress syndrome (ARDS) in terms of “linking micro-structural damage to macro-functional failure” (83.5%) and “explaining clinical manifestations through pathophysiological mechanisms” (81.9%). Open-ended feedback revealed issues with the AI tool,including “information contradiction”,“role confusion”,and “insufficient depth of reasoning”. Conclusions The capability of DeepSeek-R1 can effectively simulate the clinical reasoning process in respiratory medicine,making it a useful auxiliary tool in PBL teaching for basic medical courses.