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2026, Volume 47, Issue 10
2026,
47(10):
1-12.
doi: 10.12259/j.issn.2095-610X.S20261001
Abstract:
Drug-associated cues can evoke cravings and lead to relapse by reactivating persistent reward memories. Targeting memory reconsolidation is considered an important strategy for weakening these pathological memories. This article reviews the temporal boundaries, brain networks, and molecular mechanisms drug addiction memory reconsolidation, and compares the evidence for clinical translation of pharmacological, retrieval-extinction, and neuromodulatory interventions. Current research suggests that the transient state of vulnerability following memory retrieval is constrained by boundary conditions, including prediction error, retrieval duration, and memory age and strength. During this time window, the amygdala, hippocampus, prefrontal cortex, and nucleus accumbens form a dynamic network, while NMDAR, mTORC1, BDNF-TrkB, the ubiquitin-proteasome system, and monoaminergic neurotransmission jointly regulate destabilization and restabilization. Evidence from animal studies is relatively robust, whereas human research has focused primarily on propranolol, ketamine, and retrieval-extinction procedures. Small sample sizes, heterogeneous outcomes, and insufficient long-term follow-up limit the certainty of the evidence. This article further proposes a multilevel regulatory framework-“boundary conditions-neural circuits-molecular plasticity-intervention strategies-clinical outcomes”-to inform precision interventions for addiction-related memories and the design of clinical trials.
Drug-associated cues can evoke cravings and lead to relapse by reactivating persistent reward memories. Targeting memory reconsolidation is considered an important strategy for weakening these pathological memories. This article reviews the temporal boundaries, brain networks, and molecular mechanisms drug addiction memory reconsolidation, and compares the evidence for clinical translation of pharmacological, retrieval-extinction, and neuromodulatory interventions. Current research suggests that the transient state of vulnerability following memory retrieval is constrained by boundary conditions, including prediction error, retrieval duration, and memory age and strength. During this time window, the amygdala, hippocampus, prefrontal cortex, and nucleus accumbens form a dynamic network, while NMDAR, mTORC1, BDNF-TrkB, the ubiquitin-proteasome system, and monoaminergic neurotransmission jointly regulate destabilization and restabilization. Evidence from animal studies is relatively robust, whereas human research has focused primarily on propranolol, ketamine, and retrieval-extinction procedures. Small sample sizes, heterogeneous outcomes, and insufficient long-term follow-up limit the certainty of the evidence. This article further proposes a multilevel regulatory framework-“boundary conditions-neural circuits-molecular plasticity-intervention strategies-clinical outcomes”-to inform precision interventions for addiction-related memories and the design of clinical trials.
2026,
47(10):
13-23.
doi: 10.12259/j.issn.2095-610X.S20261002
Abstract:
Objective To explore the protective effect of ginsenoside Rg1 on alcohol-induced liver injury in tree shrews, and to reveal its molecular mechanism based on the Nrf2 signaling axis and mitochondrial apoptosis pathway, so as to provide new insights for the treatment of alcoholic liver disease. Methods Tree shrews were randomly divided into a control group, an alcohol model group and a ginsenoside Rg1 treatment group（6 animals per group）. The latter two groups were given alcohol by gavage to establish a liver injury model, while the Rg1 group was simultaneously administered ginsenoside Rg1 by gavage for 12 consecutive weeks. Hepatic ultrasonography was used to assess parenchymal changes; serum liver function indicators （ALT, AST）, oxidative stress indicator malondialdehyde （MDA） levels, and the activities of lactate dehydrogenase （LDH） and glutathione peroxidase （GSH-Px） were measured; liver tissue sections were stained with HE to observe the degree of steatosis, inflammatory cell infiltration, and ballooning degeneration; transmission electron microscopy was used to observe changes in mitochondrial ultrastructure; Western Blot was used to detect the expression of Nrf2 pathway proteins （Nrf2, Keap1） and apoptosis-related proteins （Bcl-2, Bax, Cytochrome c, total Caspase-9, total Caspase-3）. Immunohistochemistry was used to detect the protein expression and localization of Keap1, HO-1 and total Caspase-3 in liver tissue. Results Compared with the model group, the ginsenoside Rg1 group showed improved hepatic ultrasound imaging, significantly reduced serum ALT, AST, MDA levels and LDH activity （P < 0.05, F values were 327.57, 218.70, 510.07, and 331.59, respectively）, and significantly increased GSH-Px activity (P < 0.05, F = 73.56). Hepatic steatosis, inflammatory infiltration, and ballooning degeneration were all significantly attenuated; transmission electron microscopy showed repair of mitochondrial ultrastructural damage such as swelling. At the molecular level, ginsenoside Rg1 significantly upregulated Nrf2 expression and downregulated its negative regulator Keap1 （P < 0.05）; immunohistochemistry confirmed that after Rg1 intervention, Keap1-positive signals were weakened and HO-1-positive signals were significantly enhanced （P < 0.05）. Meanwhile, ginsenoside Rg1 increased the expression of the anti-apoptotic protein Bcl-2, decreased the expression of the pro-apoptotic protein Bax, and inhibited Cytochrome c release （P < 0.05）; the expression level of total Caspase-9 （precursor form） increased, and the downward trend in total Caspase-3 （precursor form） expression was reversed （P < 0.05）; immunohistochemistry showed that total Caspase-3-positive signals were significantly weakened in the ginsenoside Rg1 group （P < 0.05）. Conclusion Ginsenoside Rg1 has a definite protective effect against alcohol-induced liver injury in tree shrews. Its mechanism may involve activation of the Nrf2/Keap1/HO-1 antioxidant pathway, improvement of mitochondrial structure, regulation of Bcl-2/Bax balance, and inhibition of the caspase cascade, there by blocking the mitochondrial-dependent apoptosis pathway.
2026,
47(10):
24-44.
doi: 10.12259/j.issn.2095-610X.S20261003
Abstract:
Objective To systematically investigate the potential mechanisms of Tianlongjie in the treatment of idiopathic pulmonary fibrosis （IPF） using network pharmacology combined with machine learning methods. Methods The active components and therapeutic targets of Tianlongjie （Rhodiola rosea, Lumbricus, and Dragon’s blood） were screened using the HERB and SymMap databases. Differentially expressed genes （DEGs） associated with IPF were identified from the GEO datasets （GSE150910 and GSE32537）, and the intersection of these datasets was used to obtain potential therapeutic targets. Gene Ontology （GO） and Kyoto Encyclopedia of Genes and Genomes （KEGG） enrichment analyses were performed to elucidate their biological functions and signaling pathways, and a protein–protein interaction （PPI） network was constructed. Key targets were screened using LASSO regression and SVM-RFE algorithms and validated by ROC curve analysis. Gene set enrichment analysis （GSEA）, immune infiltration analysis, and construction of a ceRNA regulatory network were subsequently performed. Molecular docking was used to validate the binding capacity of key components to their targets, and in vivo experiments were conducted using a bleomycin-induced mouse model of pulmonary fibrosis. Results A total of 123 active components and 1, 147 potential targets were identified, yielding 135 IPF-related differentially expressed targets. GO and KEGG analyses showed that these targets were mainly enriched in lipid metabolism, responses to hypoxia, and the PPAR and IL-17 signaling pathways. Machine learning identified four key targets—VCAM1, MMP2, SPP1, and LCN2—which demonstrated a certain degree of discriminatory ability in both the training and validation sets （AUC > 0.7）. （4） Immune infiltration analysis indicated that the key targets were significantly associated with multiple immune cell types （|r| > 0.4, FDR < 0.05）. Molecular docking results showed that the candidate compounds had good binding activity with the targets. Animal experiments confirmed that Tianlongjie significantly alleviated pulmonary fibrosis, reduced the levels of inflammatory factors and the expression of fibrosis markers （P < 0.05 or P < 0.01）. Conclusion Tianlongjie may exert anti-IPF effects through the coordinated action of multiple components, targets, and pathways by regulating inflammatory responses, the immune microenvironment, and fibrosis-related signaling pathways. Its key targets include VCAM1, MMP2, SPP1, and LCN2.
2026,
47(10):
45-54.
doi: 10.12259/j.issn.2095-610X.S20261004
Abstract:
Objective To investigate the regulatory role and mechanism of miR-448 and ADAM10 in the malignant phenotype of MGC-803 gastric cancer cells. Methods RT-qPCR was used to compare the expression levels of miR-448 and ADAM10 in normal GES-1 cells and the gastric cancer cell lines MGC-803, MKN-7, NCI-N87. The targeting binding interaction between the two was validated by dual-luciferase reporter assay. After intervening with miR-448 expression in MGC-803 cells, cell proliferation, migration, and invasion capabilities were assessed via colony formation assays, scratch assays and Transwell assays. MGC-803 cells were co-transfected with miR-448 mimics/inhibitors and ADAM10 overexpression/interference plasmids. Changes in apoptosis and EMT-related molecular expression in MGC-803 cells were detected by flow cytometry, RT-qPCR, and Western blot. Results Compared with normal GES-1 cells, miR-448 was significantly downregulated while ADAM10 was significantly upregulated in MGC-803 cells （P < 0.01）. Dual-luciferase assay confirmed that miR-448 directly targets ADAM10. Furthermore, miR-448 overexpression inhibited MGC-803 proliferation, migration and invasion （P < 0.05）, and downregulated ADAM10 （P < 0.05）, thereby reducing the levels of N-cadherin, vimentin and MMP9 （P < 0.05）, which in turn inhibited MGC-803 migration and invasion. Simultaneously, miR-448 overexpression increased Bax and cleaved caspase-3 levels while decreasing Bcl-2 levels, promoting MGC-803 cell apoptosis （P < 0.05）. Conclusion miR-448 may suppress the malignant phenotype of MGC-803 cells by targeting and inhibiting ADAM10.
2026,
47(10):
55-67.
doi: 10.12259/j.issn.2095-610X.S20261005
Abstract:
Objective To investigate the effects of macrophage colony-stimulating factor （M-CSF） on chondrocyte function through macrophage polarization mediated by colony-stimulating factor 1 receptor （CSF1R） in osteoarthritis （OA）, and to elucidate the underlying mechanism. Methods Lipopolysaccharide （LPS） and interferon-gamma （IFN-γ） were used to induce mouse RAW 264.7 macrophages and primary mouse bone marrow-derived macrophages （BMDMs） to establish an OA cell model. RAW 264.7 cells were transfected with sh-NC or sh-M-CSF and treated with the CSF1R inhibitor PLX3397. Western blotting, immunofluorescence, and enzyme-linked immunosorbent assay （ELISA） were used to assess the effects of M-CSF and CSF1R on RAW 264.7 macrophage polarization. Mouse chondrocytes were co-cultured with RAW 264.7 cells or BMDMs using a Transwell co-culture system. Cell Counting Kit, Annexin V-FITC/PI apoptosis assays, ELISA, Western blotting, and immunofluorescence were used to analyze the effects of RAW 264.7 cell polarization on chondrocyte function. Results Following LPS and IFN-γ treatment , RAW 264.7 and BMDM cells underwent M1 polarization, accompanied by increased secretion of pro-inflammatory cytokines （P < 0.01） and upregulated M-CSF and CSF1R expression （P < 0.001）. Chondrocyte viability decreased （P < 0.001）, apoptosis increased （P < 0.001）, and pro-inflammatory cytokine levels rose （P < 0.001） after co-culture with induced RAW 264.7 cells or BMDMs. M-CSF knockdown or PLX3397 treatment inhibited M1 polarization （P < 0.05） and NF-κB pathway activation （P < 0.05） in RAW 264.7 cells and alleviated their damaging effects on chondrocytes （P < 0.001）. Combined M-CSF knockdown and PLX3397 treatment further inhibited M1 polarization （P < 0.01） and promoted functional recovery of chondrocytes （P < 0.001）. Conclusion M-CSF knockdown attenuates LPS- and IFN-γ-induced M1 polarization of RAW 264.7 cells by inhibiting CSF1R expression and NF-κB pathway activation, thereby alleviating chondrocyte injury.
2026,
47(10):
68-77.
doi: 10.12259/j.issn.2095-610X.S20261006
Abstract:
Objective To investigate the ameliorative effects of Ganoderma lucidum polysaccharides （GLP） on Adjuvant-induced arthritis （RA） in rats and to determine whether the mechanism is associated with modulating the MAPK/NF-κB/IL-6 signaling pathway and macrophage polarization. Methods Fifty-five male Sprague-Dawley rats were randomly divided into a control group （CON） of 10 rats, with the remaining 45 rats used to establish a rheumatoid arthritis （RA） model. The 40 successfully modeled rats were randomly divided into four groups: the RA group, the positive control group treated with methotrexate （MTX）, the GLP treatment group （GLP）, and the combined GLP+PDTC group, with 10 rats in each group. Continuous medication was administered for 5 weeks. Arthritis Index （AI） was assessed weekly. Upon completion of the experiment, paw swelling was measured. Micro-CT was used to analyze ankle joint bone microstructure [bone density （BMD）, bone surface area to bone volume ratio （BS/BV）, trabecular thickness （Tb. Th）, and trabecular separation （Tb. Sp）]. Histopathological changes in the joint were assessed using H&E staining and Safranin O/Fast Green staining. Serum levels of pro-inflammatory cytokines （IL-6; TNF-α; IL-1β） and the anti-inflammatory cytokine （IL-10） were measured by Enzyme-linked immunosorbent assay. Immunohistochemistry was performed to detect the expression of the iNOS and CD206 in the synovial tissue. Western blot analysis was used to evaluate the protein expression of key molecules in macrophage polarization markers （iNOS, CD86, CD206, Arg-1）, the MAPK pathway （p-p38, p38, p-ERK, ERK, p-JNK, JNK）, the NF-κB pathway （p-IκBα, IκBα, p-p65, p65）, and the downstream effector IL-6 in the synovial tissue. Results Compared with the RA group, the GLP group showed significantly reduced Arthritis Index （AI） scores [（6.05±0.71） vs （11.60±0.92）] and paw swelling [（14.95±0.98） mm vs （19.42±1.35） mm] （P < 0.05） in RA rats, with improved joint bone microstructure and alleviated histopathological damage. Serum pro-inflammatory cytokines IL-6, TNF-α, and IL-1β levels were downregulated （P < 0.01）, while the anti-inflammatory cytokine IL-10 level was upregulated （P < 0.01）. Immunohistochemical results demonstrated decreased positive expression of iNOS and increased positive expression of CD206 in the GLP group （P < 0.001）. Western blot analysis revealed reduced expression of M1 macrophage markers iNOS and CD86, and increased expression of M2 macrophage markers CD206 and Arg-1 in the GLP group （P < 0.001）. Phosphorylation levels of key MAPK pathway proteins p-p38/p38, p-ERK/ERK, and p-JNK/JNK were significantly inhibited （P < 0.05）. Phosphorylation levels of key NF-κB pathway proteins p-IκBα/IκBα and p-p65/p65 were significantly suppressed （P < 0.05）, with downstream IL-6 protein expression decreased （P < 0.05）. Compared with the MTX positive control group, the GLP group showed weaker effects in improving all aforementioned indicators with statistically significant differences between groups （P < 0.05）. Compared with the GLP group alone, combined treatment with the NF-κB inhibitor PDTC and GLP demonstrated synergistic enhancement, further strengthening the above effects. Conclusion GLP effectively ameliorate the arthritis symptoms in RA rats, with mechanisms potentially involving inhibition of the excessive activation of the MAPK/NF-κB signaling pathway in synovial tissue, downregulation of pro-inflammatory cytokines such as IL-6, and promotion of macrophage polarization toward M2 type, thereby rebalancing immune inflammatory equilibrium.
2026,
47(10):
78-85.
doi: 10.12259/j.issn.2095-610X.S20261007
Abstract:
Objective To investigate the risk factors for catheter-related fungal bloodstream infections in burn patients and their correlation with toll-like receptor 4 （TLR4） and nuclear factor-kappa B （NF-κB）. Methods A retrospective analysis was conducted on clinical data of 110 burn patients who underwent catheter placement admitted to the Department of Burns and Plastic Surgery, First Affiliated Hospital of Air Force Medical University from March 2021 to February 2025. Patients were divided into infection group （n = 22） and non-infection group （n = 88） based on whether catheter-related fungal bloodstream infection occurred. Pearson correlation coefficient analysis was used to analyze the correlation between TLR4 and NF-κB and catheter-related fungal infection in burn patients. ROC curve were constructed to determine optimal cutoff values for TLR4 and NF-κB. Logistic regression model was used to analyze the risk factors and a decision tree model was established. Results Pearson correlation analysis showed that both TLR4 and NF-κB were positively correlated with catheter-related fungal infection in burn patients （r = 0.579, P < 0.001; r = 0.556, P < 0.001）. ROC analysis showed that the optimal cut-off values of TLR4 and NF-κB for predicting catheter-related fungal infection in burn patients were 2.65 and 1.75, respectively. Multivariate Logistic regression analysis showed that diabetes mellitus, burn area, catheterization duration, TLR4 and NF-κB were independent risk factors for catheter-related fungal infection in burn patients （P < 0.05）. Decision tree modeling revealed that TLR4 was the most important predictor, with a classification accuracy rate of 90.00%. Conclusion Diabetes, burn area, catheterization duration, TLR4, and NF-κB are independent risk factors for catheter-related fungal infections in burn patients.
2026,
47(10):
86-93.
doi: 10.12259/j.issn.2095-610X.S20261008
Abstract:
Objective To explore the interactive effects and predictive performance of interleukin-19 （IL-19） and microRNA-320 （miR-320） for in-stent restenosis （ISR） after percutaneous coronary intervention （PCI） in patients with type 2 diabetes mellitus （T2DM） complicated with non-ST-segment elevation myocardial infarction （NSTEMI）. Methods A total of 210 patients with T2DM complicated by NSTEMI admitted to Tangshan Central Hospital from August 2022 to October 2023 were enrolled and stratified based on ISR status one year post-PCI. Clinical data were compared between the ISR group （n = 34） and non-ISR group （n = 172）. IL-19 and miR-320 levels were compared between groups on postoperative day 1 and 3 months post-operation. The correlations between IL-19 and miR-320, and Killip classification were analyzed. The predictive performance of IL-19, miR-320, and their interactive effects on postoperative ISR was evaluated. Results The Gensini score in ISR group was significantly higher than in non-ISR group （t = 4.524, P < 0.001）. IL-19 and miR-320 levels in the ISR group were higher than those in the non-ISR group （postoperative day 1 IL-19: t = -8.916, miR-320: t = -9.997; 3 months post-operation IL-19: t = -15.498, miR-320: t = -17.175; all P < 0.001）. Logistic regression analysis showed that after adjusting for Gensini score, IL-19 at 3 months post-operation （OR = 1.099, 95%CI: 1.014～1.192） and miR-320 （OR = 1.104, 95%CI: 1.019～1.196） were independent risk factors for ISR（both P < 0.001）. Significant differences in IL-19 and miR-320 levels were observed across different Killip classifications, with both parameters increasing with higher Killip grades （F = 57.143, 153.049, 86.212, 200.270; all P < 0.001）. Spearman correlation analysis revealed positive correlations between IL-19, miR-320, and Killip classification on postoperative day 1 and 3 months post-operation （P < 0.05）. Interaction analysis demonstrated a significant positive multiplicative interaction between IL-19 and miR-320 （interaction term OR = 1.042, 95%CI: 1.011～1.074, P = 0.006）. ROC curve analysis revealed AUC values of 0.742 （95%CI: 0.676～0.800）, 0.768 （95%CI: 0.705～0.824）, and 0.882 （95%CI: 0.830～0.922） for IL-19, miR-320, and their interactive effect, respectively, in predicting ISR after PCI in T2DM patients with NSTEMI, with the interactive effect showing superior predictive performance （P < 0.05）. Bootstrap internal validation showed a corrected AUC of 0.871 for the combined model, with Hosmer-Lemeshow test P = 0.412 > 0.05, indicating good calibration. The combined model provided superior clinical net benefit across a wide range of threshold probabilities. Conclusion IL-19 and miR-320 levels are associated with cardiac function classification in T2DM patients with NSTEMI and serve as independent predictive factors for ISR after PCI. Higher levels of IL-19 and miR-320 indicate increased risk of ISR after PCI in these patients. Combined detection of both biomarkers demonstrates high predictive value for ISR.
2026,
47(10):
94-108.
doi: 10.12259/j.issn.2095-610X.S20261009
Abstract:
Objective To investigate the associations of the Montreal Cognitive Assessment （MoCA）, Mini-Mental State Examination （MMSE）, and neutrophil percentage-to-albumin ratio （NPAR） with diabetic peripheral neuropathy （DPN）, as well as their discriminative performance. Methods A total of 171 patients with type 2 diabetes mellitus who visited the Department of Endocrinology at the First People's Hospital of Luliang County from July to November 2025 were recruited. According to the presence or absence of DPN, patients were divided into a diabetic peripheral neuropathy（DPN） group（n = 79）and the non-DPN group. Basic demographic data and laboratory results were collected, and MoCA and MMSE scores were assessed. Associations were analyzed using LASSO and logistic regression, and receiver operating characteristic （ROC） curves were plotted to evaluate the discriminative performance of relevant indicators for DPN. Results MoCA（OR = 0.857, 95%CI 0.807～0.910, P < 0.001） and MMSE（OR = 0.824, 95%CI 0.761～0.892, P < 0.001） scores were negatively associated with the risk of DPN, whereas NPAR was positively associated with the risk of DPN（OR = 1.020, 95%CI 1.008～1.032, P < 0.001）. Regarding discriminative performance, MoCA （AUC=0.7477 , 95%CI: 0.6741 ～0.8213 ） was comparable to MMSE （AUC=0.7454 , 95%CI: 0.6720 ～0.8188 ; DeLong test, P = 0.911）, although MoCA had higher specificity and MMSE had higher sensitivity. Compared with the basic clinical model （AUC=0.7859, 95%CI: 0.718～0.8539 ）, the MoCA+NPAR model （AUC=0.8254 , 95%CI: 0.7636 ～0.8872 ） and the MMSE+NPAR model （AUC=0.8235 , 95%CI: 0.7606 ～0.8863 ） showed significantly improved discriminative performance （DeLong test, P < 0.05）. The combined MoCA+MMSE+NPAR model had discriminative performance comparable to that of the MoCA+NPAR model （DeLong test, P > 0.05）. Conclusion MoCA, MMSE, and NPAR are associated with the risk of DPN. Combining either MoCA or MMSE with NPAR can effectively improve the discriminative performance for DPN.
2026,
47(10):
109-115.
doi: 10.12259/j.issn.2095-610X.S20261010
Abstract:
Objective To evaluate the clinical application value of metagenomic next-generation sequencing （mNGS） combined with GeneXpert MTB/RIF （Mycobacterium tuberculosis/rifampicin resistance gene detection） in the early diagnosis of tuberculous meningitis （TBM）. Methods A total of 73 patients clinically suspected of TBM who visited Kunming Third People’ s Hospital from January 2022 to June 2024 were enrolled. Cerebrospinal fluid specimens were collected for mNGS, GeneXpert MTB/RIF, Mycobacterium tuberculosis smear microscopy, culture, and PCR testing. The sensitivity, specificity, and concordance rate of each detection method were calculated. Appropriate statistical methods were used to comprehensively evaluate the diagnostic value of each method. Results （1） Among 73 clinically suspected TBM patients, 65 were diagnosed with TBM （45 confirmed bacteriologically, 20 diagnosed clinically）; and 8 had non-tuberculous meningitis. （2） Using the 65 diagnosed TBM cases as the reference standard, the sensitivity, specificity, and consistency of mNGS+GeneXpert for TBM diagnosis were 86.1%（95%CI: 75.6～92.5）, 100.0%（95%CI: 67.4～100.0）, and 87.7%（95%CI: 77.7～93.6）, respectively. The sensitivity and concordance rate of mNGS+GeneXpert were higher than those of mNGS alone [60% （95%CI: 47.9～71.0） , 64.4% （95%CI: 52.9～74.4）]and GeneXpert alone [38.5% （95%CI: 27.4～50.8）, 45.2% （95%CI: 34.2～56.6）]. Regarding sensitivity, P-values for all three detection methods were < 0.05. （3） Using 45 bacteriologically confirmed TBM cases as the reference standard, mNGS combined with GeneXpert showed the highest sensitivity of 93.3% （95%CI: 81.7～97.7）, and the highest consistency rate was 76.7% （95%CI: 65.7～85.1）. （4） Comparative analysis of mNGS+GeneXpert with mNGS and GeneXpert alone showed statistically significant differences （P < 0.001）. Conclusion Metagenomic next-generation sequencing combined with GeneXpert MTB/RIF showed high sensitivity and specificity in the early diagnosis of tuberculous meningitis, significantly improving diagnostic efficiency, and can provide clinicians with rapid and accurate etiological diagnostic evidence.
2026,
47(10):
116-125.
doi: 10.12259/j.issn.2095-610X.S20261011
Abstract:
Objective To explore the influencing factors of delirium in patients with acute exacerbation of chronic obstructive pulmonary disease （AECOPD） complicated by respiratory failure, and to construct a nomogram prediction model, and to evaluate the predictive efficacy of this model. Methods A retrospective analysis was conducted on clinical data from 210 patients with AECOPD complicated by respiratory failure admitted to the First Affiliated Hospital of Anhui Medical University from March 2023 to March 2025, serving as the observation cohort. Patients were stratified into a delirium group （n = 72） and a non-delirium group （n = 138） based on whether delirium occurred. General baseline data of the two groups were compared, and univariate and multivariate Logistic regression analyses were conducted to explore the influencing factors of delirium in patients with AECOPD with respiratory failure. With delirium occurrence designated as positive and absence of delirium as negative, receiver operating characteristic （ROC） curves were plotted to analyze the predictive value of factors with significant differences in univariate analysis for delirium development. A nomogram model was constructed to predict the risk of delirium in AECOPD patients with respiratory failure, and the predictive performance was analyzed. Results Between the two groups, significant differences were observed in mechanical ventilation duration, arterial partial pressure of oxygen （PaO2）, partial pressure of carbon dioxide （PaCO2）, serum brain-derived neurotrophic factor （BDNF）, albumin （ALB）, C-reactive protein （CRP）, and microRNA-212-5p （miR-212-5p） levels （P < 0.001）. Multivariate Logistic regression analysis showed that mechanical ventilation duration > 72 hours （OR = 1.082, 95%CI: 1.016 ～1.152, P = 0.014）, serum BDNF ≤ 0.64 μg/L （OR = 0.922, 95%CI: 0.859～0.99, P = 0.024）, ALB ≤ 35 g/L （OR = 0.920, 95%CI: 0.875～0.968, P = 0.001）, miR-212-5p relative expression≤ 0.27 （OR = 0.927, 95%CI: 0.869～0.989, P = 0.021）, and serum CRP > 76.95 mg/L （OR = 1.081, 95%CI: 1.023～1.142, P = 0.005） were all independent risk factors for delirium in AECOPD patients with respiratory failure. ROC curve results showed that mechanical ventilation duration, serum BDNF, ALB, CRP, and miR-212-5p levels had AUCs of 0.807 （0.745～0.859）, 0.841 （0.783～0.889）, 0.793 （0.730～0.847）, 0.745 （0.61～ 0.803）, and 0.826 （0.768～0.875）, respectively, all demonstrating high predictive value. Further analysis of the ROC curve revealed that the nomogram model demonstrated a good predictive ability for the risk of delirium in AECOPD patients with respiratory failure （AUC=0.852, 95%CI:0.797～0.897）. Hosmer-Lemeshow goodness-of-fit test indicated high model accuracy （χ2 = 2.309, P = 0.970）. Decision curve analysis （DCA） demonstrated that at high-risk thresholds of 0.0-0.4, the combined predictive value of mechanical ventilation duration, serum BDNF, ALB, CRP, and miR-212-5p levels for delirium risk in AECOPD patients with respiratory failure showed superior net benefit compared to individual indicators. Conclusion Prolonged mechanical ventilation duration, decreased serum BDNF, ALB and miR-212-5p levels, and the elevated serum CRP leves are all influencing factors for the occurrence of delirium in patients with AECOPD with respiratory failure. Clinically, these factors can serve as auxiliary tools for assessing delirium occurrence. these factors can be utilized to assist in the assessment of the occurrence of delirium.
2026,
47(10):
126-134.
doi: 10.12259/j.issn.2095-610X.S20261012
Abstract:
Objective To investigate the differences in tumor-infiltrating lymphocytes （TILs） and solute carrier family 35 member A2 （SLC35A2） expression in the tumor microenvironment across different molecular subtypes of breast cancer and their predictive value for neoadjuvant therapy （NAT） response. Methods A prospective study was conducted on 202 breast cancer patients scheduled for NAT admitted to the First Affiliated Hospital of Nanping, Fujian Medical University from February 2022 to May 2024. The cohort consisted of 13 cases of Luminal A subtype, 108 cases of Luminal B subtype, 39 cases of human epidermal growth factor receptor 2 （HER-2） overexpression subtype, and 42 cases of triple-negative breast cancer （TNBC）. According to the NAT response, patients were stratified into the pathological complete response （pCR） group （n = 78） and non-pCR group （n = 124）. Differences in tumor microenvironment TILs and SLC35A2 expression were compared across different molecular subtypes and NAT response status. Multivariate logistic regression analysis was performed to identify factors influencing NAT response. The predictive value of TILs and SLC35A2 for NAT response was analyzed using both the AND rule （simultaneous high expression of both TILs and SLC35A2） and the OR rule （high expression of either TILs or SLC35A2）. Results Among different molecular subtypes, high expression rates of TILs in HER-2 overexpression （61.54%） and TNBC （57.14%） were significantly higher than those in Luminal B （24.07%） and Luminal A （23.08%） subtypes （P < 0.05）. The high expression rate of SLC35A2 in Luminal A （69.23%） was significantly higher than in TNBC （23.81%, P < 0.05）. Compared to the pCR group, the non-pCR group showed significant differences in high expression rates of TILs（17.74% vs. 70.51%）, high expression rate of SLC35A2 （49.19% vs. 21.79%）, molecular subtype, treatment regimen, T stage and lymph node metastasis （all P < 0.05）. After adjusting for confounding factors by multivariate logistic regression analysis, high TILs expression was an independent protective factor for NAT response （OR = 0.589, 95%CI: 0.467～0.744, P < 0.001）, while high SLC35A2 expression was an independent risk factor （OR = 2.737, 95%CI: 1.651～4.539, P < 0.001）. Predictive value analysis demonstrated that the OR rule （high expression of either marker） achieved a sensitivity of 92.74% （95%CI: 85.21～97.18）, significantly higher than TILs alone （82.26%, adjusted P = 0.0013 ） and SLC35A2 alone （49.19%, adjusted P < 0.0001 ）. The accuracy was 83.66% （95%CI: 77.98～88.34）, significantly higher than TILs alone （77.72%, adjusted P = 0.014） and SLC35A2 alone （60.40%, adjusted P < 0.0001 ）. The AND rule （simultaneous high expression of both） achieved a specificity of 96.15% （95%CI: 90.87～98.76）, significantly higher than TILs alone （70.51%） and SLC35A2 alone （78.21%） （adjusted P < 0.0001 for both）. Conclusion TILs and SLC35A2 expression demonstrates significant differences across different molecular subtypes of breast cancer. High TILs expression is associated with superior NAT response, whereas high SLC35A2 expression predicts poor NAT response. The OR rule （high expression of either marker） enhances the predictive value for NAT response and provides valuable reference for clinical identification of patients who may benefit from NAT.
2026,
47(10):
135-144.
doi: 10.12259/j.issn.2095-610X.S20261013
Abstract:
Objective To investigate the correlation between plasma EPB41L3 gene expression level and methylation status with colorectal cancer （CRC）, and to evaluate its potential as a biomarker for early screening and risk assessment of CRC. Methods A total of 210 colorectal cancer patients diagnosed between May 2022 and October 2025 at Suqian Hospital affiliated with Jiangsu Province People’ s Hospital were enrolled as the case group, with 207 healthy individuals from the same period as the control group. Peripheral blood plasma samples were collected. The expression level of EPB41L3 gene mRNA was measured using quantitative real-time PCR （qRT-PCR）. The methylation status of the EPB41L3 gene promoter region was qualitatively detected using bisulfite conversion combined with methylation-specific fluorescent quantitative PCR （MethyLight）. Methylation positivity or negativity was determined by comparing the Ct values of samples with methylation-positive controls. Plasma EPB41L3 protein expression was measured using Western blotting. Differences in EPB41L3 expression and promoter methylation between the case and control groups were compared. A multivariate logistic regression model was used to analyze the independent association of EPB41L3 expression and methylation with CRC risk. Differences in EPB41L3 gene expression and promoter region methylation status across different clinical characteristics and their effects were analyzed, and the diagnostic efficacy of individual and combined indicators for colorectal cancer was evaluated. Results The positivity rate of EPB41L3 methylation was significantly higher in the case group than in the control group, while the relative expression levels of EPB41L3 mRNA and protein were significantly lower in the case group （all P < 0.05）. High expression of EPB41L3 gene mRNA and high expression of EPB41L3 protein were both significantly associated with decreased colorectal cancer risk （P < 0.05）. Positive methylation of EPB41L3 gene was significantly associated with increased colorectal cancer risk （P < 0.05）. EPB41L3 mRNA and protein expression levels were significantly lower in patients with advanced clinical stage （III–IV）, poor differentiation, and lymph node metastasis, while the methylation positivity rate was significantly higher in the corresponding groups （all P < 0.05）. Combined detection of EPB41L3 methylation, mRNA expression, and protein expression showed good diagnostic value for CRC and early-stage CRC （stage I–II） with AUC values of 0.913 and 0.894, respectively, showing good sensitivity and specificity. Conclusion Hypermethylation and downregulation of EPB41L3 in plasma are closely associated with an increased risk of CRC and adverse clinicopathological features. Combined detection of these three markers has important potential auxiliary value in the diagnosis of colorectal cancer, including early-stage colorectal cancer.
2026,
47(10):
145-153.
doi: 10.12259/j.issn.2095-610X.S20261014
Abstract:
Objective To explore the value of a nomogram model based on clinicopathological factors and radiomics in predicting mortality risk in elderly patients with advanced non-small cell lung cancer （NSCLC）. Methods A retrospective cohort of 290 elderly patients with advanced NSCLC admitted to Shijiazhuang Hospital of Traditional Chinese Medicine from March 2021 to March 2024 was enrolled and divided into a training set （n = 203） and validation set （n = 87） in a 7:3 ratio. One-year prognostic survival outcomes were assessed in the training set. Personal baseline characteristics, clinicopathological data, computed tomography （CT） radiomics features and scores were compared between patients with different prognoses. Cox regression analysis was performed to identify prognostic factors affecting survival in elderly patients with advanced NSCLC. A nomogram model based on radiomics was constructed to predict the prognosis survival in these patients. The predictive performance was evaluated using receiver operating characteristic （ROC） curves, calibration curves, decision curve analysis （DCA）, and clinical impact curves （CIC）. Results The Eastern Cooperative Oncology Group （ECOG） score, proportion of malnutrition, lesion diameter, differentiation grade, clinical stage, and microwave ablation （MWA） response in the deceased group showed statistically significant differences compared with the survival group （P < 0.05）. Lasso regression identified 8 optimal features. The CT radiomics score in the deceased group （0.58±0.15） was significantly higher than in the survival group （-0.42±0.13） （P < 0.05）. COX regression analysis showed that the ECOG score, lesion diameter, differentiation grade, clinical stage, MWA response, and CT radiomics score were independent prognostic factors （P < 0.05）. The nomogram model demonstrated area under the curve （AUC） values of 0.939 （95%CI: 0.905～0.972） in the training set and 0.942 （95%CI: 0.908～0.975） in the validation set. Calibration curves showed good agreement between predicted and actual outcomes. DCA curves demonstrated high clinical net benefit within the 0.2～0.8 threshold range in both sets. CIC curves showed substantial overlap between predicted and actual prognoses across the 0.8～1.0 range. Conclusion The nomogram model based on clinicopathological factors and radiomics demonstrates predictive value for mortality risk in elderly patients with advanced NSCLC, with good discrimination, calibration and clinical practicability. It can be used as an effective model for clinical prediction of mortality risk.
2026,
47(10):
154-162.
doi: 10.12259/j.issn.2095-610X.S20261015
Abstract:
Objective To investigate the relationship between serum microRNA-30d-5p （miR-30d-5p）, microRNA-146a-5p （miR-146a-5p）, regulatory T cell/helper T cell 17 （Treg/Th17） ratio and the prognosis of elderly patients with sepsis, and to construct and verify a nomogram prediction model. Methods A prospective observational study was conducted, enrolling 382 elderly sepsis patients treated at the Second People's Hospital of Lianyungang from January 2019 to December 2023. Patients were randomly divided in a 7∶3 ratio into a modeling group （n = 268） and a validation group （n = 114）. The modeling group was stratified into a survival group （n = 182） and a mortality group （n = 86） based on 90-day survival status. Serum and peripheral blood samples were collected within 24 hours of admission. Serum miRNA levels were detected using qRT-PCR, and the Treg/Th17 ratio was determined by flow cytometry. Multivariate Logistic regression analysis was used to identify independent risk factors and construct a nomogram model. The model performance was validated using ROC curves, calibration curves, and decision curve analysis （DCA）. Results Serum miR-30d-5p and miR-146a-5p levels were significantly lower in the mortality group compared to the survival group, while the Treg/Th17 ratio and APACHE II score were significantly higher （P < 0.05）. Multivariate Logistic regression analysis showed that low miR-30d-5p levels, low miR-146a-5p levels, high Treg/Th17 ratio, and high APACHE II score were independent risk factors for 90-day mortality in elderly sepsis patients. The nomogram model constructed based on these indicators showed an AUC of 0.886 （95%CI: 0.842 ～ 0.930） in the modeling group and 0.862 （95%CI: 0.795～ 0.929） in the validation group. The Hosmer-Lemeshow test yielded P = 0.652 in the modeling group and P = 0.584 in the validation group. The calibration curve showed good consistency between predicted probability and actual incidence rate. Conclusion Decreased serum miR-30d-5p and miR-146a-5p levels, and increased Treg/Th17 ratio are closely associated with adverse prognosis in elderly sepsis patients. The prediction model constructed based on these parameters demonstrates good discriminative ability and accuracy, providing a valuable reference for clinical assessment.
2026,
47(10):
163-169.
doi: 10.12259/j.issn.2095-610X.S20261016
Abstract:
Objective To explore the predictive value of soluble growth stimulating express gene 2 protein （sST2） and growth hormone （GH）/insulin-like growth factors （IGF-I） in peripheral blood for the prognosis of prostate cancer. Methods A total of 153 prostate cancer patients admitted to the Department of Urology at the First Hospital of Zhangjiakou from January 2022 to January 2023 were enrolled as study subjects. Based on the 2-year postoperative prognosis, patients were divided into a good prognosis group （n = 126） and a poor prognosis group （n = 27）. Clinical data were collected, and univariate analysis was conducted to identify adverse prognostic factors for prostate cancer. Multivariate logistic regression analysis was employed to determine independent risk factors for poor prognosis. ROC curve analysis was performed to assess the predictive value of serum sST2, GH, and IGF-I levels for poor prostate cancer prognosis. Results Among the 153 prostate cancer patients, 126 exhibited a favorable 2-year postoperative prognosis, while 27 had an unfavorable prognosis. Univariate analysis revealed that the unfavorable prognosis group had significantly higher proportions of Gleason score ≥7, preoperative PSA levels, sST2, GH, and IGF-I levels compared to the favorable prognosis group （P < 0.05）. Preoperative PSA levels, sST2, GH, and IGF-I were identified as independent risk factors for poor prostate cancer prognosis （P < 0.05）. The area under the receiver operating characteristic curve （AUC） of sST2, GH, and IGF-I alone, and in combination were 0.843 （95%CI: 0.761～0.926）, 0.768 （95%CI: 0.647～0.889）, 0.775 （95%CI: 0.674～0.875）, and 0.920 （95%CI: 0.844～0.996）, respectively. The combined AUC was significantly greater than the individual measurements （P < 0.05）. Conclusion sST2, GH, and IGF-I are independent risk factors for poor prostate cancer prognosis. Combined detection of three biomarkers demonstrates high predictive efficacy for poor prostate cancer prognosis.
2026,
47(10):
170-180.
doi: 10.12259/j.issn.2095-610X.S20261017
Abstract:
Lichen planus is a chronic, immune-mediated inflammatory disease characterized by lichenoid interface dermatitis. Its development results from interactions between genetic susceptibility and environmental factors. The immune mechanisms are predominantly T-cell mediated: IFN-γ, TNF-α, and the IL-23/Th17 axis drive inflammation, while CD8+cytotoxic T cells induce keratinocyte apoptosis via the perforin/granzyme B and Fas/FasL pathways. JAK-STAT signaling and metabolic abnormalities further amplify the inflammatory response. A systematic review of the etiology, immunopathogenesis, and clinical associations of LP provides a theoretical basis for precision subtyping and targeted therapy.
Lichen planus is a chronic, immune-mediated inflammatory disease characterized by lichenoid interface dermatitis. Its development results from interactions between genetic susceptibility and environmental factors. The immune mechanisms are predominantly T-cell mediated: IFN-γ, TNF-α, and the IL-23/Th17 axis drive inflammation, while CD8+cytotoxic T cells induce keratinocyte apoptosis via the perforin/granzyme B and Fas/FasL pathways. JAK-STAT signaling and metabolic abnormalities further amplify the inflammatory response. A systematic review of the etiology, immunopathogenesis, and clinical associations of LP provides a theoretical basis for precision subtyping and targeted therapy.
