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2026 Vol. 47, No. 8
2026, 47(8): 1-12.
doi: 10.12259/j.issn.2095-610X.S20260801
Abstract:
Aortic aneurysm and aortic dissection are life-threatening cardiovascular diseases whose occurrence and development are closely associated with phenotypic switching of vascular smooth muscle cells （VSMCs）. Recent studies have revealed significant segmental heterogeneity in aortic diseases; that is, different segments of the aorta from the aortic root to the abdominal aorta exhibit essential differences in embryologic origin, tissue architecture, molecular mechanisms, and pathological manifestations. This heterogeneity directly influence disease susceptibility, and VSMC phenotypic switching exhibits distinct regulatory networks across different segments, with molecular-level differences constituting unique "transcriptional phenotype fingerprints" for each segment. The central thesis of this review posits that elucidating the molecular mechanisms regulating VSMC phenotypic switching in different aortic segments and mapping their segment-specific regulatory networks are key to advancing the treatment of aortic disease from a "homogeneous" approach toward "segment-specific precision medicine." This review systematically summarizes recent advances in epidemiology, regulatory mechanisms of VSMC phenotypic switching, molecular diagnostics, and targeted therapeutic strategies across various aortic segments. In-depth analysis of the segment-specific regulatory networks governing VSMC phenotypic switching will provide new insights for individualized precision treatment of aortic disease.
Aortic aneurysm and aortic dissection are life-threatening cardiovascular diseases whose occurrence and development are closely associated with phenotypic switching of vascular smooth muscle cells （VSMCs）. Recent studies have revealed significant segmental heterogeneity in aortic diseases; that is, different segments of the aorta from the aortic root to the abdominal aorta exhibit essential differences in embryologic origin, tissue architecture, molecular mechanisms, and pathological manifestations. This heterogeneity directly influence disease susceptibility, and VSMC phenotypic switching exhibits distinct regulatory networks across different segments, with molecular-level differences constituting unique "transcriptional phenotype fingerprints" for each segment. The central thesis of this review posits that elucidating the molecular mechanisms regulating VSMC phenotypic switching in different aortic segments and mapping their segment-specific regulatory networks are key to advancing the treatment of aortic disease from a "homogeneous" approach toward "segment-specific precision medicine." This review systematically summarizes recent advances in epidemiology, regulatory mechanisms of VSMC phenotypic switching, molecular diagnostics, and targeted therapeutic strategies across various aortic segments. In-depth analysis of the segment-specific regulatory networks governing VSMC phenotypic switching will provide new insights for individualized precision treatment of aortic disease.
2026, 47(8): 13-27.
doi: 10.12259/j.issn.2095-610X.S20260802
Abstract:
Objective To investigate the effects of quercetin （QUE） on regulating transferrin receptor （TFRC） expression on mitochondrial function and ferroptosis in a sepsis-induced cardiomyopathy （SCM） cell model, and to elucidate the underlying regulatory mechanisms. Methods H9C2 cells were treated with 1 μg/mL LPS and co-cultured with 20 μM, 40 μM, 80 μM, or 160 μM QUE for 24 hours. H9C2 Cells treated with 80 μM QUE were transfected with sh-TFRC, pcDNA-TFRC, or treated with the ferroptosis inhibitor Ferrostatin-1 for 24 hours. The regulatory effect of QUE on TFRC expression and the effects of QUE-regulated TFRC regulation on LPS-induced mitochondrial dysfunction and ferroptosis in H9C2 cells were assessed using CCK-8 assay, flow cytometry, JC-1 staining, Western blot, Fe2+, LDH, and MDA kits, enzyme-linked immunosorbent assay （ELISA）, and RT-qPCR. QUE was intraperitoneally injected into mice and LPS was administered to establish an SCM mouse model. The effects of QUE on SCM mice were investigated using hematoxylin-eosin staining, TUNEL staining, ELISA, LDH, and MDA kits, and Western blotting. Results LPS stimulation significantly inhibited H9C2 cell proliferation, promoted cell apoptosis, and increased the levels of ROS, cleaved-caspase 3, Bax, FTH1, ACSL4, Fe2+, IL-1β, TNF-α, LDH, and CK-MB （P < 0.001）, while decreasing mitochondrial membrane potential and expression of Bcl-2 and glutathione peroxidase 4 （GPX4） proteins （P < 0.001）. Treatment with 40 μM, 80 μM, and 160 μM QUE significantly alleviated LPS-induced mitochondrial dysfunction and ferroptosis in H9C2 cells （all P < 0.05） and inhibited TFRC expression （P < 0.001）. TFRC knockdown or Ferrostatin-1 treatment further enhanced the protective effect of 80 μM QUE against H9C2 cell injury （all P < 0.05）. TFRC overexpression exacerbated LPS-induced mitochondrial dysfunction and ferroptosis in H9C2 cells, while QUE treatment alleviated the effects of TFRC overexpression on H9C2 cells. LPS stimulation increased cardiac myocyte injury and death and elevated inflammatory cytokines levels in SCM mice. QUE treatment mitigated myocardial injury and suppressed ferroptosis in SCM mice. Conclusion QUE alleviates LPS-induced mitochondrial injury in H9C2 cells and cardiac myocardial injury in mice by downregulating TFRC expression and inhibiting ferroptosis.
2026, 47(8): 28-37.
doi: 10.12259/j.issn.2095-610X.S20260803
Abstract:
Objective To investigate the potential mechanism by which neurofilament light chain （NEFL） affects the progression of Alzheimer’ s disease （AD） through its interaction with tuberous sclerosis complex 1 （TSC1）. Methods An AD model was established in adult male Sprague-Dawley rats by streptozotocin（STZ）injection. An in vitro cell model was established by treating neuronal cells with amyloid β peptide 1–42 （Aβ1–42）. Cognitive and motor functions were evaluated by the novel object recognition test and the rotarod test. The expression of NEFL and TSC1 were detected by RT-qPCR. The protein expression of NEFL, TSC1, p-TSC1, mTOR, p-mTOR, S6K1, and p-S6K1 were detected by western blot. The cell viability was detected by CCK-8 kit. The contents of IL-6, IL-1β, TNF-α, Aβ1-42, and p-Tau in cells and tissues were detected by ELISA kits. The levels of GSH, MDA, SOD, and AChE in cells and tissues were detected by biochemical kits. The apoptosis rates was detected by flow cytometry. Co-immunoprecipitation assay was used to detect the interaction between NEFL and TSC1. Results An AD rat model was successfully established. The expression of NEFL was markedly upregulated in the hippocampal tissue of AD rats, while TSC1 expression markedly downregulated. NEFL knockdown alleviated cognitive and motor dysfunction in AD rats, reduced inflammatory responses and oxidative stress injury in hippocampal tissues, and inhibited the protein expression of p-mTOR and p-S6K1 (P < 0.05). In Aβ1-42-induced neurons, NEFL expression was markedly increased (P < 0.0001 ), while TSC1 expression was markedly decreased (P < 0.0001 ). After NEFL knockdown, TSC1 expression was significantly increased (P < 0.0001 ), cell apoptosis rate was significantly reduced (P < 0.0001), and cell viability was significantly restored (P < 0.0001 ). NEFL knockdown also suppressed the levels of IL-1β, IL-6, and TNF-α induced by Aβ1-42 (P < 0.0001 ), suppressed the elevation of MDA and AChE (P < 0.0001 ), and increased the levels of GSH and SOD (P < 0.01). Compared with the sh-NC group, the protein expression levels of p-mTOR and p-S6K1 (P < 0.001) were significantly downregulated in the sh-NEFL group. Co-immunoprecipitation results showed that NEFL interacted with TSC1. Knockdown of NEFL upregulated the protein expression of TSC1 and p-TSC1 (P < 0.01), whereas overexpression of TSC1 inhibited NEFL protein expression (P < 0.05). Moreover, knockdown of TSC1 reversed the effects of NEFL knockdown. Conclusion Knockdown of NEFL not only can alleviate inflammatory response and improve oxidative stress state, but also may exert neuroprotective effects by inhibiting the mTOR/S6K1 signaling pathway.
Effects of Erianin on Ferroptosis in Prostate Cancer Cells via the Keap1/Nrf2/HO-1 Signaling Pathway
2026, 47(8): 38-47.
doi: 10.12259/j.issn.2095-610X.S20260804
Abstract:
Objectives To investigate whether erianin induces ferroptosis in prostate cancer cells by regulating the Keap1/Nrf2/HO-1 signaling pathway. Methods Human prostate cancer cell lines DU145 and PC-3 were cultured. Cell viability was detected by CCK-8 assay, cell proliferation by colony formation assay, cell invasion by Transwell assay, and cell apoptosis by flow cytometry. Intracellular reactive oxygen species （ROS） content was analyzed using the ROS-specific probe DCFH-DA, and the levels of malondialdehyde （MDA） and glutathione （GSH） were determined. Western blot was used to detect the expression of metastatic phenotypic markers （vimentin, N-cadherin, slug, snail, and MMP-9）, ferroptosis-negative regulatory proteins （GPX4, CHAC2, SLC40A1, SLC7A11, and glutaminase）, and proteins related to the Keap1/Nrf2/HO-1 signaling pathway. Results Compared with the control group, erianin significantly reduced the viability of prostate cancer cells （DU145, PC-3） and inhibited their proliferation, migration, and invasion abilities （P < 0.05）. Erianin inhibited the migration of prostate cancer cells by downregulating the mesenchymal markers （vimentin, N-cadherin, slug, snail, and MMP-9） and upregulating the epithelial marker E-cadherin. ROS accumulation, GSH depletion, and lipid peroxidation were significantly increased （P < 0.05）. Erianin-induced prostate cancer cell death could be rescued by co-treatment with the ROS inhibitor N-acetyl-L-cysteine （NAC） and glutathione （GSH）. After erianin treatment, the proportion of Phen Green SK-positive cells （detecting intracellular free Fe2+） was significantly decreased （P < 0.05）. Transmission electron microscopy （TEM） revealed mitochondrial matrix condensation and cristae enlargement in erianin-treated prostate cancer cells. Additionally, erianin treatment significantly downregulated the expression of ferroptosis-negative regulatory proteins （GPX4, CHAC2, SLC40A1, SLC7A11, and glutaminase）（P < 0.05）. Co-treatment with ferroptosis inhibitors （Liproxstatin-1, Lip-1; or Ferrostatin-1, Fer-1） blocked erianin-induced prostate cancer cell death. Erianin increased Keap1 protein expression while decreasing the expression of Nrf2, HO-1, and NQO1 proteins in cells （P < 0.05）. CPUY192018 enhanced ferroptosis in prostate cancer cells, indicating that erianin induces ferroptosis through targeting the Keap1/Nrf2/HO-1 signaling pathway. Conclusion Erianin induces cell death and suppresses prostate cancer cell migration by targeting the Keap1/Nrf2/HO-1 signaling pathway.
2026, 47(8): 48-57.
doi: 10.12259/j.issn.2095-610X.S20260805
Abstract:
Objective To explore the correlation between leukocyte ratios and nutritional indicators at admission in patients with acute exacerbation of chronic obstructive pulmonary disease （AECOPD）, and their association with patient clinical outcomes and short-term prognosis. Methods A total of 82 patients with AECOPD admitted to Nansha District People's Hospital of Guangzhou from January 2022 to December 2024 （AECOPD group） and 82 patients with stable chronic obstructive pulmonary disease （SCOPD） who had been hospitalized for AECOPD at the same hospital and had baseline stability for ≥8 weeks （SCOPD group） were selected as controls. General data, pulmonary function, neutrophil-lymphocyte ratio （NLR）, platelet-lymphocyte ratio （PLR）, serum albumin （ALB）, and prealbumin （PA） levels at admission were collected and compared between the two groups. Pearson correlation analysis was used to analyze the correlations between indicators, and multivariate Logistic regression analysis was used to identify independent factors affecting the clinical outcomes and short-term prognosis of AECOPD patients. Results There was no statistically significant difference in the baseline data between the two groups （P > 0.05）. FEV1/FVC （53.87 ± 8.96） and FEV1 （% pred） in the AECOPD group were lower than those in the SCOPD group （57.34 ± 7.25 and 51.15 ± 10.48 % pred）, while age （68.76 ± 7.24 years） was higher than in the SCOPD group （65.38 ± 7.19 years）, with statistically significant differences between groups （P < 0.05）. NLR （5.14 ± 1.15） and PLR （152.74 ± 20.39） in the AECOPD group were higher than in the SCOPD group （3.20 ± 0.73 and 127.38 ± 14.22）, while ALB （32.18 ± 6.04） g/L and PA （167.47 ± 36.29） mg/L were lower than in the SCOPD group （37.45 ± 5.12 g/L and 180.36 ± 38.18 mg/L）, with statistically significant differences between groups （P<0.05）. Correlation analysis showed that NLR was negatively correlated with ALB （r = -0.443, P < 0.05） and PA （r = -0.157, P < 0.05）, and PLR was negatively correlated with ALB （r = -0.379, P < 0.05） and PA （r = -0.263, P < 0.05）. Prior to multivariate logistic regression analysis, collinearity diagnosis of the included independent variables （age, NLR, PLR, ALB, PA） was performed using the variance inflation factor （VIF）. The results showed that all variables had VIF values <3（NLR: 2.13, PLR: 2.28, age: 1.42, ALB: 1.35, PA: 1.28）, suggesting no significant multicollinearity issues. Multivariate Logistic regression analysis showed that age （OR = 2.449, 95%CI: 1.385 ～ 4.327）, NLR （OR = 2.066, 95%CI: 1.156 ～ 3.693）, and PLR （OR = 2.233, 95%CI: 1.211 ～ 4.120） were independent risk factors for poor outcomes, while ALB （OR =0.409, 95%CI: 0.281 ～ 0.595） and PA （OR = 0.472, 95%CI: 0.423 ～ 0.526） were protective factors for good outcomes. Age （OR = 2.370, 95%CI: 1.351 ～ 4.158）, NLR （OR = 2.574, 95%CI: 1.153 ～ 5.750）, and PLR （OR = 2.959, 95%CI: 1.134 ～ 7.721） were risk factors for short-term prognosis, while ALB （OR =0.418, 95%CI: 0.276 ～ 0.632） and PA （OR = 0.453, 95%CI: 0.404 ～ 0.507） were protective factors for short-term prognosis. Conclusion At admission, AECOPD patients demonstrated significantly elevated NLR and PLR levels and significantly decreased ALB and PA levels, with inflammatory markers negatively correlated with nutritional indicators. NLR and PLR are independent risk factors for poor outcomes and adverse short-term prognosis in AECOPD patients, while ALB and PA are protective factors for good clinical outcomes.
2026, 47(8): 58-69.
doi: 10.12259/j.issn.2095-610X.S20260806
Abstract:
Objective To explore the differences in gut microbiota composition of exclusively breastfed infants with and without late-onset breast milk jaundice （LBMJ）, and to identify key bacterial taxa and metabolic pathways associated with LBMJ development and progression. Methods We selected 16 healthy full-term mother-infant pairs with exclusively breastfed infants and 15 healthy full-term mother-infant pairs diagnosed with late-onset breast milk jaundice, both groups with infants aged 0.5 to 3 months. The healthy exclusively breastfed infants were assigned to the control group （Group Z）, and those with late-onset breast milk jaundice to the jaundice group （Group H）. Fecal samples were collected under aseptic conditions and preserved at −80 °C. Differences in intestinal microbiota between the two groups were detected and analyzed using metagenomic methods. Inter-group diversity analysis was performed using the Kruskal-Wallis test, and differential analysis employed the Mann-Whitney U test, among others. Results All fecal microbial sequences were annotated into 53 phyla, 1028 genera, and 5421 species. Alpha diversity in the H group was significantly reduced compared to the Z group （P < 0.05）, while Beta diversity showed no significant difference （P < 0.05）. Species-level differential analysis between the two groups revealed that at the phylum level, group Z showed enrichment of Chlamydia, Deinococcota, Cyanobacteriota, and Spirochaetota. At the genus level, Shigella and Eggerthella were significantly increased in the Z group, while Staphylococcus and Atopobium were significantly increased in the H group. At the species level, Shigella was significantly elevated in the Z group, while unclassified Staphylococcus was significantly increased in the H group. LEfSe differential analysis revealed biomarkers for the Z group including Coriobacteriia, Hungatella, Enterocloster, Flavonifractor, Shigella, Clostridioides, Flavonifractor plautii, Enterocloster bolteae, Enterocloster unclassified, Shigella sonnei, while H group biomarkers included Bacillales, Staphylococcaceae, and Bacteriophage. Gene Ontology functional enrichment predictions showed that cellular components including cytoplasmic membrane and cytoplasm, as well as molecular functions including protein binding pathways, were significantly enriched in the Z group. The H group showed significant enrichment in UDP-glucuronic acid synthesis pathways. KEGG function predictions revealed that the Z group demonstrated advantages in dioxin degradation and Yersinia pestis infection pathways at the tertiary level, while the H group showed advantages in bacitracin biosynthesis pathways. At the quaternary level, biosynthetic metabolism-related pathways were more advantageous in the Z group. Conclusions Exclusively breastfed infants with LBMJ show significant differences from non-jaundiced infants in intestinal microbiota species composition, biomarkers, and gene function annotation.
2026, 47(8): 70-80.
doi: 10.12259/j.issn.2095-610X.S20260807
Abstract:
Objective To explore the predictive value of serum hypoxia-inducible factor-1alpha （HIF-1α） and Cystatin C （CysC） levels for 28-day mortality risk in patients with acute left heart failure （AHF） complicated with respiratory failure （RF）. Methods A retrospective analysis was conducted on clinical data from 217 AHF patients with concurrent RF admitted between January 2022 and December 2024. Patients were stratified based on 28-day survival status post-discharge into a mortality group （n = 62） and a survival group （n = 155）. General demographic data and serum HIF-1α and CysC levels were compared between the two groups. The influencing factors for 28-day mortality risk in AHF patients with RF and the relationship between serum HIF-1α, CysC levels and 28-day mortality risk were analyzed. Receiver operating characteristic （ROC） curves were used to evaluate the predictive value of HIF-1α and CysC for 28-day mortality risk in AHF with RF patients. Risk stratification and clinical validation were performed based on a combined predictive model. Results The mortality group demonstrated significantly higher Acute Physiology and Chronic Health Evaluation II （APACHE II） scores （16.59±3.05 vs 13.72±2.47, t = 7.214, P < 0.001）, Sequential Organ Failure Assessment （SOFA） scores（12.61±2.24 vs 11.89±2.15, t = 2.202, P = 0.029）, N-terminal pro-B-type natriuretic peptide （NT-proBNP） （507.41±82.44 vs 329.49±70.55 pg/mL, t = 15.975, P < 0.001）, HIF-1α （30.14±4.58 vs 21.37±3.82 ng/L, t = 14.410, P < 0.001） and CysC （1.72±0.35 vs 1.30±0.28 mg/L, t = 9.270, P < 0.001） compared with the survival group. Logistic regression analysis showed that HIF-1α （OR = 1.315, 95%CI: 1.129-1.532） and CysC （OR = 1.260, 95%CI: 1.105-1.437） were independent influencing factors for 28 day mortality risk in AHF with RF patients （P < 0.05）. Restricted cubic spline （RCS） model analysis demonstrated that after adjusting for other variables, serum HIF-1α and CysC levels remained linearly and positively correlated with 28 day mortality risk in AHF with RF patients （P < 0.05）, with mortality risk progressively increasing as serum HIF-1α and CysC levels elevated. ROC curve analysis revealed that the area under the curve （AUC） for predicting 28-day mortality risk were as follows: APACHE II score 0.737 （95% CI: 0.673–0.794）, SOFA score 0.711 （0.646–0.771）, NT-proBNP 0.768 （0.706–0.822）, HIF-1α 0.748 （0.684–0.804）, and CysC 0.753 （0.690–0.809）, with no statistically significant differences in AUC between individual indicators （P>0.05）. Interaction analysis revealed RERI=1.09, AP=0.253, and SI=2.727, indicating a positive additive interaction between HIF-1α and CysC when both were simultaneously elevated, with the combined effect exceeding the sum of individual effects. The combined predictive AUC for serum HIF-1α and CysC for 28-day mortality risk in AHF with RF patients was 0.878, significantly higher than the individual AUCs for APACHE II score, SOFA score, NT-proBNP, HIF-1α, and CysC （P < 0.05）. Calibration curves demonstrated good concordance between predicted and observed risk across the entire risk spectrum（Hosmer-Lemeshow test, χ2=2.224, P = 0.086）. Internal validation via Bootstrap resampling （1000 iterations） yielded a corrected model AUC of 0.877 （95% CI: 0.828–0.927）, with calibration curves demonstrating good agreement between predicted and actual risk. Decision curve analysis （DCA） indicated clinical net benefit within the threshold probability range of 0.2–0.8, and temporal validation demonstrated high model robustness and predictive performance. Patients stratified into low, intermediate, and high-risk groups based on the combined predictive model had actual 28-day mortality rates of 4.17%, 27.40%, and 54.17%, respectively （P<0.05）. Conclusion Serum HIF-1α and CysC levels in AHF patients with concurrent RF are closely associated with 28-day mortality risk. A combined predictive model constructed from these two markers demonstrates excellent discriminative ability.
2026, 47(8): 81-89.
doi: 10.12259/j.issn.2095-610X.S20260808
Abstract:
Objective To explore the value of microRNA-155 （miR-155） and microRNA-146a （miR-146a） in peripheral blood mononuclear cells （PBMC） in combined prediction of poor prognosis risk in uremic patients undergoing maintenance hemodialysis （MHD）. Methods A prospective study enrolled 214 uremic patients from January 2021 to November 2023 as research subjects. All patients received MHD treatment with 1-year follow-up, and prognostic outcomes were recorded. Levels of miR-155 and miR-146a in PBMC before the first hemodialysis were detected in all patients. PBMC miR-155 and miR-146a levels were compared between patients with different prognoses. Using the median levels as cutoff values, patients were stratified into high miR-155/low miR-155 and high miR-146a/low miR-146a groups, which were further divided into four subgroups: low miR-155/low miR-146a （Q1）, low miR-155/high miR-146a （Q2）, high miR-155/low miR-146a （Q3）, and high miR-155/high miR-146a （Q4）. Clinical data and cumulative incidence of poor prognosis were compared among the four groups. Logistic regression was used to analyze the effects of miR-155 and miR-146a in PBMC on poor prognosis and their interactive efficacy. Receiver operating characteristic （ROC） curve analysis was used to evaluate the predictive value of PBMC miR-155 and miR-146a for poor prognosis. Results Levels of miR-155 and miR-146a in PBMC were higher in patients with poor prognosis compared to those with good prognosis （P < 0.05）. Significant differences were observed among the four groups regarding systolic blood pressure （SBP）, diastolic blood pressure （DBP）, C-reactive protein （CRP）, neutrophil-to-lymphocyte ratio （NLR）, intact parathyroid hormone （iPTH）, and calcium-phosphorus product （P < 0.05）. Group Q4 had higher SBP, DBP, CRP, NLR, iPTH, and calcium-phosphorus product compared to Q1, Q2, and Q3 groups, while Q2 and Q3 groups were higher than Q1 （P < 0.05）. CRP and NLR in Q3 were higher than in Q2 （P < 0.05）. The cumulative incidence of poor prognosis in Q4 was 51.43%, significantly higher than Q1 （9.09%）, Q2 （30.00%）, and Q3 （25.49%）, with Q2 and Q3 higher than Q1 （P < 0.05）. Lasso-Logistic regression analysis showed that after adjusting for confounding factors, the odds ratios （OR） for poor prognosis in Q2, Q3, and Q4 compared to Q1 were 2.397, 2.735, and 5.033, respectively. Interaction analysis showed that the relative excess risk due to interaction （RERI）, attributable proportion （AP）, and synergy index （S） for miR-155 and miR-146a were 0.901, 0.179, and 1.288, respectively, indicating synergistic enhancement of poor prognosis risk with high miR-155 and high miR-146a （P < 0.05）. ROC analysis demonstrated that the area under the curve （AUC） for combined prediction of poor prognosis using both miR-155 and miR-146a was 0.870, superior to individual predictions （Z = 2.240, 2.057; P = 0.025, 0.040）. Conclusion Both miR-155 and miR-146a in PBMC are independent factors influencing poor prognosis in uremic patients undergoing MHD. These two microRNAs exhibit positive interactive effects on poor prognosis risk, and their combined detection has certain predictive value for poor prognosis.
2026, 47(8): 90-99.
doi: 10.12259/j.issn.2095-610X.S20260809
Abstract:
Objective To explore the predictive value of a nomogram model based on quantitative parameters from contrast-enhanced ultrasound （CEUS） for platinum-based chemotherapy sensitivity in breast cancer patients, providing clinical reference for treatment decisions. Methods A prospective study enrolled 275 breast cancer patients treated at Guangyuan Central Hospital from January 2021 to December 2024 as the modeling cohort, with 118 breast cancer patients from January to July 2025 selected at a 7:3 ratio as the temporal validation cohort. All patients received platinum-based chemotherapy and were stratified based on achievement of pathologic complete response （pCR） following chemotherapy into platinum-resistant group （without pCR, n = 94） and platinum-sensitive group （with pCR, n = 181）. Multivariate logistic regression was used to analyze the influencing factors of platinum-based chemotherapy sensitivity in breast cancer patients, and a nomogram prediction model was constructed. The discrimination, consistency and clinical practicability of the nomogram model were evaluated by receiver operating characteristic （ROC） curve, calibration curve and decision curve （DCA）. Results Clinical characteristics showed no significant differences between the modeling and temporal validation cohorts（P > 0.05）. In the modeling cohort, significant differences were observed between the two groups in molecular subtype, ER expression, Ki-67 expression, blood flow signal grade, lymph node status, peak time （TTP）, arrival time （AT）, and wash-in rate （WiR）（P < 0.05）. Multivariate Logistic regression analysis showed that molecular subtype, ER expression, Ki-67 expression, lymph node status, TTP, AT and WiR were all independent influencing factors for platinum chemotherapy resistance in breast cancer patients （P < 0.05）. Based on the results of Logistic regression analysis, a nomogram prediction model was constructed. ROC curve showed that the nomogram model for predicting platinum-based chemotherapy resistance had an area under the curve （AUC） of 0.886 （95%CI: 0.826～0.946）in the modeling cohort with sensitivity of 92.55% and specificity of 88.95%, and an AUC of 0.830 （95%CI: 0.780～0.880） in the temporal validation cohort with sensitivity of 91.43% and specificity of 86.75%, demonstrating good discrimination. The Hosmer-Lemeshow goodness-of-fit test showed P > 0.05, with Brier scores of 0.122 and 0.141 for calibration curves in the modeling and temporal validation cohorts, respectively. The DCA curve suggests that when the threshold probability ranges from 40% to 80%, using this nomogram model for clinical decision-making provides higher net benefit compared to "treat all" or "treat none" strategies, demonstrating good clinical utility. Conclusion A nomogram model integrating molecular subtype, ER, Ki-67, lymph node status, and CEUS quantitative parameters （TTP, AT, WiR） demonstrates good predictive efficacy for platinum-based chemotherapy resistance risk in breast cancer patients.
2026, 47(8): 100-109.
doi: 10.12259/j.issn.2095-610X.S20260810
Abstract:
Objective To investigate the risk factors for acute symptomatic seizures （ASS） in patients with viral encephalitis （VE）, and to construct and validate a risk prediction model for early identification of high-risk patients. Methods A retrospective cohort study design was employed. Data from 249 VE patients admitted to a tertiary hospital in Yunnan Province between January 1, 2020 and December 31, 2023, who met the inclusion and exclusion criteria, were collected as the modeling cohort. The occurrence of ASS during hospitalization was set as the outcome indicator. Univariate logistic regression was used for initial screening of the modeling cohort. Subsequently, LASSO regression （least absolute shrinkage and selection operator） combined with 10-fold cross-validation was applied for variable selection. A multivariable logistic regression model was constructed using the selected variables, and a nomogram prediction model was developed based on this model. The discriminative ability, calibration, and clinical utility of the model were evaluated using the area under the receiver operating characteristic curve （AUC）, calibration curve, and decision curve analysis. Additionally, an external validation was performed using 60 VE patients from another tertiary hospital in Yunnan Province between January 1, 2024, and September 1, 2024. Results Multivariate analysis showed that decreased serum sodium concentration （OR = 0.883, 95%CI: 0.789～0.989）, frontal or temporal lobe involvement （OR = 2.387, 95%CI: 1.138～5.007）, moderate to severe EEG abnormalities （moderate: OR = 6.179, 95%CI: 2.030～18.806; severe: OR = 7.875, 95%CI: 1.081～57.393）, and moderate to severe disturbances of consciousness （GCS≤12; moderate: OR = 4.282, 95%CI: 1.482～12.378; severe: OR = 6.228, 95%CI: 1.099～35.289） were independent risk factors for ASS in VE patients. The predictive model constructed based on these factors showed an AUC of 0.836 （95%CI: 0.782～0.891, sensitivity 0.886, specificity 0.565） in the modeling cohort and an AUC of 0.784 （95%CI: 0.665～0.904, sensitivity 0.848, specificity 0.711） in the validation cohort. The Brier score was 0.145 and calibration slope was 1.023 in the modeling cohort; Brier score was 0.172 and calibration slope was 0.912 in the validation cohort. Decision curve analysis demonstrated that within the threshold probability range of 0.1–0.6, the net benefit provided by the model exceeded both the "treat all" and "treat none" strategies. When the threshold probability ranged from 0.15 to 0.40, the model's net benefit advantage was most pronounced, providing higher clinical decision-making value. Conclusion This study successfully established and validated a risk prediction model for ASS following VE that incorporates four readily obtainable clinical indicators. The model demonstrates predictive capability and provides an intuitive, quantitative assessment tool for early clinical identification of high-risk patients and implementation of stratified management and intervention.
2026, 47(8): 110-117.
doi: 10.12259/j.issn.2095-610X.S20260811
Abstract:
Objective To explore the relationship between serum levels of pulmonary surfactant protein D （SP-D）, Krebs von den Lungen-6 （KL-6）, and soluble programmed death-ligand 2 （sPD-L2） and disease severity in patients with chronic obstructive pulmonary disease （COPD）. Methods A prospective study enrolled 153 COPD patients and 100 healthy controls from the First People's Hospital of Kashgar Region between June 2023 and December 2024. Based on the GOLD criteria, COPD patients were classified into Group A （n = 39）, Group B （n = 53）, and Group E （n = 61）, which were further stratified into low-risk group （Group A） and high-risk group （Group B+E）. Serum levels of SP-D, KL-6, and sPD-L2 were measured. High-resolution computed tomography （HRCT） parameters including percentage of low attenuation area （LAA%）, and bronchial wall thickness of bilateral lungs were obtained. Pulmonary function indices including forced expiratory volume in one second （FEV1）, FEV1 as percentage of predicted value （FEV1%）, and ratio of forced expiratory volume in one second to forced vital capacity （FEV1/FVC） were assessed. Pearson correlation analysis was used to evaluate associations between variables. Receiver operating characteristic （ROC） curves were constructed to assess the discriminatory efficiency of biomarkers for disease severity. Results Serum levels of SP-D, KL-6, sPD-L2, LAA%, and bronchial wall thickness were significantly higher in the COPD group compared with controls, while pulmonary function indices were significantly decreased （P < 0.05）. With increasing GOLD classification, serum biomarkers and HRCT parameters increased progressively, while pulmonary function decreased （P < 0.05）. Pearson correlation analysis revealed that SP-D, KL-6, and sPD-L2 were negatively correlated with pulmonary function indices and positively correlated with HRCT parameters. ROC curve analysis showed that the combined predictive value of the three biomarkers for COPD severity yielded an AUC of 0.896 （95%CI: 0.836-0.939）, which was significantly superior to any single biomarker alone （Z = 2.909, 2.224, 3.134; all P < 0.05）. Conclusion Serum levels of SP-D, KL-6 and sPD-L2 are associated with disease severity in COPD patients. The combined assessment using these three biomarkers demonstrates superior efficacy in evaluating disease severity in COPD patients.
2026, 47(8): 118-126.
doi: 10.12259/j.issn.2095-610X.S20260812
Abstract:
Objective To investigate the relationship between peripheral blood growth arrest-specific protein 6 （Gas6）, interleukin-18 binding protein （IL-18BP） and postoperative secondary cognitive impairment in patients with intracranial aneurysms, and to analyze its predictive value for postoperative secondary cognitive impairment. Methods A total of 287 patients with intracranial aneurysm who underwent endovascular intervention at Yancheng First People's Hospital from January 2022 to May 2025 were enrolled. Based on the presence or absence of postoperative secondary cognitive dysfunction at 3 months post-operation （3 cases lost to follow-up）, patients were divided into cognitive dysfunction group （n = 82） and normal cognition group （n = 202）. Peripheral blood levels of Gas6 and IL-18BP before and after surgery were compared between the two groups. The influencing factors of postoperative secondary cognitive dysfunction in intracranial aneurysm were analyzed. The relationship between peripheral blood Gas6, IL-18BP and postoperative secondary cognitive dysfunction in intracranial aneurysm was analyzed. The predictive value of peripheral blood Gas6 and IL-18BP for postoperative secondary cognitive dysfunction in intracranial aneurysm was analyzed. Results Peripheral blood Gas6 levels in the cognitive dysfunction group were higher at postoperative day 1, 3, and 7 compared with the normal cognition group, while IL-18BP levels were lower （P < 0.05）. After adjusting for Hunt-Hess grade, CT Fisher grade, maximum aneurysm diameter, operation time, postoperative cerebral hemorrhage/cerebral ischemia, peripheral blood Gas6 and IL-18 BP on postoperative day 7 remained independently associated with postoperative secondary cognitive dysfunction in intracranial aneurysm （P < 0.05）. Postoperative day 7 peripheral blood Gas6 levels were positively linearly correlated with postoperative secondary cognitive dysfunction in intracranial aneurysm, while IL-18BP levels were negatively linearly correlated （P < 0.05）. The area under the receiver operating characteristic curve （AUC） for combined prediction of postoperative secondary cognitive dysfunction using Gas6 and IL-18BP on postoperative day 7 was significantly higher than that of single indicators （P < 0.05）. Conclusion In patients with intracranial aneurysm, peripheral blood Gas6 levels are positively linearly correlated with postoperative secondary cognitive dysfunction, while IL-18BP levels are negatively linearly correlated. Combined detection of these biomarkers has predictive value for postoperative secondary cognitive dysfunction.
2026, 47(8): 127-136.
doi: 10.12259/j.issn.2095-610X.S20260813
Abstract:
Objective To investigate the predictive value of myocardial contrast echocardiography （MCE） combined with three-dimensional speckle tracking imaging （3D-STI） for major adverse cardiovascular events （MACEs） following percutaneous coronary intervention （PCI） in patients with non-ST-segment elevation myocardial infarction （NSTEMI）. Methods A total of 254 NSTEMI patients who underwent PCI at the 928th Hospital of the Joint Logistics Support Force, People's Liberation Army from May 2022 to March 2024 were selected. Patients were stratified into MACEs group and non-MACEs group based on the occurrence of MACEs within one year of discharge. Clinical data, conventional echocardiographic parameters, MCE parameters [peak intensity （A）, perfusion score index （PSI）, curve slope （β） and myocardial blood flow （A·β）] and 3D-STI parameters [left ventricular global area strain （LVGAS）, left ventricular global circumferential strain （LVGCS）, left ventricular global longitudinal strain （LVGLS）, left ventricular global radial strain （LVGRS）] were compared between the two groups. The relationships between MCE, 3D-STI parameters and left ventricular ejection fraction （LVEF） were analyzed. Receiver operating characteristic （ROC） curve were used to assess the predictive value of MCE and 3D-STI parameters for MACEs. Results Compared with the non-MACEs group, the MACEs group had higher levels of N-terminal pro-brain natriuretic peptide （NT-proBNP）, interleukin-6 （IL-6）, and soluble suppression of tumorigenicity 2 （sST2）, with lower LVEF and vascular endothelial growth factor （VEGF） levels （P < 0.05）. At 3 months post-operatively, the MACEs group showed lower A, β, A·β values, and higher PSI compared with the non-MACEs group, with significant differences in the changes of A, PSI, β, A·β from 3 months to 24 hours post-operatively between groups （P < 0.05）. At 3 months post-operatively, LVGAS, LVGCS, LVGLS and LVGRS were all lower in the MACEs group than in the non-MACEs group, with significant differences in the changes of these parameters from 3 months to 24 hours post-operatively （P < 0.05）. The combined AUC of MCE and 3D-STI parameters at 3 months post-operatively for predicting MACEs was 0.933 （95%CI: 0.895–0.961）, and the combined AUC using the differences in MCE and 3D-STI parameters between 3 months and 24 hours post-operatively was 0.915 （95%CI: 0.873～0.946）. Conclusion The combined quantitative parameters of MCE and 3D-STI demonstrate high predictive value for MACEs risk following PCI in NSTEMI patients. Monitoring dynamic changes in MCE and 3D-STI parameters from 3 months to 24 hours post-operatively is helpful for early identification of high-risk patients and provides evidence for developing individualized therapeutic and follow-up strategies.
2026, 47(8): 137-145.
doi: 10.12259/j.issn.2095-610X.S20260814
Abstract:
Objective To investigate the efficacy of transcranial direct current stimulation （tDCS） combined with computerized cognitive training （CCT） in treating autism spectrum disorder （ASD）. Methods A total of 208 children with ASD admitted to Longgang District Maternal and Child Health Hospital, Shenzhen from January 2021 to August 2024 were selected, and randomly divided into four groups using a random number table: CCT group （n = 52）, tDCS group （n = 52）, combination group （n = 52）, and sham stimulation group （n = 52）. All four groups received standard rehabilitation treatment. Additionally, the CCT group received CCT, the tDCS group received tDCS, the combination group received tDCS combined with CCT, and the sham stimulation group received sham tDCS combined with CCT. Therapeutic efficacy, Childhood Autism Rating Scale （CARS）, Aberrant Behavior Checklist （ABC）, Chinese Version of Psychoeducational Profile-3 （C-PEP-3）, and Children’ s Neuropsychological Behavioral Scale （abbreviated as China Children Development Scale） scores, electroencephalographic parameters [latency and amplitude of mismatch negativity （MMN） at Fz and Cz leads, frontal lobe relative θ power, sleep discharge index] before and after treatment, and the incidence of adverse reactions were compared among the four groups. Results The overall therapeutic efficacy rate showed no significant difference among the four groups （χ2 = 6.811, P = 0.078）. After 3 months of treatment, the combination group showed significantly lower scores on ABC scale dimensions （somatic motor, language, sensory, social interaction, self-care） and CARS total scores compared with the CCT, tDCS, and sham stimulation groups, and significantly higher C-PEP-3 total scores and Child Neuropsychological Behavior Examination Scale scores in language, social behavior, developmental quotient, mental age, adaptive ability, gross motor, and fine motor dimensions compared with the other three groups （F = 7.575, 14.741, 7.616, 6.817, 6.896, 21.804, 12.175, 13.034, 17.661, 11.925, 12.690, 9.691, 8.777, 13.485, P < 0.05）. No significant differences were found among the CCT, tDCS, and sham stimulation groups in ABC dimensions, CARS scores, C-PEP-3 scores, or Child Neuropsychological Behavior Examination Scale dimensions （P > 0.05）. After 3 months of treatment, the combination group showed significantly lower MMN latency in Fz and Cz leads, relative frontal theta power, and sleep discharge index, and significantly higher MMN amplitude in Fz and Cz leads compared with the other three groups （F = 15.593, 12.714, 12.072, 48.912, 6.901, 5.723, P < 0.05）. No significant differences were found among the CCT, tDCS, and sham stimulation groups in these EEG parameters （P > 0.05）. The overall incidence of adverse reactions showed no significant difference among the four groups （P = 0.123）. Conclusion tDCS combined with CCT demonstrates significant therapeutic efficacy in treating ASD, potentially improving cognitive and social functioning, reducing aberrant behaviors, and improving cerebral electrical activity in affected children.
2026, 47(8): 146-157.
doi: 10.12259/j.issn.2095-610X.S20260815
Abstract:
Objective To explore the efficacy of Stent Boost-guided percutaneous coronary intervention （PCI） in treating coronary artery disease （CAD） patients with typical angina pectoris and moderate to severe calcified lesions. Methods A prospective study enrolled 180 CAD patients with typical angina pectoris and moderate-to-severe calcified lesions from January 2022 to January 2024. Patients were randomly divided into control group （n = 90） and experimental group （n = 90）, further stratified into three subgroups: moderate calcification subgroup （n = 30）, severe calcification subgroup （n = 30）, and special population subgroup （n = 30）. The control group received standard stent implantation, while the experimental group received Stent Boost-guided visualization combined with standard stent implantation. All patients received drug-eluting stents. We compared intraoperative convenience and efficacy, cardiac function parameters[left ventricular ejection fraction （LVEF）, left ventricular end-systolic volume （LVESV）, left ventricular end-diastolic volume （LVEDV）] , and complications between the two groups. The patients were followed up for 12 months, and the target lesion revascularization and major adverse cardiovascular events （MACE） events were assessed between the two groups. Results The experimental group demonstrated superior immediate stent visibility, stent expansion rate, minimum stent lumen diameter, maximum stent edge diameter, minimal stent area （MSA）, eccentricity index, and LVEF compared to controls. Post-dilation rate, operative time, contrast volume, LVESV, and LVEDV were significantly lower in the experimental group （P < 0.05）. The experimental group showed higher proportion of Thrombolysis In Myocardial Infarction （TIMI） grade 3 flow immediately post-procedure, with lower complication and MACE rates （P < 0.05）, However, TIMI grade 3 flow proportions showed no significant difference among subgroups between groups （P > 0.05）. Complication and MACE rates were similar between groups in moderate and severe calcification subgroups （P > 0.05）, while the special population subgroup showed significantly lower complication and MACE rates in the experimental group （P < 0.05）. Conclusion For CAD patients with typical angina and moderate-to-severe calcified lesions, Stent Boost-guided PCI optimizes treatment outcomes, improves post-operative cardiac function, and reduces complications and MACE rates, particularly in patients with severe calcification and bifurcation lesions.
2026, 47(8): 158-168.
doi: 10.12259/j.issn.2095-610X.S20260816
Abstract:
Objective To construct an early warning model of upper gastrointestinal bleeding （UGIB） in patients with cirrhosis and portal hypertension （CPH） based on serum microRNA-140 （miR-140） and microRNA-335-5p （miR-335-5p） combined with clinical indicators, and to evaluate its predictive efficacy. Methods A total of 289 patients with CPH admitted to Taiyuan Central Hospital from March 2021 to August 2024 were enrolled as research subjects and divided into a training set (n = 203) and a validation set (n = 86) at a ratio of 7:3. All patients were followed up for 1 year to record the incidence of UGIB. Clinical data were collected, and serum levels of miR-140 and miR-335-5p were detected. Lasso-Logistic regression analysis was performed to screen independent predictors of UGIB in CPH patients for model construction. Calibration curves, receiver operating characteristic (ROC) curves and decision curve analysis (DCA) were used to evaluate and verify the clinical value of the early warning models. Results After 1-year follow-up, in the training set, 2 patients were lost to follow-up, 125 did not develop UGIB, and 76 developed UGIB. In the validntion set, 1 was lost to follow up, 54 did not develop UGIB, and 31 developed UGIB. Conclusion The early warning model constructed based on serum miR-140 and miR-335-5p combined with clinical indicators is an effective tool for predicting UGIB in CPH patients, enabling early risk stratification and optimization of clinical decision-making.
2026, 47(8): 169-180.
doi: 10.12259/j.issn.2095-610X.S20260817
Abstract:
Under the increasingly severe aging demographics, neurodegenerative diseases such as Alzheimer’ s disease （AD） pose serious threats to population health. AD is characterized by progressive cognitive decline and memory loss. Its pathogenic mechanisms are complex, featuring a prolonged disease course and pathological characteristics that encompass multiple aspects, including β-amyloid protein deposition, tau protein hyperphosphorylation, neuroinflammatory responses, and oxidative stress, presenting formidable challenges for AD prevention and treatment. Currently, monoclonal antibody-based targeted therapeutics for AD not only show limited efficacy but are also associated with significant adverse effects. In contrast, traditional Chinese medicine, utilizing its multi-component and multi-target systemic regulatory advantages, exhibits unique potential in intervening in the complex pathological processes of AD, particularly in modulating neuroinflammatory responses. This article systematically reviews the central role of the Wnt/β-catenin signaling pathway in regulating neuroinflammation in Alzheimer's disease and summarizes recent research advances in the treatment of AD by traditional Chinese medicine and its active components through intervention in this pathway, aiming to provide novel theoretical evidence and strategic references for AD prevention and treatment.
Under the increasingly severe aging demographics, neurodegenerative diseases such as Alzheimer’ s disease （AD） pose serious threats to population health. AD is characterized by progressive cognitive decline and memory loss. Its pathogenic mechanisms are complex, featuring a prolonged disease course and pathological characteristics that encompass multiple aspects, including β-amyloid protein deposition, tau protein hyperphosphorylation, neuroinflammatory responses, and oxidative stress, presenting formidable challenges for AD prevention and treatment. Currently, monoclonal antibody-based targeted therapeutics for AD not only show limited efficacy but are also associated with significant adverse effects. In contrast, traditional Chinese medicine, utilizing its multi-component and multi-target systemic regulatory advantages, exhibits unique potential in intervening in the complex pathological processes of AD, particularly in modulating neuroinflammatory responses. This article systematically reviews the central role of the Wnt/β-catenin signaling pathway in regulating neuroinflammation in Alzheimer's disease and summarizes recent research advances in the treatment of AD by traditional Chinese medicine and its active components through intervention in this pathway, aiming to provide novel theoretical evidence and strategic references for AD prevention and treatment.
