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28 September 2026,Issue 9 Previous Issue   
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Innovative research team achievement column
Frontier review
Basic research
Clinical research
Public health
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Innovative research team achievement column

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Study on the pro-tumorigenic function of N-acetyltransferase 10 in Ewing sarcoma and its upstream and downstream regulatory molecular mechanisms Huang Xinyu, Mo Jialin, Tang Yujie 2026, 46(9):  1155-1168.  doi: 10.3969/j.issn.1674-8115.2026.09.001 Abstract ( 7 )   HTML ( 1 )   PDF (25323KB) ( 13 )   Objective ·To investigate the expression, function, and regulatory mechanisms of N-acetyltransferase 10 (NAT10) in Ewing sarcoma (EwS). Methods ·Transcriptomic and epigenomic data from the Gene Expression Omnibus (GEO), the Genotype-Tissue Expression (GTEx), the Database of Genotypes and Phenotypes (dbGaP), and the Cancer Cell Line Encyclopedia (CCLE), as well as in-house EwS tumor tissues and cell models, control normal muscle tissues, and human mesenchymal stem cell (HMSC) models, were integrated to analyze the transcriptional expression and epigenetic regulatory mechanisms of NAT10 and related genes. Validation was performed in cell models using reverse transcription quantitative real-time PCR (RT-qPCR), Western blotting (WB), and dual-luciferase reporter assay (DLR). The dependency of EwS cell growth on NAT10 was analyzed using the Cancer Dependency Map (DepMap) database and in-house clustered regularly interspaced short palindromic repeats-associated protein 9 (CRISPR-Cas9) library screening data, and further validated by RNA interference (RNAi) experiments. N4-acetylcytidine sequencing (ac4C-seq) data from A673 cells and RNA sequencing (RNA-seq) data following NAT10 knockdown were integrated to screen for ac4C-modified target genes regulated by NAT10. Gene Ontology (GO) enrichment analysis was performed on these targets, followed by functional validation of the enriched malignant features, and subsequently an integrative screening was conducted to identify key target genes involved in regulating tumor growth. Results ·Analyses of the GEO, GTEx, dbGaP, and CCLE database, together with RT-qPCR and WB results, revealed that NAT10 was significantly upregulated at both the mRNA and protein levels in EwS tumor tissues and cell models. DLR results demonstrated that the EWS RNA-binding protein 1 and Friend leukemia integration site 1 transcription factor fusion protein (EWS-FLI1) promotes NAT10 transcriptional activation by binding to and driving the activity of the EwS-specific NAT10 gene enhancer. Gene dependency analysis and functional assays showed that NAT10 exhibited strong growth dependency across multiple EwS cell models, and knockdown of NAT10 significantly inhibited the in vitro growth and colony formation of EwS cells. Mechanistic investigation of downstream pro-tumorigenic pathways revealed that ac4C-modified target genes regulated by NAT10 in EwS cell models were significantly enriched in biological processes including the cell cycle, proliferation, migration, and the unfolded protein response (UPR). Knockdown of NAT10 induced cell cycle arrest, reduced proliferation, impaired migration, and enhanced apoptosis. Among these, inner centromere protein (INCENP), kinesin family member 11 (KIF11), kinesin family member 14 (KIF14), minichromosome maintenance complex component 5 (MCM5), non-SMC condensin Ⅰ complex subunit G2 (NCAPG2), DNA polymerase δ1, catalytic subunit (POLD1), and DNA topoisomerase Ⅱα (TOP2A) were identified as key target genes through which NAT10-catalyzed ac4C modification promotes mRNA stability, thereby regulating cell cycle and proliferation. Conclusion ·This study preliminarily reveals the pro-tumorigenic role and underlying mechanisms of the “EWS-FLI1-NAT10 modifier enzyme-ac4C-modified key target genes” regulatory network in EwS. Figures and Tables | References | Related Articles | Metrics

Frontier review

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3D printing biomimetic periosteum: from structural substitution to functional integration Yu Meixuan, Sun Lin, Fu Jingke, Hao Yongqiang, Dai Kerong 2026, 46(9):  1169-1178.  doi: 10.3969/j.issn.1674-8115.2026.09.002 Abstract ( 19 )   HTML ( 1 )   PDF (2439KB) ( 31 )   The periosteum, as the central regulatory barrier for bone regeneration, directs bone repair by supplying osteogenic progenitor cells and diverse bioactive factors; its functional loss is a key reason for the failure of bone defect repair. Conventional periosteal reconstruction methods are markedly limited in clinical practice because they cannot precisely recapitulate the periosteum′s refined hierarchical architecture and multifaceted biological functions. Leveraging its unique strengths in patient-specific high-fidelity shaping, tightly controlled multiscale microarchitectures, and spatiotemporally ordered delivery of bioactive components, 3D printing offers a transformative solution for constructing biomimetic periosteum. Both mainstream clinical bone repair therapies and traditional periosteum fabrication techniques have inherent drawbacks and fail to address the clinical challenge of large bone defect repair effectively. With the advancement of precision regenerative medicine, the developmental philosophy of biomimetic periosteum has shifted from simple structural substitution based on simple defect filling to a new stage of functional integration, characterized by multidimensional physiological simulation and dynamic modulation of the repair microenvironment. This review systematically outlines the periosteum′s core biological functions and clinical needs, focuses on key construction strategies and multi-technology integration pathways for 3D-printed biomimetic periosteum, provides an in-depth analysis of current technical bottlenecks, and envisions an artificial intelligence-driven shift of periosteal reconstruction toward a paradigm of personalized, precision repair. The goal is to provide a theoretical basis and practical reference for the clinical translation of therapies for large bone defects and the development of precision medicine. Figures and Tables | References | Related Articles | Metrics

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Roles of extracellular vesicles in pathogenesis and treatment of osteoporosis and their functionalized delivery strategies Zhang Xin, Li Dan, Yang Ju, Deng Kelei, Cao Hong 2026, 46(9):  1179-1187.  doi: 10.3969/j.issn.1674-8115.2026.09.003 Abstract ( 12 )   HTML ( 1 )   PDF (1523KB) ( 10 )   Osteoporosis is a systemic skeletal disease characterized by reduced bone mass and disrupted bone microarchitecture, representing a major cause of disability and diminished quality of life among middle-aged and older adults while imposing a substantial socioeconomic burden worldwide. Extracellular vesicles (EVs) are membrane-bound nanoparticles that mediate intercellular communication by transferring proteins, lipids, and nucleic acids between cells. In the skeletal system, EVs participate in multiple stages of bone remodeling by promoting osteogenic differentiation, inhibiting osteoclast formation and function, and regulating angiogenesis, making them promising candidates for osteoporosis therapy. Nevertheless, the therapeutic application of native EVs is restricted by rapid clearance after administration and limited bone-targeting efficiency. Recent advances in EV engineering have provided new opportunities to address these limitations. This review summarizes the biological characteristics of EVs and discusses their regulatory roles in the bone microenvironment. It further focuses on emerging strategies for EV-based osteoporosis therapy, including donor-cell preconditioning to improve the biological activity of native EVs, cargo engineering and surface modification to enhance therapeutic efficacy and bone-targeting capability, and the combination of engineered EVs with biomaterial platforms such as hydrogels and three-dimensional printed scaffolds to construct delivery systems that enable localized retention, controlled release, and synergistic tissue repair. Finally, the current challenges associated with EV-based therapeutics and the prospects for their clinical translation are discussed. This review provides a theoretical basis and research perspective for the development of effective and safe cell-free bone regeneration therapies. Figures and Tables | References | Related Articles | Metrics

Basic research

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Effects of extracellular vesicles derived from Lactobacillus rhamnosus GG on the biological properties of MC3T3-E1 cells Ye Zhiyun, Zhou Yining, Chen Huiwen, He Zhiyan, Zhou Wei, Song Zhongchen 2026, 46(9):  1188-1198.  doi: 10.3969/j.issn.1674-8115.2026.09.004 Abstract ( 8 )   HTML ( 0 )   PDF (23217KB) ( 8 )   Objective ·To observe the effects of extracellular vesicles derived from Lactobacillus rhamnosus GG (L.GG-EVs) on the proliferation, migration, and osteogenic differentiation of mouse embryonic osteoblast precursor cell line (MC3T3-E1). Methods ·After L.GG-EVs were extracted by ultracentrifugation, the morphology of L.GG-EVs was observed by transmission electron microscope (TEM), and the particle size distribution of L.GG-EVs was measured by ZETAView nanoparticle size tracker. After SDS-PAGE, Coomassie brilliant blue R-250 staining was used to observe the protein expression of L.GG-EVs. The effect of L.GG-EVs(12.5, 25, 50, and 100 μg/mL) on the viability of MC3T3-E1 cells after 1, 3, 5, and 7 d of co-culture was evaluated by a cell counting kit-8 (CCK-8) assay. The wound-healing assay was used to detect the effect of L.GG-EVs (50 and 100 μg/mL) on the migration ability of MC3T3-E1 cells after 6 and 24 h of co-culture. Alkaline phosphatase (ALP) staining was used to detect the effect of L.GG-EVs (50 and 100 μg/mL) on the ALP expression in MC3T3-E1 cells following 7 d of co-culture. Alizarin red S staining was used to detect the effect of L.GG-EVs (50 and 100 μg/mL) on calcium nodule formation in MC3T3-E1 cells after 21 d of co-culture. Quantitative real-time PCR (qPCR) was used to detect the mRNA expression of osteogenic genes, including Runt-related transcription factor 2 (Runx2), osteopontin (Opn), and bone morphogenetic protein 2 (Bmp2), in MC3T3-E1 cells after 7 d of co-culture with L.GG-EVs (50 and 100 μg/mL). A rat alveolar bone defect model was constructed and divided into the surgical group (SUR group), the pure hydrogel group [gelatin methacryloyl (GelMA) group], and the hydrogel group loaded with L.GG-EVs (GelMA-L.GG-EVs group). The alveolar bone regeneration was detected by Micro-CT. Results ·L.GG-EVs were spherical, double-layered membrane vesicles, with diameters ranging from 20 to 500 nm and an average diameter of approximately 161 nm, showing a normal distribution. A protein band was observed at a relative molecular mass of 42 000. CCK-8 assay showed that compared with the CON group, L.GG-EVs at 50 and 100 μg/mL significantly promoted the proliferation of MC3T3-E1 cells after co-culture for 3, 5, and 7 d (all P<0.05). The wound-healing assay indicated that L.GG-EVs (50 and 100 μg/mL) accelerated the migration of MC3T3-E1 cells compared with the Ctrl group (all P<0.05). After 7 d of co-culture, L.GG-EVs (50 and 100 μg/mL) markedly intensified ALP staining in MC3T3-E1 cells (both P<0.05). After 21 d of co-culture, L.GG-EVs (50 and 100 μg/mL) significantly increased calcium nodule formation in MC3T3-E1 cells (both P=0.001). After 7 d of co-culture, 50 μg/mL L.GG-EVs up-regulated the expression of Opn and Bmp2 mRNA (both P<0.05), and 100 μg/mL L.GG-EVs up-regulated the expression of Runx2, Opn, and Bmp2 mRNA (all P<0.05). In the rat alveolar bone defect model, L.GG-EVs significantly promoted alveolar bone regeneration (all P<0.05). Conclusion ·L.GG-EVs can promote the proliferation, migration, and osteogenic differentiation of MC3T3-E1 cells, and have the potential to facilitate bone tissue regeneration. Figures and Tables | References | Related Articles | Metrics

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TRPM4-mediated sodium dysregulation drives acute renal tubular injury Wang Jialing, Wang Yanzhe, Miao Naijun, Wang Xiaoxia 2026, 46(9):  1199-1211.  doi: 10.3969/j.issn.1674-8115.2026.09.005 Abstract ( 10 )   HTML ( 0 )   PDF (20482KB) ( 9 )   Objective ·To investigate dynamic changes in the expression of transient receptor potential melastatin 4 (TRPM4) in acute kidney injury (AKI), its associations with renal tubular epithelial cell death and inflammatory responses, and the protective effects of TRPM4 inhibition in vivo or small interfering RNA (siRNA)-mediated Trpm4 knockdown in vitro on renal tubular injury. Methods ·Murine ischemia-reperfusion (IR) and cisplatin-induced AKI models were established, respectively. Tubular injury was evaluated by hematoxylin-eosin (H-E) staining, and renal TRPM4 expression was assessed. In the IR model, mice received the TRPM4 inhibitor glibenclamide. Western blotting was performed to quantify renal injury markers [T cell immunoglobulin and mucin domain-containing protein 1 (TIM-1) and neutrophil gelatinase-associated lipocalin (NGAL)] and inflammasome pathway components [nucleotide-binding domain leucine‑rich repeat and pyrin domain‑containing receptor 3 (NLRP3), cleaved caspase-1 (c-CASP-1), and interleukin-18 (IL-18)]. In vitro, a human proximal tubular epithelial cell line (PTEC) and a mouse renal tubular epithelial cell line (TCMK-1) were subjected to injury stimuli including cisplatin, hydrogen peroxide (H2O2), and hypoxia/reoxygenation (H/R), followed by assessment of TRPM4 and injury-associated signaling. Quantitative PCR (qPCR) was used to examine Trpm4 and ninjurin 1 (Ninj1) transcriptional responses across a cisplatin dose gradient. In TCMK-1 cells, Trpm4 was silenced using siRNA; plasma membrane injury and intracellular Na⁺ load were quantified by propidium iodide (PI) staining and the CoroNa-AM probe using flow cytometry. RNA sequencing was conducted in siRNA-Trpm4-treated cells, with Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis performed to characterize transcriptional programs impacted by Trpm4 knockdown. Results ·① Both AKI models exhibited marked tubular injury accompanied by significant upregulation of TRPM4 in renal tubular epithelial cells. ② Glibenclamide treatment significantly reduced serum creatinine (sCr) and blood urea nitrogen (BUN) levels, alleviated IR-induced tubular damage, decreased TIM-1 and NGAL levels, and suppressed activation of the NLRP3-CASP-1-IL-18 axis. ③ In vitro exposure to cisplatin or H/R induced TRPM4 upregulation and enhanced injury-associated signaling, while increasing cisplatin doses further elevated Trpm4 and Ninj1 mRNA levels. ④ Trpm4 knockdown reduced the proportion of PI-positive cells after cisplatin challenge and significantly decreased CoroNa-AM signals [including the proportion of CoroNa-AMhigh cells and geometric mean fluorescence intensity (GeoMFI)] within the PI⁻ gate, indicating attenuation of intracellular Na⁺ overload. Conclusion ·TRPM4-mediated sodium dysregulation is a critical driver of renal tubular injury, and intracellular Na⁺ overload is involved in the amplification of NLRP3 inflammasome activation. Targeting TRPM4 may constitute a key brake on the injury-inflammation cycle in AKI. Figures and Tables | References | Related Articles | Metrics

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Design and functional characterization of VEGFA-targeted binding proteins Lu Yue, Yan Weikang, Liu Yingbin, He Yongning 2026, 46(9):  1212-1221.  doi: 10.3969/j.issn.1674-8115.2026.09.006 Abstract ( 8 )   HTML ( 1 )   PDF (14127KB) ( 9 )   Objective ·To construct vascular endothelial growth factor A (VEGFA)-targeted binding proteins by using a de novo protein design strategy, and verify the effects of these proteins on VEGFA-induced biological activities in human umbilical vein endothelial cells (HUVECs). Methods ·A multi-algorithm workflow integrating Rosetta RifDock, FastDesign, and ProteinMPNN was used to design VEGFA-targeted binding proteins. The structural plausibility of the binding proteins and their interactions with VEGFA were assessed using the AlphaFold prediction model. Yeast surface display combined with dual-fluorescence-activated cell sorting was then used to screen specific VEGFA-targeted binding proteins, which were subsequently expressed and purified using the E. coli expression system. The binding affinities between the binding proteins and VEGFA were measured using bio-layer interferometry (BLI). Finally, cell counting kit-8 (CCK-8) assays, Annexin Ⅴ/PI double-staining, Western blotting, scratch wound healing assays, and in vitro tube formation assays were performed to evaluate the effects of the binding protein on VEGFA-induced biological activities in HUVECs. Results ·VEGFA-targeted binding proteins were successfully designed and a candidate binding protein library was constructed. One protein, minibinder-3 (MB3), with moderate affinity for VEGFA was obtained after yeast surface display screening and BLI measurement. Subsequent in vitro experiments demonstrated that MB3 inhibited VEGFA-induced survival, resistance to apoptosis, migration, and angiogenesis, and also reduced the VEGFA-induced phosphorylation of protein kinase B (AKT) and extracellular signal-regulated kinase (ERK), which are downstream signaling molecules of vascular endothelial growth factor receptor (VEGFR) (all P<0.05). Conclusion ·Based on the de novo protein design workflow, MB3, a VEGFA-binding protein with moderate affinity, was obtained. In vitro experiments confirmed that MB3 inhibited VEGFA-mediated HUVEC functions and related signaling pathways, thereby demonstrating the feasibility of the design workflow for developing anti-VEGFA artificial proteins and providing new insights into tumor vascular-targeted therapy. Figures and Tables | References | Related Articles | Metrics

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Mechanism of neutrophil extracellular traps in promoting post-injury airway fibrosis Huang Danqing, Yin Yuting, Xu Li, Guo Shuliang 2026, 46(9):  1222-1232.  doi: 10.3969/j.issn.1674-8115.2026.09.007 Abstract ( 5 )   HTML ( 1 )   PDF (22703KB) ( 9 )   Objective ·To investigate the role of neutrophil extracellular traps (NETs) in aberrant repair following airway injury and the underlying mechanisms. Methods ·Patients with airway stenosis caused by granulation tissue or scarring and healthy volunteers were enrolled from The First Affiliated Hospital of Chongqing Medical University between April and October 2024. Peripheral blood, airway granulation tissue, and paracancerous normal airway tissue were collected. The levels of NETs markers—myeloperoxidase (MPO), citrullinated histone H3 (CitH3), and extracellular free double-stranded DNA (dsDNA)—in serum and tissues were detected using enzyme-linked immunosorbent assay (ELISA), immunofluorescence staining, and a dsDNA quantification kit. After stimulation of airway fibroblasts with NETs, the expression levels of α-smooth muscle actin (α-SMA) and collagen Ⅰ (COL1) were examined by real-time quantitative PCR (qPCR), Western blotting, and immunofluorescence staining. Cell proliferation and migration were evaluated using the Cell Counting Kit-8 (CCK-8) assay and Transwell migration assay. The Toll-like receptor 4 (Tlr4) gene in rat airway fibroblasts was knocked down using small interfering RNA (siRNA), and the above indices, as well as phosphorylation levels of SMAD family member 2 (SMAD2), were assessed. A rat airway scraping injury model was established. A diphenyleneiodonium chloride (DPI) pretreatment group and a control group were additionally included. Serum MPO and interleukin-8 (IL-8) levels were measured by ELISA. The expression levels of α-SMA and COL1 in airway tissue were detected by qPCR and Western blotting. Airway tissue structure and the localization and expression of CitH3 were observed using Masson staining and immunofluorescence staining, respectively. Results ·① Patients with airway stenosis exhibited higher levels of serum NETs markers than healthy controls, and increased CitH3 was observed in the granulation tissue. ② After stimulation with NETs, fibroblasts showed elevated expression of α-SMA and COL1, enhanced proliferation and migration abilities, and upregulated SMAD2 phosphorylation; these effects were inhibited by deoxyribonuclease Ⅰ (DNaseⅠ). ③ Knockdown of Tlr4 suppressed the effects induced by NETs. ④ In the rat airway scraping injury model, serum MPO and IL-8 levels were significantly elevated, airway structure was damaged with severe collagen deposition, and the expression levels of α-SMA, COL1, and CitH3 in the airway tissue were increased compared with those in the control group; DPI pretreatment partially attenuated these changes. Conclusion ·NETs may activate fibroblasts via the TLR4/SMAD2 pathway following airway injury, promoting cell migration, proliferation, and extracellular matrix deposition, thereby contributing to airway fibrosis. Figures and Tables | References | Related Articles | Metrics

Clinical research

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Effect of vaginal microbiota dysbiosis on live birth outcomes in patients with cervical incompetence Li Xue, Zhou Ling, Li Ji, Liu Juanjuan, Zhang Hong 2026, 46(9):  1233-1241.  doi: 10.3969/j.issn.1674-8115.2026.09.008 Abstract ( 5 )   HTML ( 1 )   PDF (1046KB) ( 10 )   Objective ·To investigate the impact of vaginal microbiota dysbiosis on pregnancy outcomes in patients with cervical incompetence using stabilized inverse probability of treatment weighting (sIPTW) and Logistic regression. Methods ·A retrospective analysis was conducted on the clinical data of 756 patients with cervical incompetence who visited the Department of Obstetrics and Gynecology, The Second Affiliated Hospital of Soochow University, between January 2013 and December 2023. Based on the results of vaginal secretion culture in the second trimester, the patients were divided into a microbiota dysbiosis group (pathogenic bacteria were detected and lactobacilli were absent or significantly reduced) and a normal microbiota group (lactobacilli were the dominant bacteria and no pathogenic bacteria were detected). The sIPTW method was employed to balance variables such as parity, gravidity, number of late miscarriages, and cervical length. The differences in pregnancy outcomes between the vaginal microbiota dysbiosis group and the normal microbiota group before and after sIPTW were compared, including the full-term delivery rate, live birth rate, miscarriage rate, preterm birth rate, neonatal birth weight, and gestational age at delivery. Univariate conditional Logistic regression analysis was conducted to investigate the influencing factors of live birth outcomes. Results ·A total of 756 patients with cervical insufficiency were included, including 216 cases in the microbiota dysbiosis group and 540 cases in the normal microbiota group. Prior to sIPTW, the vaginal microbiota dysbiosis group and the normal microbiota group exhibited significant differences in body mass index (BMI), cervical length, cervical internal os dilation, and whether cervical cerclage was performed (P<0.05). After sIPTW, no statistically significant differences were observed in clinical data between the two groups. Before and after sIPTW, the full-term delivery rate and live birth rate in the vaginal microbiota dysbiosis group were significantly lower than those in the normal microbiota group. The miscarriage rate and preterm birth rate were significantly higher in the microbiota dysbiosis group, while neonatal birth weight and gestational age at delivery were significantly lower (all P<0.05). Univariate conditional Logistic regression analysis showed that cervical cerclage (OR=1.090, P<0.010), abnormal physical examination (OR=0.888, P<0.001), vaginal microbiota dysbiosis (OR=0.932, P=0.003), and no history of late miscarriage (OR=0.827, P=0.008) were major factors influencing live birth outcomes. Conclusion ·Vaginal microbiota dysbiosis significantly reduces the live birth rate and full-term delivery rate in patients with cervical incompetence, and increases the risk of miscarriage and premature birth. Figures and Tables | References | Related Articles | Metrics

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Predictive value of combined biomarkers for early postoperative risk following the modified extended Morrow procedure for hypertrophic obstructive cardiomyopathy Shi Yaqiang, Bai Xiaoyu, Jiang Yongjie, Liu Jun, Qi Quan 2026, 46(9):  1242-1251.  doi: 10.3969/j.issn.1674-8115.2026.09.009 Abstract ( 6 )   HTML ( 1 )   PDF (1506KB) ( 11 )   Objective ·To investigate the predictive value of the combination of preoperative D-dimer levels and the N-terminal pro-B-type natriuretic peptide (NT-proBNP) ratio for early major adverse cardiovascular events (MACE) following the modified extended Morrow procedure in patients with hypertrophic obstructive cardiomyopathy (HOCM). Methods ·Patients with HOCM who underwent the modified extended Morrow procedure in the First Hospital of Lanzhou University between January 2015 and June 2025 were enrolled. Baseline data and perioperative data were collected for all patients. Baseline data included demographic indicators, symptoms and functional status, medical history, preoperative levels of blood biomarkers (D-dimer and NT-proBNP, with the latter calculated as an age- and sex-adjusted ratio), and preoperative echocardiographic parameters. The primary outcome was MACE within 30 days postoperatively. Four predictive models were constructed using Logistic regression: a model based on clinical baseline variables, a model combining clinical baseline variables with the NT-proBNP ratio, a model combining clinical baseline variables with D-dimer levels, and a model combining clinical baseline variables with two biomarkers (the ratio of NT-proBNP and the levels of D-dimer). Model performance was evaluated using the area under the receiver operating characteristic curve (AUC), net reclassification improvement (NRI), and integrated discrimination improvement (IDI). Calibration accuracy, prediction accuracy, and clinical applicability were assessed using calibration curves, the Brier score, and decision curve analysis (DCA). Risk stratification of patients was performed using the optimal cut-off values for the NT-proBNP ratio and D-dimer, and perioperative risks and clinical outcomes were compared. Results ·Among the 83 patients included in the final analysis, 21 (25.30%) experienced MACE within 30 days postoperatively. The combined dual-biomarker model demonstrated the best predictive performance, with an AUC of 0.935, superior to the model based on clinical baseline variables and to any model combining clinical baseline variables with a single biomarker. Compared to the clinical baseline variable model, the combined dual-biomarker model showed an NRI of 1.390 and an IDI of 0.366 (both P<0.001). It also exhibited the best calibration (Hosmer-Lemeshow test P=0.767, Brier score 0.080), and DCA indicated the highest net benefit across a wide range of threshold probabilities. Patients were stratified into three groups (“dual-low”, “single-high”, and “dual-high”) based on the optimal cut-off values of the NT-proBNP ratio and D-dimer, revealing a significant risk gradient in MACE incidence. Furthermore, patients in the “dual-high” group had a more complex perioperative course, with significantly longer cardiopulmonary bypass time, aortic cross-clamp time, postoperative mechanical ventilation time, and postoperative hospital stay compared to those in the “dual-low” group (all P<0.05). Conclusion ·The preoperative combination of an age- and sex-adjusted NT-proBNP ratio and D-dimer levels can be used to construct an efficient and robust risk prediction model for early postoperative MACE. This strategy demonstrates excellent performance in discrimination, calibration, and clinical applicability, effectively identifying patients at extremely high risk and providing an objective basis for individualised perioperative management. Figures and Tables | References | Related Articles | Metrics

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Multimodal functional magnetic resonance imaging combined with Ki-67 index for assessing pathological typing of head and neck rhabdomyosarcoma Xiao Hua, Zhang Zimin, Jiang Mengda, Guo Jiuhong 2026, 46(9):  1252-1259.  doi: 10.3969/j.issn.1674-8115.2026.09.010 Abstract ( 5 )   HTML ( 1 )   PDF (19092KB) ( 11 )   Objective ·To investigate the clinical value of multimodal functional MRI combined with the cell proliferation marker Ki‑67 in the preoperative pathological classification of head and neck rhabdomyosarcoma (RMS), based on the apparent diffusion coefficient (ADC) derived from diffusion‑weighted imaging (DWI) and time‑intensity curve (TIC) types obtained from dynamic contrast‑enhanced magnetic resonance imaging (DCE‑MRI). Methods ·Patients diagnosed with head and neck RMS who underwent surgical resection at Shanghai Ninth People′s Hospital, Shanghai Jiao Tong University School of Medicine between January 2015 and March 2026 were retrospectively enrolled. Demographic, clinical, and imaging data of all patients were collected. According to postoperative pathological types, patients were divided into three groups: embryonal RMS (n=21), alveolar RMS (n=14), and spindle cell/sclerosing RMS (n=15). Intergroup differences in multimodal functional MRI parameters (ADC values and TIC types), age, sex, and Ki‑67 index were analyzed, and the correlation between ADC values and Ki‑67 index was analyzed. Intraclass correlation coefficient (ICC) and Cohen′s κ coefficient were calculated to assess the inter‑ and intra-reader consistency of multimodal functional MRI parameters. Multinomial Logistic regression was performed to evaluate the predictive value of ADC values, TIC types, and Ki-67 index for the three pathological types, and a confusion matrix was used to assess model performance. Results ·Both ADC values and TIC types exhibited good inter‑reader and intra‑reader consistency. Statistically significant differences were observed among the three RMS pathological types in ADC values (P<0.001), Ki‑67 index (P<0.001), and TIC types (P=0.031). Spearman correlation analysis revealed a significant negative correlation between ADC value and Ki‑67 index (r=-0.362, P=0.010). Multinomial Logistic regression demonstrated that, using the embryonal RMS as the reference, the ADC value was independently associated with both the alveolar RMS and the spindle cell/sclerosing RMS, while the Ki-67 index was independently associated with the spindle cell/sclerosing RMS. The predictive accuracy of the model for embryonal, alveolar, and spindle cell/sclerosing RMS was 66.7%, 57.1%, and 93.3%, respectively, with an overall predictive accuracy of 72.0%. Conclusion ·The combination of multimodal functional MRI and Ki‑67 index enables effective prediction of pathological types of head and neck RMS, and has crucial clinical value for preoperative risk stratification and prognostic assessment. Figures and Tables | References | Related Articles | Metrics

Public health

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Burden and trends of biliary tract cancer in five Northeast Asian countries, 1990-2021 Dong Wenjun, Zhao Jingwei, Zhu Jiayun, Gong Wei, Yang Ziyi 2026, 46(9):  1260-1271.  doi: 10.3969/j.issn.1674-8115.2026.09.011 Abstract ( 10 )   HTML ( 0 )   PDF (3231KB) ( 20 )   Objective ·To evaluate the epidemiological characteristics and health inequalities of biliary tract cancer in five Northeast Asian countries (China, Japan, Republic of Korea, Democratic People′s Republic of Korea, and Mongolia) from 1990 to 2021, and to project disease burden trends through 2035, providing evidence for regional prevention and control strategies. Methods ·Data were obtained from the Global Burden of Disease Study 2021 (GBD 2021). Incidence, mortality, disability-adjusted life years (DALYs), sociodemographic index (SDI), and estimated annual percentage change (EAPC) for biliary tract cancer from 1990 to 2021 were analyzed. A Bayesian age-period-cohort (BAPC) model was applied to predict changes in disease burden from 2022 to 2035. Results ·In 2021, there were 88 861 new cases, 66 107 deaths, and 1 292 121 person-year (DALYs) attributable to biliary tract cancer in the five countries. From 1990 to 2021, the age-standardized incidence rate (ASIR) increased in China but declined in the other four countries, while the age-standardized mortality rate (ASMR) and age-standardized DALY rate (ASDR) declined in all five countries; the Republic of Korea showed EAPCs of -2.18% for ASMR and -2.71% for ASDR. Nevertheless, the absolute burden in the 5 countries continued to rise, with China showing the most pronounced increase. Males and older adults were the main high-burden groups, with incidence and mortality peaking in the 70‒74 and 75‒79 age groups, respectively. The burden of BTC remained heterogeneous across countries with different SDI levels, while between-country disparities narrowed over time and health inequalities decreased. Population aging was the dominant driver of burden growth, and in China, it contributed 53.21% of the increase in incidence, 81.31% in mortality, and 82.32% in DALYs. The BAPC model projected that by 2035, new cases, deaths, and DALYs would reach 133 706, 89 852, and 1 586 879, respectively, representing increases of 50.5%, 35.9%, and 22.8% compared with 2021. Conclusion ·From 1990 to 2021, the burden of biliary tract cancer in five Northeast Asian countries generally increased, with a heavier burden in males and older age groups. Projections suggest that the numbers of incident cases, deaths, and DALYs will continue to rise through 2035. Population aging is the primary driver of this growth, with China contributing the most. Tailored, SDI-stratified prevention and control strategies, including strengthening high-risk screening, early diagnosis, standardized treatment, and surveillance/registry quality, are needed to reduce the future burden. Figures and Tables | References | Related Articles | Metrics

Review

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Research progress in the roles and mechanisms of lysine crotonylation in diseases He Zhilin, Xu Lin, Li Yan, Wang Linzheng, Chen Wei, Li Yanbin 2026, 46(9):  1272-1282.  doi: 10.3969/j.issn.1674-8115.2026.09.012 Abstract ( 3 )   HTML ( 0 )   PDF (3348KB) ( 8 )   Lysine crotonylation (Kcr) is a novel post-translational modification of proteins that plays a critical regulatory role in the occurrence and development of various diseases, and has become a significant research hotspot in the field of disease mechanisms in recent years. This review summarizes the latest research progress in Kcr in diseases of the nervous, cardiovascular, digestive, urinary, and respiratory systems, as well as metabolic and autoimmune diseases, comprehensively presenting the range of pathophysiological roles of Kcr modification. It focuses on summarizing the molecular mechanisms by which Kcr dynamically regulates gene transcription and cellular metabolism through the "writer-eraser-reader" enzyme system. The three components act synergistically to dynamically regulate gene transcription efficiency and cellular metabolic homeostasis. Additionally, this article systematically clarifies the mechanisms by which Kcr participates in disease progression by affecting chromatin status, metabolic reprogramming, and signaling pathways. This review aims to summarize existing findings and unresolved issues, provide a theoretical basis for the prevention, diagnosis, and treatment of related diseases, and offer insights into the clinical translation of Kcr as a potential drug target. Figures and Tables | References | Related Articles | Metrics

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Postoperative complications in the treatment of upper urinary tract stones with flexible ureteroscopic lithotripsy: from preoperative assessment to postoperative management Liu Junchen, Liu Min 2026, 46(9):  1283-1289.  doi: 10.3969/j.issn.1674-8115.2026.09.013 Abstract ( 7 )   HTML ( 0 )   PDF (1034KB) ( 13 )   Flexible ureteroscopic lithotripsy (fURS-L) has become the important surgical technique for the treatment of small ureteral and renal calculi with a diameter of ≤2 cm. With the continuous advancement of endoscopic techniques, fURS-L is expected to emerge as the primary modality for upper urinary tract calculi management in the future due to its minimal invasiveness, high safety, and accessibility. Nevertheless, its postoperative complications, such as infection, ureteral stricture, stent-related discomfort, and more severe urosepsis, remain major clinical challenges that restrict improvements in its therapeutic efficacy and hinder its widespread clinical application. This review integrates relevant academic literature to elaborate on recent advances in surgical techniques and equipment innovations of fURS-L (including intelligent pressure control, negative-pressure suction systems, and novel laser applications) and their impacts on the prevention and management of complications. It analyzes preoperative risk predictors of postoperative complications, which encompass patients′ physical conditions, stone burden, and infectious status, and briefly discusses the classification and updated management strategies of postoperative complications. Furthermore, future research directions are proposed, including establishing a standardized reporting system for postoperative complications, refining prediction models based on artificial intelligence and biomarkers to enable early identification and intervention for high-risk patients, evaluating the cost-effectiveness and environmental impacts of disposable flexible ureteroscopes, and optimizing application strategies of advanced technologies in complex clinical cases. References | Related Articles | Metrics

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Research advances in role of histone deacetylase 4/5 in anxiety disorders Huo Sirui, Zhu Yongchuan 2026, 46(9):  1290-1298.  doi: 10.3969/j.issn.1674-8115.2026.09.014 Abstract ( 5 )   HTML ( 0 )   PDF (5326KB) ( 9 )   Histone deacetylase 4/5 (HDAC4/5) mediate epigenetic regulation in stress-related disorders. Class Ⅱa HDACs feature signal-dependent shuttling between the nucleus and cytoplasm. By assembling complexes with transcription factors or co-repressors, HDAC4/5 regulate the transcription of stress-responsive genes and synaptic plasticity, thereby modulating anxiety-like behaviors; they additionally regulate the threshold for synaptic plasticity within core limbic circuits including the hippocampus and amygdala. This cascade of physiological and biochemical events is closely associated with modifiable psychological processes such as fear extinction. Serving as modulators of the basal plastic state of neural circuits, HDAC4/5 lay a theoretical foundation for time-windowed interventions combining exposure therapy and behavioral training. Nevertheless, their clinical translation remains challenged by factors including interspecies differences and pathological heterogeneity. Focusing on the molecular characteristics, signal-dependent regulation, circuit-level effects, and psychology-related evidence of HDAC4/5, the present review integrates causal evidence and circuit-level findings from animal models of distinct anxiety disorder subtypes, and summarizes recent advances in basic and clinical research. Figures and Tables | References | Related Articles | Metrics

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Anatomical comparison of venous access options during cardiovascular electronic device implantation Fan Yichen, Zhuang Ruoxi, Qiu Zhaohui, Han Dan, Li Yan 2026, 46(9):  1299-1306.  doi: 10.3969/j.issn.1674-8115.2026.09.015 Abstract ( 5 )   HTML ( 0 )   PDF (3548KB) ( 9 )   Cardiovascular implantable electronic devices (CIEDs) serve as crucial tools for the treatment and prevention of arrhythmia-related diseases, and related technologies are currently developing rapidly. Common access routes for clinical CIED implantation include subclavian vein, cephalic vein, and axillary vein. The selection of surgical access routes necessitates a comprehensive evaluation of venous anatomical characteristics, the complexity of the puncture procedure, and the long-term safety and efficacy of the device. In clinical practice, surgeons should pay particular attention to the choice of venous access and its association with puncture success rates and potential complications. In addition, the application of imaging guidance techniques such as X-ray and ultrasound enables surgeons to identify the course of the veins and their adjacent structures, reduce the risk of puncture-related complications, and further improve the surgical success rates. This article, based on the anatomical features of the veins and clinical experience, summarizes common anatomical variations and associated risks of the three veins, as well as new imaging-guided techniques. It also provides anatomical references for clinical CIED implantation. Figures and Tables | References | Related Articles | Metrics

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Whole-body bone scintigraphy reveals extensive metastatic calcification secondary to hyperparathyroidism: a case report Sheng Shiwei, Luo Quanyong 2026, 46(9):  1307-1312.  doi: 10.3969/j.issn.1674-8115.2026.09.016 Abstract ( 5 )   HTML ( 0 )   PDF (1947KB) ( 9 )   This paper reports one case of a 46-year-old male patient with a 6-year history of stage 5 chronic kidney disease who had been undergoing long-term peritoneal dialysis and was admitted for generalized pain and limited movement following a minor fall. Laboratory examinations revealed severe hyperphosphatemia (2.85 mmol/L), hypocalcemia (2.04 mmol/L), and markedly elevated parathyroid hormone levels (356 pg/mL). Whole-body bone scintigraphy combined with single-photon emission computed tomography (SPECT)/CT showed extensive abnormal radiotracer accumulation in the soft tissues around the bilateral shoulder joints, hip joints, and pubic symphysis, which precisely matched the calcified masses shown on CT. Typical signs of metabolic bone disease and multiple acute fractures corresponding to traumatic injury sites were also detected. The patient was finally diagnosed with renal osteodystrophy accompanied by extensive metastatic calcification. This case suggests that whole-body bone scintigraphy combined with SPECT/CT is of great value in the comprehensive evaluation of patients with chronic kidney disease. As a one-stop imaging examination, it can simultaneously detect soft tissue calcification, evaluate the type and severity of metabolic bone disease, identify occult fractures, and provide comprehensive evidence for clinical diagnosis and treatment. Figures and Tables | References | Related Articles | Metrics