Table of Content

28 September 2025, Volume 45 Issue 9 Previous Issue   
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Guidelines and consensus
Frontier review
Basic research
Clinical research
Techniques and methods
Review
Case report


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Guidelines and consensus

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Chinese expert consensus on ultrasound-guided nerve blocks in children (2025 edition) Writing Group of Chinese Expert Consensus on Ultrasound-Guided Pediatric Nerve Blocks in Children (2025 edition) 2025, 45 (9):  1079-1098.  doi: 10.3969/j.issn.1674-8115.2025.09.001 Abstract ( 352 )   HTML ( 25 )   PDF (5963KB) ( 436 )   Ultrasound-guided nerve blocks in children have made significant progress in recent years, with improved safety and efficacy attributed to high-resolution ultrasound visualization. The widespread clinical adoption of ultrasound technology empowers clinicians to visualize pediatric neural structures and adjacent tissues clearly and individually, which permits real-time observation of local anesthetic spread, thereby markedly lowering complication risks inherent to conventional blind puncture techniques. This expert consensus is based on evidence-based medicine and clinical practical experiences, integrating the development history and current status of ultrasound-guided pediatric nerve blocks. It systematically elaborates on the anatomical characteristics of pediatric nerves and their impact on blocking techniques, clarifies the indications and contraindications for pediatric nerve blocks, and standardizes equipment preparation, drug formulation, and pediatric sedation protocols prior to nerve block administration. It also comprehensively provides the procedural guidance and technical key points for nerve blocks in different regions, including probe selection, needle insertion pathways, and real-time monitoring of local anesthetic diffusion, and analyzes the potential complications along with corresponding prevention and management strategies. Through in-depth discussions among the expert group, recommendations were formed based on jointly established criteria. The final consensus aims to provide practical guidance for the implementation of ultrasound-guided pediatric nerve blocks in clinical anesthesia and pain management, thereby promoting more effective and safer application, ultimately achieving the goal of reducing children's pain and accelerating postoperative recovery. Figures and Tables | References | Related Articles | Metrics

Frontier review

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Exploration and practice of enhanced recovery after surgery in neurocritical care CHEN Hao, TIAN Hengli 2025, 45 (9):  1099-1105.  doi: 10.3969/j.issn.1674-8115.2025.09.002 Abstract ( 253 )   HTML ( 10 )   PDF (1331KB) ( 1277 )   Neurocritical care is an important subspecialty in neurosurgery, engaged in the clinical diagnosis and treatment of various neurosurgical conditions, particularly emergencies and critical diseases. These patients often present with complex and dynamic conditions. Effectively mitigating secondary injuries to the central nervous system, reducing surgical and postoperative stress responses, and preventing and managing severe complications are critical to lowering mortality and disability rates in neurosurgical care, but remain major clinical challenges. Enhanced recovery after surgery (ERAS) employs a series of evidence-based perioperative optimization measures to reduce surgical injury and stress, promote functional recovery, shorten hospital stays, and lower medical costs, demonstrating significant advantages across multiple surgical disciplines. However, in the high-risk and complex neurocritical care patient population, there is still a lack of systematic ERAS practice and related clinical research, both domestically and internationally. Therefore, actively exploring and implementing ERAS in neurocritical care, scientifically optimizing diagnostic and therapeutic techniques, management measures, and overall clinical processes, and systematically evaluating its safety and efficacy, hold significant clinical importance. Such efforts will not only provide critical evidence-based medical support for the development of consensus on ERAS in neurocritical care and neurosurgery, but also promote the standardized application and dissemination of the ERAS concept in the field of neurosurgery in China, ultimately improving patient outcomes and enhancing the quality of medical care. Figures and Tables | References | Related Articles | Metrics

Basic research

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Effect of jaw osteoblasts on B cell development via cytokine secretion WANG Xinyu, CHEN Qianye, SUN Jiping, LU Tingwei, HUANG Xiangru, SUN Siyuan, LIU Yuanqi, PAN Houwen, DAI Qinggang, SHEN Lei, JIANG Lingyong 2025, 45 (9):  1106-1115.  doi: 10.3969/j.issn.1674-8115.2025.09.003 Abstract ( 171 )   HTML ( 9 )   PDF (6510KB) ( 929 )   Objective ·To investigate the regulatory effects and underlying mechanisms of mouse mandibular osteoblasts on B cell differentiation and development. Methods ·Single-cell suspensions from mouse mandibular bone were prepared using an optimized enzymatic digestion method and induced to differentiate into osteoblasts in vitro. Osteogenic potential was validated by real-time quantitative PCR (RT-qPCR), alkaline phosphatase (ALP) staining, and alizarin red S (ARS) staining. The spatial localization relationship between osteoblasts and B cells in mandibular tissues was examined via immunofluorescence staining. High-purity hematopoietic progenitor cells were isolated using fluorescence-activated cell sorting. A Transwell co-culture system was established to assess the regulatory effects of different osteoblast concentrations (5×104, 2.5×105, and 5×105 cells/well) on B cell differentiation (5×104 cells/well). Flow cytometry and RT-qPCR were employed to evaluate B cell viability and differentiation. Additionally, RT-qPCR was used to analyze the expression of osteoblast-secreted factors associated with B cell development during osteogenic differentiation. Results ·Mandibular osteoblasts exhibited robust osteogenic potential, as confirmed by ALP/ARS staining and high expression of osteogenic markers (Runx2, Osx, Ocn, and Alp) via RT-qPCR. Immunofluorescence revealed close spatial proximity between osteoblasts and B cells in mandibular tissues. In the co-culture system, osteoblasts promoted B cell differentiation in a concentration-dependent manner. RT-qPCR and immunofluorescence demonstrated that osteoblasts significantly upregulated key genes involved in B cell development (Ebf1, Rag1, Il7r, and Pax5; all P<0.001). Furthermore, osteoblast-derived factors (Il7, Baff, and Flt3l) were markedly elevated during osteogenic differentiation (all P<0.05). Conclusion ·Mandibular osteoblasts enhance B cell differentiation and development in a concentration-dependent manner, likely through secreting growth factors that upregulate critical B cell differentiation genes. Figures and Tables | References | Related Articles | Metrics

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Role and mechanisms of SIRT5 in pulmonary microvascular endothelial cell injury in sepsis ZHAO Shanzhi, ZHENG Xiangtao, WANG Xiaofeng, CHEN Erzhen, GONG Fangchen, CHEN Ying 2025, 45 (9):  1116-1125.  doi: 10.3969/j.issn.1674-8115.2025.09.004 Abstract ( 188 )   HTML ( 9 )   PDF (4230KB) ( 241 )   Objective ·To investigate the role and mechanism of sirtuin 5 (SIRT5) in pulmonary microvascular endothelial cell injury in sepsis. Methods ·Wild-type (WT) and Sirt5 gene knockout C57BL/6 male mice underwent cecal ligation and puncture (CLP) surgery. Following euthanasia, lung tissues were collected. Pulmonary inflammation was assessed using hematoxylin and eosin (H-E) staining; vascular leakage was evaluated by Evans blue (EB) staining; coagulation function in mice was analyzed via immunofluorescence staining of lung tissues. Immunohistochemical staining was employed to detect vascular cell adhesion molecule-1(VCAM-1) protein expression, thereby assessing endothelial inflammation in CLP-treated mice. By using gene editing technology, SIRT5 was knocked down or overexpressed in human umbilical vein endothelial cells (HUVECs), and the cells were subsequently stimulated with lipopolysaccharide (LPS) to induce endothelial inflammation. Protein expression levels of VCAM-1, tissue factor (TF), and other endothelial injury markers were detected by Western blotting, and inflammatory cytokines such as interleukin-6 (IL-6) and IL-1β, were detected by quantitative real-time PCR (qPCR). In addition, transcriptomic sequencing was performed on HUVECs overexpressing SIRT5, and key genes including F2R-like thrombin or trypsin receptor 3 (F2RL3), serpin family A member 3 (SERPINA3), and transforming growth factor β2/β3 (TGF-β2/3) were validated by qPCR. Results ·Sirt5 knockout significantly aggravated lung injury in CLP mice, reducing their survival rates (P<0.001). H-E staining showed increased inflammatory infiltration in the lung tissue of the mice, while EB staining indicated increased vascular leakage (P<0.001). Immunofluorescence revealed elevated fibrinogen deposition. In HUVECs with SIRT5 knockdown, the protein levels of VCAM-1 and TF, as well as the mRNA levels of inflammatory factors including IL-6, IL-1β, VCAM-1, and E-selectin, were significantly upregulated (all P<0.001), whereas overexpression of SIRT5 reversed these effects. Transcriptome sequencing analysis indicated that SIRT5 regulated endothelial inflammation and coagulation responses by inhibiting the F2RL3/SERPINA3/TGF‑β pathway. Conclusion ·SIRT5 negatively regulates the F2RL3/SERPINA3/TGF‑β signaling axis, thereby alleviating endothelial inflammation and promoting coagulation responses, suggesting its potential protective role in sepsis-induced lung injury. Figures and Tables | References | Related Articles | Metrics

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Mechanistic study of targeting melanoma with STING pathway deficiencies via PIKfyve inhibitor YANG Xiaoyu, HUANG Rui, WU Yijia, ZHANG Zhe, FANG Yan, SHEN Jianfeng 2025, 45 (9):  1126-1137.  doi: 10.3969/j.issn.1674-8115.2025.09.005 Abstract ( 201 )   HTML ( 7 )   PDF (4677KB) ( 758 )   Objective ·To explore the antitumor effects and potential mechanisms of combining phosphoinositide 3-kinase, FYVE-type zinc finger containing (PIKfyve) inhibitor YM201636 with the stimulator of interferon genes (STING) agonist diABZI in STINGpathway-deficient melanoma. Methods ·The mRNA and protein expression levels of STING in human cancer cell lines were obtained from the Cancer Cell Line Encyclopedia (CCLE) and UniProt databases. Based on median expression values, melanoma cell lines with high STING mRNA but low protein expression were identified. Quantitative real-time PCR (qRT-PCR) and Western blotting were performed to validate STING mRNA and protein expression in human melanoma cells. The murine melanoma cell line YUMM1.7, characterized by low STING protein expression, was selected through Western blotting. The ability of YM201636 to restore STING protein expression in YUMM1.7 cells was evaluated. STING agonist diABZI was then applied in combination with YM201636 to analyze the synergistic tumor cell-killing effect through CCK-8 assay. Western blotting was used to detect the phosphorylation of TANK-binding kinase 1 (TBK1) and interferon regulatory factor 3 (IRF3), and qRT-PCR was used to evaluate type Ⅰ interferon expression. A mouse melanoma model was established and treated with YM201636, diABZI, or their combination. Tumor volume was measured, and treatment efficacy was assessed. RNA sequencing and immunofluorescence staining were performed to analyze immune cell infiltration in the tumor microenvironment. Results ·Database analyses, qRT-PCR, and Western blotting confirmed that some human melanoma cell lines exhibited high STING mRNA expression but low STING protein levels. YM201636 significantly increased STING protein expression in YUMM1.7 cells (P<0.001). Combined treatment with YM201636 and diABZI significantly enhanced phosphorylation of TBK1 and IRF3 (P<0.05), indicating effective activation of the STING signaling pathway. This combination also promoted the expression of type Ⅰ interferons (P<0.001) and enhanced tumor cell killing in vitro. In vivo, the combination therapy markedly suppressed melanoma growth compared to monotherapy. Immune profiling of the tumor microenvironment revealed significantly increased infiltration of CD4⁺ T cells and CD8⁺ T cells in the combination treatment group (P<0.05). Conclusion ·The PIKfyve inhibitor YM201636 could restore STING protein expression in STING-deficient melanoma and enhance the antitumor efficacy of the STING agonist diABZI, offering a promising therapeutic strategy for tumors with defective STING signaling. Figures and Tables | References | Related Articles | Metrics

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Function and mechanism of suppressor of zeste 12 in hepatocellular carcinoma LI Qianyu, QIAN Yifei, LI Songling, ZHU Zijun, QIN Wenli, LIU Yanfeng, QIU Bijun 2025, 45 (9):  1138-1148.  doi: 10.3969/j.issn.1674-8115.2025.09.006 Abstract ( 164 )   HTML ( 6 )   PDF (9648KB) ( 712 )   Objective ·To explore the function and potential mechanism of suppressor of zeste 12 (SUZ12) in hepatocellular carcinoma (HCC). Methods ·The expression of SUZ12 in HCC patients was analyzed using R language in liver cancer datasets, and relevant survival curves were drawn. Stable knockdown of SUZ12 was established in the liver cancer cell lines LM3 and Huh7. The knockdown efficiency of SUZ12 was assessed using quantitative real-time PCR (qPCR) and Western blotting. Cell proliferation ability was assessed using CCK-8 assay and colony formation assay. Using the hydrodynamic tail vein injection (HTVI) method, Suz12 was knocked out in the livers of fully immunocompetent mice to explore its tumorigenic function in vivo. The molecular mechanism of SUZ12 regulating HCC was explored using The Cancer Genome Atlas (TCGA) database. R language was used to analyze the relationship between SUZ12 and the expression of cancer stem cell (CSC) markers as well as key glycolysis-related genes. Findings were validated in liver cancer cell lines and mouse tumor tissues. Results ·The expression of SUZ12 in liver cancer tissues was higher than in adjacent non-tumor tissues, and its expression increased with higher tumor stage. HCC patients with high SUZ12 expression had poorer prognoses. In LM3 and Huh7 liver cancer cell lines, stable knockdown of SUZ12 reduced cell proliferation ability. In the de novo MYC/Trp53-/- mouse liver cancer model, tumor nodule number and size, and tumor burden in liver tissue were reduced after endogenous knockout of Suz12. TCGA analysis showed that high SUZ12 expression in HCC was enriched in multiple tumor proliferation- and metabolism-related pathways. The expression of SUZ12 was positively correlated with CSC markers and key genes in glycolysis pathway. The mRNA levels of CSC markers and key genes in glycolysis pathway were decreased in liver cancer cell lines with stable SUZ12 knockdown and Suz12 knockout mouse HCC tissues. Conclusion ·The expression of SUZ12 is significantly increased in HCC patients and is associated with poor prognosis. Stable knockdown of SUZ12 weakens the proliferative ability of liver cancer cells. Knockout of Suz12 in mice in vivo can suppress the occurrence and development of HCC. The high expression of SUZ12 maintains the CSC pool, induces metabolic reprogramming, and promotes the occurrence and progression of HCC. SUZ12 can serve as a potential biomarker for poor prognosis and a novel target for potential therapeutic intervention in HCC. Figures and Tables | References | Related Articles | Metrics

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Construction of a truncated cylindromatosis tumor suppressor deubiquitinase plasmid and its regulation of the phenotypes of gastric cancer cells PAERHATI Nadina, ZHANG Pengshan, XU Yitian, CHEN Yunqi, HUANG Chen 2025, 45 (9):  1149-1160.  doi: 10.3969/j.issn.1674-8115.2025.09.007 Abstract ( 159 )   HTML ( 5 )   PDF (5054KB) ( 198 )   Objective ·To construct truncations of CYLD, and to preliminarily analyze their effects on the proliferation of gastric cancer cells. Methods ·TCGA, GTEx, and Kaplan-Meier Plotter databases were used to analyze the differences in the expression levels of CYLD between gastric cancer tissues and normal tissues, and their relationship with the prognosis of gastric cancer patients. Immunohistochemistry and Western blotting were used to detect the expression of CYLD in cancer tissues and adjacent noncancerous tissues. Western blotting and qRT-PCR were used to analyze the protein and mRNA expression levels of CYLD in gastric mucosal epithelial cells and gastric cancer cells. According to the sequence and structural characteristics of CYLD gene, primers were designed to construct its truncations. Their expression was detected and identified by agarose gel electrophoresis and Western blotting, and localization was observed by immunofluorescence. In the human gastric adenocarcinoma cells (AGS) with CYLD knockdown, blank NC was added to the control group, and the full-length CYLD, enzyme-inactivated mutant, and three truncated plasmids were added to the experimental group. The proliferation changes of cells in each group were detected by CCK-8 and plate cloning assays. Co-immunoprecipitation, deubiquitination, and Western blotting assays were performed to examine the binding ability of full-length CYLD, the enzyme-inactivated mutant, and the truncated variants to CAMK2A, the level of CAMK2A deubiquitination, and the expression of STAT3 and p-STAT3 proteins. Results ·CYLD expression in normal gastric tissues and cells was significantly higher than in gastric cancer tissues and cells, and the prognosis of patients with high expression of CYLD was better. The truncations of human CYLD were successfully constructed, and full length CYLD, enzyme-inactivated mutant, and truncations were mainly localized in the cytoplasm. Knockdown of CYLD in gastric cancer cells significantly enhanced the proliferative ability of gastric cancer cells. Reconstitution of CYLD-knockdown cells with CYLD-WT, or truncated variants containing the CAP3 or USP domains significantly inhibited the proliferation of gastric cancer cells. In addition, CYLD bound to CAMK2A mediated K63 deubiquitination modification, and inhibited CAMK2A-induced phosphorylation of STAT3. Conclusion ·The human CYLD truncation plasmids are successfully constructed, and the full length CYLD and its CAP3 and USP segments significantly inhibit the proliferation of gastric cancer cells. Figures and Tables | References | Related Articles | Metrics

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Effects of hydrogel microspheres loaded with interleukin-4 on neural functional recovery by modulating the immune microenvironment after stroke XU Tongtong, RUAN Huitong 2025, 45 (9):  1161-1170.  doi: 10.3969/j.issn.1674-8115.2025.09.008 Abstract ( 181 )   HTML ( 7 )   PDF (16180KB) ( 198 )   Objective ·To explore the effects of hydrogel microsphere (MP) loaded with the immunoregulatory factor interleukin-4 (IL-4) on the regeneration and repair after stroke injury. Methods ·IL-4-loaded nanoparticles were prepared using an emulsification method and subsequently incorporated into polyvinyl alcohol (PVA) hydrogel microspheres via an airflow technique to obtain IL-4-loaded PVA hydrogel microspheres (MP@IL-4). The morphology of MP@IL-4 was characterized by optical microscopy. BV2 microglia were cultured in vitro and treated with MP@IL-4. Cell viability and survival were detected by the CCK-8 assay and live/dead cell staining, respectively. Subsequently, BV2 microglia were further treated with lipopolysaccharide (LPS), and the expression levels of the pro-inflammatory marker inducible nitric oxide synthase (iNOS) and the anti-inflammatory marker arginase 1 (Arg-1) were detected by immunofluorescence staining. Meanwhile, a mouse stroke model was constructed using the middle cerebral artery occlusion method, and the mice were randomly divided into the sham operation group (Sham group), the ischemic stroke (IS) group and the microsphere treatment group (IS-MP@IL-4 group). The neurobehavioral functions of mice in the three groups were detected by the modified Neurological Severity Score, elevated body swing test, and hanging wire test. The brain atrophy volume was detected by cresyl violet staining. Immunofluorescence staining was used to assess the expression levels of the pro-inflammatory factor CD86 and the anti-inflammatory factor CD206 in microglia. Results ·Optical microscopy confirmed the successful fabrication of MP@IL-4 with a particle size of 200 μm, which did not affect the cell viability and survival of BV2 microglia. Both in vitro and in vivo experiments demonstrated that MP@IL-4 downregulated the expression of pro-inflammatory markers and upregulated the expression of anti-inflammatory markers in microglia. Moreover, compared with the IS group, the neurobehavioral function of mice in the IS-MP@IL-4 group was significantly improved (P<0.05), and the brain atrophy volume was reduced (P<0.001). Conclusion ·MP@IL-4 can exert a therapeutic effect on post-stroke neurofunctional injury by improving the immune microenvironment. Figures and Tables | References | Related Articles | Metrics

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Anaphase-promoting complex subunit 10 promotes hepatocellular carcinoma progression through regulation of the PI3K-AKT-mTOR signaling pathway ZHU Zijun, QIAN Yife, LI Qianyu, LI Songling, QIN Wenli, LIU Yanfeng 2025, 45 (9):  1171-1182.  doi: 10.3969/j.issn.1674-8115.2025.09.009 Abstract ( 158 )   HTML ( 6 )   PDF (6473KB) ( 415 )   Objective ·To explore the biological functions and underlying mechanisms of anaphase-promoting complex subunit 10 (ANAPC10) in the development and progression of liver hepatocellular carcinoma (LIHC, often abbreviated as HCC). Methods ·By integrating data from The Cancer Genome Atlas (TCGA)_LIHC, the hepatitis B virus-related subgroup (HBV) of the China Hepatocellular Carcinoma Genome Project (CHCC), and the Gene Expression Omnibus (GEO), the expression pattern of ANAPC10 in HCC was analyzed. Western blotting and quantitative real-time PCR (q-PCR) were used to verify the findings in HCC cell lines. shRNA-mediated knockdown of ANAPC10 was performed in MHCC-97H and SNU-398 cell lines to investigate the effect of ANAPC10 depletion on the in vitro proliferation of HCC cells. An orthotopic liver cancer model with Anapc10 knockout was constructed using the hydrodynamic tail-vein injection technique in mice to further confirm the impact of ANAPC10 deficiency in the liver on the development and progression of HCC. Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) enrichment analyses were performed on the RNA-sequencing data from TCGA_LIHC and CHCC_HBV. Results ·ANAPC10 was highly expressed in tumor tissues, and its expression level was closely related to patient survival. Downregulation of ANAPC10 in vitro and in vivo effectively inhibited HCC progression. ANAPC10 mainly reprogrammed the metabolism of tumors by affecting the PI3K-AKT-mTOR pathway. In the tumor tissues of the orthotopic liver cancer mouse model in the Anapc10 knockout group, the phosphorylation levels of Akt and S6k were decreased, and changes in the key downstream lipid metabolism proteins Fasn and Scd1 were verified. Conclusion ·ANAPC10 is highly expressed in HCC and is positively correlated with poor prognosis. It promotes HCC occurrence and progression by activating the PI3K-AKT-mTOR signaling pathway and enhancing lipid metabolism reprogramming, thereby promoting tumor cell proliferation. These findings expand the understanding of ANAPC10 in tumor progression and suggest potential therapeutic targets for HCC. Figures and Tables | References | Related Articles | Metrics

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Experimental study on novel pH-responsive manganese-based nanoprobes for ferroptosis and magnetic resonance imaging in breast cancer WANG Jingyi, DENG Jiali, ZHU Yi, DING Xinyi, GUO Jiajing, WANG Zhongling 2025, 45 (9):  1183-1193.  doi: 10.3969/j.issn.1674-8115.2025.09.010 Abstract ( 168 )   HTML ( 3 )   PDF (6917KB) ( 946 )   Methods ·BSA-MnO2@CPT (BMC) nanoprobes were prepared by biomineralization, and their physicochemical properties were characterized by transmission electron microscope (TEM) and dynamic light scattering. The magnetic resonance imaging (MRI) was used to evaluate the pH-responsive MRI T1 activation and time-dependent activation efficacy at the cellular level, with quantitative analysis of MRI T1 signal intensity. The reactive oxygen species (ROS) generation and glutathione (GSH) depletion by BMC nanoprobes were respectively detected by methylene blue (MB) and DTNB in vitro. The synergistic efficacy of chemotherapy and ferroptosis mediated by the nanoprobes in 4T1 breast cancer cells was evaluated using the Thiazolyl Blue Tetrazolium Bromide (MTT) assay. After co-incubation 4T1 cells with BMC, intracellular ROS levels were determined through the staining of ROS fluorescence indicator 2′,7′-dichlorodihydrofluorescein diacetate (DCFH-DA) and the level of lipid peroxide (LPO) expression was detected by using BODIPY581/591 C11 probe. A subcutaneous xenograft tumor model of 4T1 breast cancer was established in mice, with four experimental groups: Control group (PBS group), CPT group, BSA-MnO2(BM) group, and BMC group. The pH-responsive T1 activation effect of the BMC nanoprobes was dynamically monitored in vivo, while the ferroptosis-based antitumor efficacy was evaluated by measuring tumor volume and ferroptosis biomarkers (LPO and ROS). Results ·TEM revealed that the prepared BMC nanoprobes exhibited a spherical morphology with an average diameter of approximately 150 nm. The MRI results demonstrated that the nanoprobes were pH-activable, exhibiting progressively enhanced T1 signal intensity under acidic conditions, and displaying pH-dependent r1 relaxivity enhancement. These findings validated their dual pH/time-responsive activation efficacy at the cellular level. In vitro solution-level MB and DTNB assays demonstrated that the BMC nanoprobes effectively enhanced the generation of ROS and the consumption of GSH. Fluorescence staining with DCFH-DA and BODIPY581/591 C11 demonstrated that the combination of ferroptosis effect and chemotherapy significantly enhanced intracellular generation of ROS and LPO accumulation. The MTT assay demonstrated that the survival rate of tumor cells significantly decreased to 17% (P=0.003). In vivo MRI demonstrated that the T1 signal was significantly enhanced and reached its peak at 4 h after tail vein injection of the BMC nanoprobes. Furthermore, in vivo antitumor therapy showed that the BMC group exhibited upregulated levels of LPO and ROS in tumor tissues, accompanied by marked tumor suppression (P=0.009). Conclusion ·The pH-responsive theranostic BMC nanoprobes enhances antitumor efficacy via the synergistic interaction of chemotherapy and ferroptosis, while enabling tumor microenvironment-activated MRI. Objective· To construct a pH-responsive manganese-based nanoprobe and explore the therapeutic efficacy of chemotherapy/ferroptosis synergistic treatment in breast cancer and the effect of pH-responsive magnetic resonance-activated imaging. Figures and Tables | References | Related Articles | Metrics

Clinical research

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Clinicopathologic characteristics, gene mutation profile, and prognostic analysis of patients with adrenal diffuse large B-cell lymphoma HE Jiayin, CHEN Siyuan, SHI Qing, ZHANG Muchen, YI Hongmei, DONG Lei, QIAN Ying, WANG Li, CHENG Shu, XU Pengpeng, ZHAO Weili 2025, 45 (9):  1194-1201.  doi: 10.3969/j.issn.1674-8115.2025.09.011 Abstract ( 223 )   HTML ( 10 )   PDF (2610KB) ( 379 )   Objective ·To analyze the clinicopathologic characteristics, gene mutation profile, and prognostic factors of patients with adrenal diffuse large B-cell lymphoma (DLBCL). Methods ·From March 2002 to December 2022, a total of 105 patients with adrenal DLBCL admitted to Ruijin Hospital, Shanghai Jiao Tong University School of Medicine were retrospectively analyzed for their clinicopathological data, survival outcomes, and prognostic factors. Patients' gene mutation profiles were evaluated by targeted sequencing of 152 lymphoma-related genes. Results ·The median age of the patients was 62 (15‒82) years and the male-to-female ratio was 2.3∶1. Among them, 63 patients (60.0%) were over 60 years old, 22 patients (21.0%) had an Eastern Cooperative Oncology Group (ECOG) performance status of two or higher, 87 patients (82.9%) were staged Ann Arbor Ⅲ‒Ⅳ, 92 patients (87.6%) had elevated serum lactate dehydrogenase (LDH) levels (above the upper limit of reference), 84 patients (80.0%) had extranodal invasion in at least two organs, 67 patients (63.8%) were of non-germinal center B-cell (non-GCB) origin, and 95 patients (90.5%) had an international prognosis index (IPI) scored over 2. With a median follow-up of 28.3 (0.7‒191.9) months, the estimated 2-year overall survival (OS) rate and progression-free survival (PFS) rate were 68.3% and 53.1%, respectively. The estimated 5-year OS rate and PFS rate were 52.6% and 44.0%, respectively. Among 93 patients who could be evaluated for clinical outcomes, 62 (66.7%) got a complete response (CR). Univariate analysis and multivariate Cox analysis revealed that age over 60 years was an adverse prognostic factor for PFS, and ECOG performance status of two or higher was an adverse prognostic factor for both OS and PFS. Targeted gene sequencing in 46 adrenal diffuse DLBCL patients showed high mutation frequencies in lysine methyltransferase 2D (KMT2D; n=17, 37%), Pim-1 proto-oncogene, serine/threonine kinase (PIM1; n=17, 37%), MYD88 innate immune signal transduction adaptor (MYD88; n=15, 33%), CD79b molecule (CD79B; n=13, 28%), and BTG anti-proliferation factor 2 (BTG2; n=10, 22%). Conclusion ·Age over 60 years is an adverse prognostic factor for PFS, and ECOG performance status of two or higher is an adverse prognostic factor for both OS and PFS in patients with adrenal DLBCL. Patients exhibited high frequencies of KMT2D, PIM1, MYD88, CD79B, and BTG2 mutations, as well as an increased proportion of the MCD-like subtype. Figures and Tables | References | Related Articles | Metrics

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Using diffusion-relaxation correlation spectroscopic imaging to assess the heterogeneity of head and neck tumors and identify occult lymph node metastasis LI Siyu, CHEN Ya, HU Wentao, DAI Yongming, WU Yingwei 2025, 45 (9):  1202-1213.  doi: 10.3969/j.issn.1674-8115.2025.09.012 Abstract ( 230 )   HTML ( 5 )   PDF (6091KB) ( 257 )   Objective ·To evaluate the feasibility and diagnostic performance of diffusion-relaxation correlation spectroscopic imaging (DR-CSI) in assessing the heterogeneity of benign and malignant head and neck tumors, as well as in identifying occult lymph node metastasis (OLNM). Methods ·A prospective study was conducted from January to December 2024 at Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, enrolling patients with suspected head and neck tumors who were scheduled for surgery and had a confirmed pathological diagnosis. All patients underwent preoperative routine head and neck plain and contrast-enhanced magnetic resonance imaging (MRI) examinations, including DR-CSI sequence. Conventional imaging parameters, including maximal diameter (MD), depth of invasion (DOI) for tumors, and MD and short diameter (SD) for lymph nodes, were obtained. Post-processing was performed to obtain apparent diffusion coefficient (ADC), T2 value, and D-T2 spectra for all lesions. The compartment segmentation strategy was optimized based on the spectral peak distribution characteristics of different diseases, and the volume fraction (V i ) of each compartment was obtained. Independent sample t-tests, Mann-Whitney U tests, chi-square tests, or Fisher's exact tests were used to compare intergroup differences in clinical data and imaging metrics. Principal component analysis (PCA) and Adonis analysis were employed to evaluate the discriminative ability of imaging metrics among different subtypes of benign tumors. Receiver operating characteristic (ROC) analysis was used to evaluate the ability of univariate and multivariable models to characterize the malignancy of head and neck squamous cell carcinoma (HNSCC) and identify OLNM. Results ·A total of 97 cases were collected, including 28 benign tumors and 69 HNSCCs. Fifteen pathologically confirmed OLNMs and 20 benign lymph nodes (BLNs) were also enrolled. Among the 28 benign tumors, there were 6 cases of pleomorphic adenoma stroma-rich (PA stroma-rich), 9 cases of pleomorphic adenoma stroma-poor (PA stroma-poor), 9 cases of Warthin's tumor (WT), and 4 cases of basal cell adenoma (BCA). Statistically significant differences were observed in certain imaging parameters (ADC, T2, and DR-CSI V i ) among benign tumor subtypes. PCA analysis demonstrated a strong discriminative ability of imaging parameters in distinguishing pathological subtypes of benign tumors (R²=0.64, P<0.001). Among the 69 HNSCCs, 47 were classified as Grade 1 (well/moderately well-differentiated) and 22 as Grade 2 (moderately/poorly differentiated). Compared to Grade 1, Grade 2 showed lower ADC and higher T2 values, though differences were not statistically significant. As HNSCC malignancy increased, VA4 decreased and VB4increased significantly. OLNM showed a significant increase in SD and VA4 compared to BLNs. The combination of SD and VA4 for preoperative OLNM identification achieved a diagnostic efficiency of 0.843. Conclusion ·DR-CSI can analyze diffusion and relaxation characteristics at the sub-voxel level, offering valuable insights for characterizing benign head and neck tumor subtypes, assessing HNSCC malignancy, and identifying OLNMs. Compared to traditional parameters like ADC or T2, DR-CSI provides enhanced tissue microstructure analysis. Figures and Tables | References | Related Articles | Metrics

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Clinicopathologic characteristics, gene mutation profile, and prognostic analysis of diffuse large B-cell lymphoma with lung involvement CHEN Siyuan, SHI Qing, FU Di, WANG Li, CHENG Shu, XU Pengpeng, ZHAO Weili 2025, 45 (9):  1214-1220.  doi: 10.3969/j.issn.1674-8115.2025.09.013 Abstract ( 227 )   HTML ( 2 )   PDF (1973KB) ( 461 )   Objective ·To investigate the clinicopathologic features, gene mutation profile, and real-world survival prognosis of diffuse large B-cell lymphoma (DLBCL) with pulmonary involvement. Methods ·The clinical data of 110 patients with newly diagnosed, pathologically confirmed DLBCL and pulmonary involvement at Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, between August 2003 and December 2022 were retrospectively collected and analyzed. Evaluation of the efficacy of treatment, survival analyses, and univariate and multivariate analyses were performed in 88 patients who received a first-line regimen based on rituximab in combination with cyclophosphamide, doxorubicin/epirubicine, vincristine, and prednisone (R-CHOP). A total of 74 patients underwent targeted DNA sequencing of 55 lymphoma-related genes and were evaluated for mutations. Results ·Among the 110 patients, 72 (65.5%) were >60 years old, 52 (47.3%) were female, 92 (83.6%) presented with Ann Arbor stage Ⅲ‒Ⅳ, 20 (18.2%) had ECOG scores≥2, 75 (68.2%) had elevated lactate dehydrogenase (LDH) levels, 79 (71.8%) had ≥2 extranodal involvements, 32 (31.4%) were classified as germinal center B-cell subtype, 22 (26.8%) were diagnosed with double expressor lymphoma, and 4 (4.6%) with double-hit lymphoma. Among the patients treated with R-CHOP-based first-line regimens, the objective response rate (ORR) was 68.2%, the 5-year progression-free survival (PFS) rate was 43.7%, and the 5-year overall survival (OS) rate was 65.4%. Univariate analysis showed that elevated LDH and ECOG score≥2 were poor prognostic factors for PFS and OS, and mutations in PIM1 and CD79B were poor prognostic factors for PFS among high-frequency mutations. Multivariate analysis showed that elevated LDH was an independent adverse prognostic factor for PFS (HR=2.47, 95%CI 1.28‒4.77) and OS (HR=2.71, 95%CI 1.21‒6.07). Targeted sequencing results showed that PIM1 (25.7%), MYD88 (24.3%), TP53 (18.9%), CD79B (17.6%), KMT2D (17.6%), and TNFAIP3 (16.2%) were the high-frequency mutations with mutation rates over 15%. Conclusion ·Elevated LDH is an independent adverse prognostic factor for PFS and OS in DLBCL with pulmonary involvement. Mutations in PIM1, MYD88, TP53, CD79B, KMT2D, and TNFAIP3 are frequently observed in this population. Figures and Tables | References | Related Articles | Metrics

Techniques and methods

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Graph neural network-based auxiliary diagnostic model for gallbladder cancer on CT imaging YIN Ziming, WANG Rongqin, YANG Ziyi, LIU Yingbin, CHEN Tao, SHU Yijun, GONG Wei 2025, 45 (9):  1221-1231.  doi: 10.3969/j.issn.1674-8115.2025.09.014 Abstract ( 216 )   HTML ( 9 )   PDF (2755KB) ( 949 )   Objective ·To develop a graph neural network (GNN)-based auxiliary diagnostic model for gallbladder cancer on CT images, and validate its accuracy and feasibility. Methods ·From January 2010 to November 2023, 1 774 contrast-enhanced CT arterial-phase images were acquired from 887 patients with normal gallbladder, benign gallbladder disease, or gallbladder cancer at Xinhua Hospital and Renji Hospital, Shanghai Jiao Tong University School of Medicine. These images were randomly divided into training and testing sets at a 4∶1 ratio to develop a hybrid GNN-convolutional neural network (CNN) model, named VJK-GIN. The model constructed a pixel-level graph in which each pixel served as a node, and spatial adjacency defined the edges, enabling extraction of local texture features. In the model architecture design, VJK-GIN integrated a three-layer graph isomorphism network, augmented with virtual nodes and jump-knowledge connections; global pooling compressed node features into a graph-level representation, which was classified by a multi-layer perceptron head. Five-fold cross-validation was used to compare VJK-GIN with GNN baselines (GCN, GraphSAGE, GAT, and GIN) and CNN baselines (ViT, EfficientNetV2, and ConvNeXt) in terms of accuracy, precision, recall, F1-score, and area under the receiver operating characteristic curve (AUC). Results ·The results of five-fold cross-validation showed that VJK-GIN achieved an F1-score of 0.799 (95%CI 0.775‒0.823), recall of 0.795 (95%CI 0.773‒0.817), precision of 0.799 (95%CI 0.775‒0.823), AUC of 0.812 (95%CI 0.792‒0.832), and accuracy of 0.773 (95%CI 0.748‒0.798), surpassing all competing models across every metric. Conclusion ·The VJK-GIN model exhibits high stability and accuracy in identifying contrast-enhanced CT images of normal, benign, and malignant gallbladder conditions. Figures and Tables | References | Related Articles | Metrics

Review

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Advances in the diagnosis and treatment of inflammatory bowel disease-associated anemia in children WANG Zhiqi, WANG Ying 2025, 45 (9):  1232-1238.  doi: 10.3969/j.issn.1674-8115.2025.09.015 Abstract ( 188 )   HTML ( 8 )   PDF (1292KB) ( 730 )   Inflammatory bowel disease (IBD) is a group of non-specific chronic gastrointestinal inflammatory disorders of unknown etiology. Patients with IBD often have a variety of extraintestinal symptoms and complications. Anemia is one of the most common extraintestinal manifestations, and its incidence and prevalence in children are higher than in adults. Anemia in children with IBD not only causes non-specific symptoms such as dizziness, headache, and fatigue, but also impacts growth and development, and is closely related to the quality of life. The etiologies of IBD-associated anemia include iron deficiency, anemia of chronic disease, vitamin deficiency, hemolysis, and myelosuppression, among which iron deficiency is the most common. In recent years, in addition to conventional indicators such as hemoglobin, hematocrit, and mean corpuscular hemoglobin, many new indicators for evaluating anemia and iron deficiency have emerged, including soluble transferrin receptor (sTfR), the ratio of sTfR to log ferritin (sTfR-F) index, and reticulocyte hemoglobin content (CHr). In the treatment of IBD-associated anemia in children, oral iron supplementation is the most commonly used therapy in clinical practice, while intravenous iron therapy is not widely used. Although anemia has many negative effects on children with IBD, its diagnosis and treatment are often delayed. This article reviews the pathogenesis, diagnosis, and treatment of IBD-associated anemia in children, in order to improve clinical awareness and attention, and provide a basis for further improving the treatment effect and quality of life. Figures and Tables | References | Related Articles | Metrics

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Role of isocitrate dehydrogenase 1 mutation-mediated D-2-hydroxyglutarate metabolic reprogramming in tumor immunoregulation and progress in related drug development YANG Quanjun, BAI Dingyuan, ZHOU Yuxuan, BAI Lu, GUO Cheng 2025, 45 (9):  1239-1248.  doi: 10.3969/j.issn.1674-8115.2025.09.016 Abstract ( 171 )   HTML ( 4 )   PDF (4144KB) ( 335 )   Mutations in isocitrate dehydrogenase 1 (IDH1) can abnormally produce the oncometabolite D-2-hydroxyglutarate (D2HG), which in turn remodels the tumor immune microenvironment. In recent years, it has become a key target in the research on the interaction between tumor metabolism and immunity. D2HG competitively inhibits endogenous α-ketoglutarate-dependent dioxygenases, leading to DNA histone hypermethylation and cell differentiation arrest, thus promoting tumorigenesis, development, metastasis, and drug resistance. Meanwhile, D2HG suppresses T-cell function, promotes myeloid cell expansion and macrophage polarization, weakens immune surveillance, and creates an immunosuppressive state that affects the response to immunotherapy. In various tumors, such as glioma, acute myeloid leukemia, and cholangiocarcinoma, IDH1 mutations exhibit heterogeneity and different prognostic characteristics. Currently, small-molecule inhibitors targeting IDH1 mutations, such as ivosidenib and vorasidenib, can partially reverse immunosuppression by reducing D2HG levels and have shown certain efficacy in clinical trials. However, these inhibitors face challenges including efficacy differences, drug resistance, and safety concerns. Combination therapies with IDH1 inhibitors aim to synergistically reverse the metabolic-epigenetic-immune triple-suppression network and enhance the anti-tumor effects, attracting extensive attention. This article reviews the tumor immune regulatory network mediated by IDH1-mutation-induced D2HG metabolism and comprehensively summarizes progress in related drug development, providing new references and ideas for tumor prevention and treatment. Figures and Tables | References | Related Articles | Metrics

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Research progress on intelligent diagnosis of eye diseases based on facial photos XU Hanwen, CHEN Moxin, LIANG Xiaoyi, SHU Qin, NIE Wanqin, YANG Xuefeng, SHEN Minxuan, LI Xiaojing, CAO Yu, LI Lin 2025, 45 (9):  1249-1255.  doi: 10.3969/j.issn.1674-8115.2025.09.017 Abstract ( 177 )   HTML ( 6 )   PDF (1318KB) ( 270 )   The number of patients with eye diseases in China is enormous, and the negative effects of these conditions, such as impaired visual function, psychological burdens, and restricted social participation, are becoming increasingly severe. Due to the limited and unevenly distributed ophthalmic resources, and the significant limitations of traditional diagnostic and therapeutic approaches in terms of accuracy and efficiency, there is an urgent need for more sensitive and efficient modalities. With the rapid advancement of artificial intelligence technology, ophthalmic diagnosis has entered a new stage of intelligent transformation. Facial photos, as a noninvasive and convenient medium, show unique advantages in eye disease diagnosis. Artificial intelligence systems based on facial photo analysis have been applied to the screening and diagnosis of conditions such as myopia, strabismus, ptosis, and thyroid eye disease, showing promising results. This review introduces the workflow of intelligent diagnosis for ocular diseases based on facial photographs, with a focus on recapitulating relevant research findings both domestically and internationally in recent years. It summarizes the innovative features and application advantages of intelligent diagnosis systems for eye diseases based on facial photos, analyzes the current technical bottlenecks and challenges in application, proposes corresponding countermeasures, and discusses future development directions, aiming to provide references and new insights for the intelligent screening and diagnosis of eye diseases. References | Related Articles | Metrics

Case report

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Effect of preoperative chemotherapy combined with immunotherapy in a colorectal cancer patient with KRAS mutation JIANG Yi, HUANG Chenhao, LI Zhiliang, WU Junwei, ZHAO Ren, ZHANG Tao 2025, 45 (9):  1256-1260.  doi: 10.3969/j.issn.1674-8115.2025.09.018 Abstract ( 187 )   HTML ( 4 )   PDF (3003KB) ( 684 )   Colorectal cancer (CRC), a highly prevalent malignant tumor worldwide, has shown a continuously increasing incidence, particularly with the rise of early-onset CRC in young populations. Neoadjuvant therapy, as an important strategy for locally advanced CRC, shows significant potential to downstage tumors, improve radical surgical cure rates, and enhance prognosis. In this paper, a 39-year-old male patient with sigmoid colon adenocarcinoma at clinical stage cT4aN2aM0 (stage ⅢC) is reported. Genetic testing revealed a mutation in the oncogene KRAS (G13D) and microsatellite stability (MSS). The patient also had significantly elevated carcinoembryonic antigen (CEA), lymph node metastasis, and suspected pelvic implant nodules, with a high risk of invasiveness and potential peritoneal metastasis. Because he had a refractory subtype of CRC with poor response to traditional immunotherapy, the patient was treated with neoadjuvant therapy, comprising CapeOx regimen (capecitabine+oxaliplatin), followed sequentially by sluzumab; after 6 treatment cycles, the tumor shrank significantly, and laparoscopic radical sigmoid colon resection was successfully performed, with no residual (ypT0N0) confirmed by postoperative pathology. This case suggests that for patients with KRAS-mutated MSS CRC resistant to traditional immunotherapy, a combination of CapeOx chemotherapy followed by programmed death-1 (PD-1) inhibitors may induce a deep pathological response and provide translational treatment opportunities for locally advanced patients. However, the universality and long-term benefits of this treatment regimen still require further longitudinal studies and clinical follow-up. Figures and Tables | References | Related Articles | Metrics