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28 November 2025, Volume 45 Issue 11 Previous Issue   
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Innovative research team achievement column
Frontier review
Basic research
Clinical research
Techniques and methods
Review
Case report


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Innovative research team achievement column

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Expression of long noncoding RNA LINC00467 and its mechanism in affecting lung adenocarcinoma progression GUO Linyan, ZHANG Hailong, ZHENG Chao, LEI Ming 2025, 45 (11):  1407-1420.  doi: 10.3969/j.issn.1674-8115.2025.11.001 Abstract ( 14 )   HTML ( 3 )   PDF (54055KB) ( 7 )   Objective ·To investigate the expression of long noncoding RNA (lncRNA) LINC00467 in lung adenocarcinoma (LUAD) and its impact on the poor prognosis of patients, as well as its functional role and underlying molecular mechanisms in the occurrence and development of LUAD. Methods ·First, tumor sample data from The Cancer Genome Atlas (TCGA) database were utilized to analyze the expression levels of LINC00467 in LUAD tissues and its correlation with patient survival. Second, a stable LINC00467-knockdown LUAD cell line was established, and the effects of LINC00467 on LUAD cell proliferation, colony formation, migration, and tumorigenicity were assessed through cell phenotypic experiments (including live-cell imaging for cell proliferation analysis, plate colony formation assays, and wound healing assays) and nude mouse tumor formation experiments. Furthermore, RNA sequencing (RNA-seq), differentially expressed genes (DEGs) analysis, and hallmark gene sets enrichment analysis were performed to identify signaling pathways regulated by LINC00467, and Western blotting was used to validate its impact on tumor cell pathways. Finally, RNA pull-down combined with mass spectrometry and co-immunoprecipitation (co-IP) assays were conducted to filter and identify LINC00467-interacting proteins. Results ·Analysis of tumor sample data from the TCGA database showed that LINC00467 was highly expressed in LUAD, and its expression level was negatively correlated with overall survival in LUAD patients (P=0.004). Cell phenotypic experiments and nude mouse tumor formation experiments demonstrated that LINC00467 knockdown significantly inhibited the proliferation, colony formation, migration and in vivo tumorigenesis of LUAD cells (all P<0.05). RNA-seq, DEGs analysis, hallmark gene sets enrichment analysis, and Western blotting indicated that knockdown of LINC00467 suppressed the activation of nuclear factor kappa-B (NF-κB) signaling pathway. RNA pull-down combined with mass spectrometry and co-IP assays demonstrated that LINC00467 interacted with casein kinase 2 alpha 2 (CSNK2A2) and promoted the phosphorylation of NF-κB p65. Conclusion ·High expression of LINC00467 in LUAD tissues is negatively correlated with patient prognosis. LINC00467 can interact with CSNK2A2, promote the phosphorylation of NF-κB p65, activate the NF-κB pathway, and enhance LUAD proliferation, colony formation, migration, and in vivo tumorigenesis. Figures and Tables | References | Related Articles | Metrics

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Three-dimensional imaging of cochlear nerve fibers based on multi-scale resolution CHENG Yaqiong, DU Yiwei, LIU Sidi, JING Dian, WU Hao 2025, 45 (11):  1421-1431.  doi: 10.3969/j.issn.1674-8115.2025.11.002 Abstract ( 11 )   HTML ( 1 )   PDF (25678KB) ( 7 )   Objective ·To establish a standardized research platform for comprehensive imaging of the cochlea and its surrounding tissues through multi-scale resolution three-dimensional (3D) imaging, thereby enabling 3D visualization and analysis of the cochlea under physiological conditions. Methods ·The cochlea or combined cochlea and whole brain samples were obtained from 8‒12-week-old thymus cell antigen 1 (Thy1) -driven yellow fluorescent transgenic mice (Thy1-YFP-16 mice) after cardiac perfusion. Tissue clearing was performed using PEGASOS, followed by direct imaging of the cochlea and surrounding tissues through their entire depth using a laser confocal microscope with 4× and 10× objectives. For individual cochlear samples, whole tissue immunofluorescence staining was performed in combination with a neurofilament-200 (NF200) antibody and propidium iodide (PI) fluorescent dye, in the process of tissue clearing and embedding using PEGASOS and TESOS techniques. The entire cochlea was then subjected to serial sectioning with a paraffin microtome, and each section was imaged using a laser confocal microscope equipped with a 63× oil immersion objective. 3D reconstruction was performed using ImageJ for image stitching, followed by image processing, single-nerve-fiber tracking, and length measurement conducted in Imaris software. Fiber path curvature was calculated using MATLAB, and statistical analyses were performed with GraphPad Prism. Results ·Transparent cochlear and surrounding tissue samples were successfully prepared using tissue clearing techniques. The cochlea and its surrounding tissues were directly imaged by low- and medium-magnification objectives on the confocal microscope, which reconstructed the 3D morphology of the cochlea and delineated its spatial relationship with adjacent structures such as the vestibular nerve. Serial sectioning and imaging with a high-magnification objective enabled 3D imaging of the entire cochlear sample at single-cell resolution. This approach revealed the overall pathway of THY1+ fibers within the cochlea, extending from the hair cell region to the modiolus. Single nerve fiber tracing revealed distinct trajectory characteristics of the cochlear efferent nervous system and auditory nerve fibers near the spiral ganglion. Conclusion ·The PEGASOS and TESOS techniques enable multi-scale resolution 3D imaging of the cochlea and its surrounding tissues as an integrated whole. When combined with whole-tissue immunofluorescence staining, this methodology can be used to delineate the 3D spatial relationships between the cochlea and adjacent tissues, as well as between cells and nerve fibers within the cochlea itself. Furthermore, it allows for the tracing of individual nerve fiber pathways. Figures and Tables | References | Related Articles | Metrics

Frontier review

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Review of CAR-T cell therapy for autoimmune diseases WANG Xueyi, LI Benshang 2025, 45 (11):  1432-1442.  doi: 10.3969/j.issn.1674-8115.2025.11.003 Abstract ( 23 )   HTML ( 2 )   PDF (1941KB) ( 11 )   Chimeric antigen receptor T cell (CAR-T) therapy, which involves genetically engineering T cells to specifically recognize and efficiently eliminate target cells, has achieved groundbreaking success in treating hematological malignancies such as B-cell lymphoma and leukemia. Driven by its unique mechanism of action, research into extending its applications to other disease areas is actively underway. In particular, CAR-T therapy has shown significant potential in treating autoimmune diseases (AIDs), attracting considerable attention. Current conventional treatments for AIDs, including glucocorticoids, immunosuppressants, and biologics, are often associated with limitations such as limited efficacy, short duration of remission, and long-term toxicity. In contrast, CAR-T therapy has emerged as a highly promising treatment strategy for AIDs, owing to its advantages of precise targeting and the capacity to induce sustained, drug-free remission. This article reviews recent preclinical and clinical advances in CAR-T therapy for various AIDs, demonstrating its feasibility in eradicating pathogenic B cells and reestablishing immune tolerance. It also examines the major challenges confronting this treatment approach, including adverse effects, limited persistence, and treatment resistance in some patients. Furthermore, strategies to address these challenges are discussed, focusing on the optimization of the chimeric antigen receptor (CAR) structure, the exploration of novel specific targets, and the development of universal CAR-T products. Finally, future research directions are outlined, with the aim of providing a rational foundation for the further development and refinement of CAR-T therapy for AIDs. Figures and Tables | References | Related Articles | Metrics

Basic research

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LINC01123 promotes proliferation and glycolysis of gastric cancer via binding to ENO1 ZHANG Shuqiong, KE Xing, ZHAO Xinghe, CHEN Xiaocui, ZHENG Haodong, CHEN Hui, SHEN Lisong, YANG Junyao 2025, 45 (11):  1443-1457.  doi: 10.3969/j.issn.1674-8115.2025.11.004 Abstract ( 10 )   HTML ( 3 )   PDF (130835KB) ( 6 )   Objective ·To investigate the expression and tumor-promoting mechanism of the long non-coding RNA (lncRNA) LINC01123 in gastric cancer and evaluate its potential as a novel diagnostic biomarker and therapeutic target. Methods ·Differential expression analysis of lncRNAs between gastric cancer and normal tissues was performed based on The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) datasets (GSE95667, GSE99416) by using R software. LINC01123 was identified as the candidate of interest. Its expression was validated in gastric cancer cell lines and clinical tissue samples by using qRT-PCR. The biological effects of LINC01123 on cell proliferation and metastasis were evaluated in vitro through gene overexpression and knockdown by utilizing CCK-8, colony formation, wound healing, and Transwell migration and invasion assays. In vivo, a subcutaneous xenograft tumor model in nude mice was established to assess the effect of LINC01123 on tumor growth. ATP and lactate production were measured to evaluate the role of LINC01123 in glycolysis. Transcriptome sequencing and Gene Set Enrichment Analysis (GSEA) were conducted to explore related pathways. RNA pull-down combined with mass spectrometry was used to identify proteins interacting with LINC01123. The binding region was predicted using the catRAPID database and validated by constructing α-enolase (ENO1) protein truncation mutants and performing RNA immunoprecipitation (RIP) assays. Functional interaction studies were carried out to determine whether ENO1 mediates the oncogenic effect of LINC01123. Results ·LINC01123 was upregulated in gastric cancer tissues and cell lines and was associated with poor patient prognosis (P=0.021). Functional assays demonstrated that LINC01123 promoted proliferation, migration, invasion, and glycolysis of gastric cancer cells such as MKN-45 in vitro, and enhanced tumor growth in vivo (all P<0.05). Mechanistically, LINC01123 was predominantly localized in the cytoplasm and bound to the 97‒237 amino acid region of ENO1 protein. Further studies showed that ENO1 knockdown in LINC01123-overexpressing cells partially reversed the proliferative and migratory effects of LINC01123 (all P<0.05) , indicating that ENO1 upregulation enhances the tumor-promoting function of LINC01123. Conclusion ·LINC01123 is highly expressed in gastric cancer and promotes tumor progression by binding to ENO1 protein and enhancing proliferation, migration, invasion, and glycolysis. LINC01123 holds promise as a novel diagnostic and prognostic biomarker and a potential therapeutic target for gastric cancer. Figures and Tables | References | Related Articles | Metrics

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N-glycosylation of Cav3.2 channel in DRG neurons of myelinated A-fiber contributes to diabetic mechanical allodynia LIAO Chenlong, LI Shuo, XU Xin, ZHANG Yue, ZHANG Wenchuan 2025, 45 (11):  1458-1465.  doi: 10.3969/j.issn.1674-8115.2025.11.005 Abstract ( 7 )   HTML ( 0 )   PDF (7927KB) ( 5 )   Objective ·To investigate the association of Cav3.2 channel N-glycosylation in myelinated A-fiber dorsal root ganglion (DRG) neurons with diabetic mechanical allodynia (MA). Methods ·Diabetic rat models were induced by a single intraperitoneal injection of streptozotocin. Pain behavior assessments, including evaluations of MA and thermal hyperalgesia (TH), were conducted on a weekly basis. Diabetic rats exhibiting TH were subsequently categorized into two subcategories based on the onset of mechanical allodynia by the third week. The impact of N-glycosylation on both the expression of Cav3.2 channels in DRG neurons and pain behaviors was investigated through sequential administration of neuraminidase (NEU) and TTA-P2, a selective blocker of T-type calcium channels, after C-unmyelinated fiber blockage by the application of resiniferatoxin (RTX). The extent of Cav3.2 N-glycosylation was quantitatively compared between diabetic rats with and without MA by analyzing the N-terminal fragment of Cav3.2 following de-glycosylation. Results ·Higher levels of Cav3.2 expression in myelinated A-fiber DRG neurons were observed in diabetic rats with MA compared to those without MA (P<0.001). NEU-induced de-glycosylation led to a reduction in Cav3.2 expression across all groups, with diabetic rats with MA maintaining higher levels of the Cav3.2 expression than those without MA (P<0.05). It was observed that RTX eliminated only TH and not MA, whereas NEU had a restorative effect on both TH and MA, similar to TTA-P2. Diabetic rats with MA exhibited increased expression of N-terminal fragments compared to those without MA (P<0.001). Conclusion ·N-glycosylation of the Cav3.2 channel within DRG neurons of myelinated A-fiber is a contributing factor to diabetic MA. Figures and Tables | References | Related Articles | Metrics

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CD10+ neutrophils promote CD8+ T-cell depletion in mucosal malignant melanoma through the SELPG-SELL pathway HAO Meiling, MA Yanni, MA Xuhui, ZHANG Yanjie, ZENG Hanlin, CHEN Shanshuang 2025, 45 (11):  1466-1479.  doi: 10.3969/j.issn.1674-8115.2025.11.006 Abstract ( 9 )   HTML ( 0 )   PDF (5132KB) ( 5 )   Objective ·To compare the immune microenvironment of mucosal malignant melanoma (MM) and cutaneous malignant melanoma (CM) using single-cell transcriptome analysis system, and to elucidate the key regulatory mechanism of CD8+ T cell depletion in MM. Methods ·A total of 36 531 cells from three treatment-naïve MM surgical specimens and three CM samples were subjected to single-cell RNA sequencing. Data pre-processing included batch correction, strict quality control (based on mitochondrial gene ratio and gene number screening), unsupervised clustering, and cell-type annotation (using established marker genes). Differential gene analysis (Wilcoxon test), gene set enrichment analysis [based on Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) databases], cell-cell interaction network analysis, and prognostic association analysis using. The Cancer Genome Atlas (TCGA) were used to comprehensively analyse the heterogeneity of MM and CM tumour immune microenvironment. Results ·Compared with CM, the expression of cytotoxicity-related genes (GZMB, IFNG, etc.) in CD8+ T cells in MM was reduced (P<0.001), while the depletion markers (PDCD1, LAG3, etc.) were significantly up-regulated (P<0.001). The proportion of depleted CD8+ T cell subsets increased by nearly 6 times (CM: 3.38% vs MM: 19.26%, P<0.010), and the terminal depletion score was higher. In addition, the level of neutrophil infiltration in the MM microenvironment was significantly higher than that in CM (CM: 1.6% vs MM: 34.1%, P=0.009), and single-cell analysis further divided it into five subgroups. Among them, the CD10+ neutrophil subset (accounting for 23.52% of MM neutrophils) highly expressed pro-inflammatory molecules (S100A8/A9) and immunosuppressive molecules (MME/CD10, CD55), and the characteristic scores of myeloid-derived suppressor cells (MDSCs) in this subset were significantly higher than those of other subgroups. TCGA and MM cohort analyses further confirmed that the highly expressed genes of this subset were independently associated with poor prognosis (P=0.049), suggesting that this subset was involved in tumour immunosuppressive effects. Mechanistically, CD10+ neutrophils interacted with depleted CD8+ T cells through the SELPLG-SELL ligand-receptor pair, driving T-cell inactivation. Conclusion ·Single-cell transcriptome sequencing was performed on MM clinical samples, and the single-cell immunomes of MM and CM were systematically compared, suggesting that CD10+ neutrophils in MM induce CD8+ T-cell terminal depletion through the SELPLG-SELL pathway. The molecular mechanism of MM immunotherapy tolerance was elucidated, providing a new strategy for targeting neutrophil-T cell interaction. Figures and Tables | References | Related Articles | Metrics

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Research on the impact of in vivo liver transfection of carboxylesterase 1f gene on acute liver failure BIAN Shu, YU Qian, ZHANG Yuting, LI Dingjia, ZHANG Qiaoting, LIU Liangming 2025, 45 (11):  1480-1489.  doi: 10.3969/j.issn.1674-8115.2025.11.007 Abstract ( 9 )   HTML ( 0 )   PDF (42324KB) ( 5 )   Objective ·To explore the effects of in vivo gene transfection of Carboxylesterase 1f (Ces1f) on mice with acute liver failure (ALF) induced by lipopolysaccharide (LPS) in combination with D - galactosamine (D - GalN), as well as its impact on the expression of hepatic endocannabinoid (EC) and their specific receptors, cannabinoid receptor 1 (Cb1r) and cannabinoid receptor 2 (Cb2r). Methods ·Twenty male C57BL/6J mice were randomly divided into four groups (n=5 per group): the blank control group, the Ces1f over expression group, the ALF model group (LPS/D-GalN), and the Ces1f over expression ALF model group. Recombinant adeno-associated virus 8 (rAAV8) containing the Ces1f sequence was injected via the tail vein, while the control group received an injection of the empty viral vector. Three weeks after virus injection, an ALF animal model was established by intraperitoneal injection of LPS+D-GalN. Immunofluorescence was used to observe the transfection efficiency of Ces1f in the mouse liver. Quantitative real-time polymerase chain reaction (qPCR) and Western blotting were employed to determine the expression levels of CES1F, CB1R, and CB2R in mouse liver tissue. Hematoxylin-eosin (H-E) staining was used to observe the pathological changes in the mouse liver tissue. The enzyme-linked immunosorbent assay (ELISA) was utilized to detect the levels of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), arachidonoylethanolamide (AEA), and 2-arachidonoylglycerol (2-AG). Results ·The AAV8 virus had high transfection efficiency and significant hepatotropism in the mouse liver. Compared with the control group, the ALF model group showed decreased mRNA (P<0.001) and protein expression levels of Ces1f and Cb2r (P=0.039, P=0.012). The pathological injury score of liver tissue, the levels of serum ALT, AST, IL-1β, and TNF-α, as well as the levels of Il-1β mRNA, Tnf-α mRNA, AEA, 2-AG, Cb1r mRNA, and CB1R protein in liver tissue were significantly increased (P<0.001). Compared with the ALF model group, the Ces1f over expression ALF model group had significantly increased Ces1f mRNA (P<0.001) and CES1F protein (P=0.002) expression levels, decreased serum AST level (P=0.011), significantly decreased pathological injury scores of liver tissue (P=0.001), decreased levels of serum ALT, IL-1β, and TNF-α, and decreased levels of Il-1β mRNA, Tnf-α mRNA, AEA, and 2-AG in liver tissue (P<0.001). The levels of Cb1r mRNA (P=0.024) and CB1R protein (P=0.027) were also decreased. Conclusion ·Liver-targeted Ces1f gene transfection exerts a protective effect in the ALF mouse model induced by LPS/D-GalN. This protective effect may be achieved by downregulating the levels of hepatic endocannabinoids AEA and 2 - AG and inhibiting the expression of CB1R. Figures and Tables | References | Related Articles | Metrics

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Clinical value and transcriptional regulatory mechanism of ABCA7 in colorectal cancer SUN Ruizhuang, QIAO Kunpeng, LI Pu, XU Xiaolian, MENG Jun 2025, 45 (11):  1490-1501.  doi: 10.3969/j.issn.1674-8115.2025.11.008 Abstract ( 12 )   HTML ( 1 )   PDF (10308KB) ( 8 )   Objective ·To investigate the prognostic value of the ATP-binding cassette subfamily A member 7 (ABCA7) gene in colorectal cancer (CRC) and provide a novel molecular marker for the precise diagnosis and personalized treatment of CRC. Methods ·Single-cell transcriptome data of CRC were retrieved from the Tumor Immune Single-cell Hub (TISCH). Spatial transcriptome data of sample GSM8594571 (based on the 10x Genomics Visium platform) were downloaded from the Gene Expression Omnibus (GEO) database. Transcriptome data from the TCGA-COAD and TCGA-READ projects were extracted from The Cancer Genome Atlas (TCGA) database. Using a multi-omics integration analysis strategy, single-cell transcriptome data were employed to analyze the expression patterns of ABCA7 in different cell subpopulations and were combined with spatial transcriptome data to explore its spatial distribution characteristics in tumor and adjacent tissues. The Cox Proportional Hazards Model (Cox) was used to evaluate the prognostic value of ABCA7. The effect of ABCA7 on CRC cell proliferation was verified using Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR) knockout technology combined with the CERES algorithm. The transcriptional regulatory network between ABCA7 and the transcription factors zinc finger BTB domain-containing protein 33 (ZBTB33) and Nuclear factor-κB-repressing factor (NKRF) was constructed using chromatin immunoprecipitation sequencing (ChIP-seq) data from the Cistrome database and Pearson correlation analysis. Results ·The analysis revealed that ABCA7 was significantly overexpressed in CRC malignant cells, with further upregulation particularly in tumor tissues with high Ki-67 expression. Moreover, the mRNA expression of ABCA7 in tumor tissues was significantly higher than that in normal tissues (P<0.05), showing certain diagnostic efficacy [area under the curve (AUC) of the receiver operating characteristic (ROC) curve=0.686]. Knockout of ABCA7 significantly inhibited the proliferative capacity of CRC cell lines (e.g., C75, CL11). Patients in the ABCA7 high-expression group had significantly shorter overall survival (OS), disease-specific survival (DSS), and progression-free interval (PFI) (all P<0.05). Epigenetic analysis showed that ZBTB33 and NKRF could directly bind to the regulatory region of the ABCA7 gene, forming a ZBTB33/NKRF-ABCA7 transcriptional regulatory axis, and all three were significantly upregulated in CRC (P<0.05). Conclusion ·ABCA7 is highly expressed in CRC and associated with poor prognosis. The ZBTB33/NKRF-ABCA7 regulatory axis may be a key mechanism driving CRC progression. Figures and Tables | References | Related Articles | Metrics

Clinical research

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Effect of automatic tube current modulation on radiation dose and image quality of robotic-assisted hip CT HU Jie, YANG Xianfeng 2025, 45 (11):  1502-1506.  doi: 10.3969/j.issn.1674-8115.2025.11.009 Abstract ( 8 )   HTML ( 0 )   PDF (2630KB) ( 7 )   Objective ·To evaluate the feasibility of automatic tube current modulation (ATCM) in reducing radiation dose during preoperative CT imaging for robotic-assisted hip arthroplasty and to assess its impact on image quality. Methods ·A total of 106 patients undergoing CT scans for robotic-assisted hip arthroplasty at Nanjing Drum Tower Hospital (from November 2021 to October 2024) were prospectively enrolled. Participants were randomly divided into Group A (n=56) and Group B (n=50).The patients in Group A underwent ATCM scanning, and the patients in Group B underwent partial fixed tube current scanning for hip imaging. Radiation dose parameters included volume CT dose index (CTDIvol) and dose-length product (DLP). Image quality was evaluated using signal-to-noise ratio (SNR), contrast-to-noise ratio (CNR), and objective noise. Age, gender, body mass index (BMI), scan length, CTDIvol, DLP, SNR, CNR,noise,and image qualification rate were compared between the two groups. Results ·No statistically significant differences were observed between the two groups in baseline characteristics (gender, age, and BMI), scan length, image qualification rate, SNR, CNR, or objective noise (all P>0.05). However, Group A demonstrated significantly lower CTDIvol and DLP compared to Group B (both P<0.001). Conclusion ·The use of ATCM in preoperative CT imaging for robotic-assisted hip surgery significantly reduces radiation dose while maintaining image quality sufficient for 3D modeling requirements. Figures and Tables | References | Related Articles | Metrics

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A cone-beam computed tomographic study comparing characteristics of maxillary anterior regional alveolar bone remodeling under two reference systems LI Lulu, WU Jianyong 2025, 45 (11):  1507-1514.  doi: 10.3969/j.issn.1674-8115.2025.11.010 Abstract ( 7 )   HTML ( 0 )   PDF (9710KB) ( 4 )   Objective ·To compare differences in the bone remodeling/tooth movement ratio (B/T ratio) between the skeletal stable structure reference system and the dental long-axis reference system among extraction patients (extracted bilateral first premolars) undergoing maxillary anterior retraction and intrusion with micro-implant anchorages. Methods ·A total of 23 samples were retrospectively analyzed. Pretreatment and posttreatment cone-beam computed tomography (CBCT) data, along with pretreatment demographic (age, gender) and cephalometric parameters (ANB angle and FMA angle), were collected from patient records. All subjects underwent standardized orthodontic treatment protocols. Using Dolphin Imaging software, pretreatment and posttreatment CBCT images were superimposed. Labial inclination changes, incisal edge sagittal displacements, root apex sagittal displacements, and intrusion values were measured under skeletal stable structure reference system. For both group G (skeletal stable structure) and group Y (dental long-axis), tooth movement distances, bone remodeling distances, and B/T ratios were measured at three levels: alveolar crest (Level 1), mid-root (Level 2), and root apex (Level 3). Normalized data were compared to evaluate intergroup differences in B/T ratios. Results ·Average ANB and FMA angles were 6.00 °±2.08° and 30.24 °±5.95°, respectively, consistent with skeletal Class Ⅱ malocclusion and vertical hyperdivergence tendencies. The maxillary central incisors exhibited sagittal displacement gradients in which incisal edge displacements [right: (6.07±2.58) mm; left: (6.33±2.27) mm] exceeded apical displacements [right: (3.92±2.06) mm; left:(3.90±2.27) mm]. Concurrently, intrusion values demonstrated comparable vertical changes bilaterally [right: (2.90±1.51) mm; left: (2.87±1.80) mm], accompanied by labial inclination changes of 4.26°±9.19° (right) and 4.00°±8.84° (left). In group G, tooth movement distance progressively decreased from Level 1 to Level 3, whereas no such gradient was observed in group Y. Both groups demonstrated decreasing bone remodeling distances and B/T ratios from Level 1 to Level 3. After normalization, statistically significant intergroup differences (P<0.05) were identified across all measurement levels except for the B/T ratio at Level 1 of the left maxillary central incisor. Conclusion ·When evaluating alveolar bone remodeling during orthodontic retraction and intrusion of maxillary anterior teeth with micro-implant anchorages, the skeletal stable structure reference system provides more accurate assessments than the dental long-axis reference system, as the latter is susceptible to displacement artifacts inherent to the reference itself. Figures and Tables | References | Related Articles | Metrics

Techniques and methods

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An efficient isolation method for pericytes of the cochlear stria vascularis ZHU Yue, LI Xiaoqin, WANG Wenxiao, ZHOU Lingyun, WU Hao, TAO Yong, DU Tingting 2025, 45 (11):  1515-1526.  doi: 10.3969/j.issn.1674-8115.2025.11.011 Abstract ( 8 )   HTML ( 1 )   PDF (14921KB) ( 5 )   Objective ·To develop a stable and efficient method for isolating and obtaining pericytes from the cochlear stria vascularis while preserving their original physicochemical properties as much as possible. Methods ·Stria vascularis tissues were dissected from 6-day-old wild-type C57BL/6J mice under a microscope. Experimental conditions such as enzyme type, digestion time, and mechanical dissociation duration were optimized by evaluating single-cell yield and viability via flow cytometry (FCM). The single-cell samples were incubated with CD140b (i.e., platelet-derived growth factor receptor-β, PDGFR-β) and CD31 antibodies, and CD140b+CD31- and CD140b- cells were obtained by fluorescence-activated cell sorting (FACS). Reverse transcription quantitative polymerase chain reaction (RT-qPCR) was performed to assess the expression of pericyte markers [Pdgfrb and desmin (Desm)], endothelial cell markers [von Willebrand factor (Vwf)and glucose transporter 1 (Glut1)], and melanin-like macrophage markers [glutathione S-transferase α4 (Gsta4) and adhesion G protein-coupled receptor E1 (Adgre1)] to validate cell identity and the effectiveness of the isolation method. Results ·Flow cytometric analysis revealed that papain digestion of stria vascularis tissue caused significant cell damage and a high debris rate, cold-active protease showed low dissociation efficiency, and thermolysin combined with Accutase yielded unstable digestion efficiency and a relatively high debris rate. In contrast, Accutase alone consistently produced single-cell suspensions with relatively high yield and viability, and was therefore selected as the optimal enzyme. High-purity pericytes were successfully obtained by digesting stria vascularis tissue from 6-day-old mice with Accutase followed by sorting with CD140b and CD31 antibodies. RT-qPCR showed that CD140b+CD31- cells specifically exhibited high expression levels of pericyte markers Pdgfrb and Desm, and low expression levels of endothelial cell markers Vwf and Glut1, as well as melanin-like macrophage markers Gsta4 and Adgre1. Conclusion ·A stable and effective flow cytometry-based method for isolating pericytes from the stria vascularis is successfully established. Figures and Tables | References | Related Articles | Metrics

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Progress in applications of anti-senescence materials for tissue repair HOU Senlin, DENG Xiangtian, ZHENG Tingjia, HAN Yifei, LIU Shen 2025, 45 (11):  1527-1535.  doi: 10.3969/j.issn.1674-8115.2025.11.012 Abstract ( 12 )   HTML ( 10 )   PDF (2618KB) ( 8 )   Tissue repair is an important physiological process after tissue injury, but it is often disrupted by tissue fibrosis, oxidative stress, and other problems, accompanied by cellular senescence. Cellular senescence refers to the proliferation stagnation and function decline of cells under adverse stimuli, which plays a bidirectional regulatory role in tissue repair. In the early stage of wound healing, it can limit fibrosis and induce cell plasticity, thus promoting repair. Nevertheless, the long-term accumulation of senescent cells will interfere with the normal proliferation and differentiation of cells and hinder the repair process. In recent years, with the development of histology and cell biology, the mechanisms of tissue repair and cellular senescence have been deeply studied, providing a theoretical basis for the application of anti-senescence materials to tissue repair. Ingredients in anti-senescence materials, such as anti-senescence drugs, energy supplements, and antioxidants, play a favorable role by inducing apoptosis, activating autophagy, reversing the senescence process, and other mechanisms. The application of these anti-senescence materials provides new ideas to solve clinical problems like tissue fibrosis in chronic wounds, and is expected to become an effective means to intervene in tissue regeneration. In recent years, anti-senescence materials have been widely used in tissue regeneration and repair. This review may promote the translation and application of more fundamental research and provide references for clinical tissue repair. Figures and Tables | References | Related Articles | Metrics

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Review on the role of intrinsically photosensitive retinal ganglion cells in the onset and progression of mental disorders JIA Chenxi, ZHU Jiayi, DU Jiang, ZHAO Min 2025, 45 (11):  1536-1544.  doi: 10.3969/j.issn.1674-8115.2025.11.013 Abstract ( 10 )   HTML ( 0 )   PDF (949KB) ( 5 )   The retina is the peripheral sensor of light information and the only part of the central nervous system accessible to direct observation. It is also regarded as a “window to the brain” due to its developmental and structural similarity to the brain. Intrinsically photosensitive retinal ganglion cells (ipRGCs) within the neural retina transmit signals of environmental light changes to the brain via both intrinsic melanopsin-mediated currents and integrated signals from rod/cone input. ipRGCs project widely to multiple brain regions that regulate circadian rhythm, emotion, cognition and sleep. Numerous studies have indicated that ipRGC dysfunction may impair light-evoked emotional and sleep-wake behavioral changes, and may play a key role in the occurrence and development of insomnia, seasonal affective disorder, bipolar disorder, substance use disorder, and mental disorders associated with physical diseases. Therefore, understanding and futher exploring the function of ipRGCs may help discover potential treatment targets, which is of great value for improving the diagnosis and treatment of mental disorders. This review summarizes the physiological characteristics and functions of ipRGCs, as well as current research findings in animal models of mental disorders and in patients, aiming to provide references for future interventions targeting ipRGC function in mental disorders. References | Related Articles | Metrics

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Research progress on cognitive behavioral therapy in addressing weight regain XU Wenyi, ZHANG Zhiruo 2025, 45 (11):  1545-1551.  doi: 10.3969/j.issn.1674-8115.2025.11.014 Abstract ( 11 )   HTML ( 0 )   PDF (892KB) ( 5 )   Overweight and obesity are among the major public health concerns worldwide. Although conventional comprehensive interventions often enable short-term weight loss, weight regain remains prevalent. Cognitive behavioral therapy (CBT), a psychological intervention focused on modifying cognitions and behaviors, has been shown to help individuals with overweight or obesity achieve weight loss more effectively and healthily. It is regarded as one of the core evidence-based treatment modalities for weight management. From a neurobiological perspective, CBT enhances brain function, modulates the reward system, and alters neuroplasticity in individuals with excess weight, thereby significantly extending weight maintenance duration after intervention. Furthermore, CBT assists this population in identifying and modifying health-impairing thought patterns, fostering the adoption of healthy eating and physical activity habits, and effectively curbing weight regain. As CBT strategies are increasingly integrated into weight loss research, their application continues to evolve—shifting from traditional face-to-face sessions to digitally enabled interventions based on information and communication technologies. This transition not only improves intervention accessibility and engagement but also offers more personalized and convenient support for weight management. Future research should prioritize the local adaptation and technological innovation of CBT to enhance its scalability, positioning it as a vital tool in obesity prevention and control and thereby contributing substantially to improve public health outcomes. References | Related Articles | Metrics

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A case of primary pigmented nodular adrenocortical disease associated with germline PRKACA duplication variation ZHOU Jianhua, ZHANG Hongli, LI Xiaohua 2025, 45 (11):  1552-1558.  doi: 10.3969/j.issn.1674-8115.2025.11.015 Abstract ( 10 )   HTML ( 0 )   PDF (2533KB) ( 7 )   Primary pigmented nodular adrenocortical disease (PPNAD) is a rare subtype of adrenocorticotropic hormone (ACTH)-independent Cushing′s syndrome and the most common endocrine gland lesion in Carney complex (CNC). This article reported a case of PPNAD and CNC in an adult patient. The patient presented with speckled pigmentation around both eyes, lacked typical Cushingoid features, and exhibited symptoms of diabetes, hypertension, and osteoporosis. The circadian rhythm of blood cortisol levels disappeared, and neither the low-dose nor high-dose dexamethasone suppression tests were inhibited. The 24-hour urinary free cortisol was elevated. Enhanced adrenal computed tomography (CT) showed bilateral adrenal hyperplasia with uniform enhancement after contrast. Through genetic testing, an approximately 0.69Mbp duplication (copy number=3) was found in the 19p13.2-p13.12 region of the proband, which contained the protein kinase cAMP-dependent catalytic subunit α gene (PRKACA). The genetic test of the proband′s daughter also revealed the same genomic duplication. The patient was eventually diagnosed with PPNAD and CNC and underwent laparoscopic right adrenalectomy. Intraoperative pathology showed adrenal cortical hyperplasia and gray-brown nodules. Post-operative pathology confirmed adrenal cortical hyperplasia with abundant lipofuscin in the cytoplasm. The patient received short-term replacement therapy with prednisone acetate tablets, which was discontinued after 3 months. Currently, the patient′s condition is stable and further follow-up is in ongoing. Figures and Tables | References | Related Articles | Metrics