The hand constitutes a pivotal anatomical structure associated with human labor and mobility, and its morphological study holds significant value in fields such as anthropology and forensic medicine. The existing literature on hand morphology primarily encompasses the following aspects: sex, age, and population-based morphological variations; the determinants underlying morphological differences; the characterization of hand morphometric features; and the interdisciplinary applications of hand morphology research. By synthesizing empirical datasets and interpretive frameworks from pivotal studies, this paper delineates the patterns of morphological variation and the standardized measurement approaches employed in the field and examines the progress of domestic research in China and proposes prospective directions for future inquiry .

The convergence of 3D printing, virtual/augmented reality, and biosensing technologies has transformed medical teaching models from static anatomical displays into multi-dimensional platforms capable of dynamic functional simulation and pathological progression recapitulation. This review systematically examines high-quality studies from three key perspectives—technological integration, functional advancement, and disciplinary coverage— aiming to clarify innovative applications and educational effectiveness in both preclinical and clinical settings. Mounting evidence indicates that these novel models significantly improve students’ comprehension and retention of anatomical structures, physiological mechanisms, and disease processes, while also enhancing procedural accuracy, shortening learning curves, and boosting clinical competence. Nevertheless, challenges persist, including material performance constraints, a lack of standardized protocols, and cost-effectiveness imbalances that hinder widespread adoption. Future directions should prioritize intelligent models that integrate “structure–function–metabolism” linkages, hybrid training systems combining physical and virtual environments, affordable high-fidelity simulators, and the establishment of multi-center collaborative validation frameworks with interdisciplinary governance. These efforts will provide empirical evidence and strategic guidance for optimizing medical education resource allocation and facilitating broader technological adoption among the medic al training institutions.

Objective: To investigate whether high-intensity interval training (HIIT) promotes cerebral cortical angiogenesis in mice through the lactate/G-protein-coupled rece ptor 81 (GPR81)/extracellular signal-regulated kinase (ERK) signaling pathway. Methods: Nine-week-old C57BL/6J mice were randomly assigned to a control group or a HIIT group subjected to a 6-week training regimen. Mouse cerebral vascular endothelial cells (bEnd.3) were divided to control group, lactate group, lactate+ERK inhibitor group, GPR81 agonist group and GPR81 agonist+ERK inhibitor group. Cortical microvascular density and length were evaluated by immunofluorescence staining. Protein expression of collagen Ⅳ, GPR81, total ERK, and phosphorylated ERK (p-ERK) was analyzed by Western blotting. Cell migration, proliferation, and tube-forming ability were assessed by wound healing, CCK-8, and Matrigel tube formation assays, respectively. Results: A single bout of HIIT significantly elevated blood lactate levels. After the 6-week intervention, HIIT enhanced cortical angiogenesis, as indicated by increased microvascular density and length, and upregulation of collagen Ⅳ, GPR81, and p-ERK expression. In vitro, both lactate and GPR81 activation enhanced bEnd.3 cell proliferation, migration, and tube formation. Notably, ERK inhibition attenuated the lactateand GPR81 agonist-induced enhancement of these cellular functions. Conclusion: HIIT induces angiogenesis in the mouse cerebral cortex through the lactate/GPR81/ERK signaling p athway.

Objective: To explore the effects of ropivacaine (Rop) on labor pain in rats by regulating the protein kinase C epsilon (PKCε)/transient receptor potential vanilloid 1 (TRPV1) signaling pathway. Methods: Pregnant rats were randomly divided into control (normal delivery, intrathecal catheter injection of 0.9% normal saline), L-Rop, M-Rop, and H-Rop (intrathecal catheter injection of 0.5, 1.0, and 2.0 mg/kg Rop, respectively), and DCP-LA group (intrathecal catheter injection of 2 mg/kg Rop combined with intraperitoneal injection of 2.1 mg/kg DCP-LA, a PKCε/TRPV1 signaling pathway activator). The hot water tail-flick method was used to detect the threshold of labor pain. Sedation was assessed with the Richmond Agitation-Sedation Scale. ELISA was performed to detect serum levels of 5-hydroxytryptamine (5-HT), dynorphin (DYN), and glutathione (GSH). Immunohistochemical staining was adopted to measure brain-derived neurotrophic factor (BDNF) in spinal cord of rats. Western blotting was applied to detect PKCε/TRPV1 signaling pathway-related proteins in rat spinal cord. Results: Compared with the control group, the L-Rop, M-Rop, and H-Rop groups showed increased pain threshold, DYN, and GSH levels and decreased Richmond Agitation-Sedation Scale score, 5-HT, BDNF, PKCε, and TRPV1 expression. Compared with the H-Rop group, the DCP-LA group exhibited decreased pain threshold, DYN, and GSH levels, and increased Richmond Agitation-Sedation Scale score, 5-HT, BDNF, PKCε, and TRPV1 expression. Conclusion: Ropivacaine may alleviate labor pain in rats, which may be related to the inhibition of t he PKCε/TRPV1 signaling pathway.

Objective: To investigate the effect of long noncoding RNA (lncRNA) CALML3-AS1 on the proliferation and invasion of nasopharyngeal carcinoma cells and its underlying molecular mechanism. Methods: The lnCAR database was used to analyze the expression level of CALML3-AS1 in nasopharyngeal carcinoma tissues and its correlation with the clinical stage of nasopharyngeal carcinoma patients. The expression level of CALML3- AS1 in nasopharyngeal carcinoma cell lines (5-8F, C666-1, SUNE-1, CNE-2Z, and 6-10B) was detected by RTqPCR. CALML3-AS1 overexpression plasmid or corresponding control plasmid was transfected into C666-1 cells through liposome transfection technology and designated as the CALML3-AS1 group and NC group, respectively. Cell proliferation and invasion of C666-1 cells were detected by CCK-8 assay and Transwell assay. The targeting relationship between CALML3-AS1 and let-7i-5p was verified by dual-luciferase reporter gene experiment. The correlation between CALML3-AS1 and let-7i-5p expression in nasopharyngeal carcinoma tissues was analyzed by lnCAR database. RT-qPCR was used to detect the effect of CALML3-AS1 on the expression of let-7i-5p in C666-1 cells. Western blotting was adopted to detect the effect of CALML3-AS1 on the expression of proliferation and invasion-related proteins in C666-1 cells. Results: The expression of CALML3-AS1 was significantly lower in nasopharyngeal carcinoma tissues than that in adjacenttissues. The expression level of CALML3-AS1 was negatively correlated with the clinical stage of nasopharyngeal carcinoma patients. Compared with immortalized nasopharyngeal carcinoma NP69 cells, CALML3-AS1 was expressed at low levels in various nasopharyngeal carcinoma cells. Compared with the NC group, overexpression of CALML3-AS1 could inhibit the proliferation of C666-1 cells. The number of invading cells was (141.00±7.26) in the NC group and (25.30±6.07) in the CALML3-AS1 group, indicating that overexpression of CALML3-AS1 could significantly inhibit the invasion of C666-1 cells. CALML3-AS1 could directly target and bind to let-7i-5p. The expression of CALML3-AS1 was negatively correlated with let-7i-5p in nasopharyngeal carcinoma tissues. Overexpression of CALML3-AS1 could downregulate the expression of let-7i-5p. Compared with the NC group, the expression of proliferation-related proteins (cyclin E and cyclin-dependent kinase 2) in C666-1 cells in the CALML3- AS1 group and invasion-related proteins (transforming growth factor-β and fibronectin) decreased. Conclusion: Overexpression of CALML3-AS1 can inhibit the proliferation and invasion of nasopharyngeal carcinoma C666-1 cells, and its mechanism may be related to the tar geted downregulation of let-7i-5p expression.

Objective: To explore the effect of Poria cocos polysaccharide on gastric mucosal injury in rats with chronic atrophic gastritis (CAG) and explore its potential mechanism involving the interleukin (IL)-10(IL-10)/JAK1/ STAT3 signaling pathway. Methods: SD rats were randomly divided into the following groups: control, model, Poria cocos polysaccharide, Poria cocos polysaccharide+RO8191 (a JAK/STAT3 signaling pathway activator), and Poria cocos polysaccharide+IL-10 neutralizing antibody. A CAG rat model was established by using N-methyl-N’-nitro-Nnitrosoguanidine (MNNG) combined with irregular feeding. After intervention with Poria cocos polysaccharides, the pH value of rat gastric juice was measured. ELISA was applied to measure serum levels of gastric function-related indicators and inflammatory cytokines. H-E staining was performed to evaluate gastric mucosal histopathological change. Immunohistochemical staining was employed to detect the numbers of G cell and D cell in the gastric mucosa of rats. TUNEL staining was applied to detect apoptosis of gastric mucosal tissue cells of rats. Western blotting was adopted to detect the IL-10/JAK1/STAT3 signaling pathway-related proteins in the gastric mucosal tissues of rats. Results: Compared with the control group, the model group showed significant pathological damage in gastric mucosa, with increased gastric juice pH value, gastric mucosal tissue cell apoptosis index, IL-8 and IL-6 levels, and elevated p-JAK1/JAK1 and p-STAT3/ STAT3 ratios, while gastrin, motilin, G cell and Dcell optical density values, and serum and tissue protein expression of IL-10 were decreased. Compared with the model group, the Poria cocos polysaccharide group exhibited alleviated gastric mucosal damage, decreased gastric juice pH value, gastric mucosal tissue cell apoptosis index, IL-8 and IL-6 levels, and p-JAK1/JAK1 and p-STAT3/ STAT3 ratios, along with increased gastrin, motilin, G cell and D cell optical density values, and IL-10 expression. Compared with the Poria cocos polysaccharide group, both the Poria cocos polysaccharide+RO8191 and the Poria cocos polysaccharide+IL-10 neutralizing antibody groups showed aggravated pathological damage to gastric mucosal tissue, increased gastric juice pH value, gastric mucosal tissu e cell apoptosis index, IL-8 and IL-6 levels, and p-JAK1/ JAK1 and p-STAT3/STAT3 ratios, while decreased gastrin, motilin, G cell and D cell optical density values, and IL- 10 serum and protein expression. Conclusion: Poria cocos polysaccharide can alleviate gastric mucosal injury in CAG rats, possibly by modulating the IL-10/JAK1/ST AT3 signaling pathway.

Objective: To investigate the molecular mechanisms by which nuclear factor erythroid 2-related factor 2 (Nrf2), highly expressed in nasopharyngeal carcinoma (NPC), leads to M2 polarization and promotes tumor proliferation in NPC by regulating the Nrf2/NADPH oxidase 2(NOX2)/spleen tyrosine kinase(SYK)/Src homology 2 domain-containing protein tyrosine phosphatase 2(SHP2) signaling pathway in tumor-associated macrophages (TAMs). Methods: The GSE12452 dataset from the GEO database was selected for bioinformatics analysis to investigate the effect of Nrf2 expression level on NPC progression. THP-1 cells were selected for analysis and induced with PMA to differentiate into macrophages. The induced macrophages were divided into the following groups: control (NC group), Nrf2-knockdown (Nrf2-KD), Nrf2-KD+SYK inhibitor, and Nrf2+SHP2 agonist groups. Nrf2, NOX2, SYK, and SHP2 protein expression levels were detected by Western blotting. q-PCR was performed to detect the mRNA expression of M1 and M2 markers. Cell proliferation, migration, and invasion abilities were assessed by Transwell assays. Results: Nrf2 and SHP2 protein expression decreased and NOX2 and SYK protein expression increased in the Nrf2-KD group compared with the NC group. Compared with the Nrf2-KD group, NOX2 and SYK protein expression decreased and SHP2 protein expression increased in the Nrf2-KD+SYK inhibitor group. Compared with the NC group, the mRNA expression of the M1 markers (IL-1β, TNFα, and IL-8) was upregulated, and the mRNA expression of the M2 markers(Arginase-1, CD206, and YM-1) was down-regulated in the Nrf2-KD group. Administration of a SYK inhibitor reversed this effect, decreasing M1 markers and increasing M2 markers compared to the Nrf2-KD group. Knockdown of Nrf2 reduced cell proliferation and invasion capabilities, compared to the NC group. However, the addition of a SYK inhibitor enhanced proliferation and invasion, which was reversed by an SHP2 agonist. Conclusion: Nrf2 in NPC promotes M2 polarization of TAMs by regulating the NOX2/SYK/SHP2 signaling pathway in TAMs, thereby enhancing the proliferation and invasion abilities of NPC cells .

Objective: To investigate the effect of long noncoding RNA00852 (LINC00852) on the malignant progression of esophageal squamous cell carcinoma (ESCC) cells by regulating the microRNA-671-5p (miR-671-5p)/ SET domain-containing protein 5 (SETD5) axis. Methods: RT-qPCR was used to measure the expression levels of LINC00852, miR-671-5p, and SETD5 mRNA in the ESCC tissues and adjacent non-tumor tissues from 56 ESCC patients who underwent surgery in our hospital from March 2023 to March 2024. Human esophageal squamous cell carcinoma cell line TE11 cells were selected as research objects and divided into five groups: Control, sh-NC, sh- LINC00852, sh-LINC00852+anti-NC, and sh-LINC00852+anti-miR-671-5p. EdU staining, Transwell assay, and flow cytometry were applied to detect the effects of LINC00852 silencing on the proliferation, migration, invasion, and apoptosis of TE11 cells. Western blotting was employed to measure the expression of PCNA, SETD5, MMP-9, and Bax proteins in TE11 cells. Dual-luciferase reporter gene assay was utilized to determine the interaction between LINC00852 and miR-671-5p, and between miR-671-5p and SETD5. Results: The expression of LINC00852 and SETD5 mRNA in ESCC tissues was higher than that in adjacent non-tumor tissues, while the expression of miR-671-5p was lower. The EdU-positive cell rate, migration and invasion numbers, LINC00852, SETD5 mRNA and protein levels, PCNA and MMP-9 protein levels in the sh-LINC00852 group were lower than those in the sh-NC group and the Control group, while the apoptosis rate, miR-671-5p, and Bax protein levels were higher than those in the sh-NC group and the Control group. Compared with the sh-LINC00852 group and the sh-LINC00852+anti-NC group, the sh-LINC00852+anti-miR-671-5p group showed increased EdU-positive cell rate, migrationand invasion numbers, SETD5 mRNA and protein levels, PCNA and MMP-9 protein expression, but decreased apoptosis rate, miR-671-5p expression, and Bax protein expression. Conclusion: LINC00852 promotes the malignant progression of ESCC cells by regulating the miR-671-5p/SETD5 ax is.

Objective: To investigate the effects of polydatin on the proliferation, migration, invasion, and radiation sensitivity of esophageal cancer cells by regulating the Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signaling pathway. Methods: Human esophageal cancer cells (KYSE-150) in logarithmic growth phase were randomly divided into blank group, 50 and 100 μmol/L polydatin groups, polydatin (100 μmol/L) + pcDNA-NC (transfected with pcDNA-NC plasmid) group, and polyd atin (100 μmol/L) + pcDNA-JAK2 (transfected with pcDNA-JAK2 plasmid) group. MTT assay was used to detect cell proliferation. Wound healing assay was performed to detect cell migration. Transwell chamber experiment was adopted to detect cell invasion. Clonogenic survival assay was applied to detect cell radiation sensitivity. RT-qPCR was utilized to detect the expression of JAK2 and STAT3 mRNA in cells. Western blotting experiments were employed to detect JAK2 and STAT3 proteins and their phosphorylation levels in cells. Results: Compared with the blank group, the OD490nm value, cell migration rate, number of invading cells, post-radiation cell survival fraction, JAK2 and STAT3 mRNA expression, and p-JAK2/JAK2 and p-STAT3/STAT3 levels of cells in the 50 μmol/L and 100 μmol/L polydatin groups decreased, with more pronounced effects observed at 100 μmol/L group. Compared with polydatin+pcDNA-NC group, the polydatin+pcDNA-JAK2 group showed increased OD490nm values, cell migration rate, number of invading cells, postradiation cell survival fraction, JAK2 and STAT3 mRNA expression, and the ratios of p-JAK2/JAK2 and p-STAT3/ STAT3, with no significant difference between the polydatin+pcDNA-NC group and the 100 μmol/L polydatin group. Conclusion: Polydatin suppresses the proliferation, migration, and invasion of esophageal cancer cells, and enhances radiation sensitivity, likely through inhibiting the JAK2/STAT3 signaling pathway.

Objective: To explore the effects of isovitexin on cisplatin resistance in esophageal cancer cells and its potential molecular mechanism. Methods: EC109/DDP cells were divided into control group, isovitexin group (16 μmol/L), cisplatin group (10 μmol/L), isovitexin+cisplatin group (16 μmol/L isovitexin+10 μmol/L cisplatin), and isovitexin+Wnt/β-catenin pathway activator (LiCl) group (16 μmol/L isovitexin+20 mmol/L LiCl). Flow cytometry was applied to observe the cell cycle distribution and apoptosis of EC109/DDP. Transwell assay was adopted to detect the invasion and migration of EC109/DDP cells. RT-qPCR was employed to determine the mRNA expression of drug resistance genes multidrug resistance-associated protein 1 (MRP1) and glutathione S-transferase π (GST-π) in EC109/DDP cells. Western blotting was utilized to assess the expression of Wnt, β-catenin, E-cadherin, Vimentin, and P-glycoprotein (P-gp) proteins in EC109/DDP cells. Results: Compared with the control group, isovitexin treatment significantly reduced the viability of EC109/DDP cells exposed to various concentrations of cisplatin. The IC50 of the control group was 34.72 μmol/L, and the IC50 of the isovitexin group was 13.06 μmol/L, with a reversal index (RI) of 2.66. Compared with the control group, the apoptosis rate of EC109/DDP cells and the expression of E-cadherin protein in the isovitexin group, cisplatin group and isovitexin+cisplatin group were significantly increased, while the proportions of cells in S phase and G2/M phase, and the numbers of cell invasion and migration were significantly reduced. The proportion of cells in G0/G1 phase was significantly increased, while the mRNA expressions of MRP1, GST-π and the protein expression of Vimentin, Wnt, and β-catenin were significantly decreased. Compared with isovitexin group and cisplatin group, the above indexes of EC109/DDP cells in isovitexin+cisplatin group were more pronounced. LiCl partially reversed the effect of isovitexin on cisplatin resistance in EC109/DDP cellsConclusion: Isovitexin may inhibit the Wnt/β-catenin pathway, reducing the malignant biological behavior of EC109/ DDP cells and the expression of drug resistance genes, and counter acting cisplatin resistance in EC109/DDP cells.

目的：探讨长链基因间非编码RNA1018（LINC01018）对非小细胞肺癌（NSCLC）A549 细胞增殖、侵 袭、迁移和凋亡的影响及其机制。方法：将体外培养A549 细胞分为未转染组（ 正常培养）、空载体组（ 转染 pcDNA3.1 空载体质粒）和LINC01018 组（ 转染LINC01018-pcDNA3.1 过表达质粒），采用Real-time PCR 检测 细胞中LINC01018 和微小RNA（miR）-346 水平，MTT 法和克隆形成实验检测细胞增殖能力，Transwell 小室 检测细胞侵袭和迁移，流式细胞术检测细胞凋亡情况。生物信息学软件预测、双荧光素酶实验检测LINC01018 和miR-346 的关系。结果：与BEAS-2B 细胞比较，LINC01018 在A549 细胞中表达降低。与未转染组比较， LINC01018 组细胞中LINC01018 的表达和细胞凋亡率明显升高，而细胞存活率、克隆形成率和miR-346 的表达水 平明显降低，且侵袭细胞数、迁移细胞数明显减少；但空载体组和未转染组之间上述指标差异均无统计学意义。 双荧光素酶报告基因实验证实LINC01018 可直接与miR-346 靶向结合。结论：LINC01018 通过靶向调控miR-346 抑制NSCLC细胞的增殖、迁移、侵袭，并发挥促凋亡的作用。Objective: To investigate the effects of long intergenic non-coding RNA 1018 (LINC01018) on proliferation, invasion, migration and apoptosis of non-small cell lung cancer (NSCLC) A549 cells and its underlying mechanism. Methods: Cultured A549 cells were divided into three groups: non-transfected (normal culture), empty vector (transfected with pcDNA3.1 empty vector plasmid) and LINC01018 groups (transfected with LINC01018- pcDNA3.1 overexpression plasmid). The expression levels of LINC01018 and microRNA (miR)-346 in the cells were detected by real-time PCR, cell proliferation by MTT and colony formation assays, cell invasion and migration by Transwell chamber, and apoptosis by flow cytometry. The targeting relationship between LINC01018 and miR- 346 was predicted by bioinformatics software and verified by dual-luciferase reporter assay. Results: Compared with BEAS-2B cells, the expression level of LINC01018 in A549 cells decreased significantly. Compared with the nontransfected group, the expression level of LINC01018 and apoptosis rate in LINC01018 group were significantly increased, while the cell survival rate, colony formation rate, and miR-346 expression level were significantly reduced. The number of invading and migrating cells was significantly reduced. However, there were no statistically significant differences in the above indicators between the empty vector and the non-transfected groups. The dualluciferase reporter assay confirmed that LINC01018 could directly target and bind to miR-346. Conclusions: LINC01018 inhibits proliferation, migration and invasion, and promotes apoptosis in NSCLC cells by directly targeting and negatively regulating miR-346.

Objective: To explore the relationship between the ratio of index finger length (2D) to ring finger length (4D) and simple eye-hand reaction time（ SERT）in college students. Methods: According to standard anthropometric methods, the lengths of the index and the ring fingers were measured by using a digital vernier caliper. An eye-hand reaction time tester was used to measure SERT. Results: For both males and females, the 2D of the left and right hand was shorter than the 4D, with a statistically significant difference. There were statistically significant differences in the 2D∶4D ratio between the left and right hands in both genders, whereas no significant sex differences were observed in either left- or right-hand 2D∶4D. For males, the SERT of the left hand was (244.00±31.72) ms, which was lower than that of the right hand (248.75±34.39) ms, showing a significant difference. Notably, a positive correlation was identified between the right-hand 2D∶4D and SERT in male students. Conclusion: The correlation between 2D∶4D and SERT in college students presents obvious gender and hand-specific patterns. Specifically, a positive correlation was observed between right-hand 2D∶4D and SERT in male college students, which could provide a foundational reference for the screening of characteristic indicators in athletic talent identification and selection. Nevertheless, further studies are required to verify its feasibility as a reference indicator for sports talent selection.

Spatially resolved transcriptomics (SRT) technologies, with its advantages of high resolution and highthroughput sequencing, allows for the quantitative and spatial visualization of gene expression and positional information of different cell types within tissues, offering significant value in histopathological research. This review summarizes the development of SRT technologies and its applications in oncology, tissue pathology, and developmental biology. The paper focuses on the exploration of tumor heterogeneity, optimization of tissue pathological diagnostics, and the discovery of new cell types, while also discussing the potential of SRT technology for clinical translation.

Parkinson’s disease (PD) is the second most prevalent neurodegenerative disease of the central nervous system worldwide, with its core feature being the loss of dopaminergic neurons in the substantia nigra of the midbrain. Protein homeostasis dysfunction constitutes a critical pathogenic event, mainly caused by disorders of the protein clearance system. Among them, abnormal aggregation of α-synuclein (α-syn) induced by functional abnormalities of the ubiquitin-proteasome system (UPS) and autophagy-lysosome system (ALS) is an important factor driving the pathological process of PD. This review focuses on the association between UPS and ALS dysfunction and the pathogenesis of PD, and systematically summarizes the research achievements on the role of protein clearance system disorders in the pathogenesis of PD. Studies have shown that in hereditary PD, mutations in the Parkin and UCH-L1 genes can disrupt the normal protein degradation function of UPS; in sporadic PD, decreased levels and activity of key UPS components enhance the vulnerability of dopaminergic neurons in the substantia nigra; different types of ALS dysfunction play heterogeneous roles in α-syn degradation and Lewy body formation, and the dual role of autophagy affects the therapeutic effect of PD. Disorders of the protein clearance system composed of UPS and ALS are closely related to the occurrence and development of PD, and in-depth clarification of its mechanism of action can provide an important theoretical basis for the prevention, treatment strat egies and new drug research and development of PD.

Post-stroke depression (PSD) is closely associated with the phenotypic polarization of microglia in the central nervous system and the regulation of immuno-inflammatory responses, offering new perspectives for the prevention and treatment of PSD. To systematically elucidate the roles of M1 and M2 microglial phenotypes and their associated inflammatory cytokines in PSD. This review systematically elucidates the roles of the M1 and M2 microglial phenotypes and their associated inflammatory cytokines in PSD, outlines key signaling pathways regulating the activation and polarization of M1 and M2 phenotypes, and highlights the central role of M1/M2 imbalance in the progression of neuroinflammation in PSD. This provides a theoretical foundation for understanding the immunoinflammatory mechanisms underlying PSD and offers insights for the identification of potential novel therapeutic targets.

Objective: To compare the effects of two different staining methods, drop staining and immersion staining, on rhodanine staining effect for copper granules in liver tissue specimens. Methods: A total of 42 pathological specimens with positive copper rhodanine staining diagnosed at our department from 2019 to 2024 were included. The specimens were stained by using the immersion staining method and the drop staining method. The positive staining rate, staining intensity, and integrated optical density (IOD) of rhodanine-stained copper granules were compared between the two met hods. The Student’s t-test was used to compare the IOD values of the two groups; the McNemar’s test was used to analyse the positive rates of the two groups; and Pearson’s chi-square test was used to analyse the expression intensities of the two groups. Results: Both staining methods exhibited no significant difference in the positive rate of the copper rhodanine staining. However, the drop staining method resulted in stronger positive expression intensity and higher IOD values. Conclusion: The drop staining method in rhodanine staining for copper granules achieves diagnostic efficacy comparable to that of the immersion method, while offering advantages such as broader positive staining areas, deeper color intensity, ease of interpretation, and lower cost. It is thus worthy of wider clinical promotion.