The foot is a critical weight-bearing and locomotive organ of human body, with its morphological and dimensional variations influenced by factors such as gender, age and ethnicity. The morphological characteristics and dimensions of the foot during different periods also have a significant impact on athletic performance and competitive abilities. Current research on foot morphology encompasses age, gender, and ethnic differences in foot morphology; factors influencing foot morphology; methods for collecting foot-related data; and applications of foot morphology. This review summarizes research data and conclusions from existing literature, outlines the current state of foot morphology variation studies and related measurement methods, and examines domestic research progress while offering future prospects.

Objective: To investigate whether melatonin can alleviate ferroptosis induced by RAS-selective lethal small molecule 3 (RSL3) in AML12 cells and the role of melatonin receptor 1 (MT1) in the process. Methods: A ferroptosis model of AML12 cells was established via RSL3 induction. Cell viability was assessed by CCK-8 staining. Intracellular ferrous ion (Fe2+), reactive oxygen species (ROS), and lipid peroxidation levels were detected through fluorescent probe staining. Expressions of MT1 and ferroptosis-related proteins, namely long-chain acyl- CoA synthetase 4 (ACSL4) and glutathione peroxidase 4 (GPX4), were measured by Western blotting. The impact of MT1 knockdown on the effects of melatonin was observed using the broad-spectrum receptor antagonist of melatonin, N-acetyl-2-benzyltryptamine (Luz) and small RNA interference technology. Results: After RSL3 induction, AML12 cell viability decreased, GPX4 expression was reduced, and ACSL4 expression was increased, along with elevated levels of intracellular Fe2+, ROS, and lipid peroxidation. Melatonin pretreatment antagonized the changes in cell viability, ferroptosis-related proteins, intracellular Fe2+, ROS, and lipid peroxidation. RSL3 induction led to a decrease in MT1 expression in AML12 cells, which was rescued by melatonin administration. Luz and MT1 knockdown could both antagonize the protective effect of melatonin on AML12 cell ferroptosis. Conclusion: Melatonin may alleviate RSL3-induced ferroptosis in AML12 cells via MT1.

Objective: To investigates the role of Wnt/β-catenin signaling pathway in the phenotypic transformation of astrocytes in diabetic encephalopathy. Methods: A diabetic mouse model was established by feeding the mice with high-fat diet for 12 weeks. Twelve C57BL/6 mice were randomly divided into control group and diabetic groups. The blood glucose level and body weight of the mice were detected at 0 and 12 weeks. Immunofluorescence was used to detect the expression of A1 astrocyte marker C3 and A2 astrocyte marker S100A10 in the hippocampus. C8- D1A astrocyte cell line was used to establish three groups: control, palmitic acid (PA)-treated, and PA+Wnt pathway activator (SKL2001). cell viability at various PA concentrations (0, 50, 100, 200, 300 μmol/L) was assessed through the CCK-8 assay. Lipid accumulation in C8-D1A astrocytes was evaluated by using Oil Red O staining. Western blotting analysis was performed to measure the protein expression levels of GFAP, C3, S100A10, Wnt3a, β-catenin, p-GSK3β and GSK3β. Immunofluorescencewas used to visualize the expression of C3/GFAP, S100A10/GFAP, Wnt3a and β-catenin in astrocytes. Results: Compared with the control group, the blood glucose level and body weight of the diabetic group were significantly increased. The fluorescence intensity of C3 in the hippocampus of diabetic mice was significantly higher than that of the control group, but the fluorescence intensity of S100A10 was not significantly different between the two groups. Compared with the control group, PA treatment significantly inhibited the cell viability in a concentration-dependent manner. Oil Red O staining showed orange-red lipid droplets in the cytoplasm of C8-D1A cells in PA-treated groups. Western blotting results showed that the protein expressions of GFAP and C3 in the PA group were significantly higher than those in the control group, while the protein expressions of Wnt3a, β-catenin, and p-GSK3β/GSK3β in the PA group were significantly lower than those in the control group. In the PA+SKL2001 group, SKL2001 partially reversed the PA-induced changes in protein expression. No significant differences were found in S100A10 protein expression among the three groups. Immunofluorescence results confirmed that compared with the control group, the fluorescence intensity of C3/GFAP in the PA group was increased. Compared with the PA group, the fluorescence intensity of C3/GFAP was decreased in the PA+SKL2001 group, while the fluorescence intensity of S100A10 did not differ significantly between groups. Compared with the control group, the fluorescence intensity of Wnt3a and the translocation of β-catenin into the nucleus in the PA group decreased. Compared with the PA group, both indicators above were increased in the PA+SKL2001 group. Conclusion: In diabetic encephalopathy, the transformation of astrocyte phenotype may be caused by inhibiting the expression of Wnt/β-catenin signaling pathway-related proteins, leading to the transformation of astrocytes into type A1, thereby exacerbating disease progression.

Objective: To investigate the changes in levels of ubiquitin-specific protease 39 (USP39) and homeobox protein hox B13 (HOXB13) in lung cancer tissues and their relationship with clinical pathological characteristics and prognosis of patients. Methods: A total of 102 cases of patients diagnosed with lung cancer in our hospital from August 2018 to August 2020 were collected. A three-year prognosis follow-up was conducted on the patients. ELISA method was applied to detect the levels of USP39 and HOXB13 in adjacent normal and lung cancer tissues. Immunohistochemical staining was adopted to detect the expression of USP39 and HOXB13 in adjacent normal and lung cancer tissues. Kaplan-Meier analysis was performed to analyze the relationship between USP39 and HOXB13 levels in lung cancer tissue and prognosis. COX regression was employed to analyze the influencing factors of prognosis in lung cancer. Results: The expression levels of USP39 and HOXB13 in the lung cancer group were obviously higher than the adjacent group. The positive expression rates of USP39 and HOXB13 in the lung cancer group were obviously higher than those in the adjacent group. The expression of USP39 and HOXB13 was correlated with clinical TNM staging, differentiation degree, and lymph node metastasis. Kaplan-Meier curve analysis showed that the survival rate of lung cancer patients with positive expression of USP39 and HOXB13 was obviously lower than that of patients with negative expression. COX analysis results showed that lymph node metastasis, USP39, and HOXB13 expression levels were prognostic factors for lung cancer patients. Conclusion: USP39 and HOXB13 are highly expressed in lung cancer tissues, which are associated with the clinical pathological characteristics and prognosis of patients.

Objective: To investigate the effect of long non-coding RNA (lncRNA) cancer susceptibility candidate 9 (CASC9)/miR-874-3p/a disintegrin and metalloproteinase 19 (ADAM19) axis on the proliferation, migration and invasion of retinoblastoma (RB) cells. Methods: Real-time fluorescence quantitative PCR method was applied to detect the expression levels of CASC9, miR-874-3p, and ADAM19 mRNA in RB tumor tissues and cells. Immunohistochemistry was used to detect the expression of ADAM19 protein. CCK-8 method and Transwell assay were applied to evaluate the cell proliferation, migration, and invasion. Western blotting was used to detect the expression of E-cadherin, N-cadherin, Vimentin and ADAM19 proteins. Dual-luciferase reporter assays were employed to verify the relationship between miR-874-3p and CASC9 or ADAM19. Results: CASC9 and ADAM19 were highly expressed in RB tumor tissues, while miR-874-3p showed low expression. Knockdown of CASC9 inhibits cell proliferation, migration, and invasion, and reduced the expressions of ADAM19, N-cadherin and Vimentin, while promoting the expression levels of miR-874-3p and E-cadherin. Inhibition of miR-874-3p weakened the effects of knockdown of CASC9 on cell proliferation, migration, invasion and protein expression. CASC9 targeted and negatively regulated miR-874-3p expression, while miR-874-3p targeted and negatively regulated ADAM19 expression. Conclusion: Knocking down CASC9 may inhibit the expression of ADAM19 protein by up-regulating miR-874-3p, thereby inhibiting the proliferation, migration, and invasion of doi ： 10.3969/j.issn.1001-1633.2025.03.005 ·论 著· RB cells

Objective: To investigate the impacts of long non-coding RNA KCNQ1 overlapping transcript 1 (LncRNA KCNQ1OT1) on proliferation and radiation sensitivity of glioma cells, and its regulatory mechanism on the miR-181a-5p/TRIM71 pathway. Methods: Human glioma cells U251 were divided into NC group (untransfected plasmid), si-NC group (transfected with KCNQ1OT1 negative control), si-KCNQ1OT1 group (transfected with si-KCNQ1OT1), si-KCNQ1OT1+miR-NC group (co-transfected with si-KCNQ1OT1 and miR-181a-5p negative control), si-KCNQ1OT1+miR-181a-5p inhibitor group (co-transfected with si-KCNQ1OT1 and miR-181a-5p inhibitor). After 48 hours of transfection, cells selected from each group were irradiated with 6 Gy radiation. RT-qPCR method was applied to detect the levels of KCNQ1OT1, miR-181a-5p, and TRIM71 mRNA of cells in each group. CCK-8 method and colony formation assay were applied to assess the proliferation activity of transfected cells in each group. Flow cytometry was adopted to detect the apoptosis of transfected cells in each group. Western blotting was performed to measure the relative expression levels of TRIM71 protein in transfected cells of each group. Dual luciferase reporter gene assay was applied to verify the targeting relationship between miR-181a-5p and KCNQ1OT1, TRIM71. Results: Compared with the si-NC group, the expression levels of KCNQ1OT1 and TRIM71 mRNA, cell survival rate, and number of clones formed in the si-KCNQ1OT1 group decreased, while the expression l e v e l o f m i R - 1 8 1 a - 5 p i n c r e a s e d . A f t e r v e r t i c a l irradiation with 6 Gy of radiation, the survival rate of transfected cells in all groups decreased, while the apoptosis rate increased. Among them, the survival rateof cells in the si-KCNQ1OT1+6Gy group was lower than that in the si-NC+6Gy group, while the apoptosis rate was higher in the si-NC+6Gy group. The rescue experiment demonstrated that miR-181a-5p inhibitor reversed the effects of KCNQ1OT1 knockdown on cell proliferation and radiotherapy sensitivity. Dual luciferase activity confirmed the targeting relationship between miR-181a-5p and KCNQ1OT1, or TRIM71. Conclusion: KCNQ1OT1 knockdown can inhibit the proliferation of glioma cells and improve their radiotherapy sensitivity by up-regulating miR-181a-5p and down-regulating TRIM71 expression.

Objective: To investigate the molecular mechanism by which the long non-coding RNA (lncRNA) LINC01510 promotes the proliferation, metastasis and invasion of osteosarcoma cells by targeting cyclin-dependent kinase 14 (CDK14). Methods: The differences in expression of LINC01510 and CDK14 between normal and tumor tissues of osteosarcoma patients, and between human normal osteoblasts and osteosarcoma cell lines were investigated by RT-qPCR and Western blotting. Cell transfection, SRB staining, and colony formation assays were performed to investigate the effects of LINC01510 knockdown on osteosarcoma cell proliferation. The impact of LINC01510 knockdown on the cell metastasis and invasion of osteosarcoma cells was assessed by using cell transfection techniques and Transwell assays. Bioinformatics tools and methods were employed to identify the miRNAs that interact with LINC01510 and CDK14. RNA immunoprecipitation assays and RT-qPCR techniques were utilized to examine the binding interactions between LINC01510, CDK14 and miR-339-5p. The dual luciferase reporter gene system, cell transfection technique and RT-qPCR technique were adopted to examine the regulatory mechanisms of LINC01510, CDK14 and miR-339-5p. Results: The expression levels of LINC01510 and CDK14 were significantly upregulated in patients’ osteosarcoma tissues and immortalized osteosarcoma cell lines. Knockdown of LINC01510 inhibited the proliferation, metastasis and invasion of osteosarcoma cells. LINC01510 knockdown suppressed CDK14 expression by up-regulating miR-339-5p targeting the 3'-UTR of CDK14. LINC01510/miR- 339-5p/CDK14 signaling axis regulated proliferation, invasion and metastasis of osteosarcoma cells. Conclusion: LINC01510 regulates CDK14 expression by targeting the 3’-UTR region via miR-339-5p, eventually regulating the proliferation, invasion and metastasis of osteosarcoma cells.

Objective: To investigate the effects of propofol on the proliferation, migration and invasion of gastric cancer cells by targeting glucose-6-phosphate dehydrogenase (G6PD) through microRNA-613 (miR-613). Methods: Gastric cancer cells SGC7901 were cultured in vitro and divided into control group, propofol group, propofol+inhibitor NC group, propofol+miR-613 inhibitor group, propofol+miR-613 inhibitor+si-NC group, and propofol+miR-613 inhibitor+si-G6PD group. Real-time fluorescence quantitative PCR (RT-qPCR) was applied to detect the miR-613 expression. CCK-8 experiment was applied to detect cell proliferation. Flow cytometry was employed to detect cell apoptosis. Transwell assay was adopted to detect cell migration and invasion. Western blotting was performed to detect the expression of G6PD and epithelial mesenchymal transition (EMT) marker proteins, and dual-luciferase reporter assay was utilized to confirm the targeting relationship between miR-613 and G6PD. Results: Compared with the control group, the numbers of SGC7901 cell migration and invasion was decreased significantly, along with a significant decrease in OD450 value, G6PD, and N-cadherin expression in the propofol group, while the apoptosis rate, miR-613, and E-cadherin expression were obviously increased. Inhibiting the expression of miR- 613 weakened the inhibitory effect of propofol on the proliferation, migration, and invasion of gastric cancer cells. The low expression of G6PD reversed the promoting effect of miR-613 silencing on the proliferation, invasion, and migration of gastric cancer cells. Conclusion: Propofol may inhibit the proliferation, migration, and invasion of gastric cancer cells by targeting G6PD through miR-613.

Objective ：To investigate the effect of fasudil on the proliferation, apoptosis and angiogenesis of bladder cancer cells by regulating RhoA/ROCK signaling pathway. Methods ： T24 cells of bladder cancer were divided into control group, low-dose fasudil group, medium-dose fasudil group, high-dose fasudil group, and high-dose fasudil + Naciclassine (RhoA activator) group. MTT and EdU assays were adopted to detect cell proliferation. Transwell assay was applied to detect cell migration and invasion. Flow cytometry was employed to detect cell apoptosis rate. Threedimensional Matrigel culture was performed to observe angiogenesis. Western blotting was utilized to detect the expression levels of vascular endothelial growth factor A (VEGF-A), vascular endothelial cadherin (VE cadherin), Ki-67, MMP-9, caspase-3, RhoA, and ROCK proteins in cells. Results ： The control group cells had good lumen structure. Compared with the control group, the lumen structure of T24 cells in the low, medium, and high-dose fasudil groups showed varying degrees of damage, and the OD490 values (at 24 h and 48 h), cell viability, numbers of cell migration and invasion, the expression of VEGF-A, VE cadherin, Ki-67, MMP-9, RhoA, and ROCK proteins were obviously reduced, while the apoptosis rate and the expression of caspase-3 protein were obviously increased. Naciclassine partially reversed the inhibitory effect of fasudil on T24 cells. Conclusion ： Fasudil can inhibit the malignant biological behavior of bladder cancer cells, possibly by blocking the RhoA/ROCK signaling pathway activation.

Objective ：To explore the association between single nucleotide polymorphisms (SNPs) in five loci (rs77640775, rs2051935, rs3823720, rs1125413, rs846266) of GLI zinc finger 3 gene (GLI3) and the second to fourth digit ratio (D2/4). Methods ：A total of 807 college students (405 females and 402 males) of Han nationality in Ningxia were selected as subjects. Photos of both hands were captured using a digital camera, and then the length of the index finger (2D) and ring finger (4D) were measured respectively by the Image-Pro Plus 6.0 software. Multiplex PCR assays were used to detect the genotype of 5 SNP sites of GLI3 gene. The relationship between D2/4 and GLI3 gene polymorphisms was evaluated by one-way analysis of variance. Results ：The left hand D2/4 (LD2/4) and right hand D2/4 (RD2/4) were significantly higher in female university students in Ningxia than those in males. There were no statistically significant differences in genotype and distribution of allele frequencies in the five loci of GLI3 gene between males and females. There was no significant association between the five loci SNPs of the GLI3 gene and the digit ratio (D2/4) of both hands among different genders. Conclusion ：There are significant gender differences of D2/4 in the university students in Ningxia, and polymorphism in the GLI3 loci have not yet been found to be associated with the formation of D2/4.

Objective: To compare the correlation and difference of body type index and physical forms of the Wa nationality in China and Myanmar across different age groups and genders, and to clarify the body type characteristics of the Wa nationality in China and Myanmar. Methods: The Heath-Carter somatotype evaluation method was used to determine and evaluate the body types of 508 Wa people (326 males and 182 females) from China and 368 Wa people (242 males and 126 females) from Myanmar. Results: The average body size values of Chinese and Burmese Wa males were 2.3-5.6-2.7 and 2.2-5.7-3.5, respectively. The average body size values of Chinese and Burmese Wa females were 4.3-5.2-2.1 and 4.2-5.4-2.4, respectively. The endomorphic component values of Chinese Wa males and females were slightly higher than those of Myanmar Wa nationality, while the mesomorphic and ectomorphic component values were lower than those of Myanmar Wa nationality. For males in both groups, there were no significant differences in the three somatotype components across different age groups. Similarly, for females, there were no significant correlations in the three somatotype components across age groups. However, bone development, muscle strength, fat and linearity of the body were significantly different across different age groups, showing statistical significance. There was no significant difference in average somatotype values between the Wa nationality in China and Myanmar. Conclusion: The male of Sino-Burmese Wa nationality has higher linearity and slender body shape. The female of Sino-Burmese Wa nationality have a more pronounced distribution of subcutaneous fat, resulting in a more curvaceous physique. Overall, males predominantly exhibit a mesomorphic ectomorphic somatotype, while females predominantly exhibit a mesomorphic endomorphic somatotype.

The protective effect of exercise on the heart and its benefits in promoting cardiovascular health have been widely recognized. Exercise induces physiological hypertrophy of the myocardium, improves mitochondrial metabolism and function, regulates the balance of the cardiovascular autonomic nervous system. These mechanisms enhance cardiovascular fitness, improves cardiovascular metabolism and function, and reduce the risk of various cardiovascular diseases, playing a positive biological role in disease prevention and treatment. Exercise also has a beneficial health effect on the structure and function of the cardiovascular system by promoting the secretion of related exercise factors, inducing and activating related signaling pathways, improving insulin sensitivity and metabolism of the cardiovascular system, and enhancing antioxidant capacity. Studying the mechanisms of exercise-mediated benefits on cardiovascular structure and function and its role in disease prevention and treatment offers valuable theoretical insights for designing effective exercise-based health promotion strategies and holds great promise for clinical applications.