The integration of sports and medicine provides powerful support and significant avenues for the Healthy China initiative, aiming to promote health, prevent and treat diseases through the deep integration of sports science and medicine. Exercise preconditioning (EP) exhibits myocardial protective effects, including reducing the size of myocardial infarction, alleviating exercise-induced myocardial ischemia/hypoxia injury, improving cardiac function, and decreasing the incidence of malignant arrhythmias caused by exhaustive exercise. EP acts as a bridge between sports science and medicine, representing a novel pathway for the integration of sports and medicine in the context of building a healthy and sports-strong nation. This article provides a comprehensive review of the origins and current status of EP, its relationship with cardiac rehabilitation, ischemic heart disease, as well as the prospects of EP for public fitness programmes. This article aims to provide updated insights that advance the integration of sports and medicine and support national strategies for building China into a strong sports nation.

Objective: To prepare acute hippocampal brain slices and investigate the non-genomic effects of testosterone (T), dihydrotestosterone (DHT) and testosterone BSA (T-BSA) on dendritic spine density and synaptic proteins [synaptophysin (SYN) and postsynaptic density protein 95 (PSD95)] in hippocampal brain slices. Methods: The brains of 3-month-old SD male rats were extracted after anesthesia, and the hippocampal tissue was dissected in artificial cerebrospinal fluid to prepare 300 μm coronal slices. DAPI and PI staining were applied at 0, 15, 30, 60 min and 120 min to evaluate neuronal viability. Acute hippocampal brain slices were randomly divided into control (CON), T (10 nmol/L), DHT (10 nmol/L) and T-BSA (0.36 nmol/L) groups. The density of dendritic spines was observed by Golgi-Cox staining, and the synaptic proteins SYN and PSD95 were examined through immunofluorescence histochemical staining and Western blotting after 1 h administration. Results: DAPI and PI staining showed that there was no significant difference in the percentage of active cells at all 5 time points. Golgi-Cox staining showed that the density of dendritic spines in T group, DHT group and T-BSA group was significantly increased compared with CON group. There was no significant difference in dendrite spine density among T group, DHT group and T-BSA group. Immunofluorescence histochemical staining and Western blotting assay revealed that compared with CON group, the expression of SYN and PSD95 protein in T group, DHT group and T-BSA group were significantly increased. There were no significant differences in the expression of SYN and PSD95 protein among T group, DHT group and T-BSA group. Conclusion: Acute hippocampal slices maintain excellent and stable neuronal viability within 2 h. Androgens increase the density of dendritic spines and the expression of synaptic proteins SYN and PSD95 inacute hippocampal brain slices through non-genomic effects.

Objective: To investigate the effects of geniposide (Gen) on the spontaneous pain behavior, pain threshold, apoptosis, inflammatory response, and toll-like receptor 4 (TLR4)/nuclear transcription factor kappa B (NF-κB) pathway of spinal cord in neuropathic pain (NPP) model mice. Methods: Mice were randomly divided into sham surgery group, CCI group, and Gen group. The NPP model was established by chronic constriction injury (CCI) of the sciatic nerve. The Gen group was intraperitoneally injected with Gen for 7 consecutive days after surgery. The autogenous pain behavior score, paw withdrawal thermal latency (PWTL) and paw withdrawal cold latency (PWCL) of mice were observed. Immunofluorescence staining was used to detect the expression of cleaved caspase-3 in spinal cord. RT-qPCR was applied to detect the expression of TNF-α, IL-1β, IL-6, and IL-10 mRNA in the spinal cord. ELISA was adopted to determine the protein levels of TNF-α, IL-1β, IL-6, and IL-10 in the spinal cord. Western blotting was utilized to detect the expression of TLR4, p-NF-κB p65, and NF-κB p65 proteins in the spinal cord. Results: Compared with the model group, the Gen group mice showed reduced autogenous pain behavior score, elevated PWTL and PWCL, and decreased pain sensitivity. The expression of cleaved caspase-3 protein in the spinal cord was reduced in the Gen group, with reduced mRNA and protein expression levels of TNF-α, IL-1β, and IL-6, while the expression of IL-10 was increased at both mRNA and protein levels in the Gen group. The expression of TLR4 and p-NF-κB p65 proteins was reduced, with no difference in the expression of NF-κB p65, the ratio of p-NF-κB p65 to NF-κB p65 decreased, and the activity of the TLR4/NF-κB pathway was decreased. Conclusion: Gen can alleviate spinal cord— 288 — apoptosis, inflammatory response, and TLR4/NF-κB pathway in NPP mice, exerting analgesic ef fects.

Objective: To investigate whether baicalin can improve lung injury in multidrug-resistant Pseudomonas aeruginosa (MDR-PA) pneumonia rats through the TLR4/MyD88/NF-κB signaling pathway. Method: 40 rats were randomly divided into four groups: blank group (blank group), MDR-PA pneumonia rat model group (MDR-PA group), MDR-PA pneumonia rat group treated with baicalein (BI group), and MDR-PA pneumonia rat group treated with baicalein and TLR4 agonist lipopolysaccharide (BI+LPS group), with 10 rats in each group. The lung index （LI）and lung wet/dry weight ratio of rats in each group, inflammatory cytokine levels (detected by ELISA), and histopathological changes in lung tissue (evaluated with haematoxylin–eosin staining) were measured. Western blotting was applied to determine the protein expression of TLR4, MyD88, NF-κB p65, and p-NF-κB p65 in lung tissue. Comparison of mRNA expression of TLR4, MyD88, NF-κB p65, and p-NF-κB p65 in uterine tissue was detected by RT-qPCR. Results: Compared with the blank group, the lung index, wet/dry weight ratio, serum levels of IL-6, IL-1β, TNF-α, and the protein expression of TLR4 and MyD88, the ratio of p-NF-κB p65/NF-κB p65, and mRNA expression of TLR4, MyD88, and NF-κB p65 were significantly increased in the MDR-PA group. Compared with the MDR-PA group, such parameters in the BI group were significantly reduced. By contrast, these parameters in the BI+LPS group were significantly higher than those in the BI group. Conclusion: Baicalinmay alleviate lung injury in MDR-PA pneumonia rats by inhibiting the TLR4/MyD88/NF-κB signaling pathway to suppress inflammatory response.

Objective: To investigate the mechanism by which dexmedetomidine (DEX) improves lung tissue injury in rats with thoracic trauma by regulating the PI3K/Akt/Nrf2 signaling pathway. Methods: Male Sprague Dawley rats were randomly grouped into control group, model group, low-dose DEX (DEX-L, 10 μg · kg-1 · d-1 DEX) group, highdose DEX (DEX-H, 50 μg · kg-1 · d-1 DEX) group, and high-dose DEX+LY294002 (DEX-H+LY, 50 μg · kg-1 · d-1 DEX+5 mg · kg-1 · d-1 PI3K inhibitor LY294002) group. The ratio method was applied to determine the lung index of rats. The wet/dry weight ratio of the lungs was measured. ELISA was used to measure the inflammatory factor levels in rat bronchoalveolar lavage fluid. H-E staining was applied to determine pulmonary histopathology. Western blotting was applied to determine the expression of PI3K/Akt/Nrf2 pathway proteins. Results: Compared with the control group, the lung tissue of the model group rats showed inflammatory infiltration, loose arrangement, and thickening of alveolar walls, with the lung index, lung wet/dry weight ratio, levels of IL-1β, IL-6, TNF-α in bronchoalveolar lavage fluid, and inflammation score increased, while the expression of PI3K, Akt, and Nrf2 proteins decreased. Compared with the model group, the DEX-L and DEX-H groups showed reduced lung tissue injury in rats, with the lung index, lung wet/dry weight ratio, levels of IL-1β, IL-6, TNF-α in bronchoalveolar lavage fluid, and inflammation score decreased, while the expression of PI3K, Akt, and Nrf2 increased. Compared with the DEX-H group, the lung tissue injury in the DEX-H+LY group worsened, with the lung index, lung wet/dry weight ratio, levels of IL-1β, IL-6, TNF-α in bronchoalveolar lavage fluid, and inflammation score increased, while the expression of PI3K, Akt, and Nrf2 decreased. Conclusion: DEX may improve lung tissue injury in rats with thoracic trauma by activating the PI3K/Akt/Nrf2 signaling pathway

Objective: To investigate the impacts of honokiol (Hon) on interleukin (IL)-1β induced mitochondrial autophagy in chondrocytes by regulating PTEN induced putative kinase 1 (PINK1)/Parkin signal pathway. Methods: Rat chondrocytes were cultured in vitro. After screening the optimal concentration of Hon, they were randomly divided into control group, model group, honokiol (Hon) group, cyclosporin A (CsA) group, and Hon+CsA group. Except for the control group, the other groups were treated with 10 ng/mL IL-1β to construct an in vitro osteoarthritis (OA) model. After the respective treatments, the following were measured: cell proliferation, apoptosis, ultrastructure, autophagy, relative content of reactive oxygen species (ROS), production levels of tumor necrosis factor-α (TNF-α) and IL-17, expression of autophagy and PINK1/Parkin pathway related protein of cells in each group. Results: Compared with the control group, the ultrastructure of chondrocytes in the model group was severely damaged, with the survival rate, the relative proportion of autophagosomes, the expression of microtubule-associated protein 1A/1B-light chain 3 (LC3) Ⅱ /LC3Ⅰ , coiled-coil myosin-like BCL2-interacting protein (Beclin-1), PINK1, and Parkin proteins obviously lower, while the apoptosis rate, the relative content of ROS, and the levels of TNF-α and IL-17 were obviously higher. Compared with the model group, the ultrastructural damage of chondrocytes in the Hon group was reduced, with the survival rate, the relative proportion of autophagosomes, the expression of Beclin-1, PINK1, and Parkin proteins, LC3Ⅱ /LC3Ⅰ obviously higher, while the apoptosis rate, the relative content of ROS, and the levels of TNF-α and IL-17 were obviously lower. CsA treatment reversed Hon's effects, exacerbating all injury parameters. Conclusion: Hon can enhance mitophagy, suppress IL-1β-induced inflammation, reduce oxidative stress, and promote chondrocyte survival in OA through the activation of the PINK1/Parkin pathway.

Objective: To investigate the effects of irisin on oxidized low-density lipoprotein (ox-LDL) induced inflammation and apoptosis of human umbilical vein endothelial cells (HUVECs) by regulating the reactive oxygen species (ROS)/p38 mitogen activated protein kinase (p38 MAPK) signaling pathway. Methods: Cultured HUVECs were divided into control group, ox-LDL group, low-dose irisin group, medium-dose irisin group, high-dose irisin group, Anisomycin group. Cell viability was assessed by MTT assay. Apoptosis was detected by flow cytometry. CFH-DA fluorescent probe was used to detect ROS levels. The expression of P-selectin (P-selectin), intercellular adhesion molecule-1 (ICAM-1), vascular endothelial cell adhesion molecule-1 (VCAM-1) and E-selectin (E-selectin) were detected by ELISA. Western blotting was applied to detect protein expression. Results: ox-LDL exposure markedly decreased HUVEC viability and increased apoptosis rate, ROS positive cells, expresion of P-selectin, ICAM-1, VCAM-1, E-selectin, Bax/Bcl-2, p-p38 MAPK/p38 MAPK, cleaved caspase-3. Irisin decreased HUVEC apoptosis rate, ROS positive cells, expresion of P-selectin, ICAM-1, VCAM-1, E-selectin, Bax/Bcl-2, p-p38 MAPK/ p38 MAPK, cleaved caspase-3 in a concentration-dependent manner. These protective effects were abolished by Anisomycin. Conclusion: Irisin can inhibit ox-LDL-induced endothelial inflammation and apoptosis of HUVEC, and its mechanism may be achieved by inhibiting the ROS/p38 MAPK signaling pathway.

Objective: To investigate the effects of long non-coding RNA (lncRNA) AK035396 on lipopolysaccharideinduced vascular endothelial cell injury by regulating the miR-217-5p/chloride intracellular channel protein 4 (CLIC4) signaling pathway. Methods: Human umbilical vein endothelial cells (HUVECs) were cultured in vitro. An injury model was established through induction of 1 μg/mL lipopolysaccharide. The HUVECs were divided into the control group (infected with lentivirus lenti-si-NC) and the si-AK035396 group (infected with lentivirus lenti-si-AK035396). Quantitative real-time PCR was used to analyze the expression levels of AK035396, miR-217-5p and CLIC4 mRNA. MTT method and flow cytometry were adopted to detect the viability and apoptosis of HUVECs cells respectively. Dual luciferase assay was utilized to verify the targeting relationship between AK035396 and miR-217-5p. Western blotting was applied to detect the expression levels of CLIC4, Caspase-3, Caspase-9, and Bax proteins. Results: Compared with the control group, the expression of AK035396 in HUVECs cells in the si-AK035396 group was reduced. The viability of HUVECs cells in the si-AK035396 group was significantly higher than that in the control group. The apoptosis rate of cells in the si-AK035396 group was significantly lower than that in the control group. AK035396 can directly target and bind to miR-217-5p. Compared with the control group, the expression of miR-217-5p in HUVECs in the si-AK035396 group was significantly increased, with the expression of CLIC4 mRNA significantly decreased, and the proteins of CLIC4, Caspase-3, Caspase-9, and Bax significantly decreased. Conclusion: AK035396 silencing alleviates lipopolysaccharide-induced vascular endothelial cell injury by regulating the miR-217-5p/CLIC4 signaling pathway.

Objective: To investigate the associations of the expression of histone lylsine demethylase 5B (KDM5B), kallikrein (KLK) 11, and prospero-related homeobox 1 (PROX1) in non-small cell lung cancer (NSCLC) tissues with the clinical pathological characteristics and prognosis. Methods: NSCLC patients admitted to the Nanyang Central Hospital from July 2019 to June 2021 were selected as the study subjects. Immunohistochemistry was applied to detect the expression of KDM5B, KLK11, and PROX1 in cancer tissues and adjacent tissues. Patients were classified into deceased or surviving cohorts based on 3-year follow-up data. Multivariate Cox regression was applied to analyze the influencing factors of NSCLC prognosis. Kaplan-Meier curve was applied to analyze the relationship between the expression of KDM5B, KLK11, PROX1 with the prognosis of NSCLC. Results: The positive expression rates of KDM5B, KLK11, and PROX1 in cancer tissues were obviously higher than those in adjacent tissues. The tumor diameter of NSCLC patients was related to the expression of KDM5B and PROX1, while the elevated expression of all three markers was associated with advanced TNM stage and lymph-node metastasis. Compared with the survival group, the proportions of TNM stage Ⅲ and lymph node metastasis in the death group were obviously higher. Compared with the survival group, the positive expression rates of KDM5B, KLK11, and PROX1 were obviously higher in the cancer tissues in the death group. Multivariate Cox regression showed that TNM stage Ⅲ (OR=2.369), lymph node metastasis (OR=1.843), KDM5B positivity (OR=2.014), KLK11 positivity (OR=1.562), and PROX1 positivity (OR=1.986) were all risk factors for poor prognosis in NSCLC. Patients positive for KDM5B, KLK11, or PROX1 had significantly lower 3-year OS than their negativecounterparts (Log-rank χ2=11.108, 8.468, and 10.697, respectively). Conclusion: KDM5B, KLK11, and PROX1 have high positive expression rates in NSCLC tissues, and their expression levels are closely related to the pathological characteristics and prognosis of NSCLC.

Objective: To investigate the relationship between the humeral neck-shaft angle in adults and the success rates of medial buttress screw placement during locking-plate fixation of proximal humeral fractures, and to provide anatomical and technical guidance for pre-operative planning. Methods: A digital locking-plate model was created and its spatial relationship with virtual medial buttress screws was analysed. Images of normal humeri from X-ray examinations of the proximal humerus conducted between January 2019 and May 2019 were collected. The angles of the neck-shaft of normal humeri were measured. The digital plate was superimposed onto each radiograph to simulate screw insertion, and the success rate of medial buttress screw placement was calculated for different neckshaft angle ranges. Results: No statistical significance was observed in the average humeral neck-shaft angle between males (136.1°±4.5°) and females (135.8°±4.8°). A humeral neck-shaft angle between 130° and 135° was found to be more favorable for the implantation of medial buttress screws, while excessively large or small neck-shaft angles were prone for implantation failure. Conclusions: A humeral neck-shaft angle between 130° and 135° represents an optimal range for predictable placement of medial buttress screws in proximal humeral locking-plate fixation and should be incorporated as a key parameter in pre-operative planning.

Objective ： To evaluate the academic level and the quality of Chinese Journal of Anatomy by analyzing the cited papers from 2016 to 2024. Methods ： According to the information of China National Knowledge Internet (CNKI), the teaching research papers published in Chinese Journal of Anatomy from 2016 to 2024 were surveyed. The number of papers, the cited frequency, the distributions of the authors were analyzed by bibliometrics and citation analysis. Results ： Of the total 474 teaching research papers, the cited frequency of 402 papers was 2 825, the average cited frequency was 7.03, the top was 92. There were199 papers which were cited more than 5 times. There were 23 authors whose published works had been cited at least 21 times, with their 23 papers accumulating a total of 745 citations. Among these, 7 were ideological and political education papers, accounting for 30.43% of the total, and the average number of citations per paper was 32.39. Conclusions ： Chinese Journal of Anatomy is anatomy journals with higher academic quality teaching research papers in China.

The dopaminergic system regulates the body’s pain response through its widely distributed neural projections that interconnect multiple pain-processing regions. Due to the heterogeneous distribution of dopaminergic neurons, their distinct functional phenotypes, and the diversity of dopamine-receptor subtypes, this system exhibits significant heterogeneity and complexity in pain modulation. This article focuses on summarizing the roles of dopaminergic neurons in pain regulation across different neural pathways, as well as the mechanisms of D1 and D2 receptors in pain perception. By analyzing these mechanisms, this paper provides a theoretical basis for targeted interventions of dopaminergic system in pain treatment and highlights the importance of in-depth research into the role of dopamine receptors in pain modulation for developing personalized pain treatment plans.

Colorectal cancer (CRC) is one of the common malignant tumors of the digestive tract in clinical practice, but its etiology remains unclear. Recent studies have shown a close relationship between gut microbiota dysbiosis and CRC. To explore how gut microbiota dysbiosis contributes to the occurrence and progression of CRC, and to provide novel insights for the prevention and treatment of CRC, this article conducted a comprehensive analysis by retrieving recent literature, elucidating the mechanisms through which gut microbiota dysbiosis influences the development and progression of CRC. Research findings indicate that the gut microbiota participates in the initiation and advancement of CRC through various pathways, including inflammatory responses, metabolic byproducts, and oxidative stress. Dysbiosis of the gut microbiota emerges as a significant driving factor in the occurrence and development of CRC. Consequently, it is proposed that targeted modulation of the gut microbiota or its metabolic products may represent a novel strategy for CRC intervention, and further in-depth research holds promise for the development of innovative therapeutic approaches.