Human anatomy has emerged from humanity’s practical exploration of the human body. Anatomy has played an irreplaceable role in the advancement of medicine, from the mummification practices of ancient Egypt to Leonardo da Vinci’s anatomical sketches during the Renaissance, from Vesalius’s De humani corporis fabrica to modern digital anatomical atlases. The history of this discipline not only reflects continuous innovations in science and technology but also embodies the deepening of human self-understanding. However, with the rapid advancement of modern medicine, traditional anatomical research faces many challenges, and its role and future direction within the medical system have sparked widespread academic reflection. Based on the realities of traditional anatomy and integrating historical evolution with contemporary medical needs, this article explores new pathways for anatomical research. It emphasizes the critical value of clinical applied anatomy, analyzes the synergistic relationship between human anatomy and surgery, and envisions future directions for anatomical research empowered by modern technologies, thereby providing insights for innovative development in the field.

Objective: To systematically delineate the afferent and efferent connectivity patterns of temporal association cortex (TeA), with particular focus on elucidating its divergent upstream inputs relative to primary auditory cortex (Au1). Methods: Using adult C57BL/6J wild-type mice, we performed bidirectional viral tracing through stereotaxic injections. For retrograde tracing, AAV2/retro-hSyn-mCherry was injected into either TeA or Au1 to label and quantify upstream input neurons. For anterograde tracing, HSV1-H129 was injected specifically into TeA to map and quantify its downstream projection targets. Results: Both Au1 and TeA received extensive upstream inputs, including ipsilateral and contralateral auditory cortices, thalamus and other cortical regions. Compared with Au1, TeA received more inputs from the limbic system and entorhinal cortex. Downstream projections showed that TeA targeted auditory cortex, auditory thalamus, amygdala, pontine nuclei and other brain regions. Conclusion: In contrast to Au1, TeA, as a multisensory integration hub, receives more inputs from the limbic system and cerebral cortex, and widely projects to brain regions related to emotion, movement and sensory regulation, suggesting its potential key role in sensory-motor integration networks.

Objective: To investigate the therapeutic effect and potential mechanism of AdipoRon on peri-implantitis of tooth. Methods: A rabbit peri-implantitis model of tooth was constructed with integrated titanium implants and divided into two groups: Control group and AdipoRon treatment group. Rabbit bone marrow mononuclear cells were induced into M2-type macrophages and were also divided into control group and administration group. CCK- 8 assay was used to detect cell viability. Transwell assay was adopted to measure cell migration. The levels of interleukin-4 (IL-4) and interleukin-13 (IL-13) were measured by ELISA. The mRNA expression of cyclin-dependent kinase 1 (CDK1), proliferating cell nuclear antigen (PCNA), Ki67, interleukin-1 (IL-1), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were detected using RT-qPCR. Western blotting was employed to determine the protein expression of AMP-activated protein kinase (AMPK) and its phosphorylated form (p-AMPK), sirtuin 1 (Sirt1), inhibitor of nuclear factor-κB (IκBα) and nuclear factor-kappa B (NF-κB) p65, as well as its phosphorylated form. Results: Compared with the Control group, the AdipoRon-treated group had significantly less peri-implant inflammation and significantly increased osseous integration. The levels of IL-4 and IL-13 in periodontal tissues significantly increased. AdipoRon promoted the viability and migration of M2 type macrophages. AdipoRon significantly increased the expression levels of p-AMPK, Sirt1 and IκB, inhibited the nuclear translocation of phosphorylated NF-κB p65, and significantly decreased the mRNA levels of downstream factors IL-1, IL-6 and TNF-α in the NF-κB pathway. Conclusion: AdipoRon can promote the proliferation and migration of M2- type macrophages, possibly by activating the AMPK/ Sirt1 pathway to inhibit M1 macrophage polarization,thereby improving peri-implantitis.

Objective: To investigate the effect of Tangeretin (TAN) on high glucose (HG)-induced apoptosis in trophoblast cells by regulating the Ras homologous gene family member A (RhoA)/Rho-associated coiled-coil forming protein kinase (ROCK) signaling pathway. Methods: Human chorionic trophoblast cells (HTR8-SVneo) were cultured in vitro and randomly divided into control group (conventional culture), HG group (25 mmol/L glucose), L-TAN, M-TAN, H-TAN groups (25, 50, and 100 μg/mL TAN, respectively), and PMA group (100 μg/mL TAN+100 ng/mL RhoA/ROCK signaling pathway activator PMA). MTT method and colony formation assay were applied to detect cell proliferation. ELISA was applied to detect the levels of interleukin (IL) 1β (IL-1β), tumor necrosis factor-α (TNF-α), IL-6 and IL-8. Flow cytometry was applied to detect apoptosis. Western blotting was used to detect the expression of proliferating cell nuclear antigen (PCNA), apoptosis-associated proteins (Bcl-2, Bax, cleaved caspase-3), and proteins related to the RhoA/ROCK signaling pathway (RhoA, ROCK). Results: Compared with the control group, the A490 of cells, clone number, the PCNA, Bcl-2 protein expression in the HG group were decreased, while the IL-1β, TNF-α, IL-6, IL-8, apoptosis rate, cleaved caspase-3, Bax, RhoA, ROCK protein expression were elevated. Compared with the HG group, the A490 of cells, clone number, the PCNA, Bcl-2 protein expression in the L-TAN, M-TAN, and H-TAN groups were increased, while the IL-1β, TNF-α, IL-6, IL-8, apoptosis rate, cleaved caspase-3, Bax, RhoA, ROCK protein expression were decreased. Compared withH-TAN group, the A490 of cells, clone number, the PCNA, Bcl-2 protein expression in PMA group were decreased, while the IL-1β, TNF-α, IL-6, IL-8, apoptosis rate, cleaved caspase-3, Bax, RhoA, ROCK protein expression were elevated. Conclusion: Tangeretin may attenuate high glucose-induced inflammatory responses in trophoblast cells by inhibiting the RhoA/ROCK signaling pathway, thereby promoting cell proliferation and inhibiting cell apoptosis.

Objective: To investigate the effect and mechanism of safflower injection in alleviating oxidative stressinduced testicular damage in diabetic male rats. Methods: Male SD rats were randomly divided into three groups: a normal group, a model group, and a treatment group. The general condition and testicular mass of the rats were compared bamong the groups, plus the levels of superoxide dismutase (SOD) and malondialdehyde (MDA) in testicular tissue. Histological structure, cell morphology, and the rate of proliferating cell nuclear antigen (PCNA)- positive cells in testicular tissue were also evaluated. Results: Compared with the normal group, the model group exhibited poorer mental state, dull and yellowish fur, increased food and water intake, more urination and defecation, significantly reduced testicular mass, and markedly decreased SOD levels and increased MDA levels in the testicular tissue. Through the observation under a light microscope, there was decreased and disordered arrangement of spermatogenic cells in the testes along with a lower rate of PCNA-positive cells. Compared with the model group, the treatment group showed improved responsiveness, less pronounced dull and yellowish fur, reduced food and water intake, and less urination, significantly increased testicular mass, elevated SOD levels, and significantly decreased MDA levels in testicular tissue. Morphological lesions in testicular tissue were alleviated, and the rate of PCNApositive cells was increased. Conclusion: Safflower injection can improve the testicular damage in male diabetic rats, and its mechanism may be related to the regulation of MDA and SOD in the oxidative stress system.

Objective: To investigate the effects of remimazolam on sepsis-induced myocardial injury in rats by regulating the NOD-like receptor thermal protein domain associated protein 3 (NLRP3)/interleukin (IL)-1β signaling pathway. Methods: Mice were randomly divided into seven groups: cecal ligation and puncture (CLP) group, control group, low-dose remimazolam group, high-dose remimazolam group, ampicillin group, and high-dose remimazolam+ NLRP3 activator (DDC) group. Except for the control group, sepsis models were induced in the other groups via CLP surgery. After successful modeling, drug administration was performed once a day for two consecutive days. The changes in left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS) in mice were detected. ELISA was performed to detected the levels of lactate dehydrogenase (LDH), creatine kinase (CKMB), and cardiac troponin I (cTnI) in serum, and the levels of IL-6, IL-18, and tumor necrosis factor alpha (TNF-α) in myocardial tissue. H-E staining was utilized to assess myocardial pathology. TUNEL staining was employed to measure cell apoptosis in myocardial tissue. Western blotting was conducted to measure p53, Bcl-2 associated X protein (Bax), NLRP3, and IL-1β protein in myocardial tissue. Results: Remimazolam can improve myocardial injury in mice, as evidenced by increased LVEF and LVEF and decreased levels of LDH, CK-MB, cTNI in serum, along with the decreased levels of IL-6, IL-18, TNF-α in myocardial tissue. It also decreased the apoptosis rate and the levels of p53, Bax, NLRP3, and IL-1β protein. DDC reversed the inhibitory effect of high-dose remimazolam on inflammation and cell apoptosis in mice with sepsis-induced myocardial injury. Conclusion: Remimazolam may alleviate sepsis-induced myocardial injury by inhibiting the NLRP3/IL-1β signaling pathway, thereby reducing inflammation and apoptosis in mice.

Objective: To investigate the expression of ubiquitin-like with PHD and ring finger domain 1 (UHRF1), thrombospondin 2 (THBS2), and B-cell translocation gene 2 (BTG2) in ovarian cancer tissues, and their correlation with pathological parameters and prognosis. Methods: Cancer tissues and adjacent normal tissues ( ＞ 5 cm from the tumor) were collected from 113 patients with ovarian cancer treated in our hospital between March 2017 and June 2019. Immunohistochemistry detection of positive expression of UHRF1, THBS2, and BTG2 in cancer tissues as well as paracancerous tissues. The relationship between the expression of UHRF1, THBS2, and BTG2 in cancer tissues and clinical pathological parameters in ovarian cancer patients was analyzed. Kaplan-Meier survival curves were plotted to assess the association between the expression of UHRF1, THBS2, and BTG2 in cancer tissues of ovarian cancer patients and prognosis survival rate. Clinicopathological parameters were compared between patients with favorable and poor prognosis. Cox regression was adopted to analyze the influencing factors of poor prognosis in ovarian cancer patients. Results: The positive expression rates of UHRF1 and THBS2 in ovarian cancer cancer tissues were significantly higher than those in paracancerous tissues, while the positive expression rate of BTG2 was prominently lower than that in paracancerous tissues. The expression of UHRF1, THBS2, and BTG2 in cancer tissues of ovarian cancer patients was associated with International Federationof Gynecologyand Obstetrics (FIGO) staging, differentiation degree, and lymph node metastasis. The 5-year survival rates of patientswith the positive expression of UHRF1 and THBS2 were prominently lower than those of the negative expression groups, while the 5-year survival rate of the BTG2 positive expression group was significantly higher than those of the negative expression group. There were statistically obvious differences in FIGO staging, pathological type, differentiation degree, lymph node metastasis, expression of UHRF1, THBS2, and BTG2 between the poor and the good prognosis groups. Cox regression analysis showed that lymph node metastasis, UHRF1, THBS2, and BTG2 were independent factors affecting poor prognosis in ovarian cancer patients. Conclusion: The positive expression rates of UHRF1 and THBS2 in cancer tissues of ovarian cancer patients are prominently increased, while the positive expression rate of BTG2 is prominently decreased. These three factors are closely related to pathological parameters such as FIGO staging, differentiation, lymph node metastasis, and 5-year survival rate, and they serve as factors affecting poor prognosis.

Objective: To investigate whether artesunate affects the proliferation, migration and invasion of thyroid cancer cells through the circ_0085616/miR-338-3p pathway. Methods: RT-qPCR method was used to detect the expression of circ_0085616 and miR-338-3p in thyroid cancer tissues and adjacent non-cancerous tissues. Pearson correlation method was used to analyze the correlation between circ_0085616 and miR-338-3p expressions in thyroid cancer tissues. Human thyroid cancer SW579 cells were cultured in vitro and treated with different doses of artesunate. Cells were transfected with si-NC, si-circ_0085616, pcDNA, or pcDNA-circ_0085616. After transfection of pcDNA or pcDNA-circ_0085616, cells were treated with 90 μmol/L artesunate. CCK-8 method, plate colony formation experiment, Transwell experiment, and Western blotting assay were used to detect proliferation, colony formation, migration, invasion, and protein expression changes of SW579 cells, respectively. The dual luciferase reporter experiment, RNA pull-down assay and RNA immunoprecipitation assay were used to verify the targeting relationship between circ_0085616 and miR-338-3p. Results: The expression of circ_0085616 in thyroid cancer tissues was higher than that in adjacent tissues, while the expression of miR-338-3p was lower than that in adjacent tissues. A negative correlation was observed between circ_0085616 and miR-338-3p expression. Artesunate reduced the expression of circ_0085616 and the protein level of N-cadherin, decreased the number of colony formation, migrating and invading cells, while increasing the inhibition rate of cell proliferation, the expression of miR-338-3p and the protein level of E-cadherin. circ_0085616 targeted the expression of miR-338-3p. Transfection of sicirc_ 0085616 inhibited cell proliferation, clone formation, migration and invasion, while transfection of pcDNA-circ_0085616 attenuated the inhibitory effects of artesunate on the proliferation, clone formation,migration and invasion of SW579 cells. Conclusion: Artesunate inhibits the proliferation, migration and invasion of thyroid cancer cells by regulating the expression of circ_0085616/miR-338-3p.

Objective: To investigate the effects of isorhamnetin (ISO) on proliferation, invasion, and apoptosis of esophageal cancer cells and its mechanism of action. Methods: Human esophageal cancer EC109 cells were divided into control group, low, medium, and high concentration isorhamnetin group (ISO-L, ISO-M, ISO-H group), and ISO-H + KI696 group. CCK-8 assay was applied to detect the proliferation ability. Transwell assay was utilized to determine their invasive ability. Flow cytometry was employed to measure their apoptosis rate. RT-qPCR method was adopted to detect the mRNA expression levels of p62, Kelch-like ECH associated protein 1 (Keap1), and nuclear factor erythroid 2-related factor 2 (Nrf2). Western blotting was used to detect the expression levels of p62, Keap1, and Nrf2 proteins. Results: Compared with the control group, the ISO-treated groups exhibited significantly reduced proliferation and invasion abilities, lower levels of p62 and Nrf2 mRNA and proteins, while showing higher apoptosis rates and mRNA and protein levels of Keap1. These effects were dose-dependent. However, KI696, an inhibitor of the Keap1-Nrf2 axis, reversed the inhibitory effects of ISO on cell proliferation and invasion. Conclusion: ISO inhibits the proliferation and invasion of esophageal cancer cells, and promotes their apoptosis by downregulating p62 expression and enhancing Keap1-mediated inhibition of Nrf2 signaling.

Objective: To investigate the effects of Rab25 overexpression on the growth, invasion, migration, and JAK2/STAT3 signaling pathway in human rectal cancer HCT116 cells. Methods: HCT116 cells were randomly divided into three groups: Control group, pcDNA group, and Rab25 group. The mRNA level of Rab25 was detected by RT-qPCR. Cell proliferation was assessed by clone formation assay. Cell invasion was evaluated by Transwell assay. Cell migration was determined by scratch healing assay. The protein expression levels of Ki67, Survivin, JAK2, p-JAK2, STAT3, and p-STAT3 were analyzed by Western blotting. Results: Compared with the Control group, the Rab25 group exhibited significantly increased mRNA and protein levels of Rab25. Conversely, the Rab25 group demonstrated significant reduction in the number of colonies formed, protein expression levels of Ki67 and Survivin, the number of invasive cells, the wound healing rate, and ratios of p-JAK2/JAK2 and p-STAT3/STAT3. All these differences were statistically significant. Conclusion: Overexpression of Rab25 inhibits the proliferation, invasion, and migration of HCT116 cells, and the underlying mechanism may be related to the suppression of the JAK2/STAT3 signaling pathway.

Objective: To investigate the effect of remifentanil（REM） on spinal cord dorsal horn neuron injury in rats with neuropathic pain by regulating the high mobility group box 1 (HMGB1)-receptor for advanced glycation end products (RAGE) signaling pathway. Methods: SD rats were divided into sham surgery group, model group, lowdose remifentanil (REM-L) group, high-dose remifentanil (REM-H) group, and REM-H + rHMGB1 (recombinant protein HMGB1) group. A neuropathic pain rat model was established by spinal nerve ligation. The pain behavior of rats, the levels of tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-10, histopathological damage and neuronal apoptosis in the spinal dorsal horn, the expression of HMGB1 mRNA and RAGE mRNA, as well as the levels of HMGB1, RAGE, nuclear factor-κB (NF-κB), phosphorylated NF-κB (p-NF-κB), B-cell lymphoma-2 (Bcl-2), and Bcl-2 associated X protein (Bax) proteins were detected. Results: After the REM-L and REM-H treatments, the paw retraction threshold and thermal sensitivity latency, IL-10, and Bcl-2 expression were increased, while the expression of TNF-α and IL-1β, apoptosis rate of neurons, HMGB1 and RAGE mRNA and protein expression, the protein expression of p-NF-κB/NF-κB and Bax were reduced. The recombinant protein rHMGB1 was able to partially reverse the therapeutic effect of REM on neuropathic pain in rats. Conclusion: REM can alleviate the spinal dorsal horn nerve tissue damage in rats with neuropathic pain, which may be related to the inhibition of HMGB1-RAGE signaling pathway.

Oligodendrocytes (OLs) wrap axons to form myelin sheaths in the central nervous system. The Wnt/ β-catenin signaling pathway influences the differentiation and maturation of OLs, thereby regulating myelin formation and regeneration. Aberrant activation of this pathway is implicated in the pathogenesis of various diseases, including cancer, neurodegenerative disorders, and dysregulated myelin development/repair. This review synthesizes recent studies on the role of Wnt/β-catenin signaling in OLs development and remyelination, elucidates its regulatory mechanisms during these processes, and summarizes key regulatory factors and potential therapeutic targets.