Starting from the introduction of the new changes of physical anthropology, this paper reviews the development of medical anthropology and the birth of biomedical anthropology, focusing on the core contents of contemporary medical anthropology, as well as the new theories, methods, hotspots and applications in current research. Finally, it proposes new challenges facing medical anthropology, presents a new mission for the discipline of anatomy, and discusses the significance of medical anthropology in advancing disciplinary theory, medical education, and the construction of a Healthy China.

Objective: To explore the anterior extraperitoneal anatomical targeted surgical approach for acetabular fractures and to meet the requirements for precise minimally invasive robotic-assisted orthopedic surgery. Methods: Fresh adult Chinese cadavers were used with arterial perfusion. Based on the clinical needs of internal fixation of acetabular fractures, five most common fracture sites of acetabulum were selected, including anterior column, anterior wall, acetabular roof, medial quadrilateral surface and greater ischial notch. The distribution and density of blood vessels with diameter ≧ 2.0 mm were measured in the above areas. The shortest linear distance between blood vessels and bone was categorized as follows: Grade Ⅰ (extremely hazardous, 0–5.0 mm), Grade Ⅱ (highly hazardous, 5.0–10.0 mm), or Grade Ⅲ (moderately hazardous, 10.0–20.0 mm). Venous and arterial distribution density ≥ 10, 8, 6 vessels within a 30.0 mm radius was classified as Grade A (extremely hazardous), Grade B (highly hazardous), or Grade C (moderately hazardous). According to the above measurements, the vascular protection levels for5 regions were drawn up. The extraperitoneal targeted minimally invasive surgical pathways were summarized to avoid important blood vessels. Results: Grade I vessels included the corona mortis, obturator artery and vein, femoral artery and vein, superior gluteal artery and vein, which required level Ⅰ protection. Grade Ⅱ vessels comprised iliolumbar artery and vein, internal iliac artery and vein and their branches, external iliac artery and vein, inferior gluteal artery and vein, which needed level Ⅱ protection. Grade Ⅲ vessels consisted of deep inferior epigastric artery and vein, umbilical artery and vein, testicular artery and vein, which called for level Ⅲ protection. Grade A area was located at the greater sciatic notch. Grade B area was located at the obturator area of the superior pubic ramus, the acetabular roof and the medial quadrangle. Grade C area was located on the anterior wall. Blood vessels with a diameter ≧ 5.0mm could cause rapid fatal hemorrhage after injury, including common iliac artery and vein, external iliac artery and vein, and internal iliac artery and vein. The vascular protection levels for the five regions were as follows: level ⅠA (superior gluteal artery and vein, obturator artery and vein, and coronary artery of death), level IB (Femoral artery and vein), level ⅡA (internal iliac artery and vein, external iliac artery and vein), level ⅡB (inferior gluteal artery and vein), level ⅢB (testicular artery and vein, uterine round ligament artery and vein, umbilical artery and vein). Five extraperitoneal targeted minimally invasive pathways for acetabular fractures were identified in superior pubic ramus, anterior wall (2 sites), acetabulum roof, and the greater sciatic notch area of arcuate line. Three newly discovered arteries, with 1.0–1.5 mm in diameter, which were not described in previous anatomical works and literature, were named as the pubic posterior trophic branch of the coronary artery of death, the psoas major branch and peritoneal branch of the superior gluteal artery, and the acetabular parietal trophic branch of the iliacus vessel. Conclusion: This study provides five targeted pathways for robotic-assisted orthopedic surgery to achieve precise and minimally invasive treatment of acetabular fractures, which can allow rapid access to the five targeted fracture sites of the acetabulum and reduce the iatrogenic damage to normal tissues in non-fracture areas. The three newly discovered vessels enrich anatomical understanding of acetabular vasculature and are of significant significance to avoid intraoperative vascular injury and bleeding.

Objective: To observe the clinical anatomical features of the superior rectal artery (SRA) under digital subtraction angiography (DSA) and provide an anatomical basis for transvascular interventional therapy in hemorrhoidal disease. Methods: Non-hemorrhoid volunteers undergoing vascular interventional therapy were enrolled. A total of 24 volunteers (12 males and 12 females) were included. SRA imaging data were obtained through DSA to analyze clinical characteristics, SRA origin, initiation, morphology, branching patterns, and distribution. Results: The SRA trunk and branches appeared with complete visualization. The primary branching pattern was bifurcation type (left and right branches from the main trunk), accounting for 87.5%. Morphological subtypes based on terminal branches were as follows: type 22 (left 2, right 2 branches): 29.2%; type 12 (left 1, right 2 branches): 25.0%; type 31 (left 3, right 1 branch): 8.3%; type 13 (left 1, right 3 branches): 13.0%; type 21 (left 2, right 1 branch) and type 23 (left 2, right 3 branches): 8.3% each; type 14 (left 1, right 4 branches) and type 32 (left 3, right 2 branches): 4.2% each. The mean numbers of secondary, tertiary, and quaternary branches before reaching the anorectal junction were (3.9±1.3), (3.5±1.9), and (1.5±2.2), respectively. At the anorectal junction, the average number of branches was (5.5±1.3), and at the dentate line, the average number of branches was (2.3±1.1), with (1.0±0.7) on the left side and (1.4±0.7) on the right side. Conclusion: DSA-based clinical anatomy of the SRA and its branches better evaluates its origin, initiation, morphology, branching patterns, and distribution. These findings provide critical references for selecting target vessels and embolic agent dosage in superselective arterial embolization ablation, as well as offer theoretical support for optimizing procedural protocols.

Objective: To investigate the anatomical course of the renal plexus nerves and provide anatomical basis for clinical renal sympathetic nerve ablation in the treatment of resistant hypertension. Methods: Dissections were performed on the bilateral kidneys and perirenal arteries of 30 cadavers to observe the types of renal plexus nerve courses and their positional relationships with the renal arteries. The lengths of renal plexus nerve branches not adhering to the renal arteries and the distances between these branches and the renal arteries were measured and statistically analyzed. Results: In terms of side numbers, it occupied 60% that all nerves of renal plexus travelling around the main renal artery surface, and 30% that part of nerves bypassed the main renal artery proximally, and 10% that part of nerves bypassed the main renal artery entirely. In terms of individual cases, all nerves of both side of renal plexus were travelling around the main renal artery accounted for 40%, and 60% individuals have the situation that nerves bypassed the main renal artery in single or both sides of renal plexus. The length of renal plexus branches bypassed partly is about 35 mm, with a distance of about 12 mm from the renal artery. The length of renal plexus branches bypassed entirely is about 46 mm, with a distance of about 13 mm from the renal artery. There was no statistical significance in the difference between male and female or between the left and right renal plexuses. Conclusion: The individual difference of renal plexus travelling, which part of nerves in single or both sides bypassed the main renal artery proximally or entirely, is probably one of the c

Objective: To investigate the effects of exercise-induced lncRNA MSTRG.19096.5 on ventricular remodeling in mice with acute myocardial infarction (MI). Methods: Through lncRNA sequencing, we identified the lncRNAs that were highly expressed in myocardial tissue after exercise. The significantly upregulated lncRNA MSTRG.19096.5 was selected for further study. The mice were divided into the sham group, Lv-NC+MI group, Lv- MSTRG.19096.5+MI group, and Lv-sh-RNA-MSTRG.19096.5+MI group. Thirty days later, the effects on post- MI ventricular remodeling were evaluated through cardiac Masson staining (relative length of myocardial scar, myocardial fibrosis ratio), echocardiography [left ventricular ejection fraction (EF), left ventricular fractional shortening (FS)], ELISA [plasma brain natriuretic peptide (BNP) levels], and Western blotting (protein expression levels of left ventricular myocardial fibrosis markers). Results: LncRNA MSTRG.19096.5, which was highly expressed in the mouse myocardial group after exercise, was screened through lncRNA sequencing. Compared to the Lv-NC+MI group, the Lv-MSTRG.19096.5+MI group showed a significant reduction in the relative length of myocardial scar and myocardial fibrosis ratio, a significant increase in EF and FS, a significant decrease in BNP levels, and a significant reduction in the expression levels of myocardial fibrosis markers Collagen Ⅰ , Collagen Ⅲ , α-SMA, and TGF-β1. Conclusion: Exercise-induced lncRNA MSTRG.19096.5 plays a protective role in post-acute myocardial infarction ventricular remodeling by reducing myocardial fibrosis and improving cardiac function.

Objective: To investigate the effects of Tuina on mitochondrial metabolism and apoptosis in the liver tissue of rats with exercise-induced fatigue, and to explore the underlying molecular mechanisms. Methods: Male Sprague-Dawley rats were selected, divided into the control group, the model group and the Tuina intervention group. Tissue injury, expression of mitochondrial metabolism-related molecules and apoptosis-related molecules in liver tissue were measured by using H-E staining, Western blotting, RT-qPCR. Results: In the model group, significant damage of mitochondrial function occurred in the liver tissue and the level of cell apoptosis markedly up-regulated. After Tuina, the mitochondrial function was significantly restored, and the level of cell apoptosis also showed a trend of alleviation. Conclusion: Tuina can effectively ameliorate exercise-induced hepatic injury in rats. This effect may be mediated by regulating mitochondrial function through the AMPK/PGC-1α signaling pathway and modulating apoptosis via the caspase-3/cytochrome C pathway.

Objective: To investigate the therapeutic effect of Nobiletin (CCPS) on deep vein thrombosis (DVT) in rats by regulating the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) signaling pathway. Methods: Rats were randomly grouped into sham operation group, model group, low-dose Nobiletin (CCPS-L) group, high-dose Nobiletin (CCPS-H) group, and high-dose Nobiletin+cGAS-STING signaling pathway activator (CCPS-H+DMXAA) group. Fully automatic coagulation analyzer was applied to detect plasma prothrombin time (PT), activated partial prothrombin time (APTT), thrombin time (TT), fibrinogen (Fib) levels, and D-dimer. Fully automatic blood rheometer was utilized to measure rat plasma viscosity and hematocrit. ELISA was adopted to detect the levels of IL-1β, IL-8, IL-10, and TNF-α in lung tissue. H-E staining was used to observe the tissue morphology of venous thrombotic segments. Western blotting was employed to detect vascular tissue factor (TF), tissue factor pathway inhibitor (TFPI), antithrombin Ⅲ (ATⅢ ), cGAS, and STING protein expression. Results: Compared with the sham operation group, the venous lumen of rats in the model group showed obvious damage. The PT, APTT, TT, the level of serum IL-10, and the expression level of ATⅢ protein in the inferior vena cava tissue were significantly reduced, while the levels of Fib and D-dimer, plasma viscosity and hematocrit, the levels of serum IL-1β, IL-8, TNF-α, thrombus mass, the protein expression levels of TF, TFPI, cGAS, and STING in the inferior vena cava tissue were significantly increased. Compared with the model group, the venous lumen injury of rats in the CCPS-L and CCPS-H groups was significantly reduced, while the PT, APTT, TT, the level of serum IL-10, and the expression levelof ATⅢ protein in the inferior vena cava tissue were significantly increased. The levels of Fib and D-dimer, plasma viscosity and hematocrit, the levels of serum IL-1β, IL-8, TNF-α, thrombus mass, the protein expression levels of TF, TFPI, cGAS, and STING in the inferior vena cava tissue were significantly reduced. DMXAA attenuated the effect of Nobiletin on DVT rats. Conclusion: Nobiletin may reduce inflammation, improve coagulation function, and inhibit DVT formation by inhibiting the cGAS-STING signaling pathway.

Objective: To investigate the effects and mechanism of emodin in improving glucose and lipid metabolism and inflammatory response in rats with gestational diabetes mellitus (GDM). Methods: The model of gestational diabetes rats was established by combining a high sugar and high fat diet with streptozotocin injection. The model rats were randomly divided into model group (GDM group), low, medium and high dose emodin groups, and metformin group, with an additional normal control group. Histopathological changes and apoptosis of pancreatic cells were detected by H-E and Annexin V-FITC/DAPI staining. Fasting blood glucose (FBG), fasting insulin (FINS), the level of triglycerides (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), highdensity lipoprotein cholesterol (HDL-C), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), iron ions, and the expression of advanced glycation end products (AGEs)-receptor for advanced glycation end products (RAGE) pathway proteins were detected, respectively. Results: Compared with the GDM group, the pathological injury of the metformin group and the emodin group was improved. The levels of FBG, the apoptosis rate of pancreatic tissue, serum TG, TC, LDL-C, TNF-α, IL-6, IL-1β, MDA, iron ion levels and AGES-AGE signal pathway protein expression were decreased significantly, while serum FINS, the level of SOD and GSH-Px in pancreatic tissue were increased significantly. Conclusion: Emodin can improve glucose-lipid metabolism and systemic inflammatory response in GDM rats, reduce pancreatic tissue apoptosis, and may achieve these effects by modulating the AGEs-RAGE signaling pathway.

Objective: To investigate the effect of tea polyphenols (TP) on the inflammatory response in keratinocytes from condyloma acuminatum (CA) by regulating the Hippo/Yes-associated protein 1 (YAP1) pathway. Methods: Hacat cells with stable expression of HPV16E6 (HPV-Hacat) were cultured and were divided into control group, L-TP group (50 μg/mL TP), M-TP group (100 μg/mL TP), H-TP group (200 μg/mL TP), H-TP+TDI-011536 group (200 μg/mL TP+3 μmol/L Hippo pathway activator TDI-011536). MTT and EdU methods were applied to determine cell proliferation. Cell scratch assay and Transwell test were adopted to determine the migration and invasion of cells, respectively. ELISA method was employed to determine the contents of TNF-α and IL-6. Western blotting was utilized to determine the expression of Hippo/YAP1 pathway proteins and migration proteins in cells. Results: The survival rate of HPV-Hacat cells gradually decreased with the increase in TP concentration and showed a dose-dependent relationship. Compared with the control group, the proliferation, migration, invasion, TNF-α, IL-6 levels, YAP1, and matrix metalloproteinase (MMP)-2 and MMP-9 protein expression of HPV-Hacat cells in the L-TP group, M-TP group, and H-TP group were all reduced, with more pronounced effects observed at higher doses of TP. Compared with the H-TP group, the H-TP+TDI-011536 group showed an increase in HPV-Hacat proliferation, migration, invasion, TNF-α, IL-6 levels, YAP1, MMP-2, and MMP-9 protein expression. Conclusion: TP can effectively inhibit the proliferation, invasion, migration, and inflammatory response of HPV-Hacat cell, and its mechanism may be related to the inhibition of Hippo/YAP1 signaling pathway activation.

Objective: To investigate the effect and mechanism of serine protease inhibitor E2 (SERPINE2) on the proliferation and invasion of melanoma cells. Methods: The expression of SERPINE2 in nevi, melanoma tumors and metastases was analyzed through TCGA database and immunohistochemical staining of clinical samples. After the knockdown of SERPINE2 expression in melanoma cell A375, SERPINE2 mRNA and protein expression were detected by RT-qPCR and Western blotting. CCK8 assay was used to detect cell proliferation, Transwell assay to detect cell invasion, and Western blotting to measure E-cadherin (CDH1), N-cadherin (CDH2), SNAI1, matrix metalloprotease (MMP) 3 and MMP9 protein expression. Results: TCGA database analysis revealed that SERPINE2 expression was higher in melanoma compared with normal tissues. Immunohistochemical staining analysis confirmed that SERPINE2 was highly expressed in primary and metastatic melanoma. Knockdown of SERPINE2 significantly inhibited the proliferation and invasion of A375 cells and affected the expression of EMT pathway molecules. Specifically, the expression of CDH1 was significantly increased, while the expression of CDH2, SNAI1, MMP3 and MMP9 were significantly decreased. Conclusion: SERPINE2 promotes the proliferation and invasion of melanoma cells by regulating the expression of epithelial-mesenchymal transition-related molecules and targeting SERPINE2 and may be a promising strategy for inhibiting melanoma tumor progression.

Objective: To investigate the impacts of long non-coding RNA carbonyl reductase 3-AS1 (CBR3-AS1) on the malignant biological behavior of colon cancer cells by regulating microRNA-145-5p (miR-145-5p)/S-phase kinase-associated protein 1 (SKP1) axis. Methods: Colon cancer cell line SW480 was divided into five groups: control group, si-NC group, si-CBR3-AS1 group, si-CBR3-AS1+anti miR-NC group, and si-CBR3-AS1+anti miR- 145-5p group. The RT-qPCR was applied to detect the expression of CBR3-AS1, miR-145-5p, and SKP1 mRNA in cells. CCK-8 assay was applied to detect cell proliferation. Transwell assay was utilized to detect cell migration and invasion abilities, and the flow cytometry was employed to detect the level of cell apoptosis. Western blotting was adopted to detect the expression levels of SKP1, B-cell lymphoma protein 2 (Bcl-2)-associated X (Bax), and B-cell lymphoma protein 2 (Bcl-2) in cancer cells. Dual-luciferase reporter assay was applied to verify the interaction between miR-145-5p and CBR3-AS1, as well as between miR-145-5p and SKP1 mRNA. Results: Compared with the control group and si-NC group, the miR-145-5p, apoptosis rate, and the expression of Bax protein in SW180 cells in the si-CBR3-AS1 group were increased, while the expression of SKP1 mRNA, CBR3-AS1, OD450 values (24, 48, 72 h), numbers of migrating and invading cells, and the expression of Bcl-2 protein were decreased. Down-regulation of miR-145-5p weakened the inhibitory effects of low-expressed CBR3-AS1 on the proliferation, migration, and invasion of SW480 cells, and also inhibited cell apoptosis. CBR3-AS1 targeted and negatively regulated the miR- 145-5p expression, while miR-145-5p targeted and negatively regulated the SKP1 mRNA expression. Conclusion: The CBR3-AS1/miR-145-5p/SKP1 axis can inhibit proliferation, migration, and invasion of SW480 cells, and promote apoptosis in SW480 cells.

Objective: To investigate the inhibitory effect of Empagliflozin on human renal clear cell adenocarcinoma cells and its related mechanisms. Methods: Bioinformatics analysis was used to screen differential genes and pathways. In vitro experiments were conducted using 786-O cells, which were divided into a control group and an Empagliflozin group (combined with the AMPK inhibitor BAY-3827 or agonist Nilotinib). Western blotting and q-PCR were used to detect the expression of AMPK, PTEN, HDAC11, YAP, BRD4 proteins and epithelial-mesenchymal transition (EMT) markers. Scratch and Transwell assays were performed to evaluate cell migration and invasion capabilities. A nude mouse tumorigenesis experiment was conducted to validate the regulatory role of the AMPK pathway. Results: Bioinformatics analysis screened 1384 differentially expressed genes (800 up-regulated, 584 downregulated), enriched in PI3K-Akt, chemokines and Rap1 pathway; Engleretin significantly up-regulated p-AMPK, PTEN, HDAC11, while inhibiting YAP/BRD4 nuclear expression; down-regulated Snail, Slug mRNA, and enhanced E-cadherin expression; Emgleretin reduced cell migration and invasion, which were reversed by BAY-3827 but further inhibited by Nilotinib. In vivo studies showed Empagliflozin suppressed tumor growth, with AMPK-KD mice exhibiting larger tumor and AMPK-OE mice smaller tumors. Conclusion: Empagliflozin inhibits the progression of renal clear cell adenocarcinoma by activating the AMPK/PTEN/HDAC11 pathway, suppressing YAP/BRD4 nuclear localization and the EMT process, providing new mechanistic insights for clinical treat ment.

Stroke is a common neurological disorder caused by cerebrovascu lar events. Central post-stroke pain (CPSP) is a refractory complication of stroke characterized by variable onset times and diverse clinical manifestations. Its clinical management often yields poor therapeutic outcomes, significantly impairing patients' quality of life and even leading to suicidal tendencies in some cases. The pathogenesis of CPSP remains elusive. Current clinical treatments, including pharmacotherapy and adjunctive neuromodulatory therapies, have shown limited efficacy. This paper reviews recent advances in CPSP research from the perspectives of tissue, cellular, and molecular levels. It also discusses CPSP clinical treatment methods, aiming to provide new perspectives for both basic research and clinical management of CPSP.