In recent years, functional imaging techniques have gradually attracted widespread attention in the field of anatomical research. Unlike traditional methods that primarily rely on cadaver dissection or static structural imaging, functional imaging enables real-time monitoring of the metabolic status, hemodynamics, and neural conduction in living organisms. This provides a new perspective and technological platform for a deeper understanding of the correlation between “structure and function”. This article, following the theme of “transition from structural observation to functional understanding”, systematically reviews the research progress and application examples of representative functional imaging techniques such as functional magnetic resonance imaging, positron emission tomography/computed tomography, ultrasound, and optical imaging. It also summarizes their value in clinical preoperative planning, precision treatment, scientific research, and education, and discusses the current challenges such as in standardization, data fusion, and atlas construction.

Objective: To investigate the distribution of sexual dimorphism of skinfold thickness in the youth of Han nationality and its association with environmental factors. Methods: Data were obtained from the 2010 and 2014 Chinese School Student Physical Fitness and Health Surveillance surveys, which included 47 466 males and 47 611 females. Sexual dimorphism indices (SDI) were calculated for triceps, subscapular, and abdominal skinfold thickness. We also analyzed the correlation between SDI and sexual dimorphism in body size and body composition, alongside environmental factors. Results: The SDI of upper limbs skinfold thickness was higher than that of trunk skinfold thickness. The SDI of skinfold thickness was lower in 2014 compared with 2010 among the youth. The SDI of trunk skinfold thickness showed low to moderate positive correlations with the SDI of body mass and body composition. No significant differences were found between southern and northern populations, which is consistent with weak correlations with natural environmental factors. The SDI of skinfold thickness exhibited low to moderate positive linear correlations with social environmental factors. Conclusion: Sexual dimorphism in skinfold thickness varies between the upper limbs and the trunk, which is related to sex-hormonal regulation of subcutaneous fat distribution. The close association between sexual dimorphism in skinfold thickness and social environmental factors suggests divergent adaptive responses between males and females to societal changes

Objective: To investigate the characteristics of body composition among the Tibetan population and to analyze the impact of overweight and obesity on serum alanine aminotransferase (ALT) and uric acid (UA) levels. The study also aimed to explore the correlations between body composition and ALT/UA among overweight and obese Tibetan individuals. Methods: A cluster random sampling method was used to select adult Tibetan residents in Lhasa, Tibet. Height and body composition were measured, and biochemical indicators including ALT and UA were assessed. The abnormal detection rates of ALT and UA were calculated. Results: Among Tibetan adults, the rates of overweight and obesity were 33.22% and 13.22% in males, and 39.65% and 20.19% in females, respectively. The abnormal detection rates of ALT and UA in males were 40.00% and 32.20%, and 17.27% and 12.90% in females. In overweight males, ALT levels were significantly positively correlated with height, body weight, fat mass, subcutaneous fat mass, and trunk fat mass. UA levels in overweight males were significantly positively correlated with trunk muscle mass and right upper limb muscle mass; In obese males, UA levels were significantly positively correlated with body mass index and body fat percentage. In overweight females, UA levels were significantly positively correlated with body fat percentage, visceral fat mass, trunk fat mass, and fat percentages of the left and right lower limbs. In obese females, UA levels were significantly positively correlated with visceral fat mass. Conclusion: The abnormal detection rates of ALT and UA were higher in overweight and obese Tibetan adult males compared with females. ALT levels were significantly positively correlated with muscle and fat indicators in overweight males. UA levels showed significant positive correlations with muscle indicators in overweight males and with fat-related indicators in obese males as well as in both overweight and obese females.

Objective: To investigate the pathologic changes of primary age-related tauopathy (PART) and early stage of Alzheimer’s disease (pre-AD) in Chinese human brain samples, with the aim to provide a basis for the clinical diagnosis and pathological classification. Methods: Demographic, anatomical, neuropathological, and clinical data of PART and pre-AD samples were collected, and pathological diagnosis was performed through various morphological staining methods including hematoxylin-eosin (H-E) staining, special staining and immunohistochemistry, followed by statistical analysis of relevant data. Results: There were statistically significant differences between the PART and pre-AD groups in the pathological changes of cerebral amyloid angiopathy (CAA). CAA was present in only one case in the PART group, while the proportion of the pre-AD group reached 25.9%. The expression rates of TDP43 and p62 in the pre-AD group were higher than those of the PART group. No statistically significant differences were found between the groups in brain weight, cerebrospinal fluid pH, or Braak stage. Conclusion: Differences in certain pathologic indicators between PART and pre-AD in Chinese brain samples may be related to age at death.

Objective: To investigate the impacts of pterostilbene on inflammation and apoptosis of human periodontal ligament fibroblasts (PDLFs) by regulating the AMP-activated protein kinase (AMPK)/nuclear factorkappa B (NF-κB)/nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) signaling pathway. Methods: Human PDLFs cells were divided into six group: control group, lipopolysaccharide (LPS) group, differentdose (5, 10, and 20 μmol/L) pterostilbene groups, and pterostilbene (20 μmol/L)+AMPK inhibitor (1 μmol/L Compound C) group. After 2 h of pretreatment with pterostilbene and Compound C, the cells were cultured in medium containing 1 mg/L LPS for 24 h. CCK-8 assay was used to detect the viability of PDLFs cells. ELISA was applied to determine interleukin (IL)-6, tumor necrosis factor α (TNF-α), and IL-1β levels in PDLFs. Flow cytometry was adopted to detect apoptosis in PDLFs. RT-qPCR was utilized to measure the mRNA expression of AMPK, NF-κB, and NLRP3 in PDLFs. Western blotting was performed to observe the expression of AMPK, p-AMPK, NF-κB, p-NF-κB, and NLRP3 proteins in PDLFs. Results: Compared with the control group, the OD450 value, AMPK mRNA, and p-AMPK/AMPK of PDLFs in LPS group reduced, while the IL-6, TNF-α, IL-1β, apoptosis rate, NF-κB and NLRP3 mRNA, p-NF-κB/NF-κB and NLRP3 proteins increased. Compared with the LPS group,the OD450 value, AMPK mRNA, and p-AMPK/AMPK of PDLFs in Pterostilbene groups (5, 10, and 20 μmol/L) increased, while the IL-6, TNF-α, IL-1β, apoptosis rate, NF-κB and NLRP3 mRNA, p-NF-κB/NF-κB and NLRP3 proteins reduced. Compared with the 20 μmol/L Pterostilbene group, the OD450 value, AMPK mRNA, and p-AMPK/ AMPK of PDLFs in pterostilbene+Compound C group reduced, while the IL-6, TNF-α, IL-1β, apoptosis rate, NF-κB and NLRP3 mRNA, p-NF-κB/NF-κB and NLRP3 proteins increased. Conclusion: Pterostilbene activates AMPK to downregulate NF-κB and NLRP3, thereby inhibiting inflammation and apoptosis of PDLFs cells.

Objective: To investigate the effect of alpinetin on inflammatory injury in nephrotic syndrome (NS) rats by regulating the Hippo/Yes-associated protein (YAP) signaling pathway. Methods: A NS model was established by injecting doxorubicin hydrochloride, and rats were randomly divided into NS group, different-dose alpinetin groups, prednisone group, alpinetin + Hippo/YAP inhibitor verteporfin (VP) group, and the control group which was injected with normal saline. The assay kit was used to detect the urine protein of rats; the biochemical analyzer was used to measure the serum creatinine (Scr) and blood urea nitrogen (BUN); the ELISA kit was used to detect the levels of monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6); both kidneys were collected, and the kidney index was measured; H-E staining was used to detect renal histopathological changes; the terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) method was used to detect apoptosis of renal tissue cells. Finally, real-time quantitative polymerase chain reaction (RT-qPCR) and Western blotting were employed to detect the mRNA and protein expressions of YAP and transcriptional co-activator PDZ-binding motif (TAZ). Results: Compared with the control group, the levels of Scr, urinary protein, BUN, IL-6, TNF-α, MCP-1, kidney index, pathological score, apoptosis rate, p-YAP/YAP, TAZ and mRNA expression in the NS group were significantly increased. Compared with the NS group, the levels of Scr, urinary protein, BUN, IL-6, TNF-α, MCP-1, kidney index, pathological score, apoptosis rate, p-YAP/YAP, TAZ mRNA and protein expression in the different-dose alpinetin groups and prednisone group were significantly reduced, and therewere differences among different doses of alpinetin. Compared with the 160 mg/kg alpinetin group, the levels of Scr, urinary protein, BUN, IL-6, TNF-α, MCP-1, kidney index, pathological score, apoptosis rate, p-YAP/YAP, TAZ mRNA and protein expression in the alpinetin+VP group obviously reduced. Conclusion: Alpinetin has an effect on inflammatory injury in NS rats by regulating the Hippo/YAP signaling pathway.

Objective: The aim of this study was to investigate the role of Src-homology domain 2 containing protein tyrosine phos-phatase-1 (SHP-1) expression in macrophages in breast cancer and its potential mechanisms. Methods: GEO database was used for bioinformatics analysis, and a nude mouse tumor model was constructed to detect the effects of SHP-1 and Spi-1 proto-oncogene (PU.1) overexpression in macrophages on tumor progression. THP-1 cells were stimulated under different conditions and divided into six groups: NC group, SHP-1-OE group, NC+SP1 inhibitor group, SHP-1-OE+SP1 inhibitor group, NC+SP1 inhibitor+SYK inhibitor group and SHP-1-OE+SP1 inhibitor+SYK inhibitor group. These THP-1 cells were co-cultured with breast cancer MCF-7 cells. The protein expression levels of SHP-1, nuclear SP1, DNA methyltransferase-1 (DNMT1), PU.1 and phosphorylated spleen tyrosine kinase (p-SYK) were detected by Western blotting. The levels of oxidative stress and the polarization of M1 and M2 macrophages in THP-1 cells were detected by RT-qPCR. TUNEL assay was utilized to detect the apoptosis level of tumor cells. Results: Bioinformatics analysis showed that SHP-1 (PTPN6) inhibited ROS expression, while SP1 promoted DNMT1 expression.The transplanted tumors in SHP-1 overexpressed nude mice were significantly larger than those in the control group, while PU.1 overexpression resulted in smaller tumors. The expression of nuclear SP1, DNMT1, arginase-1, and CD206 was significantly higher in SHP-1 overexpression group compared with the control group, while PU.1, p-SYK, NOX2, NOX4, IL-1β, and TNF-α levels were significantly decreased. After the treatment of SP1 inhibitor, the expression of nuclear SP1, DNMT1, arginase-1, and CD206 was significantly decreased, while the expression of PU.1, p-SYK, NOX2, NOX4, IL-1β, and TNF-α was significantly increased. When the expression of SP1 inhibitor and SYK inhibitor were applied, the expression of arginase-1 and CD206 was significantly increased, while the expression of NOX2, NOX4, IL-1β, and TNF-α was markedly decreased. SHP-1 overexpression significantly decreased the apoptosis rate of tumor cells. Apoptosis increased notably upon SP1 inhibitor treatment but decreased again when both SP1 and SYK inhibitors were applied. Conclusion: Overexpression of SHP-1 in tumor-associated macrophages promotes the activation of SP1/DNMT1 signaling pathway, which subsequently down-regulates the expression of PU.1 and SYK, and inhibits oxidative stress-induced inflammatory responses, thereby promoting breast cancer progression.

Objective: To explore the impacts of protosappanin A (PrA) on the proliferation, apoptosis and radiosensitivity of breast cancer cells by modulating the AMP-activated protein kinase (AMPK)/acetyl-CoA carboxylase (ACC) signaling pathway. Methods: Breast cancer cells (MCF-7) were cultured in vitro and randomly divided into control group (normal culture), L-PrA group, M-PrA group, H-PrA group (treated with 400, 800, 1 600 μmol/L PrA), and Compound C group (treated with 1 600 μmol/L PrA and 1 μmol/L Compound C, an AMPK/ ACC pathway inhibitor). Cell proliferation was assessed by CCK-8 assay to select appropriate PrA concentrations and to compare proliferative activity across groups. The colony formation experiment was performed to detect cell radiosensitivity. Scratch wound-healing and Transwell assays were adopted to measure cell migration and invasion. Flow cytometry was utilized to assess the apoptosis of cells in each group. Western blotting was employed to analyze the proteins associated with proliferation, migration, invasion, apoptosis, and the AMPK/ACC signaling pathway in cells. Results: Compared with the control group, PrA treatment groups showed dose-dependent decreases in cell survival fraction (SF), proliferation rate, migration rate, invasion number, and expression of PCNA, MMP-2, MMP-9, and Bcl-2, and increases in sensitization enhancement ratio (SER), apoptosis rate, and expression of Bax, cleaved caspase-3, p-AMPK/AMPK, and p-ACC/ACC. Compared with the H-PrA group, the Compound C group exhibited significant rises in SF, proliferation rate, migration rate, invasion number, and expression of PCNA, MMP-2, MMP-9, and Bcl-2, while demonstrating decreases in SER, apoptosis rate, and expression of Bax, cleaved caspase-3, p-AMPK/AMPK, and p-ACC/ ACC. Conclusion: PrA may activate the AMPKACC signaling pathway, thereby inhibiting breast cancer cell proliferation, migration and invasion, promoting cell apoptosis, and enhancing radiosensitivity

Objective: To investigate the impacts of remifentanil on the proliferation, migration, invasion, and apoptosis of cervical cancer cells by regulating the CC-chemokine ligand 2 (CCL2)/CC chemokine receptor 2 (CCR2) signaling pathway. Methods: Human cervical cancer HeLa cells were divided into six groups: control group, low-, medium-, and high-concentration remifentanil group, remifentanil+NC group, and remifentanil+CCL2 group. EdU assay was used to detect cell proliferation. The wound healing experiment was applied to determine HeLa cell migration. Transwell method was utilized to observe HeLa cell invasion. Flow cytometry was adopted to detect apoptosis in HeLa cells. RT-qPCR was employed to detect the mRNA expression of CCL2, CCR2A, and CCR2B. Western blotting was used to analyze the expression of CCL2 and CCR2 proteins. Results: Compared with the control group, the EdU positive rate, migration rate, and number of invasive cells in the low-, medium-, and high-dose remifentanil groups were all reduced, and the mRNA expression of CCL2, CCR2A and CCR2B and the protein expression of CCL2 and CCR2 were all decreased, while the cell apoptosis rate was increased, with these effects more pronounced with higher concentrations, and there was a prominent difference among different concentration groups. Compared with the remifentanil+NC group, the EdU positive rate, migration rate, and number of invasive cells in HeLa cells in the remifentanil+CCL2 group were all increased, and the mRNA expression of CCL2, CCR2A and CCR2B and the protein expression of CCL2 and CCR2 were all up-regulated, while the cell apoptosis rate was decreased. Conclusion: Remifentanil may inhibit the proliferation, migration, and invasion and promote apoptosis in cervical cancer cells by suppressing the CCL2/CCR2 pathway.

Objective: To investigate the effects of Pueraria lobata total flavonoids on autophagy, apoptosis and PI3K/c-Myc pathway in multiple myeloma RPMI-8226 cells. Methods: The multiple myeloma RPMI-8226 cells were divided into a blank control group, low (40 μg/mL), medium (80 μg/mL), high (160 μg/mL) dose groups of Pueraria lobata total flavonoids and a positive control group (doxorubicin, 75 nmol/L). CCK-8 method was used to detect cell survival rate, flow cytometry to detect cell apoptosis rate, Transwell test method to detect cell migration, GFP-LC3 puncta formation assay to determine autophagy, and Western blotting to observe B-cell lymphoma 2 (Bcl-2), Bcl-2- associated X protein (Bax), microtubule-associated protein 1A/1B- light chain 3 (LC3)Ⅱ/Ⅰ, Beclin1, PI3K and c-Myc protein expression. A mouse model of transplanted tumors was established and divided into a blank control group, a low-dose group of kudzu root total flavonoids (10 mg/kg), a medium-dose group (20 mg/kg), a high-dose group (40 mg/kg), and a positive control group (bortezomib, 0.5 mg/kg). The tumor weight and volume were measured, as well as the expression of PI3K and c-Myc proteins in the tumor tissue. Results: Compared with the blank control group, the cell survival rate, migration capacity, Bcl-2, PI3K and c-Myc protein expression level of multiple myeloma RPMI- 8226 cell in the low-, medium-, and high-dose groups of Pueraria lobata total flavonoids and the positive control group were significantly deceased, while the apoptosis rate, number of LC3 spot, expression of Bax, Beclin1 and LC3Ⅱ/Ⅰ were significantly increased. The tumor volume, tumor weight, and the expression levels of PI3K and c-Myc proteins in the tumor tissue were significantly reduced. The effect of total flavonoids of Pueraria lobata in each dose group was dose-dependent. The high-dose group of total flavonoid and the positive control group showed similar effects, with no statistically significant differences. Conclusion: Pueraria lobata total flavonoids canpromote autophagy and apoptosis in multiple myeloma RPMI-8226 cells, potentially by inhibiting the expression of proteins associated with the PI3K/c-Myc signaling pathway.

Objective: To explore the effect of Xuefuzhuyu decoction on retinal neovascularization in diabetic retinopathy (DR) rats by regulating the Wnt family member (Wnt)/β-catenin signaling pathway. Methods: A DR model was constructed, and the successfully modeled rats were divided into four groups: DR group, low-dose Xuefuzhuyu decoction group, high-dose Xuefuzhuyu decoction group, and LiCl group. A control group was also set up. An automatic biochemical analyzer was used to measure the fasting blood glucose (FPG) and triglyceride (TG) levels. Fluorescein fundus angiography method was applied to detect retinal angiogenesis in each group. ELISA method was applied to measure the levels of angiopoietin 1 (Ang-1), vascular endothelial growth factor (VEGF), and inflammation related factors such as tumor necrosis factor-α (TNF-α) and interleukin (IL)-1β in the serum of rats in each group. Western blotting was applied to detect the expression of Wnt1 and β-catenin proteins in each group. Results: Compared with the control group, the FPG, TG, Ang-1, VEGF, TNF-α, IL-1β, Wnt1, and β-catenin in the DR group were obviously higher, with an obvious increase in retinal neovascularization and severe leakage of fluorescein. Compared with the DR group, the FPG, TG, Ang-1, VEGF, TNF-α, IL-1β, Wnt1, and β-catenin in the low- and high-dose groups decreased in a dose-dependent manner, with retinal neovascularization and the leakage of fluorescein gradually decreased. Compared to the high-dose group, the LiCl group reversed these effects. Conclusion: Xuefuzhuyu decoction may reduce blood glucose, inflammation levels, and retinal neovascularization in DR rats by inhibiting the Wnt/β-catenin pathway, thereby alleviating DR symptoms

Objective: This paper aims to explore the influences of age, cause of death, medical history on the quality of cadaver fixation. Methods: Forty-five cadavers accepted by our facility from January to October 2021 were selected. Relevant information was collected, and operations such as flushing, disinfection, and fixed preservation were carried out. One year later, the fixation status of the skin, muscles, and internal organs was evaluated and a fixation grade was assigned for each. The Fisher’s exact method was used to analyze the data such as age group, gender, medical history and age respectively. Spearman’s correlation analysis method was used to examine the correlations of age group, medical history, and cause of death, with fixation status. Results: The age of the 45 cadavers was (62.13±12.94) years old, including 28 males (62.22%) and 17 females (37.78%). There are statistically significant differences in the fixation status concerning the cadaver's age and medical history. Age and medical history are positively correlated with the fixation of corpses. Gender and cause of death have no correlation with the fixation of the body. Conclusions: Different ages, disease types and severity may all be related to their fixation outcomes. When receiving cadavers, special attention should be paid to donors of advanced age or with complex medical histories, and their intended use should be arranged accordingly.

This article systematically reviews the anatomical variations of the brachial plexus and its major terminal branches, encompassing abnormalities in the number and course of nerve roots, trunks, divisions, cords, and branches, as well as variations in the distribution of communicating branches. Based on anatomical observations, Meta-analyses, and clinical data from both domestic and international literature, the study emphasizes key variations—such as prefixed and postfixed brachial plexuses, alterations in the number of trunks (e.g., two-trunk and four-trunk configurations), and multi-root origins of terminal nerves—along with their respective incidence rates. The paper research aims to provide anatomical reference for brachial plexus injury repair, nerve block procedures, and surgical planning, thereby reducing diagnostic and therapeutic risks and improving clinical accuracy

Drug delivery remains a significant challenge for treating central nervous system (CNS) diseases, especially for macromolecular drugs that are difficult to deliver into the neural system via conventional routes. Intranasal administration has emerged as a novel approach, gaining attention for leveraging the unique anatomical and physiological features of the nasal mucosa. This review systematically reviews recent research progress in the application of intranasal administration for treating CNS diseases, summarizes key findings, analyzes existing challenges, and proposes future research directions.