To accurately identify the anatomical structures of the cystic triangle, scientifically evaluate the degree of adhesion, rationally select the surgical approach, and implement the “zero bile duct injury” philosophy, this review systematically summarizes the anatomical basis of the cystic triangle and the mechanisms underlying adhesion formation, outlines commonly used classification systems for severe adhesions, and discusses surgical approach selection guided by these classifications. This work aims to provide an anatomical foundation for the safe performance of difficult cholecystectomy and the achievement of zero bile duct in jury.

Objective: To investigate the morphological features of the intermetatarsal facet of the first metatarsal bone in modern Chinese population. Methods: A total of 355 first metatarsal bone specimens from 277 modern adult individuals (132 males, 145 females) from the Beijing region were included. Morphological observation and threedimensional digital measurement methods were employed to analyze the anatomical variations of the intermetatarsal facet. Results: The intermetatarsal facet was observed in 20 metatarsal specimens from 19 individuals, with an individual prevalence of 6.86% and a specimen prevalence of 5.63%. The facet predominantly exhibited an elongated oval shape and was located in the upper-middle two-thirds of the lateral surface of the metatarsal base. It could be categorized into two types: adjacent type (11 specimens) and separated type (9 specimens). The mean values of the long diameter, short diameter, and surface area of the facets were 10.7 mm, 6.6 mm, and 49.4 mm2, respectively. Conclusion: This study fills the gap in data regarding intermetatarsal facet variations in the Chinese population and provides important anatomical insights for sur gical planning in foot and ankle procedures.

Objective: To investigate the effects of dihydrotanshinone Ⅰ (DHT) on viability and apoptosis of cardiomyocytes induced by hypoxia/reoxygenation (H/R) by regulating the Pink1/Parkin signaling pathway. Methods: H9c2 cells were used to establish an H/R injury model and divided into model, low-dose DHT (L-DHT), medium-dose DHT (M-DHT), high-dose DHT (H-DHT), and DHT+inhibitor groups. Untreated cells served as the normal group. CCK- 8 assay was used to detect cell viability. Flow cytometry was applied to detect apoptosis. JC-1 mitochondrial membrane potential assay was employed to determine mitochondrial membrane potential. The colorimetric method was adopted to determine the content of malondialdehyde (MDA). RT-qPCR was utilized to assess the expression of Pink1 and Parkin mRNA. Western blotting was performed to observe the expression of Pink1 and Parkin proteins. Results: Compared with the normal group, the OD value of H9c2 cells, mitochondrial membrane potential, Pink1 and Parkin mRNA and protein expression in the model group were lower, while the apoptosis rate and MDA content were higher. Compared with the model group, the OD values of H9c2 cells, mitochondrial membrane potential, Pink1 and Parkin mRNA and protein expression in the L-DHT, M-DHT, and H-DHT groups were higher, while the apoptosis rate and MDA content were lower. The effect of DHT on H9c2 increased as the concentration rises. The autophagy inhibitor 3-MA greatly increased the mRNA and protein expression levels of Pink1 and Parkin in H9c2 cells and reversed the effects of DHT on H9c2 cell viability, apoptosis, mitochondrial membrane potential, and MDA content. Conclusion: DHT may promote mitochondrial autophagy in H9c2 cells by activating the Pink1/Parkin signaling pathway, thereby promoting viability and inhibiting apoptosis.

Objective: To explore the effects of puerarin on cerebral ischemia-reperfusion (I/R) injury in rats and to elucidate its mechanism mediated by miR-130a-5p. Methods: SD rats were randomly divided into sham operation group, model group, puerarin group, puerarin+antagomiR-negative control (antagomiR-NC) group and puerarin+antagomiR-130a-5p group. Longa five-point scale method was used to evaluate the neurological deficit in rats. The pathological changes of hippocampus in rats were observed by H-E staining. TUNEL staining was performed to detect the level of apoptosis in hippocampus of rats. RT-qPCR was adopted to detect the expression of miR-130a-5p in rat hippocampus. Western blotting was utilized to detect the expression of high mobility group box 2 (HMGB2), Toll-like receptor 4 (TLR4), and myeloid differentiation factor 88 (MyD88) proteins in hippocampus of rats. Results: Compared with the sham operation group, the neurological deficit score, the level of apoptosis in hippocampus and the expressions of HMGB2, TLR4 and MyD88 in hippocampus in model group were significantly increased, while the pathological damage in hippocampus was aggravated and the expression of miR-130a-5p in hippocampus was significantly decreased. Compared with the model group, puerarin group and antagomiR-NC group significantly reduced the neurological deficit score, the level of apoptosis and the expression of HMGB2, TLR4 and MyD88 proteins in hippocampus, with alleviated pathological damage of hippocampus and significantly increased expression of miR-130a-5p in hippocampus. Compared with puerarin group and antagomiR-NC group, antagomiR- 130a-5p group significantly increased the neurological deficit score, the level of apoptosis and the expression of HMGB2, TLR4 and MyD88 proteins in hippocampus, while demonstrating aggravated pathological damageof hippocampus, and significantly decreased the expression of miR-130a-5p in hippocampus. Conclusion: Puerarin improves I/R-induced brain injury and hippocampal neuron apoptosis by up-regulating the expression of miR-130a- 5p, and its mechanism may be achieved by suppressing HMGB2 expression and inhibiting activation of the TLR4/ MyD88 signaling pathway.

Objective: To investigate the impacts of long noncoding RNA (lncRNA) differentiation antagonizing non-protein coding RNA (DANCR) on the proliferation, autophagy and invasion of breast cancer MCF7 cells by targeting microRNA-125a-5p (miR-125a-5p). Methods: Breast cancer MCF7 cells were selected as research objects, and were divided into five groups: control, silenced-NC, silenced-DANCR, silenced-DANCR+inhibitor NC, and silenced-DANCR+miR-125a-5p inhibitor. The expression of DANCR and miR-125a-5p, cell proliferation, apoptosis, migration, invasion, autophagy, and the Beclin and LC3-Ⅱ/Ⅰ protein expression were detected by using RT-qPCR, CCK-8, flow cytometry, scratch assay, Transwell, monodansylcadaverine (MDC) staining, and Western blotting, respectively. A dual luciferase reporter assay was employed to validate the targeting relationship between DANCR and miR-125a-5p. Results: Compared with control and silence-NC groups, DANCR expression, optical density (OD) value, scratch healing rate, and number of invasive cells were reduced in the silenced-DANCR group, while miR-125a-5p expression, apoptosis rate, proportion of MDC-positive cells, and protein levels of Beclin and LC3-Ⅱ/Ⅰ were increased. Compared with silenced-DANCR and silenced-DANCR+inhibitor NC group, OD value, scratch healing rate, and number of invasive cells in the silencing-DANCR+miR-125a-5p inhibitor group were increased, while miR-125a-5p expression, apoptosis rate, proportion of MDC-positive cells, and protein levels of Beclin and LC3-Ⅱ/Ⅰ were decreased . DANCR was confirmed to have a targeted relationship with miR-125a-5p. Conclusion: Silencing the expression of DANCR can increase the expression of miR-125a-5p, thereby affecting the proliferation, autophagy and invasion of MCF7 cells in breast cancer.

Objective: To investigate the interaction between Src homology 2 domain-containing protein tyrosine phosphatase 1 (SHP1) and signal regulatory protein α (SIRPα) and the regulatory effects of related signaling factors on breast cancer progression, which may identify novel potential targets for tumor immunotherapy. Methods: Bioinformatics analysis was applied to predict and analyze the relationships among SHP1, SIRPα, and downstream signaling factors. A co-culture model of breast cancer MCF-7 cells and monocyte THP-1 cells was established. The co-cultured cells were treated with corresponding lentiviral transfection and heat shock factor 1 (HSF1) agonist (HSF1A) and then were divided into 8 groups: NC, SHP1-OE, HSF1A+NC, HSF1A+SHP1-OE, SIRPα-KD+NC, SIRPα-KD+SHP1-OE, SIRPα-KD+HSF1A+NC, and SIRPα-KD+HSF1A+SHP1-OE groups. Western blotting was used to detect protein expressions in THP-1 cells. RT-qPCR was used to detect mRNA expression of polarization markers of M2 macrophage in THP-1 cells. Transwell assays were conducted to assess MCF-7 cell migration and invasion. CCK-8 assays were performed to evaluate MCF-7 cell proliferation. Results: Bioinformatics analysis suggested that SHP1 might stabilize SP1 by inhibiting JNK, thereby promoting HSF1 expression, and that it was associated with the SIRPα/SHP2/STATs/PD-L1 signaling axis. Experimental results indicated that overexpression of SHP1 or treatment with an HSF1 agonist upregulated the expression of nuclear HSF1, SIRPα, membrane p-SHP2, p-STAT3, p-STAT6, PD-L1 and cathepsin L, elevated the mRNA expression of arginase-1, CD206 and YM-1, and promoted the proliferation, migration, and invasion of MCF-7 cells; whereas knockdown of SIRPα reversed these effects. Conclusion: SHP1 can accelerate breast cancer progression by activating SIRPα-dependent M2macrophage polarization mediated by the SP1/HSF1/SHP2/STATs/PD-L1 pathway.

Objective: To investigate the effects of long noncoding RNA (lncRNA) nuclear-enriched abundant transcript 1 (NEAT1) on the malignant biological behavior of gastric cancer cells by regulating the microRNA-433- 3p (miR-433-3p)/Golgi membrane protein 1 (GOLM1) axis. Methods: Gastric cancer MKN45 cells were randomly divided into five groups: Control group (normal culture), sh-NC group (transfected with sh-NC), sh-NEAT1 group (transfected with sh-NEAT1), sh-NEAT1+inhibitor-NC group (co-transfected with sh-NEAT1 and inhibitor-NC), and sh-NEAT1+miR-433-3p inhibitor group (co-transfected with sh-NEAT1 and miR-433-3p inhibitor). RT-qPCR was applied to detect the expression of lncRNA NEAT1, miR-433-3p, and GOLM1 mRNA of MKN45 cells. EdU staining, Transwell assay, and flow cytometry were employed to assess the effects of MKN45 cell proliferation, migration, invasion, and apoptosis, respectively. Western blotting was adopted to determine the expression of proliferating cell nuclear antigen (PCNA) and GOLM1 proteins in MKN45 cells. Dual luciferase reporter gene experiment was utilized to verify the interaction between lncRNA NEAT1 and miR-433-3p, and between miR-433-3p and GOLM1. Results: The EdU positive cell rate, migration number, invasion number, the expression of lncRNA NEAT1, GOLM1 mRNA and protein, and PCNA protein expression in the sh-NEAT1 group were lower than those in the sh-NC and Control groups, while the apoptosis rate and miR-433-3p expression were higher. The EdU positive cell rate, migration number, invasion number, GOLM1 mRNA and protein, and PCNA protein expression in the sh-NEAT1+miR-433-3p inhibitor group were higher than those in the sh-NEAT1 and sh-NEAT1+inhibitor-NC groups, while the apoptosis rate and miR-433-3p expression were lower. NEAT1 was found to negatively regulate miR-433-3p by direct targeting, and miR-433-3p was found to negatively regulate GOLM1 by direct targeting. Conclusion: LncRNA NEAT1 may promote the malignant biological behavior of gastric cancer cells by regulating the miR-433-3p/GOLM1 axis.

Objective: To investigate the biological function and prognostic value of miR-491-5p in gastric cancer. Methods: Eighty pairs of gastric cancer tissues and adjacent normal tissues were collected for this study. RT-qPCR was conducted to determine the expression level of miR-491-5p and evaluate its prognostic significance. Functional validation of miR-491-5p was performed in the gastric cancer AGS cell line by using CCK-8 and Transwell assays. Furthermore, RT-qPCR and Western blotting were used to detect the mRNA and protein expression levels of N-cadherin, β-catenin, vimentin, and interferon-induced transmembrane protein 2 (IFITM2). The in vivo effect of miR-491-5p was evaluated by using a nude mouse xenograft tumor model. Results: Patients with high levels of miR- 491-5p had better prognoses, and high miR-491-5p expression reduced the ability of cells to proliferate, migrate, and invade. In the nude mouse xenograft tumor model, high miR-491-5p expression inhibited tumor development. Additionally, miR-491-5p inhibited the expression of epithelial-mesenchymal transition-related markers, cell adhesion genes, and IFITM2. Conclusions: MiR-491-5p serves as a tumor suppressor in GC both in vitro and in vivo and functions as a significant prognostic biomarker for GC diag nosis and treatment.

Object ive: To i n v e s t i g a t e t h e c o r r e l a t i o n o f m i c r o R N A ( m i R ) - 2 9 b - 3 p a n d n i c o t i n a m i d e N-methyltransferase (NNMT) expression in ovarian cancer tissues with lymph node metastasis and prognosis. Methods: A retrospective study was conducted on patients with epithelial ovarian cancer treated in our hospital from January 2020 to October 2021, including 53 patients with poor prognosis and 86 patients with good prognosis followed up for 3 years. The cancer tissues and adjacent non-cancerous tissues of ovarian cancer patients were collected during intraoperative resection. RT-qPCR was used to measure miR-29b-3p and NNMT mRNA expression levels in tissues. Immunohistochemistry was used to detect NNMT protein expression in patient tissues. Logistic regression analysis was performed to analyze the influencing factors of poor prognosis in ovarian cancer patients. Receiver operating characteristic (ROC) curve was employed to assess the predictive value of miR-29b-3p and NNMT expression in cancer tissues for the prognosis of ovarian cancer patients. Results: Compared with adjacent non-cancerous tissues, the expression of miR-29b-3p in cancer tissues was lower, while the expression of NNMT mRNA and protein was higher. There was a potential binding site between miR-29b-3p and the NNMT 3’UTR region, and their expression was negatively correlated in ovarian cancer tissues. The lymph node metastasis group had lower miR-29b-3p expression and higher NNMT mRNA expression than those in the non-lymph node metastasis group. The poor prognosis group had higher FIGO stages Ⅲ - Ⅳ , poorly differentiated tumors, lymph node metastasis rate, and higher NNMT mRNA expression, and lower miR-29b-3p expression compared with good prognosis group. Multivariate analysis showed that FIGO stages Ⅲ- Ⅳ , poorly differentiated tumors, lymph node metastasis, and high NNMT mRNA expression were risk factors for poor prognosis, while high miR-29b-3p expression wasa protective factor. The area under the curve (AUC) of the combined miR-29b-3p and NNMT mRNA for predicting poor prognosis in ovarian cancer patients was 0.939, which was significantly greater than that of either alone. Conclusion: Low expression of miR-29b-3p and high expression of NNMT in ovarian cancer tissues are associated with lymph node metastasis and poor prognosis. These two markers combined have high predictive value for poor prognosis.

Objective: To investigate the effects of kaempferol (KAE) on lipopolysaccharide (LPS)-induced inflammatory damage and osteogenic differentiation in human dental pulp stem cells (hDPSCs) by modulating the Wnt/β-catenin signaling pathway. Methods: HDPSCs were exposed to LPS to establish an in vitro inflammatory model. After 48 h of treatment with graded concentrations of KAE (0, 12.5, 25, 50, 100, 200 μmol/L), CCK-8 assay was used to detect cell proliferation activity to determine the optimal treatment concentration of kaempferol. HDPSCs cells were divided into control group, LPS group, low-, medium-, and high-dose kaempferol groups (KAE-L, KAE-M, KAE-H), and high-dose kaempferol+Wnt inhibitor DKK1 group (KAE-H+DKK1). Enzyme-linked immunosorbent assay was utilized to detect changes in inflammat ory factors such as tumor necrosis factor -α (TNF-α), interleukin (IL)-6, and IL-1β. Alkaline phosphatase (ALP) staining was adopted to detect cellular ALP activity. Alizarin red staining was performed to observe the formation of mineralized nodules in cells. Western blotting was employed to measure the expression of osteogenesis-related proteins including Runt related transcription factor 2 (RUNX2), osteocalcin (OCN), bone morphogenetic protein 2 (BMP2), and Wnt/β-catenin pathway-related proteins. Results: Compared with the control group, the LPS group showed an obvious decrease in ALP activity, mineral nodule count, and the protein levels of RUNX2, OCN, BMP2, Wnt3a, and β-catenin, while exhibiting a prominent increase in TNF-α, IL-6, and IL-1β. Compared with the LPS group, the KAE-trea ted groups dose-dependently showed a prominent increase in ALP activity, mineral nodule count, and levels of RUNX2, OCN, BMP2, Wnt3a, and β-catenin proteins, while demonstrating a significant decrease in TNF-α, IL-6, and IL-1β levels. Comparedwith the KAE-H group, the KAE-H+DKK1 group showed a significant decrease in ALP activity, mineral nodule count, and levels of RUNX2, OCN, BMP2, Wnt3a, and β-catenin proteins, while indicating a marked increase in TNF-α, IL-6, and IL-1β levels. Conclusion: Kaempferol can alleviate LPS-induced inflammatory damage and inhibit osteogenic differentiation in hDPSCs, possibly achieved through activation of the Wnt/β-catenin signaling pathway.

Objective: To perform morphological observations on two unnamed structures in the human atria, namely the olivary pouch and the ostium secundum fossa, so as to provide reference data for anatomy, embryology and clinical application. Methods: The lateral wall of the right atrium and the posterior wall of the left atrium were opened for direct observation. Measurements were taken with a vernier caliper and probes. Results: The occurrence rate of the olivary pouch in the right atrium was about 62.96%, and its position was constant. The ostium secundum fossa was present in 100.00% of the left atrial specimens and also occupied a constant position. Based on morphology, it could be divided into three types: primitive, transitional and fused types. Some specimens exhibited an atrial septal pouch in association with the ostium secundum fossa. Conclusion: The olivary pouch was formed by the confluent openings of a number of anterior cardiac veins, while the ostium secundum fossa was the remnant of the ostium secundum in the primary septum.

MicroRNA (miRNA) target and regulates mitochondrial function, participates in cell death, and modulate the onset and progression of diseases. Nevertheless, systematic dis section of their regulatory networks remains insuf ficient to date. On the basis of summarizing existing research findings , this paper integrated the regulatory patterns underlying miRNA-mediated mitochondrial function and cell death, elucidated the cross-regulatory characteristics of distinct miRNAs across multiple forms of cell death, and compared the shared and disease-specific mechanisms by which miRNAs govern mitochondrial homeostasis and cell death in diverse disorders. This work is expected to provide systematic theoretical references and innovative insights for subsequent fundamental research and clinical targeted therapy development.