BACKGROUND:Post and core restoration is a common choice for tooth defects,but the repair effects of various post and core materials are different. OBJECTIVE:To evaluate the stress distribution at the post and core,tooth root,and bonding agent site of post and core models made of different elastic modulus post and core materials using finite element method. METHODS:A three-dimensional root canal treated maxillary central incisor model was built using three-dimensional modeling software,which was restored with a full ceramic crown.The post and core materials in the restoration used nanoceramic resin(elastic modulus=12.8 GPa),composite resin(elastic modulus=16 GPa),hybrid ceramic(elastic modulus=34.7 GPa),glass ceramic(elastic modulus=95 GPa),titanium alloy(elastic modulus=112 GPa),and zirconia(elastic modulus=209.3 GPa).The model was fixed in cortical bone.A 100 N concentrated force of 45° from the long axis of the tooth was applied to 1/3 of the crown and tongue side of the central incisor.The stress distribution of the post and core,dentin,and tooth-root bonding agent in the model was repaired by the maximum principal stress criterion. RESULTS AND CONCLUSION:(1)When the post and core materials with higher elastic modulus was used,the post-core stress in the repair model was more concentrated.When the elastic modulus of the post and core materials(nanoceramic resin and composite resin)was close to dentin,the stress distribution of the post and core was more uniform.The stress distribution of dentin in all restoration models was similar regardless of post and core materials.When the post and core with higher elastic modulus was used,more stress concentration was shown at the post and root bonding agent in the repair model.(2)The maximum stress values at the post and core,tooth root,and the bonding agent site of post and tooth root in the nanoceramic resin model were 31.00,33.21,and 0.51 MPa,respectively.The maximum stress values at the post and core,tooth root,and the bonding agent between the post and tooth root in the composite resin model were 36.84,33.14,and 0.59 MPa,respectively.In the mixed ceramic model,the maximum stress values at the post and core,tooth root,and the bonding agent between the post and tooth root were 64.05,32.83,and 1.00 MPa,respectively.In the glass ceramic model,the maximum stress values at the post and core,tooth root,and the bonding agent between the post and tooth root were 112.30,32.69,and 1.73 MPa,respectively.In the titanium alloy model,the maximum stress values of the post and core,tooth root,and the bonding agent between the post and tooth root were 120.00,32.17,and 1.86 MPa,respectively.In the zirconia model,the maximum stress values of the post and core,tooth root,and the bonding agent between the post and tooth root were 148.80,31.85,and 2.28 MPa,respectively.(3)The higher the elastic modulus of the post and core material,the higher the maximum stress at the post and core during restoration.The elastic modulus of the post and core material had no significant effect on the maximum stress of the dental bonding agent and dentin.

Exercise-induced metabolic remodeling is a fundamental adaptive process whereby the body reorganizes systemic and cellular metabolism to meet the dynamic energy demands posed by physical activity. Emerging evidence reveals that such remodeling not only enhances energy homeostasis but also profoundly influences immune function through complex molecular interactions involving glucose, lipid, and protein metabolism. This review presents an in-depth synthesis of recent advances, elucidating how exercise modulates immune regulation via metabolic reprogramming, highlighting key molecular mechanisms, immune-metabolic signaling axes, and the authors’ academic perspective on the integrated “exercise-metabolism-immunity” network. In the domain of glucose metabolism, regular exercise improves insulin sensitivity and reduces hyperglycemia, thereby attenuating glucose toxicity-induced immune dysfunction. It suppresses the formation of advanced glycation end-products (AGEs) and interrupts the AGEs-RAGE-inflammation positive feedback loop in innate and adaptive immune cells. Importantly, exercise-induced lactate, traditionally viewed as a metabolic byproduct, is now recognized as an active immunomodulatory molecule. At high concentrations, lactate can suppress immune function through pH-mediated effects and GPR81 receptor activation. At physiological levels, it supports regulatory T cell survival, promotes macrophage M2 polarization, and modulates gene expression via histone lactylation. Additionally, key metabolic regulators such as AMPK and mTOR coordinate immune cell energy balance and phenotype; exercise activates the AMPK-mTOR axis to favor anti-inflammatory immune cell profiles. Simultaneously, hypoxia-inducible factor-1α (HIF-1α) is transiently activated during exercise, driving glycolytic reprogramming in T cells and macrophages, and shaping the immune landscape. In lipid metabolism, exercise alleviates adipose tissue inflammation by reducing fat mass and reshaping the immune microenvironment. It promotes the polarization of adipose tissue macrophages from a pro-inflammatory M1 phenotype to an anti-inflammatory M2 phenotype. Moreover, exercise alters the secretion profile of adipokines—raising adiponectin levels while reducing leptin and resistin—thereby influencing systemic immune balance. At the circulatory level, exercise improves lipid profiles by lowering pro-inflammatory free fatty acids (particularly saturated fatty acids) and triglycerides, while enhancing high-density lipoprotein (HDL) function, which has immunoregulatory properties such as endotoxin neutralization and macrophage cholesterol efflux. Regarding protein metabolism, exercise triggers the expression of heat shock proteins (HSPs) that act as intracellular chaperones and extracellular immune signals. Exercise also promotes the secretion of myokines (e.g., IL-6, IL-15, irisin, FGF21) from skeletal muscle, which modulate immune responses, facilitate T cell and macrophage function, and support immunological memory. Furthermore, exercise reshapes amino acid metabolism, particularly of glutamine, arginine, and branched-chain amino acids (BCAAs), thereby influencing immune cell proliferation, biosynthesis, and signaling. Leucine-mTORC1 signaling plays a key role in T cell fate, while arginine metabolism governs macrophage polarization and T cell activation. In summary, this review underscores the complex, bidirectional relationship between exercise and immune function, orchestrated through metabolic remodeling. Future research should focus on causative links among specific metabolites, signaling pathways, and immune phenotypes, as well as explore the epigenetic consequences of exercise-induced metabolic shifts. This integrated perspective advances understanding of exercise as a non-pharmacological intervention for immune regulation and offers theoretical foundations for individualized exercise prescriptions in health and disease contexts.

Background::Triple-negative breast cancer (TNBC) is a type of highly invasive breast cancer with a poor prognosis. According to new research, long noncoding RNAs (lncRNAs) play a significant role in the progression of cancer. Although the role of lncRNAs in breast cancer has been well reported, few studies have focused on TNBC. This study aimed to explore the biological function and clinical significance of forkhead box C1 promoter upstream transcript (FOXCUT) in triple-negative breast cancer.Methods::Based on a bioinformatic analysis of the cancer genome atlas (TCGA) database, we detected that the lncRNA FOXCUT was overexpressed in TNBC tissues, which was further validated in an external cohort of tissues from the General Surgery Department of the First Affiliated Hospital of Nanjing Medical University. The functions of FOXCUT in proliferation, migration, and invasion were detected in vitro or in vivo. Luciferase assays and RNA immunoprecipitation (RIP) were performed to reveal that FOXCUT acted as a competitive endogenous RNA (ceRNA) for the microRNA miR-24-3p and consequently inhibited the degradation of p38. Results::lncRNA FOXCUT was markedly highly expressed in breast cancer, which was associated with poor prognosis in some cases. Knockdown of FOXCUT significantly inhibited cancer growth and metastasis in vitro or in vivo. Mechanistically, FOXCUT competitively bounded to miR-24-3p to prevent the degradation of p38, which might act as an oncogene in breast cancer. Conclusion::Collectively, this research revealed a novel FOXCUT/miR-24-3p/p38 axis that affected breast cancer progression and suggested that the lncRNA FOXCUT could be a diagnostic marker and therapeutic target for breast cancer.

Objective lo investigate the protective effect of dihydromyricetin(DHM)against exercise-induced muscle damage(EIMD)in mice and its potential mechanism. Methods Adult male C57BL/6J mice were randomly divided into control group(CG),exercise group(EG),and exercise+100 mg/kg weightd DHM(DHM)group.The intervention lasted for four weeks,during which the animals in the EG and DHM groups were subjected to exercise training for 1 h per day.The day after the training,a 90-min treadmill exercise(slope:0 and speed:18 m/min)was conducted in both EG and DHM groups.Samples of blood and gastrocnemius muscles were harvested from the three groups 24 h after the exercise,followed by the measurement of serum creatine kinase(CK)and lactate dehydrogenase(LDH)activities,total superoxide dismutase(T-SOD)activity,malondialdehyde(MDA),and skeletal muscle mitochondrial enzyme complex Ⅰ and Ⅱ activities.Histological changes in the skeletal muscle were observed by transmission electron microscopy,and the protein expressions of mitochondrial function-related pathways were detected by Western blotting. Results Skeletal muscle morphological changes and mitochondrial damage were alleviated in the DHM group compared to those in the EG.The activities of EIMD markers CK and LDH and the level of lipid peroxidation were notably repressed and the serum T-SOD activity was enhanced after DHM intervention.Western blotting demonstrated that the expressions of sirtuin type 3(SIRT3),estrogen-related receptor alpha,and peroxisome proliferator-activated receptor-gamma coactivator-1 alpha in the skeletal muscle of mice increased after the DHM intervention. Conclusion DHM can relieve EIMD in mice,possibly by promoting the recovery of the mitochondrial structure and function in the skeletal muscle of mice after high-intensity exercise via the activation of the SIRT3 signaling pathway.

ObjectiveTo investigate the effect of mucin 1 (MUC1) on the proliferation and apoptosis of nasopharyngeal carcinoma (NPC) and its regulatory mechanism. MethodsThe 60 NPC and paired para-cancer normal tissues were collected from October 2020 to July 2021 in Quanzhou First Hospital. The expression of MUC1 was measured by real-time quantitative PCR (qPCR) in the patients with PNC. The 5-8F and HNE1 cells were transfected with siRNA control (si-control) or siRNA targeting MUC1 (si-MUC1). Cell proliferation was analyzed by cell counting kit-8 and colony formation assay, and apoptosis was analyzed by flow cytometry analysis in the 5-8F and HNE1 cells. The qPCR and ELISA were executed to analyze the levels of TNF-α and IL-6. Western blot was performed to measure the expression of MUC1, NF-кB and apoptosis-related proteins (Bax and Bcl-2). ResultsThe expression of MUC1 was up-regulated in the NPC tissues, and NPC patients with the high MUC1 expression were inclined to EBV infection, growth and metastasis of NPC. Loss of MUC1 restrained malignant features, including the proliferation and apoptosis, downregulated the expression of p-IкB、p-P65 and Bcl-2 and upregulated the expression of Bax in the NPC cells. ConclusionDownregulation of MUC1 restrained biological characteristics of malignancy, including cell proliferation and apoptosis, by inactivating NF-κB signaling pathway in NPC.

ObjectiveTo explore the mechanism of treadmill exercise against type 2 diabetes mellitus (T2DM) with non-alcoholic fatty liver disease (NAFLD) based on the regulator effects of exercise on ferroptosis. MethodsEight 8-week-old male m/m mice were used as control group (Con, n=8), and db/db mice of the matched age were randomly divided into T2DM model group (db/db, n=8), exercise group (db+Exe, n=8), p38 mitogen-activated protein kinase (MAPK) inhibitor group (db+SB203580, n=8) and exercise combined with p38 MAPK inhibitor group (db+Exe+SB203580, n=8). After one-week adaptive feeding, the mice in the db+Exe group and db+Exe+SB203580 group underwent moderate intensity treadmill exercise for 40 min/d, 5 d/week lasting 8 weeks. The db+SB203580 group and db+Exe+SB203580 group were treated with SB203580 (a specific inhibitor of p38 MAPK) with a dose of 5 mg/kg, 5 d/week for 8 weeks. And the exercise intervention was performed 2 h later after the intraperitoneal injection of SB203580. The body weight and fasting blood glucose of mice were measured regularly every week during the experiment. After 24 h of the last intervention, the mice were weighted, the liver tissues were taken, weighted and the liver index was calculated. The pathological changes of liver were determined by Oil Red O and hematoxylin-eosin (HE) staining. The levels of blood lipids, liver function, Fe²⁺ and oxidative stress markers of liver were measured by enzyme linked immunosorbent assay (ELISA). The related mRNA expression levels of lipogenesis and inflammation were evaluated by quantitative reverse transcriptase-mediated PCR (qRT-PCR). The related protein expression levels of lipogenesis and ferroptosis in liver were determined by immunohistochemical (IHC) staining and Western blot. ResultsThe body weight, fasting blood glucose, liver index, blood lipid and transaminase levels in the db/db group were significantly increased compared with the Con group. HE and Oil Red O staining showed severe lipid accumulation and ballooning change in the liver of db/db mice. Biochemical tests showed that Fe²⁺ and MDA level of liver constitution homogenate increased, while GSH level decreased significantly. The results of qRT-PCR showed that the mRNA levels of MCP-1, IL-6, SREBF1 and ACC1 in liver tissue of db/db mice were all significantly increased. Western blot results showed that the expression levels of SREBF1, ACC1 increased, ferroptosis relative proteins were significantly decreased. The 8 weeks of exercise significantly reduced the rise in body weight, blood glucose, liver index and blood lipid levels in db/db mice. Exercise intervention also alleviated hepatic steatosis and reduced the expression levels of Fe²⁺, MDA, MCP-1, IL-6, ACC1 and SREBF1, upregulated the expression levels of GSH, NRF2, HO-1, SLC7A11 and GPX4 in liver tissue of db/db mice. The intervention of exercise combined with SB203580 significantly down-regulated the mRNA expression levels of ACC1, MCP-1, IL-6, reduced the levels of Fe²⁺ and MDA, and up-regulated the level of GSH in db/db mice. Compared with the db+Exe group, the expression of Fe²⁺, MDA, MCP-1, and SREBF1 in the liver of the db+Exe+SB203580 group mice significantly increased, while the expression level of GSH and expression levels of ferroptosis relative proteins also significantly decreased. In addition, compared with db+SB203580 group, the iron accumulation and lipid peroxidation in the liver of db+Exe+SB203580 group were significantly improved. ConclusionThe8-week treadmill exercise can effectively alleviate liver injury and steatosis, and its mechanism may be related to the inhibition of hepatocyte ferroptosis through p38 MAPK signal.

Objective:To explore the effect of accurately localized mini anterolateral thigh perforator flap in repairing medium-sized skin and soft tissue defects in fingers.Methods:The study was a retrospective observational study. From December 2019 to September 2022, 15 patients with medium-sized skin and soft tissue defects who met the inclusion criteria in fingers were admitted to the Second Affiliated Hospital of Wenzhou Medical University, including 12 males and 3 females, aged 23 to 62 years. After debridement, the wounds were all accompanied by exposed tendons, bones, vessels and nerves, with an area from 4.0 cm×3.0 cm to 8.0 cm×3.5 cm. Computed tomography angiography and color Doppler ultrasonography examinations were performed on both lower limbs of the patient before surgery to accurately locate the anterolateral thigh perforators. When the flap with area from 6.0 cm×3.0 cm to 11.0 cm×4.0 cm was harvested, the flap was thinned. The artery and vein perforators of the flap were anastomosed respectively with the digital artery and dorsal metacarpal vein. If there was avulsion injury, infection, or burn in the recipient area, the main arterial and veinous vessels carried by the skin flap was anastomosed with the radial artery and accompanying vein. The lateral thigh cutaneous nerve carried by the flap was anastomosed with the stump of the digital nerve. The types of perforators of the lateral thigh artery were observed during operation and compared with the location of the vessels before operation. After operation, the survival and adverse complication of the flap were closely observed. During follow-up, the skin flap color, texture, and shape were observed; the wound healing in donor area was observed. At the last follow-up, the two-point discriminative distance of the affected finger pulp was measured, and the function of the affected finger was evaluated using the trial standard for the evaluation of functions of upper limbs of Hand Surgery Society of Chinese Medical Association, and the interphalangeal joint movement of the affected finger was observed; the patients' complaints about the adverse effects of flap resection on lower limbs were recorded.Results:During the operation, it was observed that the perforators of the flaps in 11 patients were the descending branch of the lateral circumflex thigh artery, in two patients, the perforators of skin flaps were the oblique branch of the lateral thigh artery, and the perforators in another two patients were the transverse branch of the lateral circumflex thigh artery, which were consistent with the preoperative vascular localization. After operation, all flaps survived without vascular crisis and infection. The patients were followed up for 6-12 months, the flaps had excellent color, texture, and appearance; only linear scars remained on the donor wound. At the last follow-up, the two-point discrimination distance in the finger pulp was 7-11 mm; the affected finger function was rated as excellent in 6 cases, good in 6 cases, and fair in 3 cases; the flexion and extension function of the finger was not affected; two patients complained of numbness in the lateral thigh after excision of the skin flap, and the other 13 patients had no complain of adverse complaints.Conclusions:The perforating branch in lateral thigh region can be accurately located by computed tomography angiography and color Doppler ultrasonography, accurate positioning of perforators before operation can reduce the damage to the donor area during the incision of the flap, the appearance and function of the affected finger can be restored to the maximum extent by thinning the transplanted flap and rebuilding the finger sensation. Therefore, it is an effective and reliable way to repair the medium-sized skin and soft tissue defects of fingers with the mini thigh anterolateral perforator flap.

Calcified lesions increase the difficulty of interventional therapy for coronary heart disease,and increase the risk of perioperative and long-term complications.Pretreatment of calcified lesions is very important.Coronary lithotripsy(IVL)is used more and more in calcified lesions,and many clinical trials have proved its effectiveness and safety.Stent underexpansion is an important risk factor for stent thrombosis and restenosis,which increases the incidence of complications.At present,there is no effective coping strategy or clear consensus or guidelines for the treatment of stent underexpansion caused by calcified lesions.There are few reports about the treatment of stent under expansion by IVL,and most of them are case reports and small sample studies.In this paper,two cases of stent under expansion were reported.After stent implantation,stent under expansion was found,and IVL was used to treat the cases,which achieved good results.This paper reports 2 cases of stent under expansion to explore the efficacy and safety of IVL in the treatment of such lesions.

Objective:To identify the risk factors affecting the healing of defective bony nonunion.Methods:The studies reporting the risk factors for healing of defective bony nonunion between January 2000 and March 2022 were retrieved by computer from the VIP, Wanfangdata, CNKI, Web of Science, PubMed, and Medline databases. The Newcastle-Ottawa Scale (NOS) was used to evaluate the quality of the included studies. the RevMan 5.3 software was used to perform a meta-analysis of the general factors, injuries and surgical-related factors affecting the healing of defective bony nonunion.Results:Included in this Meta analysis were 17 studies with 1,236 patients. The NOS score of the included studies was from 5 to 8. The meta-analysis showed the following: age ( MD=-4.27, 95% CI: -8.29 to 2.91, P < 0.01), smoking ( OR=3.56, 95% CI: 2.81 to 6.32, P < 0.01), soft tissue defect ( OR=3.54, 95% CI: 2.21 to 5.69, P < 0.01), combined ipsilateral fibular fracture ( OR=4.18, 95% CI: 1.24 to 14.03, P=0.02), venous thrombosis ( OR=4.27, 95% CI: 1.05 to 17.44, P=0.04), and postoperative infection ( OR=2.96, 95% CI: 1.97 to 4.47, P < 0.01) were significant risk factors for the healing of defective bone nonunion. Minor bone defect ( SMD=-0.67, 95% CI: -1.25 to -0.10, P=0.02), proximal to distal bone transport ( OR=-0.42, 95% CI: 0.22 to 0.77, P < 0.01), short-term external fixation ( MD=-3.92, 95% CI: -7.10 to -0.73, P=0.02), and autologous bone grafting ( OR=0.39, 95% CI: 0.16 to 0.95, P=0.04) were protective factors for the healing of defective bony nonunion. Conclusions:High age (senility), smoking, soft tissue defect, ipsilateral fibular fracture, venous thrombosis, and postoperative infection are risk factors affecting the healing of defective bony nonunion. Minor bone defect, proximal to distal bone transport, short-term external fixation, and autologous bone grafting are protective factors affecting the healing of defective bony nonunion. Surgeons can predict early the prognosis of patients with defective bony nonunion based on the above factors.

AIM To establish an HPLC method for the simultaneous content determination of 3′-hydroxy-puerarin,hydroxysafflor yellow A,puerarin,puerarin apigenin,3′-methoxypuerarin,daidzein,stilbene glycoside,luteolin side,genistein side,luteolin B and rosmarinic acid in Naomaitai Capsules.METHODS The analysis was performed on a 30℃ thermostatic Kromasil C18 column(250 mm×4.6 mm,5 μm),with the mobile phase comprising of acetonitrile-water(containing 1.0 g/L phosphoric acid)flowing at 0.8 mL/min in a gradient elution manner,and the detection wavelength was set at 280 nm.Subsequently,principal component analysis and cluster analysis were made.RESULTS Twelve components showed good linear relationships within their own ranges(r＞0.999 0),whose average recoveries were 97.00%-99.00% with the RSDs of 0.86%-1.82% .Ten batches of samples were clustered into four categories,the accumulative variance contribution rate of four principal components reached 86.262% .CONCLUSION This simple,stable,reliable and accurate method can be used for the quality control of Naomaitai Capsules.