Objective To investigate the role of luteolin(Lut)in regulating reactive oxygen species(ROS)levels through nuclear factor erythroid 2-related factor 2(NFE2L2)/cystine glutamate antitransporter(x-CT)/glutathione peroxidase 4(GPX4)signaling axis to inhibit the viability of glioblastoma and promote apoptosis.Methods U87 MG and U251 cells were cultured in vitro.The CCK-8 assay was used to detect cell survival rates after 48 hours of treatment with different concentrations(0,6.25,12.5,25,50 and 100 μmol/L)of Lut.According to whether cells were treated with Lut,cells were divided into the U87 control group,the U87 Lut group,the U251 control group and the U251 Lut group.The half-maximal inhibitory concentration(IC50)at 48 hours was used as the unified treatment concentration for subsequent experiments.The apoptosis level of cells was detected by flow cytometry double staining method.Changes of reactive oxygen species(ROS)levels in cells were detected by the DCFH-DA method.Molecular docking was conducted using AutoDock software to verify the proteins related to the Lut and oxidative stress pathway.Real-time fluorescence quantitative reverse transcription(RT-qPCR)was used to detect the mRNA levels of NFE2L2 and GPX4.The expression levels of NFE2L2,x-CT and GPX4 proteins were detected by Western blot assay.Results After U87 MG and U251 cells were treated with Lut for 48 hours,the cell viability was significantly inhibited,and with the increase of Lut concentration,the cell viability decreased(P＜0.05).Compared with the U87 control group and the U251 control group respectively,the apoptosis rate of cells increased in the U87 Lut group and the U251 Lut group,the green fluorescence intensity was enhanced,and the intracellular ROS level was upregulated(P＜0.05).Results of molecular docking showed that Lut was tightly bound to NFE2L2,x-CT and GPX4.The results of RT-qPCR and Western blot assay showed that compared with the U87 control group and the U251 control group respectively,the protein and mRNA levels of NFE2L2 and GPX4 in cells of the U87 Lut group and the U251 Lut group,as well as the expression level of x-CT protein,decreased(P＜0.05).Conclusion Lut regulates ROS levels through the NFE2L2/x-CT/GPX4 signaling axis to inhibit the viability of glioblastoma and promote cell apoptosis.

Objective To analyze the serum 25-hydroxy vitamin D[25(OH)D]levels and vitamin D nutri-tional status of 0-14 years old children in Hangzhou,and to provide scientific basis for the prevention of vita-min D deficiency.Methods A total of 26 225 healthy children aged 0 to 14 who were tested in Hangzhou Dian Medical Diagnosis Center from January 1,2021 to December 31,2023 were selected as the study objects.The 25(OH)D levels were detected by direct chemiluminescence method,and the 25(OH)D levels and vitamin D nutritional status of children with different genders,ages and seasons were analyzed and compared.Results The level of 25(OH)D in girls was slightly higher than that in boys,and the difference was statisti-cally significant(P＜0.05).With the increase of age,the level of 25(OH)D continued to decline,and the pro-portion of vitamin D deficiency and vitamin D insufficiency gradually increased.The level of 25(OH)D was the highest in children＜3 years old and the lowest in children 10-14 years old.There was statistical significance in the proportion of vitamin D nutritional status between boys and girls aged 10 to 14(P＜0.05).In the four seasons,children's 25(OH)D level is the highest in spring and the lowest in summer.The difference of 25(OH)D level and vitamin D nutritional status in different seasons was statistically significant(P＜0.05).The proportion of vitamin D deficiency and vitamin D insufficiency in winter was higher than that in other seasons,and the difference was statistically significant(P＜0.05).Conclusion The nutritional status of vitamin D in 0-14 year old children in Hangzhou is good,but the importance of vitamin D supplementation for children should not be ignored,and active publicity and education should be carried out to prevent vitamin D deficiency.

The reconstruction of the temporomandibular joint presents a multifaceted clinical challenge in the realm of head and neck surgery, underscored by its relatively infrequent occurrence and the lack of comprehensive clinical guidelines. This review aims to elucidate the available approaches for TMJ reconstruction, with a particular emphasis on recent groundbreaking advancements. The current spectrum of TMJ reconstruction integrates diverse surgical techniques, such as costochondral grafting, coronoid process grafting, revascularized fibula transfer, transport distraction osteogenesis, and alloplastic TMJ replacement. Despite the available options, a singular, universally accepted 'gold standard' for reconstructive techniques or materials remains elusive in this field. Our review comprehensively summarizes the current available methods of TMJ reconstruction, focusing on both autologous and alloplastic prostheses. It delves into the differences of each surgical technique and outlines the implications of recent technological advances, such as 3D printing, which hold the promise of enhancing surgical precision and patient outcomes. This evolutionary progress aims not only to improve the immediate results of reconstruction but also to ensure the long-term health and functionality of the TMJ, thereby improving the quality of life for patients with end-stage TMJ disorders.
Humans ; Temporomandibular Joint/surgery* ; Temporomandibular Joint Disorders/surgery* ; Transplantation, Autologous ; Arthroplasty, Replacement/methods* ; Joint Prosthesis ; Plastic Surgery Procedures/methods*

Objective: This study aimed to elucidate the mechanisms underlying the impaired bone healing capacity in type 1 diabetes (T1DM) by investigating the role of the Hedgehog (Hh) signaling pathway in the impaired healing of cranial defects caused by T1DM. Methods: This study was approved by the experimental animal ethics committee of our hospital. A cranial defect model was established using Akita transgenic mice with spontaneous type I diabetes. The impact of T1DM on osteogenic differentiation and the Hh signaling pathway during cranial defect healing was explored by MicroCT scanning and immunohistochemical (IHC) analysis of osteocalcin (Ocn), Indian Hedgehog (Ihh), Patched1 (Ptch1), and zinc finger protein GLI1 (Gli1). Subsequently, the Hh signaling pathway was activated using smoothened agonist (SAG) (10 mg/kg, gavage), and its potential to improve cranial defect healing in T1DM was assessed by MicroCT and IHC staining. Finally, the ability of SAG (1 000 nmol/L) to counteract the inhibitory effects of a high-glucose environment (25 mol/L) on osteogenic differentiation of mouse bone marrow mesenchymal stem cells (BMSCs) was investigated through in vitro experiments. Detection methods included Alkaline Phosphatase and Alizarin Red staining, as well as quantitative real-time PCR (qPCR) analysis of the osteogenesis-related genes Alp, Spp1, Bglap, and Sp7. Results: Akita mice exhibited early, stable, and significant spontaneous T1DM characteristics. On postoperative day 21, the newly formed bone in the cranial defect area of Akita mice showed significant decreases in the bone volume-to-tissue volume ratio, volumetric bone mineral density, and Ocn expression (P < 0.05), with significant downregulation of Ihh, Ptch1, and Gli1 (P < 0.05). Activation of the Hh signaling pathway by SAG significantly mitigated the negative impact of T1DM on cranial defect healing in Akita mice (P < 0.05). Moreover, after SAG treatment, the inhibitory effects of the high-glucose environment on the alkaline phosphatase activity and in vitro mineralization capacity of BMSCs were significantly alleviated (P < 0.05), and the expression levels of osteogenic differentiation-related genes were significantly upregulated (P < 0.05). Conclusion T1DM inhibits cranial defect healing in Akita mice by suppressing the expression of the Hh signaling pathway, whereas activation of the Hh signaling pathway promotes osteogenesis and ameliorates the inhibitory effects of T1DM on bone healing.

Objective To investigate the therapeutic effect and potential mechanisms of allogeneic renal subcapsular transplantation of CD24+renal epithelial cells for the treatment of acute kidney injury(AKI)induced by ischemia-reperfusion(I/R).Methods CD24+renal epithelial cells were isolated from mouse kidneys using flow cytometric sorting and expanded by passaging.C57BL/6N mice were randomly divided into three groups:the normal control group(n=8,sham surgery only),the model control group(n=8,unilateral kidney I/R plus contralateral nephrectomy),and the CD24+cell treatment group(n=8,AKI model followed by renal subcapsular transplantation of CD24+cells).Mice were euthanized at 24 h after modeling and serum was collected to measure biochemical markers[serum creatinine(Scr),blood urea nitrogen(BUN),tumor necrosis factor-α(TNF-α),and interleukin-6(IL-6)].Renal tissues were subjected to pathological evaluation and macrophage staining.An M1-polarized macrophage model was established using mouse bone marrow-derived macrophages co-cultured with CD24+renal epithelial cells.The polarization state of macrophages was assessed by quantitative real-time polymerase chain reaction(qPCR)and flow cytometry.Results CD24+renal epithelial cells were successfully isolated and passaged stably.Compared with the normal control group,the model control group exhibited significantly elevated Scr and BUN levels and renal pathological damage.In contrast,the CD24+cell treatment group showed significant reduction in serum biochemical markers and pathological injury compared with the model control group,along with reduction in M1 macrophage infiltration in the kidneys(P<0.05,P<0.01).In vitro co-culture experiments demonstrated that in the CD24+co-culture group,the expression of M1 polarization-related markers in macrophages was significantly lower than that in the non-co-culture group,and the proportion of CD80+M1 macrophages in the co-culture group decreased(P<0.05,P<0.01).Conclusion Allogeneic renal subcapsular transplantation of CD24+renal epithelial cells can alleviate I/R-induced AKI by inhibiting M1 macrophage polarization through paracrine mechanisms.