The intervertebral disc is a complex structure composed of the central nucleus pulposus, the peripheral annulus fibrosus, and the cartilaginous endplates located at the top and bottom. This unique arrangement effectively isolates the nucleus pulposus from the host’s immune system. Additionally, specific substances within the intervertebral disc exhibit inhibitory effects on the infiltration of immune cells and cytokines, which has led to the recognition of the intervertebral disc as an immune-privileged tissue. However, during intervertebral disc degeneration (IDD), the physical barriers that maintain this immune privilege are compromised. As a result, the nucleus pulposus may be perceived as a foreign antigen by the immune system. Simultaneously, inflammatory cytokines released by the degenerating disc attract a significant influx of immune cells, disrupting the delicate immunological balance within the nucleus pulposus and exacerbating the progression of IDD. Recent studies have confirmed the infiltration of immune cells such as macrophages and mast cells into the degenerative intervertebral disc, and the phenotypic characteristics and quantitative changes of these immune cells are closely related to the process of IDD. In terms of treatment strategies, biological agents such as mesenchymal stem cell therapy, gene therapy and growth factors that regulate the immune microenvironment of degenerative intervertebral discs have entered the stage of animal experiments. At the same time, small molecule drugs have shown unique regulatory potential in restoring the immune-privileged status of intervertebral discs.

Intervertebral disc degeneration (IDD) is largely attributed to impaired endogenous repair. Nucleus pulposus-derived stem cells (NPSCs) senescence leads to endogenous repair failure. Small extracellular vesicles/exosomes derived from mesenchymal stem cells (mExo) have shown great therapeutic potential in IDD, while whether mExo could alleviate NPSCs senescence and its mechanisms remained unknown. We established a compression-induced NPSCs senescence model and rat IDD models to evaluate the therapeutic efficiency of mExo and investigate the mechanisms. We found that mExo significantly alleviated NPSCs senescence and promoted disc regeneration while knocking down thioredoxin (TXN) impaired the protective effects of mExo. TXN was bound to various endosomal sorting complex required for transport (ESCRT) proteins. Autocrine motility factor receptor (AMFR) mediated TXN K63 ubiquitination to promote the binding of TXN on ESCRT proteins and sorting of TXN into mExo. Knocking down exosomal TXN inhibited the transcriptional activity of nuclear factor erythroid 2-related factor 2 (NRF2) and activator protein 1 (AP-1). NRF2 and AP-1 inhibition reduced endogenous TXN production that was promoted by exosomal TXN. Inhibition of NRF2 in vivo diminished the anti-senescence and regenerative effects of mExo. Conclusively, AMFR-mediated TXN ubiquitination promoted the sorting of TXN into mExo, allowing exosomal TXN to promote endogenous TXN production in NPSCs via TXN/NRF2/AP-1 feed-forward circuit to alleviate NPSCs senescence and disc degeneration.

Spinal tuberculosis(STB)is an infectious disease characterized by osteolytic destruction,associated with high rates of disability and mortality.When severe bone destruction leads to spinal instability and subsequent significant neurological impairment,surgical bone grafting becomes a necessary treatment.The choice of bone graft material is closely related to surgical outcomes,as different materials have their respective advantages and disadvantages,which directly determine postoperative effi-cacy and clinical prognosis.With the continuous advancement of bone graft materials,the emergence of composite materials has expanded clinical treatment options and significantly improved patient outcomes.Tailored selection of bone graft materials based on individual patient clinical profiles is crucial for optimizing treatment efficacy in STB patients.Therefore,this article reviews the classification of bone graft materials(bone-based materials,metallic materials,and bioactive materials),their strengths and limitations,and recent developments,aiming to provide a reference for clinicians in selecting appropriate bone graft materials.

The intervertebral disc is a complex structure composed of the central nucleus pulposus, the peripheral annulus fibrosus, and the cartilaginous endplates located at the top and bottom. This unique arrangement effectively isolates the nucleus pulposus from the host’s immune system. Additionally, specific substances within the intervertebral disc exhibit inhibitory effects on the infiltration of immune cells and cytokines, which has led to the recognition of the intervertebral disc as an immune-privileged tissue. However, during intervertebral disc degeneration (IDD), the physical barriers that maintain this immune privilege are compromised. As a result, the nucleus pulposus may be perceived as a foreign antigen by the immune system. Simultaneously, inflammatory cytokines released by the degenerating disc attract a significant influx of immune cells, disrupting the delicate immunological balance within the nucleus pulposus and exacerbating the progression of IDD. Recent studies have confirmed the infiltration of immune cells such as macrophages and mast cells into the degenerative intervertebral disc, and the phenotypic characteristics and quantitative changes of these immune cells are closely related to the process of IDD. In terms of treatment strategies, biological agents such as mesenchymal stem cell therapy, gene therapy and growth factors that regulate the immune microenvironment of degenerative intervertebral discs have entered the stage of animal experiments. At the same time, small molecule drugs have shown unique regulatory potential in restoring the immune-privileged status of intervertebral discs.

Spinal tuberculosis(STB)is an infectious disease characterized by osteolytic destruction,associated with high rates of disability and mortality.When severe bone destruction leads to spinal instability and subsequent significant neurological impairment,surgical bone grafting becomes a necessary treatment.The choice of bone graft material is closely related to surgical outcomes,as different materials have their respective advantages and disadvantages,which directly determine postoperative effi-cacy and clinical prognosis.With the continuous advancement of bone graft materials,the emergence of composite materials has expanded clinical treatment options and significantly improved patient outcomes.Tailored selection of bone graft materials based on individual patient clinical profiles is crucial for optimizing treatment efficacy in STB patients.Therefore,this article reviews the classification of bone graft materials(bone-based materials,metallic materials,and bioactive materials),their strengths and limitations,and recent developments,aiming to provide a reference for clinicians in selecting appropriate bone graft materials.

Objective To investigate the effect of folic acid-modified liposome quercetin(FLQ)on the proliferation and apoptosis of triple negative breast cancer(TNBC)cells and explore its underlying mech-anism.Methods CCK-8 was used to detect the effect of FLQ on TNBC cell viability.Colony formation assay was conducted to detect the effect of FLQ on TNBC cell proliferation.Flow cytometry was performed to detect the effect of FLQ on TNBC cell apoptosis,the levels of intracellular ROS,and mitochondrial membrane potential.Western blot analysis was conducted to detect the expression levels of JAK2/STAT3 signaling pathway-related and apoptosis-related proteins.Results FLQ inhibited the proliferation and promoted the apoptosis of MDA-MB-231 cells(P=0.023,P<0.001).It promoted mitochondrial membrane potential collapse and increased the intracellular ROS levels of MDA-MB-231 cells(P=0.003,P=0.034);inhibited the phosphorylation levels of JAK2 and STAT3;upregulated the expression levels of the proapo-ptotic proteins Bax,Bak,cytochrome C,and Cleaved-Caspase-3(P<0.001,P<0.001);and downregulated the expression levels of the antiapoptotic proteins Bcl2 and Bcl-xL(P=0.037,0.028).Conclusion FLQ inhibits the proliferation and induces the apoptosis of MDA-MB-231 cells.These effects may be related to the activa-tion of the mitochondrial apoptosis pathway through the inhibition of the JAK2/STAT3 signaling pathway.

Tuberculosis(TB)is an infectious disease caused by Mycobacterium tuberculosis(MTB).Autophagy plays an im-portant role in eliminating MTB which can interfere with host autophagy through a variety of mechanisms,therefore,escape the killing of macrophages to survive and reproduce in the host cells for a long time.There are many kinds of differential expressed non-coding RNAs(ncRNAs)in macrophages upon MTB infection.These ncRNAs can affect the elimination of MTB by regula-ting the expression of autophagy-related genes in multiple processes of autophagy.Elucidating these regulatory networks are of great significance for the development of new anti-TB drugs.Therefore,the known mechanisms of ncRNAs that regulates the autophagy of MTB infected macrophages were summarized,and the process of autophagy and the main regulatory functions of ncRNAs were introduced in this review,in order to provide new perspectives for the pathogenesis of TB and the development of anti-TB drugs.

Chondrosarcoma(CHS)is the second most common primary bone malignancy in human.Recurrence and metasta-sis are common among patients,and the efficacies of radiotherapy and chemotherapy are limited.The development of CHS treat-ment method has stagnated in the past 30-40 years,and surgical treatment is still the dominant option.Research on the patho-genesis mechanism of CHS is still not clear,and there is no specific drug.Therefore,it is of great significance to explore the pathogenesis of CHS,so as to find new treatment methods and drug targets for clinical treatment.Some studies have shown that epigenetic factor play an important role in the pathogenesis of CHS.Epigenetics refers to changes in the expression level and function of a gene without the change in its DNA sequence,leading to a heritable phenotype.The mechanisms of epigenetics mainly include DNA methylation,non-coding RNA regulation,histone modification,and chromatin remodeling.In this review,the recent progress in the field of epigenetics in CHS is summarized,which provides a direction for further research on CHS and searching for new therapeutic targets.

Objective:To investigate the role and molecular mechanism of sensory neuron-derived exosomes (nExo) in mediating intervertebral disc degeneration (IDD).Methods:A rat IDD model was constructed, with nExo injected into the intervertebral disc. After 4 weeks, the degenerative grades of operated discs were evaluated using histological staining, while the senescent phenotype of nucleus pulposus stem cells (NPSC) in the tissue was evaluated using immunofluorescence staining. For in vitro experiments, 24 hours after the treatment of nExo to NPSC, immunoblotting, flow cytometry, or senescence-associated β-galactosidase staining was applied to evaluate the senescent phenotype of NPSC. Transcriptomics analysis was applied to identify the key molecules that mediate nExo-induced cells senescence. After 4 weeks of injecting nExo and TXN into the rat tail disc degeneration model.Results:nExo increased the degenerative grades of IDD and increased the proportion of TEK +p16 + and TEK +p21 + cells (from 36.32% ±4.04%, 33.69% ±4.56% in IDD group to 56.41% ±5.26%, 50.14% ±8.49% in IDD+nExo group, respectively; t=7.420, P<0.001; t=4.184, P<0.0019, respectively) in the disc tissue. Besides, nExo promoted the expression of p16 and p21 in NPSC and increased the percentage of cells with positive senescence-associated β-galactosidase staining (from 7.32%±1.73% to 58.22%±11.38%, t=7.658, P=0.002), while the percentage of G2/M cells was downregulated (from 18.10%±1.32% to 1.60%±0.67%, t=19.290, P<0.001). Transcriptomic analysis showed that the differential genes of CTRL vs. nExo were closely related to cell senescence, and TXN was screened by intersecting the differential gene set with the cellular senescence gene sets from the published database. Furthermore, we verified that nExo decreased the content of TXN in NPSC, while exogenous TXN downregulated the expression of p16 and p21 in NPSC, reduced the positive cell rate of senescence-associated β-galactosidase staining (from 58.84%±3.99% to 21.68%±8.16%, t=7.048, P=0.021), increased the percentage of G2/M cells (from 1.21%±0.34% to 15.26%±2.60%, t=9.259, P=0.001). TXN significantly reduced the grade of disc tissue degeneration (histological score: 14.33±0.82 in the nExo group; 8.17±1.17 in the nExo+TXN group, t=10.590, P<0.001), significantly increased the content of extracellular matrix (from 10.94±4.35 μg/mg to 50.55±12.16 μg/mg, t=7.512, P<0.001), and reduced the proportion of TEK +p16 + and TEK +p21 + double-positive cells (from 54.92%±4.21% and 60.31%±9.02% to 27.93%±3.26% and 33.75%±8.07%, respectively; t=12.430, P<0.001; t=5.375, P<0.001, respectively). Conclusion:nExo promotes cell senescence and IDD by downregulating TXN in NPSC.

Our understanding of facial anatomy has changed significantly over the past decade. With the emergence of numerous minimally invasive facial rejuvenation techniques, facial anatomy theory witnesses continuous development. Nowadays, temporal region-related surgeries are developing towards being with less trauma and higher safety, and further in-depth anatomical studies are conducted on the temporal branch of the facial nerve. Familiarity with the course direction, branch distribution, and position of body surface projection of the temporal branch of the facial nerve is of great importance to protect the temporal branch of the facial nerve and its branches from injury. This article summarizes and analyzes the current relevant literature thus provides critical morphological data for head and neck plastic surgery and aesthetic surgery, along with some guidance in clinical application.