Osteosarcoma (OS) [1] is the most prevalent primary bone cancer and is highly prone to both local invasion and metastasis. FAM162A, a protein implicated in cell growth transformation, is recognized as an oncogene in various cancers. Its role in osteosarcoma, however, remains poorly understood. This study investigates the role of FAM162A in the OS development. We identified that FAM162A was observably upregulated in osteosarcoma and inversely correlated with the prognosis of patients using bioinformatics and immunohistochemical analysis. The CCK-8, colony formation, scratch, and trans-well migration assays were performed to detect the effects of FAM162A on OS cell proliferation and migration. Then we found FAM162A-associated pathways in OS using GO and KEGG analyses and verified and used the downstream factor HIF-1α inhibitor to restore the OS cell proliferation induced by FAM162A overexpression to detect the mechanism of FAM162A in OS. Mechanistically, FAM162A facilitates glycolysis by activating HIF-1α and subsequently PKM2, a critical glycolytic gene, thereby advancing OS progression. These insights elucidated FAM162A's involvement in OS and its impact on glucose metabolism reprogramming, underscoring its potential as a therapeutic target.

ObjectiveTo investigate the role of matrix metalloproteinase-2 (MMP-2) and the imbalance between vascular endothelial growth factor (VEGF) and Endostatin in the pathogenesis of steroid-induced osteonecrosis of femoral head (SONFH).MethodsClinical samples and animal models were combined to systematically analyze the impact of VEGF/Endostatin imbalance on angiogenesis and osteogenesis. Clinical samples from SONFH patients and femoral neck fracture controls were analyzed for VEGF, Endostatin and MMP-2 expression. The SONFH model in C57BL/6J mice was established to evaluate the effects of an imbalanced VEGF/Endostatin axis on angiogenesis and osteogenesis, assessed by micro-CT based vascular imaging, calcein labeling, and bone density analysis. MMP-2 intervention experiments were conducted to explore its role in the VEGF/Endostatin ratio.ResultsClinical data revealed significantly lower VEGF/Endostatin ratio (P < 0.001) and higher MMP-2 levels (P < 0.05) in necrotic regions of SONFH patients compared to the controls. In animal models, decreased VEGF/Endostatin ratio caused by Endostatin supplementation could further suppress angiogenesis and osteogenesis (P < 0.05). Mechanistically, MMP‑2 disrupts the VEGF/Endostatin balance by decreasing VEGF expression (P < 0.05) and increasing Endostatin levels (P < 0.05), which is associated with the suppression of PI3K/AKT/HIF‑1α pathway.ConclusionsOur findings reveal that the imbalance of VEGF/Endostatin is a key driver of SONFH through impaired angiogenesis and osteogenesis. We further demonstrate that MMP‑2 contributes to this imbalance, likely linked to suppression of the PI3K/AKT/HIF‑1α pathway. These results support the VEGF/Endostatin ratio as a potential diagnostic biomarker and suggest that targeting MMP‑2 or Endostatin may represent promising therapeutic strategies.

Cartilage degeneration in osteonecrosis of the femoral head (ONFH) is closely associated with chondrocyte heterogeneity. Single-cell RNA sequencing was performed on 50,851 chondrocytes from 10 ONFH patients and 10 controls. The findings were further validated using an in vitro chondrocyte injury model induced by dexamethasone. Nine chondrocyte subtypes were identified, among which COL1A1⁺ chondrocytes (exhibiting fibrotic features and Hippo-YAP pathway activation) and COL2A1⁺ chondrocytes (displaying a reparative hyaline cartilage phenotype) were significantly enriched in ONFH. Immunohistochemistry and in vitro functional assays confirmed the upregulation of signature proteins and key transcription factors in these subtypes. Pseudotime analysis revealed that CCL20⁺ progenitor cells differentiate toward fibrotic or reparative fates via PRG4 or SOX5, respectively. Key ligand-receptor pairs, including FGF2-FGFR1 and TNFRSF11B-TNFSF11, mediated intercellular communication. This study elucidates the cellular and molecular basis of the “fibrosis-repair” imbalance in ONFH cartilage degeneration, offering a theoretical foundation for targeting chondrocyte fate regulation.

Traumatic brain injury (TBI) is a severe central nervous system injury, but the current diagnostic methods have limitations. Identifying plasma biomarkers and developing precise and convenient detection methods are of great significance for diagnosis and prognosis prediction. This study analyzed publicly available plasma miRNA sequencing data from post-TBI samples using bioinformatics to identify potential TBI-specific miRNAs and validated them in TBI model rats. Subsequently, the study developed a biosensor based on floating gate carbon nanotubes field effect transistor (FGCNT FET) functionalized with target miRNA probes for detecting plasma miRNA concentrations and compared its performance with PCR methods. Through bioinformatics analysis, we found that plasma rno-miR-323-3p levels significantly increased after TBI, suggesting its potential as a biomarker for TBI. PCR results indicated that plasma rno-miR-323-3p concentrations were elevated in TBI rats and positively correlated with injury severity. The developed biosensor exhibited excellent electrical and sensing performance. Specifically for rno-miR-323-3p detection, the biosensor exhibited high sensitivity and specificity, good reproducibility, and a wide detection range (1 fM to 1 mu M). Compared to traditional qPCR methods, the biosensor offers the advantages of directly using plasma as the input sample, simple operation, a lower detection limit, and reduced measurement error, which indicate the significant clinical application potential.

Meniscal posterior root tears disrupt knee joint mechanics and can lead to early-onset osteoarthritis if untreated. Surgical repair is crucial to restore meniscal integrity, yet challenges remain, including achieving anatomical fixation, reducing neurovascular risks, and avoiding growth plate interference in young patients. Traditional transtibial pullout repair for medial meniscal posterior root tear is less biomechanically effective than suture anchor techniques, while conventional posteromedial portal approaches for anchor placement have risks. Repairing lateral meniscal posterior root tears in adolescents is even more challenging due to concerns about physeal damage and peroneal nerve proximity. We present an arthroscopic technique for meniscal root repair applicable to both medial and lateral tears, utilizing a single high posterolateral portal. It features 2 key innovations: the percutaneous exchange rod technique for accurate portal localization, enhancing minimally invasive access and reducing peroneal nerve injury risk, and the use of all-suture anchors for fixation, minimizing hardware-related cartilage trauma while ensuring biomechanical stability. This technique enables anatomical reattachment without transosseous tunnels, making it suitable for adult patients with medial meniscal posterior root tear and adolescents with lateral meniscal posterior root tear.

Osteonecrosis of femoral head (ONFH) is characterized not only by ischemic bone tissue necrosis but also by cartilage degeneration, which plays an essential role in the pathogenesis of ONFH. The molecular communication between tissues contributes to disease progression, however the communication between cartilage and subchondral bone in the progression of ONFH remains unclear. In this study, we integrated transcriptomic data from ONFH cartilage and subchondral bone, exploring common differentially expressed genes (DEGs), pathway and function enrichment analyses, the protein-protein interaction (PPI) network, and hub genes to comprehensively study molecular integration. Additionally, we explored the molecular crosstalk between and within cartilage and subchondral bone using ligand-receptor pairs and ONFH cartilage proteomic data. Finally, key genes and ligand-receptor pairs were validated by quantitative real-time PCR (qRT-PCR). There were 27 common DEGs and five hub genes in cartilage and subchondral bone. The defined hub genes included COL1A1, COLIA2, CTSK, SPARC, and MXRA5. Notably, pathways related to ossification, extracellular matrix, and collagen formation were significantly altered in ONFH. Ligand-receptor data combined with DEGs revealed 60 differentially expressed ligands and 51 differentially expressed receptors in cartilage and four ligands and three receptors in subchondral bone. In inter-tissue comparisons, ligands from chondrocytes predominantly paired with receptors on osteoblasts in the subchondral bone, such as FN1, MMP2, and FGF1. Conversely, ligands from osteoblasts and osteocytes in the subchondral bone frequently paired with chondrocyte receptors, including FN1, COL1A1, and SEMA7A. At the protein level, we identified thirteen ligands and one receptor, with COL3A1 being the most highly expressed ligand and CD82 the only differentially expressed receptor in ONFH. This study highlights common molecular mechanisms and ligand-receptor crosstalk between and within cartilage and subchondral bone in ONFH, offering new insights into the disease's pathophysiology and potential molecular targets for therapeutic intervention.

In the present study, a new type of DSPE-PEG2000 polymeric liposome for the brain-targeted delivery of poorly water-soluble anticancer drugs was successfully prepared and characterized. The nanoparticles were formed by the self-assembly of an amphiphilic polymer consisting of hydrophilic 1,2-distearoyl-sn-glycero-3-phosphoethanolamine-N-[methoxy(polyethylene glycol)-2000] (DSPE‑PEG2000). These nanoliposomes served as a safe delivery platform for the simultaneous delivery of quercetin (QUE) and temozolomide (TMZ) to rat brains. The 2-in-1 PEG2000‑DSPE nanoliposomes containing QUE and TMZ (QUE/TMZ-NLs) were rapidly taken up by the U87 glioma cells in vitro, whereas at the same concentrations, the amounts of the free drugs taken up were minimal. The QUE/TMZ-NLs showed an enhanced potency in the U87 cells and the TMZ-resistant U87 cells (U87/TR cells), possibly due to the high intracellular drug concentration and the subsequent drug release. In vivo biodistribution experiments revealed a significant accumulation of QUE/TMZ-NLs in the brain, with significantly increased plasma concentrations of QUE and TMZ, as well as delayed clearance in our rat model of glioma. The results were not so significant for the QUE-loaded nanoliposomes (QUE-NLs) and free TMZ. The findings of our study establish the DSPE‑PEG2000 polymeric liposome as a novel and effective nanocarrier for enhancing drug delivery to brain tumors.

Background: Magnesium (Mg) and its alloys are receiving increasing attention in peripheral nerve regeneration, but they were limited due to the low corrosion resistance and rapid degradation. In this study, GDNF-Gel/HA-Mg was prepared and its value in peripheral nerve defects repairment was explored both in vitro and in vivo. Methods: A hydroxyapatite (HA) coating was first applied to the pure Mg surface, followed by the formation of gelatin methacrylate (GelMA) loaded with glial cell-derived neurotrophic factor (GDNF) on the HA-coated Mg surface. GDNF-Gel/HA-Mg corrosion resistance was explored. The effect of GDNF-Gel/HA-Mg conduit on Schwann cell proliferation and migration abilities were investigated. And sciatic nerve defects models were established to explored the role of GDNF-Gel/HA-Mg conduit in peripheral nerve defects repairment. Findings: The electrochemical, immersion, and hydrogen evolution experiments indicated that the corrosion resistance in phosphate buffer saline (PBS) of pure Mg was significantly improved by the GDNF-Gel/HA coating. Cell cycle, Cell Count Kit-8 (CCK-8), and clone formation assays indicated that GDNF-Gel/HA-Mg promoted the proliferation of Schwann cells. Scratch and Transwell assay results demonstrated that GDNF-Gel/HA-Mg promoted Schwann cell migration ability dose-dependently. GDNF-Gel/HA-Mg was found to enhance the secretion of nerve growth factor (NGF) and the expression of p75NTR. Flow cytometry results showed that GDNF-Gel/HA-Mg could reduce H2O2-induced oxidative stress and Schwann cell apoptosis. GDNF-Gel/HA-Mg inhibited M1 macrophage polarization while facilitated M2 macrophage polarization in a concentration-dependent manner. The in vivo studies demonstrated that GDNF-Gel/HA-Mg conduit could significantly promote the regeneration and myelination of sciatic nerve, as well as the recovery of denervated gastrocnemius atrophy. Interpretation: The GDNF-Gel/HA-Mg conduit prepared in this study exhibited good hydrophilicity and corrosion resistance and greatly enhanced the proliferation, migration, and invasion abilities of Schwann cells, as well as peripheral nerve regeneration.

To recommend serum Vitamin D3(VD3) levels for osteoarthritis patients and susceptible populations by analyzing the dose-effect relationship between VD3 and the risk of osteoarthritis(OA) and between life's essential 8 and VD3 in OA patients. This study analyzed the National Health and Nutrition Examination Survey (NHANES) 2007-2018 cross-sectional data, excluding incomplete cases. Weighted baselines were calculated, and multiple logistic regression was used to assess the VD3-OA risk relationship. Multiple linear regression explored the VD3-LE8 score association in general and OA populations. Curve associations were modeled with restricted cubic splines, followed by subgroup and sensitivity analysis, and segmented regression based on the spline outcomes. Of 18,107 participants, OA patients had higher VD3 (76.79 nmol/L) and lower LE8 (64.70) than normal participants (65.96 nmol/L, 70.02). VD3 levels (Q1-Q4) correlated with OA risks of 9.82%-19.77%. Higher VD3 increased OA risk (Estimate = 0.006, P < 0.0001 per 1nmol/L), but RCS and segmented regression showed a U-shaped association (cutoff: 41 nmol/L). In OA patients and normals, VD3 positively correlated with LE8 (Estimate = 0.035, P < 0.001 for per 1nmol/L), with a linear RCS relationship. Sensitivity analysis confirmed these results. Our findings reveal a U-shaped association between VD3 levels and the risk of osteoarthritis (OA), while a positive association between VD3 and LE8 score. Based on these observations, we recommend maintaining moderate serum VD3 levels, for both OA-susceptible individuals and patients to optimize its overall health benefits.

Background: We aim to investigate the possible causal association between Hashimoto's thyroiditis (HT) and rheumatoid arthritis (RA) using Mendelian randomization (MR) methods.Methods: A bidirectional MR analysis was conducted to evaluate the causal association between HT and RA. We obtained summary statistics data from two extensive genome-wide association studies (GWAS) comprising 15,654 cases of HT and 14,361 cases of RA. The primary effect estimate utilized in this study was the inverse-variance weighted (IVW) method. To ensure the reliability and stability of the results, we employed several additional methods for testing, including MR-Egger, weighted median, simple mode, weighted mode, and MR-PRESSO.Results: Our study revealed compelling evidence of bidirectional causality between HT and RA. When HT was considered as an exposure factor and RA was considered as an outcome factor, this study revealed a positive correlation between HT and RA (IVW: odds ratio [OR] = 2.4546, 95% confidence interval [CI], 1.1473-5.2512; p = 0.0207). Conversely, when we examined RA as the exposure factor and HT as the outcome factor, we still found a positive correlation between them (IVW: OR = 1.2113, 95% CI, 1.1248-1.3044; p = 3.9478 x 10-7).Conclusions: According to our research findings, there exists a bidirectional positive causal relationship between HT and RA among European populations. This implies that individuals with HT have an elevated risk of developing RA, and conversely, individuals with RA have an increased risk of developing HT.

Background:Zinc-finger E-box-binding homeobox-1(ZEB1)is predominantly found in type-H vessels.However,the roles of ZEB1 and type-H vessels in steroid-induced osteonecrosis of the femoral head(SONFH)are unclear. Methods:Human femoral heads were collected to detect the expression of ZEB1 and the levels of type-H vessels.Then,the SONFH model was developed by injecting C57BL/6 mice with lipopolysaccharide and methylprednisolone.Micro-computed tomography,angiography,double calcein labeling,immunofluorescence,immunohistochemistry,quantitative real-time polymerase chain reaction,and Western blotting were performed to detect the expression of ZEB1,the Wnt/β-catenin pathway,type-H vessels,and the extent to which ZEB1 mediates angiogenesis and osteogenesis.Human umbilical vein endothelial cells were also used to explore the relationship between ZEB1 and the Wnt/β-catenin pathway. Results:We found thatZEB1 expression and the formation of type-H vessels decreased in SONFH patients and in a mouse model.The number of vascular endothelial growth factors in the femoral heads also decreased.Moreover,the bone mineral density,trabecular number,mineral apposition rate,and expression of genes related to osteogenesis decreased.After ZEB1 knockdown,angiogenesis and osteogenesis decreased.However,the numbers of type-H vessels and the extent of angiogenesis and osteogenesis improved after activation of the Wnt/β-catenin pathway. Conclusions:The ZEB1 expression decreased in SONFH,causing a decrease in type-H vessel,and it mediated angiogenesis and osteogenesis by regulating the Wnt/β-catenin pathway,ultimately accelerating the process of SONFH.

Magnesium (Mg) -based conduits have gained more attention in repairing peripheral nerve defects. However, they are limited due to poor corrosion resistance and rapid degradation rate. To tackle this issue, glial cell line -derived neurotrophic factor (GDNF)- Gelatin methacryloyl (Gel)/hydroxylapatite (HA) -Mg nerve conduit was developed and implanted in sciatic nerve defect model in Sprague-Dawley (SD) rats. The sciatic functional index measurement showed that the GDNF-Gel/HA-Mg nerve conduit effectively promoted the recovery of sciatic nerve function. The pathological examination results showed that there were more regenerated nerve tissues in GDNF-Gel/HA-Mg group, with a higher number of regenerating axons, and the thickness of the myelin sheath was significantly larger than that of control group (NC group). Immunofluorescence results revealed that the GDNF-Gel/HA-Mg conduit significantly promoted the expression of genes associated with nerve repair. RNA-seq and molecular test results indicated that GDNF-Gel/HA-Mg might be involved in the repair of peripheral nerve defects by regulating PPAR-g/ RhoA/ROCK signaling pathway. Biological sciences; Neuroscience; Molecular neuroscience; Techniques in neuroscience

Varus malalignment increases the susceptibility of cartilage to mechanical overloading, which stimulates catabolic metabolism to break down the extracellular matrix and lead to osteoarthritis (OA). The altered mechanical axis from the hip, knee to ankle leads to knee joint pain and ensuing cartilage wear and deterioration, which impact millions of the aged population. Stabilization of the remaining damaged cartilage, and prevention of further deterioration, could provide immense clinical utility and prolong joint function. Our previous work showed that high tibial osteotomy (HTO) could shift the mechanical stress from an imbalanced status to a neutral alignment. However, the underlying mechanisms of endogenous cartilage stabilization after HTO remain unclear. We hypothesize that cartilage-resident mesenchymal stem cells (MSCs) dampen damaged cartilage injury and promote endogenous repair in a varus malaligned knee. The goal of this study is to further examine whether HTO-mediated off-loading would affect human cartilage-resident MSCs' anabolic and catabolic metabolism. This study was approved by IACUC at Xi'an Jiaotong University. Patients with medial compartment OA (52.75±6.85 yrs, left knee 18, right knee 20) underwent open-wedge HTO by the same surgeons at one single academic sports medicine center. Clinical data was documented by the Epic HIS between the dates of April 2019 and April 2022 and radiographic images were collected with a minimum of 12 months of follow-up. Medial compartment OA with/without medial meniscus injury patients with unilateral Kellgren /Lawrence grade 3–4 was confirmed by X-ray. All incisions of the lower extremity healed well after the HTO operation without incision infection. Joint space width (JSW) was measured by uploading to ImageJ software. The Knee injury and Osteoarthritis Outcome Score (KOOS) toolkit was applied to assess the pain level. Outerbridge scores were obtained from a second-look arthroscopic examination. RNA was extracted to quantify catabolic targets and pro-inflammatory genes (QiaGen). Student's t test for two group comparisons and ANOVA analysis for differences between more than 2 groups were utilized. To understand the role of mechanical loading-induced cartilage repair, we measured the serial changes of joint space width (JSW) after HTO for assessing the state of the cartilage stabilization. Our data showed that HTO increased the JSW, decreased the VAS score and improved the KOOS score significantly. We further scored cartilage lesion severity using the Outerbridge classification under a second-look arthroscopic examination while removing the HTO plate. It showed the cartilage lesion area decreased significantly, the full thickness of cartilage increased and mechanical strength was better compared to the pre-HTO baseline. HTO dampened medial tibiofemoral cartilage degeneration and accelerate cartilage repair from Outerbridge grade 2 to 3 to Outerbridge 0 to 1 compared to untreated varus OA. It suggested that physical loading was involved in HTO-induced cartilage regeneration. Given that HTO surgery increases joint space width and creates a physical loading environment, we hypothesize that HTO could increase cartilage composition and collagen accumulation. Consistent with our observation, a group of cartilage-resident MSCs was identified. Our data further showed decreased expression of RUNX2, COL10 and increased SOX9 in MSCs at the RNA level, indicating that catabolic activities were halted during mechanical off-loading. To understand the role of cartilage-resident MSCs in cartilage repair in a biophysical environment, we investigated the differentiation potential of MSCs under 3-dimensional mechanical loading conditions. The physical loading inhibited catabolic markers (IL-1 and IL-6) and increased anabolic markers (SOX9, COL2).Knee-preserved HTO intervention alleviates varus malalignment-related knee joint pain, improves daily and recreation function, and repairs degenerated cartilage of medial compartment OA. The off-loading effect of HTO may allow the mechanoregulation of cartilage repair through the differentiation of endogenous cartilage-derived MSCs.

Epidural steroid injection for the treatment of sciatica caused by disc herniation is increasingly used worldwide, but its effectiveness remains controversial. The review aiming to analyze the efficacy of epidural steroid injection on sciatica caused by lumbar disc herniation. Randomized controlled trials (RCTs) investigating the use of epidural steroid injections in the management of sciatica induced by lumbar disc herniation were collected from PubMed and other databases from January, 2008 to December, 2023, with epidural steroid injection in the test group and epidural local anesthetic and/or placebo in the control group. Pain relief rate, assessed by numerical rating scale (NRS) and visual analogue scale (VAS) scores, and function recovery, evaluated by Roland Morris Disability Questionnaire (RMDQ) and Oswestry Disability Index (ODI) scores, were recorded and compared. Meta-analysis was performed by Review Manager. In comparison to the control group, epidural steroid injections have been shown to be effective for providing short- (within 3 months) [MD = 0.44, 95%CI (0.20, 0.68), p = 0.0003] and medium-term (within 6 months) [MD = 0.66, 95%CI (0.09,1.22), p = 0.02] pain relief for sciatica caused by lumbar disc herniation, while its long-term pain-relief effect were limited. However, the administration of epidural steroid injections did not lead to a significant improvement on sciatic nerve function in short- [MD = 0.79, 95%CI = (0.39, 1.98), p = 0.19] and long-term [MD = 0.47, 95% CI = (−0.86, 1.80), p = 0.49] assessed by IOD. Furthermore, the analysis revealed that administering epidural steroid injections resulted in a reduction in opioid usage among patients with lumbar disc herniation [MD = −14.45, 95% CI = (−24.61, −4.29), p = 0.005]. The incidence of epidural steroid injection was low. Epidural steroid injection has demonstrated notable efficacy in relieving sciatica caused by lumbar disc herniation in short to medium-term. Therefore, it is recommended as a viable treatment option for individuals suffering from sciatica.

Osteoarthritis (OA) is a disease that affects the entire joint. To treat OA, it may be beneficial to inhibit the activity of TGF-β in the subchondral bone. However, delivering drugs to the subchondral bone using conventional methods is challenging. In this study, we developed an extracellular vesicle delivery system. The utilization of macrophage-derived extracellular vesicles as a drug-carrying platform enables drugs to evade immune clearance and cross biological barriers. By incorporating targeting peptides on the surface of extracellular vesicles, the drug platform becomes targeted. The combination of these two factors results in the successful delivery of the drug to the subchondral bone. The study evaluated the stability, cytotoxicity, and bone targeting capability of the engineered extracellular vesicle platform (BT-EV-G). It also assessed the effects of BT-EV-G on the differentiation, proliferation, and migration of bone mesenchymal stem cells (BMSCs). Additionally, the researchers administered BT-EV-G to anterior cruciate ligament transection (ACLT)-induced OA mice. The results showed that BT-EV-G had low toxicity and high bone targeting ability both in vitro and in vivo. BT-EV-G can restore coupled bone remodeling in subchondral bone by inhibiting pSmad2/3-dependent TGF-β signaling. This work provides new insights into the treatment of OA.

Background Proteasome inhibition is a promising strategy for cancer therapy. Bortezomib, which primarily targets the chymotrypsin-like activity of PSMB5, has demonstrated efficacy in various tumors. However, there is variable sensitivity to bortezomib, which could be attributed, in part, to variations in the expression of proteasome subunits. Methods and results In this study, we investigated whether miR-383 affects the expression of proteasome subunits in osteosarcoma (OS) cells, and if so, whether OS cells display differential sensitivity to bortezomib concerning miR-383 expression. We detected a decreased miR-383 expression in OS cells and tissues. Then we found a negative correlation between the cytotoxicity of bortezomib and the expression level of the proteasome 20S core particle subunit β5 (PSMB5). Intriguingly, we identified PSMB5 as a direct target of miR-383. Increased expression of miR-383 resulted in decreased PSMB5 expression and increased sensitivity to bortezomib in OS cells. Conclusions In summary, our findings present the initial comprehensive analysis of the function of miR-383 in OS. The outcomes indicate that miR-383 may augment the anticancer effect of bortezomib through PSMB5 repression, offering a novel therapeutic approach in OS and a fresh pathway for proteasome regulation.

Objective:Hip ankylosis is a prevalent condition in patients with Ankylosing spondylitis (AS) that can significantly impact their psychological well-being. This study aimed to investigate the impact of Total Hip Arthroplasty (THA) on anxiety and depression among AS patients.Methods:62 AS patients undergoing primary THA were recruited and separated into two groups based on preoperative hip motion. The 40 patients with hip mobility of 0° were assigned to group A, and others were assigned to group NA. Self-rating Anxiety Scale (SAS), Self-rating Depression scale (SDS), Harris hip scores (HHS) and 36-Item Short Form Survey (SF-36) were obtained one week before and there, six and twelve months after THA.Results:The study found that AS patients in group A had significantly higher levels of anxiety and depression (SAS score = 75.05±2.79, SDS index score = 0.74±0.02) compared to group B (SAS score = 54.58±3.35, SDS index score= 0.64±0.03, P=0.01). However, both groups showed significant improvements in anxiety and depression scores from there to twelve months after THA (P<0.001). Correlation analyses revealed that the improvement in group NA was associated with hip pain relief (p<0.001), while the improvement in group A was related to joint function, disease duration, age at THA and spine imaging lesions (p<0.001).Conclusion:Some degree of anxiety and depression was present in both groups of AS patients. Levels of depression and anxiety were higher in patients with combined hip ankylosis. And their improvement was associated with improved hip function and quality of life after THA. Hip pain relief played a significant role in patients without hip joint ankylosis. The impact of the degree of lesion on spinal imaging on psychological status needs to be considered in both groups.

BACKGROUND Osteoporosis is a systemic chronic disease characterized by bone mineral density (BMD) reduction. This study aimed to assess the prevalence of osteoporosis and fracture risks in northwestern China and investigate the related anthropometric risk factors. MATERIAL AND METHODS Between July 2022 and August 2022, 1429 participants (1295 females, 134 males) with measured BMD were recruited to participate in this cross-sectional study. Data on height, weight, and T score were collected. Spearman's correlation and multiple linear regression analysis were used to investigate the relationships between various demographic factors and BMD and the 10-year risk of major osteoporotic fracture (MO) and hip fracture (HP). RESULTS The overall prevalence of osteoporosis in northwest China was 42.34%, with 44.56% in females and 20.90% in males. Age negatively affects females' T scores (r=-0.304, P<0.05), and height positively influences both sexes' T scores (r=0.059 P<0.05). Age (r=0.148, P<0.05) and height were positive predictors of MO (r=0.027, P<0.05), while weight was a negative predictor (r=-0.035, P<0.05). The conclusion for HP was consistent with that of MO, except for the T score, which was a positive predictor of HP (r=0.014, P<0.05). CONCLUSIONS The prevalence of osteoporosis in northeast China is high. The association between anthropometric parameters and osteoporosis in adults in northwest China is different between sexes.

Surgery is the primary treatment for recurrent patellar dislocation. However, there is still a lack of consensus regarding the choice of combined surgical methods due to the complexity of the anatomical factors. This study aimed to investigate the efficacy and radiological changes in medial patellofemoral ligament reconstruction (MPFLR) and lateral retinacular release (LRR) with and without tibial tubercle osteotomy (TTO) for recurrent patellar dislocation in patients with a tibial tubercle-trochlear groove (TT-TG) distance of 15 to 20 mm. Fifty-four patients were enrolled in this retrospective study between 2010 and 2014. The average patient age was 21.6 +/- 5.0 years. All patients underwent MPFLR and LRR, and in 18 patients, these procedures were combined with TTO. Patients were evaluated preoperatively and postoperatively for patellar lateral shift, patellar tilt angle, TT-TG distance, Q-angle, Caton-Deschamps index (CDI), Kujala, and Lysholm scores. The minimally clinical important difference was used to compare clinical outcomes between two groups. In the mean follow-up of 82.6 +/- 15.9 months, functional scores improved significantly in both groups ( p < 0.01). There were no significant differences in postoperative function scores between the two groups (Kujala, p = 0.25, mean difference = 1.5, 95% confidence interval [CI]: -1.4-4.4; Lysholm, p = 0.76, mean difference = -0.6, 95% CI: -5.9-4.7). Additionally, TTO significantly decreased Q-angle (23.6 +/- 2.4 vs. 17.4 +/- 2.9, p < 0.01), TT-TG (17.1 +/- 1.5 vs. 10.4 +/- 1.8, p < 0.01), and CDI (1.18 +/- 0.12 vs. 1.08 +/- 0.07, p < 0.01). Combined MPFLR and LRR with and without TTO are both effective techniques for recurrent patellar dislocation. Additional osteotomy can correct patellar alta and tibial tubercle lateralization. However, given that there were no significant differences in postoperative functional scores or recurrence rate between groups, we may not recommend TTO in addition to MPFLR and LRR in patients with TT-TG of 15 to 20 mm. Long-term and prospective cohort studies are required to assess further outcomes.