Panyu Zhou

Background: Metabolic syndrome (MetS) has been widely accepted as a significant risk factor for osteoarthritis (OA). Nevertheless, the molecular links between these conditions have not been fully characterized. These molecular pathways are critical for the development of targeted therapies and the improvement of patient outcomes. Methods: Epidemiological analysis was based on NHANES 2007–2016. Survey‐weighted logistic regression was used to analyze the association between MetS and OA. To investigate key molecular features associated with OA and MetS, GEO gene expression profiles were analyzed by differentially expressed gene (DEG) analysis, weighted gene coexpression network analysis (WGCNA), and functional enrichment analysis. Diagnostic genes were further identified via machine learning and protein–protein interaction (PPI) network analysis. Their expression, diagnostic performance, predictive value, and associations with immune cell infiltration were evaluated. To study cell‐specific hub gene expression, single‐cell RNA sequencing (scRNA‐seq) was performed, followed by validation using quantitative real‐time polymerase chain reaction (qRT‐PCR) and immunofluorescence. Results: According to NHANES 2007–2016, MetS was significantly associated with higher odds of prevalent OA. Integrated transcriptomic analysis revealed 27 common genes among DEGs in OA, DEGs in MetS, and disease‐associated genes identified using WGCNA. Based on machine learning models and PPI network analysis, MMP9 and JUN were identified as hub genes and showed diagnostic utility in the nomogram. Immune infiltration analysis revealed changes in immune cell composition. Hub gene expression patterns were confirmed by scRNA‐seq analysis and further verified by qRT‐PCR and immunofluorescence. Conclusion: This investigation revealed JUN and MMP9 as important genes connected to the advancement of MetS‐associated OA, and these genes were significantly related to disease progression. New targets are suggested by these findings for the early diagnosis and possible treatment strategies of this comorbidity.

Purpose: Acute lung injury (ALI) is a common clinical syndrome with high mortality. The chemokine ligand 25 (CCL25) is involved in inflammation, leukocyte trafficking and immunoregulation. However, the role and mechanism of CCL25 in ALI are not fully understood yet. The aim of this study was to explore the relationship between acute lung injury and CCL25. Patients and Methods: In this study, we first examined chemokine expression in sepsis patients and found that serum CCL25 expression levels were relatively high in sepsis patients compared to healthy individuals. Based on this, we designed in vitro and in vivo experiments to verify the validity of the theory. In vitro, we used lipopolysaccharide-stimulated human pulmonary microvascular endothelial cells (HPMECs). In vivo, we established male C57BL/6 mice cecal ligation puncture (CLP) model of sepsis. Results: In vitro, we used lipopolysaccharide-stimulated human pulmonary microvascular endothelial cells (HPMECs) and found significantly higher expression of CCL25 by enzyme-linked immunosorbent assay. Inhibition of CCL25 resulted in a significant decrease in the expression of inflammatory cytokines in HPMECs. In addition, we found that CCL25 promoted increased endothelial permeability by reducing the expression of tight junction proteins and was associated with activation of the P38 MAPK pathway by measuring the transepithelial electrical resistance and fluorescence intensity of fluorescein isothiocyanate. Results from luciferase assays and chromatin immunoprecipitation assays showed that inhibition of NF-κB activity in HPMECs decreased CCL25 expression, but addition of recombinant CCL25 increased cell permeability and inflammatory cytokine expression. In vivo, we established male C57BL/6 mice cecal ligation puncture (CLP) model of sepsis. We found that inhibition of CCL25 significantly reduced inflammatory cytokine expression in a CLP-induced sepsis model, thereby alleviating lung tissue damage in mice. Conclusion: Our study suggests that CCL25 contributed to the development of ALI by modulating the functions of microvascular endothelial cells.

Background: Defects of articular cartilage represent a common condition that usually progresses to osteoarthritis with pain and dysfunction of the joint. Current treatment strategies have yielded limited success in these patients. Stem cells are emerging as a promising option for cartilage regeneration. We aim to summarize the developmental history of stem cells for cartilage regeneration and to analyse the relevant trends and hotspots.Methods: We screened all relevant literature on stem cells for cartilage regeneration from Web of Science during 2010–2020 and analysed the research trends in this field by VOSviewer and CiteSpace. We also summarized previous clinical trials.Results: We screened 1,011 publications. China contributed the largest number of publications (317, 31.36%) and citations (81,376, 48.61%). The United States achieved the highest H-index (39). Shanghai Jiao Tong University had the largest number of publications (34) among all full-time institutions. The Journal of Biomaterials and Stem Cell Research and Therapy published the largest number of studies on stem cells for cartilage regeneration (35). SEKIYA I and YANG F published the majority of articles in this field (14), while TOH WS was cited most frequently (740). Regarding clinical research on stem cells for cartilage regeneration, the keyword “double-blind” emerged in recent years, with an average year of 2018.75. In tissue engineering, the keyword “3D printing” appeared latest, with an average year of 2019.625. In biological studies, the key word “extracellular vesicles” appeared latest, with an average year of 2018.9091. The current research trend indicates that basic research is gradually transforming to tissue engineering. Clinical trials have confirmed the safety and feasibility of stem cells for cartilage regeneration.Conclusion: Multiple scientific methods were employed to reveal productivity, collaborations, and research hotspots related to the use of stem cells for cartilage regeneration. 3D printing, extracellular vesicles, and double-blind clinical trials are research hotspots and are likely to be promising in the near future. Further studies are needed for to improve our understanding of this field, and clinical trials with larger sample sizes and longer follow-up periods are needed for clinical transformation.

Background: Lateral malleolus fractures occur frequently. The common techniques for fixing purely lateral malleolus fractures are often challenging, owing to the extent of soft tissue damage and fracture non-union. Herein, we report a new treatment that entails minimally invasive insertion and continuous compression of the broken ends as a novel technique, and evaluate its clinical results. Methods: This study enrolled 21 patients (13 males and 8 females; mean age 32.06±3.45 years, range 23–69 years) with purely lateral malleolus fractures. Each patient underwent open reduction treatment with a mini locking plate for internal fixation and compression of the fracture end with an Arched Shape-Memory Connector (ASC). The clinical assessments were made using the American Orthopedic Foot and Ankle Society (AOFAS) scores, which were recorded at the final follow-up visit. Results: The patients were followed for an average of 14.7±1.2 months (range, 12–18 months). None of the patients showed surgical failure, and all of the purely lateral malleolus fractures healed in an average of 12.6±1.5 weeks (range, 10–16 weeks). The mean AOFAS score was 88.94 (range, 83–90). Conclusions: The new treatment had beneficial outcomes for purely lateral malleolus fractures. Mini locking plates are minimally invasive for surgical intervention, and combined with continuous concentrated compression with an ASC to accelerate osseous healing, they aid in restoration of function and enable early rehabilitation with a low incidence of postoperative complications.

Iron overload is a common stress in the development of cells. Growing evidence has indicated that iron overload is associated with osteoporosis. Therefore, enhancing the understanding of iron overload would benefit the development of novel approaches to the treatment of osteoporosis. The purpose of the present study was to analyze the effect of iron overload on osteoblast cells, via the MC3T3‐E1 cell line, and to explore its possible underlying molecular mechanisms. Ferric ammonium citrate (FAC) was utilized to simulate iron overload conditions in vitro. FAC‐induced iron overload strongly suppressed proliferation of osteoblast cells and induced apoptosis. Moreover, iron overload strongly suppressed the expression of dual‐specificity phosphatase 14 (DUSP14). Additionally, overexpression of DUSP14 protected osteoblast cells from the deleterious effects of iron overload, and this protective effect was mediated by FOXO3a. Additionally, matrine rescued the function of DUSP14 in osteoblast cells. Most importantly, our analysis demonstrated the essential role of the PI3K/AKT/FOXO3a/DUSP14 signaling pathway in the defense against iron overload in osteoblast cells. Overall, our results not only elucidate deleterious effects of iron overload, but also unveil its possible signaling pathway in osteoblast cells.

Accurate puncture of the renal collecting system is crucial to the success of percutaneous nephrolithotomy and presents a technical challenge for urologists. Here, we introduced the Surgical Approach Visualization and Navigation (SAVN) system, a novel navigation system to assist puncture and reduce intraoperative radiation.