Exploring m6A-linked aging genes in osteoarthritis and broad cancer spectrum: Prospects for diagnostic and therapeutic advancements.

Osteoarthritis (OA) is a prevalent degenerative joint disease that significantly impacts individuals and healthcare systems worldwide. However, the exploration of N6-methyladenosine (m6A)-related aging genes in OA pathogenesis remains largely underexplored. This study aimed to elucidate the role of m6A-related aging genes in OA and to develop a robust diagnostic model based on their expression profiles. Leveraging publicly available gene expression datasets, we conducted consensus clustering to categorize OA into distinct subtypes, guided by the expression patterns of m6A-related aging genes. Utilizing XGBoost, a cutting-edge machine learning approach, we identified key diagnostic genes and constructed a predictive model. Our investigation extended to the immune functions of these genes, shedding light on potential therapeutic targets and underlying regulatory mechanisms. Our analysis unveiled specific OA subtypes, each marked by unique expression profiles of m6A-related aging genes. We pinpointed a set of pivotal diagnostic genes, offering potential therapeutic avenues. The developed diagnostic model exhibited exceptional capability in distinguishing OA patients from healthy controls. To corroborate our computational findings, we performed quantitative real-time polymerase chain reaction analyses on two cell lines: HC-OA (representing adult osteoarthritis cells) and C-28/I2 (representative of normal human chondrocytes). The gene expression patterns observed were consistent with our bioinformatics predictions, further validating our initial results. In conclusion, this study underscores the significance of m6A-related aging genes as promising biomarkers for diagnosis and prognosis, as well as potential therapeutic targets in OA. Although these findings are encouraging, further validation and functional analyses are crucial for their clinical application.

Rapid and Severe Idiopathic Aseptic Necrosis of the Contralateral Femoral Head after Unilateral Total Hip Arthroplasty.

BACKGROUND: Osteonecrosis of the femoral head (ONFH) is a multifactorial disease, and agnogenic ONFH, otherwise known as idiopathic ONFH, is rare in clinic. Idiopathic ONFH that exhibits severe necrosis and progresses extremely rapidly is called rapidly destructive hip disease (RDHD). RDHD greatly affects patients but is rarely reported in clinical practice and literature. CASE PRESENTATION: In this study, a 64-year-old male patient with complete collapse and necrosis of the right femoral head complicated with severe bone destruction at 10 months after left total hip arthroplasty (THA) was reported. The period from the intact structure of the right femoral head to the first discovery of its complete collapse, according to imaging results, was 7 months. The duration from the occurrence of symptoms in the right hip joint to the first discovery of complete collapse and necrosis of the femoral head was only 5 months. At present, the cause has not been determined based on medical history, symptoms, signs, imaging evaluation results, laboratory examination results, and pathological examination results, though it has been identified as severe idiopathic aseptic necrosis of the femoral head with rapid progression, or RDHD. Finally, right THA was performed, and a good outcome was observed in the patient at present. CONCLUSIONS: As a rare hip joint disease, RDHD greatly influences the normal life of patients. RDHD of the contralateral side after unilateral THA is even scarcer. Left THA may be one of the important factors accelerating the necrosis of the right femoral head. Hopefully, with this case report, more attention will be paid to the contralateral hip joint in patients undergoing unilateral THA by clinicians and rehabilitation physicians, and a clinical reference will be provided for the research on RDHD.

No difference in postoperative efficacy and safety between autograft and allograft in anterior cruciate ligament reconstruction: a retrospective cohort study in 112 patients.

Background: Arthroscopic anterior cruciate ligament reconstruction (ACLR) is the best treatment choice for returning to pre-injury activities following ACL rupture. Although allografts are considered an effective alternative to autografts, there is still controversy regarding the safety and effectiveness of this procedure, especially concerning the risk of postoperative infection and disease transmission. The purpose of this study was to compare the efficacy outcomes and safety between allografts and autografts in primary ACLR. Methods: The retrospective analysis involved 112 patients (58 patients received allogeneic tendons and 54 patients received autologous hamstring tendons) who underwent primary ACLR. All patients were followed up and evaluated on admission and at 1 week, 3 months, 6 months, and 1 year postoperatively. The efficacy outcome of the ACLR was evaluated by International Knee Documentation Committee (IKDC) score and physical examinations (Lachman test, anterior drawer test, and pivot shift test). The safety outcome of allografts and autografts was compared by investigating the occurrence of postoperative complications, including postoperative inflammation and potential disease transmission. The benefits of each operation for surgeons and patients were also analyzed, including the length of surgical incision and operative time. Results: There was no significant difference in the demographic and clinical characteristics between the allograft and autograft groups. The two cohorts proved to be similar in terms of the acute or chronic nature of the cruciate ligament and the incidence of concomitant meniscal surgery. Arthroscopic ACLR was performed in all patients. The physical examinations were all positive before surgery and negative immediately after the operation. The KT-1000 and IKDC scores of two groups significantly decreased than pre-operative ones (P<0.05), but the difference between the two groups was not statistically significant (P>0.05). At final follow-up, all patients had returned to their pre-injury activities. Allografts showed no increased risk for postoperative infection or potential disease transmission relative to autografts. Conclusions: The outcomes of reconstructed ACL with allografts were similar to those of autographs. Moreover, the safety of allografts showed to be comparable to that of autografts, especially concerning postoperative infection and disease transmission. Therefore, the surgical option should be chosen wisely according to the patient's condition.

Antibacterial, antioxidant and anti-inflammatory PLCL/gelatin nanofiber membranes to promote wound healing.

Epigallocatechin-3-O-gallate (EGCG) is a green biomedical agent for promoting wound healing, which possess excellent antibacterial, antioxidant and anti-inflammatory activities. For improving the low bioavailability challenges of EGCG in vivo, we had successful created a low-cost and simple wound dressing Poly (L-Lactic-co-caprolactone) (PLCL)/Gelatin/EGCG/Core-shell nanofiber membrane (PGEC) with drug sustained release capacity through coaxial electrospinning technology. In vitro experimental indicated that the core-shell structure wound dressing had excellent biocompatibility, antibacterial and antioxidant ability, which could support cell viability and proliferation, encourage re-epithelialization during the healing process, inhibit subsequent wound infection and thus promote wound regeneration. In vivo experimental demonstrated that PGEC wound dressing could promote wound healing, the histological results further demonstrated that PGEC not only facilitated early wound closure but also influenced cellular differentiation and tissue organization. Meanwhile, PGEC had excellent hemostatic ability. Taken all together, we believed that the PGEC wound dressing, which could localize delivery of EGCG, had high potential clinical application for promoting wound healing, hemostasis or other related clinical applications in the future.

Role of the Alarmin S100A9 protein in inducing Achilles tendinopathy in rats.

BACKGROUND: This study aimed to investigate the correlation between the Alarmin S100A9 protein and Achilles tendinopathy (AT), and to reveal the role of this protein in inducing AT. METHODS: In this study, 40 male Sprague-Dawley rats were randomly divided into four groups: Control group (received no treatment), Injury group (Achilles tendon tissues were cut intraoperatively), S100A9 group (received a subcutaneous injection of rhS100A9 solution), and S100A9 + Paquinimod group [received a subcutaneous injection of rhS100A9 and Paquinimod (1:1 ratio) into the Achilles tendon]. At 1 week postoperatively, the four groups of rats were euthanized, and the Achilles tendon tissues were isolated for histological staining, immunohistochemistry (IHC), immunofluorescence, Sirius Red (SR) staining, and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay. RESULTS: Compared with both the Control and S100A9 + Paquinimod groups, the Injury and S100A9 groups exhibited higher expression levels of S100A9 protein, matrix metalloproteinase-3 (MMP-3), and inflammatory factors. Regarding histomorphology [hematoxylin-eosin (HE) staining and Safranin O/fast green (SOFG; fast green and Safranin) training], the Achilles tendon tissues in the Injury and S100A9 groups showed AT-like changes, and the fibers were extremely disorderly, non-bundled, and ruptured, and some nuclei were spindles. As for collagen (Col) remodeling, a large number of fresh collagen fibers had formed, the amounts of Col-I and Col-II were lower, and a large quantity of Col-III was present. Additionally, a large number of tendon cells had died in both the Injury and S100A9 groups. CONCLUSIONS: This study showed that Alarmin S100A9 can induce AT-like morphological changes and local inflammatory reactions, trigger collagen fiber remodeling and tendon cell apoptosis, and ultimately induce AT.