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Background This study aims to evaluate the prognostic significance of preoperative paraspinal sarcopenia (PS) on long-term clinical outcomes in patients with intervertebral disc degeneration (IDD) undergoing unilateral biportal endoscopy discectomy (UBED), and to identify independent risk factors of postoperative chronic low back pain. Methods A retrospective cohort study was conducted on 148 IDD patients who underwent UBED, classified into sarcopenia ( n  = 65) and non-sarcopenia ( n  = 83) groups based on psoas muscle index (PMI) thresholds. Radiographic parameters, including PMI, erector spinae muscle index (EMI), multifidus muscle index (MMI), multifidus fat infiltration (MFI), erector spinae fat infiltration (EFI), and multifidus muscle density (MMD), were assessed via CT/MRI. Clinical outcomes were evaluated using the Visual Analog Scale (VAS) and Oswestry Disability Index (ODI) preoperatively and postoperatively at 1 month, 6 months, and final follow-up (≥ 12 months). Univariate and multivariate logistic regression analyses identified risk factors for chronic low back pain. Results The sarcopenia group exhibited significantly lower muscle indices (PMI, EMI, MMI; all P  < 0.001) and higher fat infiltration (MFI, EFI; P  < 0.05) compared to the non-sarcopenia group. While both groups demonstrated improvements in VAS and ODI scores postoperatively, the sarcopenia group had higher VAS (3.21 ± 0.92 vs. 2.75 ± 0.72, P  < 0.001) and ODI (22.19 ± 4.37% vs. 19.08 ± 3.43%, P  < 0.001) at final follow-up. Elevated BMI, lower BMD, reduced muscle indices (PMI, EMI, MMI), and severe MFI were significant predictors of chronic low back pain ( P  < 0.05). Conclusions PS is a modifiable risk factor for postoperative chronic low back pain after UBED. Preoperative identification of high-risk patients and targeted interventions to improve muscle function may enhance clinical outcomes. These findings underscore the importance of integrating muscle health assessments into spine care pathways.

Overproduction of reactive oxygen species (ROS), elevated synovial inflammation, synovial hyperplasia and fibrosis are the main characteristic of microenvironment in rheumatoid arthritis (RA). Macrophages and fibroblast-like synoviocytes (FLSs) play crucial roles in the progression of RA. Hence, synergistic combination of ROS scavenging, macrophage polarization from pro-inflammatory M1 phenotype towards M2 anti-inflammatory phenotype, and restoring homeostasis of FLSs will provide a promising therapeutic strategy for RA. In this study, we successfully synthesized metformin-derived carbon dots (MCDs), and investigated the antirheumatic effect in vivo and in vitro. Designed MCDs could target inflamed cells and accumulate at the inflammatory joints of collagen-induced arthritis (CIA) rats. In vivo therapeutic investigation suggested that MCDs reduced synovial inflammation and hyperplasia, ultimately prevented cartilage destruction, bone erosion, and synovial fibrosis in CIA rats. In addition, MCDs eliminated the cellular ROS in M1 phenotype macrophages in RA microenvironment through the enzyme-like catalytic activity as well as inhibiting NOD-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome signaling pathway, effectively polarizing them into the M2 phenotype to realize the anti-inflammatory effect. Furthermore, MCDs could inhibit the proliferation, migration, and fibrosis of inflamed FLSs. Mechanistically, MCDs restored the homeostasis of FLSs while reducing the level of synovial inflammation by blocking IL-6/gp130 signaling pathway. Combined with preferable biocompatibility, MCDs offer a prospective treatment approach for RA.

Tendon injury, resulting from repetitive strain or acute trauma, often leads to pain, reduced mobility, and impaired healing due to the limited regenerative capacity of tendon tissue. Adipose-derived stem cells (ADSCs) exosomes show therapeutic promise, though their mechanisms are unclear. We demonstrated that ADSC-Exos delivers miR-212-5p to tendon-derived stem cells (TDSCs), thereby enhancing their proliferation, migration, and tenogenic differentiation. miR-212-5p directly suppresses forkhead box protein O1 (FOXO1) by binding to its 3′UTR. This downregulation relieves transcriptional repression of protein phosphatase 1A (PP1A ), thereby increasing its expression and leading to dephosphorylation and activation of Yes-associated protein 1 (YAP1) signaling. In vivo, ADSC-derived exosomal miR-212-5p promotes tendon repair in male C57BL/6 mice by downregulating FOXO1 and activating YAP1 signaling. Taken together, these findings demonstrate that ADSC-derived exosomal miR-212-5p promotes tendon repair by downregulating FOXO1 to modulate the PP1A/YAP1 axis, highlighting a exosome-based regulatory mechanism and suggesting potential therapeutic targets for tendon injury management. Exosomal miR-212-5p from adipose stem cells promotes tendon repair by regulating FOXO1 and activating YAP1 signaling, highlighting a functional axis involved in tendon stem cell proliferation and differentiation.

Objective The aim of this study was to identify risk factors for surgical site infections and to quantify the contribution of independent risk factors to the probability of developing infection after definitive fixation of tibial plateau fractures in adult patients. Methods A retrospective analysis was performed at a level I trauma center between January 2004 and December 2010. Data were collected from a review of the patient’s electronic medical records. A total of 251 consecutive patients (256 cases) were divided into two groups, those with surgical site infections and those without surgical site infections. Preoperative and perioperative variables were compared between these groups, and risk factors were determined by univariate analyses and multivariate logistic regression. Variables analyzed included age, gender, smoking history, diabetes, presence of an open fracture, presence of compartment syndrome, Schatzker classification, polytrauma status, ICU stay, time from injury to surgery, use of temporary external fixation, surgical approach, surgical fixation, operative time, and use of a drain. Results The overall rate of surgical site infection after ORIF of tibial plateau fractures during the 7 years of this study was 7.8 % (20 of 256). The most common causative pathogens was Staphylococcus aureus ( n  = 15, 75 %). Independent predictors of surgical site infection identified by multivariate analyses were open tibial plateau fracture (odds ratio = 3.9; 95 % CI = 1.3–11.6; p  = 0.015) and operative time (odds ratio = 2.7; 95 % CI = 1.6–4.4; p  < 0.001). The presence of compartment syndrome (odds ratio = 3.4; 95 % CI = 0.7–15.9; p  = 0.119), use of temporary external fixation (odds ratio = 0.5; 95 % CI = 0.2–1.7; p  = 0.298), and ICU stay (odds ratio = 1.0; 95 % CI = 1.0–1.1; p  = 0.074) were not determined to be independent predictors of surgical site infection. Conclusions Both open fracture and operative time are independent risks factors for postoperative infection.

Talar neck fractures are usually the result of high-energy trauma. It remains controversial whether talar neck fractures require emergent treatment. Most surgeons recommend the use of dual surgical approaches, anteromedial and anterolateral, to allow accurate visualization and anatomic reduction. It is important to carefully preserve any remaining talar blood supply. Obtaining satisfactory clinical results, while avoiding complications, presents a unique challenge in the treatment of talar neck fractures. Common complications include posttraumatic arthritis, avascular necrosis, malunion, and nonunion.

The present study aims to explore the therapeutic effect of Stefin B on gouty arthritis (GA) and the polarization of macrophages in mice. Stefin B-overexpressed or knockdown M0 macrophages were constructed. The GA model was established in mice by injecting 25 mg/mL MSU, followed by a single injecting of Stefin B-overexpressing adenovirus vector (GA model + Stefin B OE) or an empty vector (GA model + Stefin B OE NC). Stefin B was found lowly expressed in M1 macrophages. CD206 was markedly upregulated and IL-10 release was signally increased in Stefin B-overexpressed macrophages. In gouty arthritis mice, marked redness and swelling were observed in the ankle joint. Dramatical infiltration of inflammatory cells was observed in the GA model and GA model + Stefin B OE NC groups, which was suppressed in the Stefin B OE group. Increased proportion of F4/80 + CD86 + cells observed in GA mice was markedly repressed by Stefin B overexpression, accompanied by the declined level of Caspase-1 and IL-17. Collectively, Stefin B alleviated the GA in mice by inducing the M2 polarization of macrophages.

Occasional beer spoilage incidents caused by false-negative isolation of lactic acid bacteria (LAB) in the viable but non-culturable (VBNC) state, result in significant profit loss and pose a major concern in the brewing industry. In this study, both culturable and VBNC cells of an individual Lactobacillus harbinensis strain BM-LH14723 were identified in one spoiled beer sample by genome sequencing, with the induction and resuscitation of VBNC state for this strain further investigated. Formation of the VBNC state was triggered by low-temperature storage in beer (175 ± 1.4 days) and beer subculturing (25 ± 0.8 subcultures), respectively, and identified by both traditional staining method and PMA-PCR. Resuscitated cells from the VBNC state were obtained by addition of catalase rather than temperature upshift, changing medium concentration, and adding other chemicals, and both VBNC and resuscitated cells retained similar beer-spoilage capability as exponentially growing cells. In addition to the first identification of both culturable and VBNC cells of an individual L. harbinensis strain from spoiled beer, this study also for the first time reported the VBNC induction and resuscitation, as well as verification of beer-spoilage capability of VBNC and resuscitated cells for the L. harbinensis strain. Genes in association with VBNC state were also identified by the first genome sequencing of beer spoilage L. harbinensis . The results derived from this study suggested the contamination and spoilage of beer products by VBNC and resuscitated L. harbinensis strain BM-LH14723.