Yucheng Lin

Background/Objectives: The optimal surgical timing for rotator cuff tears (RCTs) remains controversial, particularly regarding how tear etiology influences the final functional recovery. This study aimed to compare the clinical outcomes of early versus delayed arthroscopic repair stratified by etiology, providing evidence for etiology-specific surgical timing. Methods: A retrospective cohort study was conducted on 183 patients who underwent arthroscopic rotator cuff repair for isolated full-thickness supraspinatus tears. Patients were stratified into traumatic (n = 74) and degenerative (n = 109) groups based on etiology. They were further divided into early-repair and delayed-repair subgroups based on symptom duration (traumatic cut-off: 3 months; degenerative cut-off: 6 months). Clinical outcomes were assessed preoperatively and at the final follow-up using the Visual Analog Scale (VAS) for pain, American Shoulder and Elbow Surgeons (ASES) score, University of California at Los Angeles (UCLA) score, and range of motion. Complications, including retear rates and stiffness, were recorded. Results: In the traumatic group, early repair yielded significantly better postoperative pain relief (VAS) and higher functional scores (ASES and UCLA) compared to delayed repair. Notably, the delayed traumatic group exhibited a significantly higher retear rate compared to the early group (16.7% vs. 2.6%; p = 0.039). Conversely, in the degenerative group, comparisons between early and delayed repair revealed no significant differences in the final functional scores, pain levels, or complication rates (p > 0.05). Conclusions: Surgical timing significantly impacts outcomes in traumatic RCTs, where early repair is critical to optimize functional recovery and minimize retear risks. In contrast, delayed arthroscopic repair for degenerative tears yielded comparable outcomes to early repair, suggesting that an initial trial of conservative management is safe and does not compromise final surgical outcomes.

OBJECTIVE: Intervertebral disc (IVD) degeneration (IDD) is a well-known consequence of low back pain, as characterized by aberrant cell proliferation and apoptosis of nucleus pulposus (NP) cells. In the present study, we aimed to investigate the effect of lncRNA small nucleolar RNA host gene 6 (SNHG6) on deregulated functions of degenerative NP cells. MATERIALS AND METHODS: After the establishment of rat IDD models, the mRNA and protein levels of collagen-I (Col-I) and collagen II (Col-II), and mRNA level of SNHG6 were detected by using reverse transcription quantitative Real Time-PCR (RT-qPCR) and Western blot. We further investigated the role and molecular mechanisms of SNHG6 by overexpressing or silencing it in degenerative NP cells. Cell proliferation was measured by MTT assay and EdU staning, and apoptosis was measured by flow cytometry. The target of SNHG6 was identified by starBase and Dual-Luciferase reporter assay. RESULTS: Upregulation of SNHG6 was found in IDD NP cells than in normal cells, associated with higher level of Col-I and lower level of Col-II. Overexpression of SNHG6 inhibited cell proliferation and enhanced apoptosis, accompanied by increased expression of Bax, caspase-3, and p21, as well as decreased expression of Bcl-2, which was in reverse to the treatment of SNHG6 silencing. Moreover. miR101-3p was indicated as a target of SNHG6, and inhibition of miR-101-3p reversed the effects on proliferation and apoptosis induced by SNHG6. CONCLUSIONS: SNHG6 suppressed cell proliferation and induced apoptosis by increasing expression of Bax. caspase-3, p21 and decreasing Bcl-2 through targeting miR-101-3p. which suggested that SNHG6 could be a potential target in the treatment of IDD.

Patients with diabetes mellitus (DM) often suffered with many musculoskeletal disorders, such as tendon rupture and tendinopathy. However, the understanding of the pathogenesis of these alternations is limited. This study was designed to investigate the role of tendon-derived stem cells (TDSCs) in histopathological alterations of DM tendons. Forty-two SD rats were randomly and equally divided into a diabetes group (DG) and control group (CG). DM was induced by streptozotocin (65 mg/kg). The patellar tendons were isolated at weeks 1, 2, and 4 for histological analysis. TDSCs were isolated at week 2 for osteo-chondrogenic differentiation analysis. Mann-Whitney U test was used with SPSS. p < 0.050 was statistically significant. Micro-tears of collagen fibers and altered appearance of tendon cells were observed in DG tendons. DG tendons exhibited significantly higher expression of OPN, OCN, SOX9, and Col II and decreased expression of Col I and tenomodulin (TNMD) at week 2. Diabetic TDSCs (dTDSCs) demonstrated significantly decreased proliferation ability and increased osteogenic and chondrogenic differentiation ability. Osteo-chondrogenic markers BMP2, ALP, OPN, OCN, Col II, and SOX9 were also significantly increased while tenogenic markers Col I and TNMD were decreased in dTDSCs. These results suggested the erroneous differentiation of dTDSCs might account for the structural and non-tenogenic alternations in DM tendons, which provided new cues for the pathogenesis of tendon disorders in DM.

Background: Aberrant apoptosis in nucleus pulposus (NP) cells is the primary cause of intervertebral disc degeneration (IDD). In contrast, a large number of studies have confirmed that autophagy may protect NP cells from apoptosis. Sinomenine is an alkaloid monomer, which has been reported to stimulate cell autophagy. Therefore, the aim of the present study was to investigate the effects of sinomenine on IDD. Methods: The effects of sinomenine on the proliferation and apoptosis of NP cells were evaluated with the CCK-8 assay and Annexin V/PI staining, respectively. Results: The data obtained from the present study demonstrated that sinomenine could notably reverse TBHP-induced growth inhibition and apoptosis in rat NP cells. In addition, sinomenine significantly induced autophagy in rat NP cells, which was completely inhibited by 3-methyladenine (3MA). In addition, the protective effect of sinomenine against TBHP in rat NP cells was abolished following treatment with 3MA. Finally, an in vivo study further confirmed that sinomenine could ameliorate rat IDD. Conclusion: Taken together, the results of the present study indicated sinomenine could ameliorate rat IDD via induction of autophagy in vitro and in vivo. These findings suggest the therapeutic potential of sinomenine in the prevention of IDD.