Evaluation of the Association between Low-Density Lipoprotein (LDL) and All-Cause Mortality in Geriatric Patients with Hip Fractures: A Prospective Cohort Study of 339 Patients.

BACKGROUND: Many factors affect the prognosis of hip fractures in the elderly. Some studies have suggested a direct or indirect association among serum lipid levels, osteoporosis, and hip fracture risk. LDL levels were found to have a statistically significant nonlinear U-shaped relationship with hip fracture risk. However, the relationship between serum LDL levels and the prognosis of patients with hip fractures remains unclear. Therefore, in this study, we assessed the influence of serum LDL levels on patient mortality over a long-term follow-up period. METHODS: Elderly patients with hip fractures were screened between January 2015 and September 2019, and their demographic and clinical characteristics were collected. Linear and nonlinear multivariate Cox regression models were used to identify the association between LDL levels and mortality. Analyses were performed using Empower Stats and R software. RESULTS: Overall, 339 patients with a mean follow-up period of 34.17 months were included in this study. Ninety-nine patients (29.20%) died due to all-cause mortality. Linear multivariate Cox regression models showed that LDL levels were associated with mortality (HR = 0.69, 95%CI: 0.53, 0.91, p = 0.0085) after adjusting for confounding factors. However, the linear association was unstable, and nonlinearity was identified. An LDL concentration of 2.31 mmol/L was defined as the inflection point for prediction. A LDL level < 2.31 mmol/L was associated with mortality (HR = 0.42, 95%CI: 0.25, 0.69, p = 0.0006), whereas LDL > 2.31 mmol/L was not a risk factor for mortality (HR = 1.06, 95%CI: 0.70, 1.63, p = 0.7722). CONCLUSIONS: The preoperative LDL level was nonlinearly associated with mortality in elderly patients with hip fractures, and the LDL level was a risk indicator of mortality. Furthermore, 2.31 mmol/L could be considered a predictor cut-off for risk.

[Treatment of aseptic ulnar diaphyseal nonunion with locking compression plate and autogenous iliac bone graft].

OBJECTIVE: To investigate the clinical results of locking compression plate combined with autologous iliac bone graft in the treatment of aseptic ulnar nonunion. METHODS: From March 2009 to July 2017, 22 patients with aseptic ulnar diaphyseal nonunion with complete follow-up data were treated with surgery, including 12 males and 10 females, aged from 16 to 58 (39.7±9.9) years old and ranging in course of disease from 10 to 192 (39.4±55.7) months. There were 15 atrophic nonunions, 5 hypertrophic nonunions and 2 synovial pseudo-articular nonunions. After debridement of the nonunion, locking compression plate was used to fix the nonunion and autogenous iliac bone graft was given. Bone healing rate, surgical complications and clinical results were evaluated. RESULTS: All the patients were followed up, and the duration ranged from 13 to 42 months, with a mean of (22.5±8.2) months, and 1 patient did not heal. Visual analogue pain scores ranged from 0 to 3 (0.9±0.9). Pronation of forearm was 47 to 86 (69.0±14.7) degrees, supination was 35 to 85 (63.0±9.4) degrees, wrist flexion was 20 to 80 (51.0±10.2) degrees, wrist flexion was 32 to 88 (71.0±11.7) degrees, elbow flexion contracture was 0 to 25 (9.0±5.6) degrees, further flexion was 105 to 150 (134.0±13.9) degrees, and grip strength was 87% on the opposite side. According to the Anderson scoring system, 8 cases were excellent, 11 were satisfied, 2 were not satisfied, and 1 was failed. CONCLUSIONS: LCP combined with autologous iliac bone graft can effectively treat aseptic ulna diaphyseal nonunion.

Knockdown of PRMT1 suppresses IL-1ß-induced cartilage degradation and inflammatory responses in human chondrocytes through Gli1-mediated Hedgehog signaling pathway.

Osteoarthritis (OA) is characterized by articular cartilage degradation and joint inflammation. The purpose of the present study is to elucidate the role of the specific function of PRMT1 in chondrocytes and its association with the pathophysiology of OA. We observed that the expression of PRMT1 was apparently upregulated in OA cartilage, as well as in chondrocytes stimulated with IL-1ß. Additionally, knockdown of PRMT1 suppressed interleukin 1 beta (IL-1ß)-induced extracellular matrix (ECM) metabolic imbalance by regulating the expression of MMP-13, ADAMTS-5, COL2A1, and ACAN. Furthermore, silencing of PRMT1 dramatically declined the production of prostaglandin E2 (PGE2) and nitric oxide as well as the level of pro-inflammatory cytokine IL-6 and TNF-α. Mechanistic analyses further revealed that IL-1ß-induced activation of the Hedgehog/Gli-1 signaling is suppressed upon PRMT1 knockdown. However, the effects of inhibition of PRMT1-mediated IL-1ß-induced cartilage matrix degradation and inflammatory response in OA chondrocytes were obviously abolished by Hedgehog agonist Purmorphamine (Pur). Our data collectively suggest that silencing of PRMT1 exerts anti-catabolic and anti-inflammatory effects on IL-1ß-induced chondrocytes via suppressing the Gli-1 mediated Hedgehog signaling pathway, indicating that PRMT1 plays a critical role in OA development and serves as a promising therapeutic target for OA.