Expression of adiponectin in the subchondral bone of lumbar facet joints with different degrees of degeneration.

BACKGROUND: Osteoarthritis research has been most commonly performed in the setting of the articular cartilage of the knee. To the best of our knowledge, no studies have evaluated the role of adiponectin in osteoarthritis of the lumbar facet joint (FJOA). Therefore, in this study, we explored whether adiponectin was expressed in the lumbar facet joints and evaluated the role of adiponectin in FJOA. METHODS: We enrolled patients who underwent lumbar computed tomography (CT) and magnetic resonance imaging (MRI) at the Orthopedic Department of the First Affiliated Hospital of Nanchang from May 2015 to June 2016. Lumbar facet joints were obtained from 135 patients at the time of lumbar fusion surgery and divided into three groups according to the Weishaupt grade. Cytokine levels in the subchondral bones were evaluated by enzyme-linked immunosorbent assays (ELISAs), and adiponectin levels were determined by immunohistochemistry, western blotting, and quantitative polymerase chain reaction (qPCR). RESULTS: By ELISA, adiponectin levels were examined in the subchondral bone for lumbar facet joint, and adiponectin was found to be negatively correlated with BMI in 52 patients (p < 0.001, r = -0.861). By immunohistochemistry analysis, adiponectin was found to be expressed in the subchondral bone of the lumbar facet, whereas the cartilage area was negative for adiponectin expression. Immunostaining intensity and area was related to the degeneration of the lumbar facet joint, and, in our research, considerably decreased staining intensity and area were observed in more severely degenerated lumbar facet joints. Furthermore, the expression of adiponectin was also reduced in degenerated lumbar facet joints, and the level of decline corresponded to degeneration detected by western blotting and qPCR analysis (n = 27, p < 0.0001). CONCLUSIONS: Adiponectin expression was observed in the subchondral bone of the lumbar facet joint and decreased as the degree of degeneration increased. Thus, the results of this study provide new insights into the relationship between adiponectin and osteoarthritis.

Heme oxygenase-1 restores impaired GARPCD4⁺CD25⁺ regulatory T cells from patients with acute coronary syndrome by upregulating LAP and GARP expression on activated T lymphocytes.

BACKGROUND: Accumulating evidence shows that the pathological autoreactive immune response is responsible for plaque rupture and the subsequent onset of acute coronary syndrome (ACS). Naturally occurring CD4(+)CD25(+)regulatory T cells (nTregs) are indispensable in suppressing the pathological autoreactive immune response and maintaining immune homeostasis. However, the number and the suppressive function of glycoprotein-A repetitions predominant (GARP) (+) CD4(+) CD25(+) activated nTregs were impaired in patients with ACS. Recent evidence suggests that heme oxygenase-1 (HO-1) can regulate the adaptive immune response by promoting the expression of Foxp3. We therefore hypothesized that HO-1 may enhance the function of GARP(+) CD4(+) CD25(+)Tregs in patients with ACS and thus regulate immune imbalance. METHODS: T lymphocytes were isolated from healthy volunteers (control, n=30) and patients with stable angina (SA, n=40) or ACS (n=51). Half of these cells were treated with an HO-1 inducer (hemin) for 48 h, and the other half were incubated with complete RPMI-1640 medium. The frequencies of T-helper 1 (Th1), Th2, Th17 and latency-associated peptide (LAP) (+)CD4(+) T cells and the expression of Foxp3 and GARP by CD4(+)CD25(+)T cells were then assessed by measuring flow cytometry after stimulation in vitro. The suppressive function of activated Tregs was measured by thymidine uptake. The levels of transforming growth factor-1 (TGF-ß1) in the plasma were measured using enzyme-linked immunosorbent assay (ELISA). The expression levels of the genes encoding these proteins were analyzed by real-time polymerase chain reaction. RESULTS: Patients with ACS exhibited an impaired number and suppressive function of GARP(+) CD4(+) CD25(+)Tregs and a mixed Th1/Th17-dominant T cell response when compared with the SA and control groups. The expression of LAP in T cells was also lower in patients with ACS compared to patients with SA and the control individuals. Treatment with an HO-1 inducer enhanced the biological activity of GARP(+) CD4(+) CD25(+)Tregs and resulted in increased expression of LAP and GARP by activated T cells. CONCLUSIONS: The reduced number and impaired suppressive function of GARP(+) CD4(+) CD25(+)Tregs result in excess effector T cell proliferation, leading to plaque instability and the onset of ACS. HO-1 can effectively restore impaired GARP(+) CD4(+) CD25(+)Tregs from patients with ACS by promoting LAP and GARP expression on activated T cells.

Towards low-temperature dendrite-free zinc anode by constructing functional MXene buffer layer with duplex zincophilic sites.

Dendrite growth and side reactions of zinc metal anode have severely limited the practical application of aqueous zinc ion batteries (AZIBs). Herein, we introduce an artificial buffer layer composed of functional MXene (Ti3CN) for zinc anodes. The synthesized Ti3CN exhibits superior conductivity and features duplex zincophilic sites (N and F). These characteristics facilitate the homogeneous deposition of Zn2+, accelerate the desolvation process of hydrated Zn2+, and reduce the nucleation overpotential. The Ti3CN-protected Zn anode demonstrates significantly enhanced reversibility compared to bare Zn anode during long-term cycling, achieving a cumulative plating capacity of 10,000 mAh cm-2 at 10 mA cm-2. In Ti3CN-Zn||Cu asymmetric cell, it maintains nearly 100 % Coulombic efficiency over 2500 cycles at 2 mA cm-2. Furthermore, the assembled Ti3CN-Zn//δ-K0.51V2O5 (KVO) full cell exhibit a low capacity decay rate of 0.002 % per cycle at 5 A/g. Even at 0 °C, the Ti3CN-Zn symmetric cell maintains steady cycling for 2000 h. This study introduces a novel approach for designing artificial solid electrolyte interlayers for commercial AZIBs.

Lumbar spinal canal osteosarcoma: A case report.

RATIONALE: Osteosarcoma is a rare neoplasm in the lumbar spine. Although osteosarcoma can arise in any portion of the skeleton, it very rarely arises in the spinal canal, which accounts for <0.1% of all cases of adult sarcomas. Here, we describe a case of osteosarcoma arising in the L4-5 spinal canal. PATIENT CONCERNS: The present report describes the case of a 55-year-old female patient with osteosarcoma of the L4-5 spinal canal. DIAGNOSES: The patient was initially diagnosed with lumbar spinal stenosis and underwent lumbar fusion at a local hospital. At the 4-month follow-up, the patient reported a marked increase in numbness and pain in the lumbar region and lower limbs. Based on magnetic resonance imaging, we diagnosed a postoperative infectious lesion of the lumbar spine. INTERVENTIONS: The patient underwent surgery for complete removal of the mass lesion. The mass measured 3 × 2.5 × 0.7 cm in size and was located in the L4-5 spinal canal. OUTCOMES: Based on histological and immunohistochemical findings, the diagnosis of osteosarcoma was confirmed by an expert pathology consultant. The patient then received chemotherapy. Postoperative follow-up at 6 months revealed no evidence of recurrent disease or residual side effects from therapy. LESSONS: Osteosarcoma in the L4-5 spinal canal is extremely rare and very difficult to distinguish histologically from benign nervous and fibrous tissue. This is a very valuable case, which highlights the need for orthopedic surgeons to consider this when diagnosing patients with spinal tumors.

Risk factors for acute surgical site infections after lumbar surgery: a retrospective study.

BACKGROUND: Currently, many scholars are concerned about the treatment of postoperative infection; however, few have completed multivariate analyses to determine factors that contribute to the risk of infection. Therefore, we conducted a multivariate analysis of a retrospectively collected database to analyze the risk factors for acute surgical site infection following lumbar surgery, including fracture fixation, lumbar fusion, and minimally invasive lumbar surgery. METHODS: We retrospectively reviewed data from patients who underwent lumbar surgery between 2014 and 2016, including lumbar fusion, internal fracture fixation, and minimally invasive surgery in our hospital's spinal surgery unit. Patient demographics, procedures, and wound infection rates were analyzed using descriptive statistics, and risk factors were analyzed using logistic regression analyses. RESULTS: Twenty-six patients (2.81%) experienced acute surgical site infection following lumbar surgery in our study. The patients' mean body mass index, smoking history, operative time, blood loss, draining time, and drainage volume in the acute surgical site infection group were significantly different from those in the non-acute surgical site infection group (p < 0.05). Additionally, diabetes mellitus, chronic obstructive pulmonary disease, osteoporosis, preoperative antibiotics, type of disease, and operative type in the acute surgical site infection group were significantly different than those in the non-acute surgical site infection group (p < 0.05). Using binary logistic regression analyses, body mass index, smoking, diabetes mellitus, osteoporosis, preoperative antibiotics, fracture, operative type, operative time, blood loss, and drainage time were independent predictors of acute surgical site infection following lumbar surgery. CONCLUSIONS: In order to reduce the risk of infection following lumbar surgery, patients should be evaluated for the risk factors noted above.

Digoxin reduces atherosclerosis in apolipoprotein E-deficient mice.

BACKGROUND AND PURPOSE: Numerous in vitro studies have suggested that digoxin suppresses inflammation and alters lipid metabolism. However, the effect of dioxin on atherosclerosis is poorly understood. The present study was conducted to determine whether digoxin affects the development of atherosclerosis in a murine model of atherosclerotic disease. EXPERIMENTAL APPROACH: Apolipoprotein E-deficient mice maintained on a Western-type diet were administered PBS (control), low-dose digoxin (1 mg · kg(-1) · day(-1)) or high-dose digoxin (2 mg · kg(-1) · day(-1)) via i.p. injection for 12 weeks. KEY RESULTS: Digoxin dose-dependently reduced atherosclerotic lesion formation and plasma lipid levels (reductions of 41% in total cholesterol, 54% in triglycerides and 20% in low-density lipoprotein cholesterol in the high-dose digoxin-treated group). Moreover, treatment with digoxin markedly attenuated IL-17A expression and IL-17A-related inflammatory responses and increased the abundance of regulatory T cells (Tregs). CONCLUSIONS AND IMPLICATIONS: Our data demonstrate that digoxin acts as a specific antagonist of retinoid-related orphan receptor-γ to decrease atherosclerosis by suppressing lipid levels and IL-17A-related inflammatory responses.

Lanatoside C Promotes Foam Cell Formation and Atherosclerosis.

Lanatoside C's impact on atherosclerosis is poorly understood. The present study was conducted to determine whether lanatoside C affects the development of atherosclerosis in apolipoprotein E-deficient (ApoE(-/-)) mice. ApoE(-/-) mice were administered either phosphate-buffered saline (PBS) containing 0.1% DMSO (the vehicle control group) or lanatoside C at low (1 mg/kg per day) or high (2 mg/kg per day) doses, and fed a Western diet for 12 weeks. Lanatoside C dose-dependently aggravated the development of atherosclerosis in the ApoE(-/-) mice compared with the vehicle control group. In an effort to determine the mechanism by which lanatoside C increased atherosclerosis, we found that lanatoside C significantly promoted the uptake of oxidised low-density lipoprotein (oxLDL) and increased foam-cell formation by upregulation of scavenger receptor class A (SR-A) and the class B scavenger receptor (CD36) in macrophages. Meanwhile, the effects of lanatoside C were abolished using small interfering RNA (siRNA) inhibition of peroxisome proliferator-activated receptors ß/δ (PPARß/δ). Overall, our data demonstrate that lanatoside C aggravates the development of atherosclerosis by inducing PPARß/δ expression, which mediates upregulation of SR-A and CD36, and promotes oxLDL uptake and foam-cell formation.