Melatonin attenuates intervertebral disc degeneration by restoring mitochondrial homeostasis through PGC-1α signaling pathway.

Intervertebral disc degeneration (IVDD) is a major cause of low back pain (LBP) and poses a substantial economic burden worldwide. Mitochondrial dysfunction, associated with oxidative stress and apoptosis, is linked to various degenerative diseases. Melatonin has emerged as a potential therapeutic agent for preventing IVDD because of its capacity to regulate cellular rhythms.

Development of a Novel Inflammatory-Associated Gene Signature and Immune Infiltration Patterns in Intervertebral Disc Degeneration.

Background: Both inflammatory factors and immune response play important roles in the pathogenesis of intervertebral disc degeneration (IDD). However, a comprehensive analysis of interaction between inflammatory response-associated genes (IRGs) and immune microenvironment in patients with IDD remains lacking. Hence, the current research is aimed at investigating the correlations between IRG signatures and immune cells in the progression of IDD.

VDR promotes nucleus pulposus cell mitophagy as a protective mechanism against oxidative stress injury.

Intervertebral disk degeneration (IDD) is a common aging disease. Excessive apoptosis of nucleus pulposus (NP) cells has been widely considered a main contributor to IDD. Emerging science has shown that autophagy plays a protective role against apoptosis under oxidative stress.

The efficacy of bipolar sealer on blood loss in spine surgery: a meta-analysis.

Objective: The purpose of this meta-analysis of randomized controlled trials (RCTs) and non-RCTs was to gather data to evaluate the efficacy and safety of bipolar sealer versus standard electrocautery in the management of spinal disease.

Methods: The electronic databases including Embase, PubMed and Cochrane library were searched to identify relevant studies published from the time of the establishment of these databases up to January 2017. The primary outcomes were total blood loss, requirement of transfusion (rate and amount), and operation time.

High-mobility group box-B1 (HMGB1) mediates the hypoxia-induced mesenchymal transition of osteoblast cells via activating ERK/JNK signaling.

High-mobility group box 1 (HMGB1) is a nuclear protein that involves the binding with DNA and influences chromatin regulation and transcription. HMGB1 activates monocytes and neutrophils, which are involved in inflammation during wounding. In this study, we investigated the promotion of HMGB1 under hypoxia and determined the regulatory role of HMGB1 on the fibrosis of mouse osteoblast-like MC3T3-E1 cells or of human osteoblast MG-63 cells.

EGCG ameliorates the hypoxia-induced apoptosis and osteogenic differentiation reduction of mesenchymal stem cells via upregulating miR-210.

The healing process of fractured bone is affected by the multiple factors regulating the growth and differentiation of osteoblasts and bone mesenchymal stem cells (MSCs), however, such markers and molecular events need to be orchestrated in details. This study investigated the effect of polyphenol(-)-epigallocatechin-3-gallate (EGCG) on the hypoxia-induced apoptosis and osteogenic differentiation of human bone marrow-derived MSCs, examined the miR-210 induction by EGCG, explored the target inhibition of the expression of receptor tyrosine kinase ligand ephrin-A3 (EFNA3) by miR-210, and then determined the association of the miR-210 promotion with the hypoxia-induced apoptosis and osteogenic differentiation. Results demonstrated that EGCG treatment significantly inhibited the hypoxia-induced apoptosis in MSCs and promoted the level of alkaline phosphatase (ALP), bone morphogenetic protein 2 (BMP-2), propeptide of type I procollagen I (PINP) and runt-related transcription factor 2 (RUNX2) in MSCs under either normoxia or hypoxia.

Spontaneous spinal epidural haematoma.

Spontaneous spinal epidural haematoma (SSEH) is a rare clinical condition with unknown aetiology. Prompt diagnosis and treatment are paramount because of the risk of permanent neurological deficits without appropriate intervention. We described a case of a 48-year-old man presenting with complete quadriplegia and hypoesthesia.