Revisiting the immune landscape post spinal cord injury: More than black and white.

Spinal cord injury (SCI) induced catastrophic neurological disability is currently incurable, especially in elderly patients. Due to the limited axon regeneration capacity and hostile microenvironment in the lesion site, essential neural network reconstruction remains challenging. Owing to the blood-spinal cord barrier (BSCB) created immune cells and cytokines isolation, the immune elements were incorrectly recognized as innocent bystanders during the SCI pathological process traditionally.

Is Tranexamic Acid Beneficial in Open Spine Surgery? and its Effects Vary by Dosage, Age, Sites, and Locations: A Meta-Analysis of Randomized Controlled Trials.

Background: The role of tranexamic acid (TXA) in controlling blood loss during spine surgery remains unclear. With the publication of new randomized controlled trials (RCTs), we conducted a meta-analysis to determine the safety and efficacy of TXA in spine surgery.

Methods: PubMed, Embase, Web of Science, and Cochrane databases were searched for relevant studies through 2022.

Predictive risk factors for recollapse of cemented vertebrae after percutaneous vertebroplasty: A meta-analysis.

Background: As one of the most common complications of osteoporosis, osteoporotic vertebral compression fracture (OVCF) increases the risk of disability and mortality in elderly patients. Percutaneous vertebroplasty (PVP) is considered to be an effective, safe, and minimally invasive treatment for OVCFs. The recollapse of cemented vertebrae is one of the serious complications of PVP.

Morphologic analysis of Chinese lumbar endplate by three-dimensional computed tomography reconstructions for helping design lumbar disc prosthesis.

Lumbar disc prostheses have been used increasingly in recent years. The successful design of lumbar disc prostheses depends on accurate morphometric parameters. However, the morphologic dimensions of lumbar endplate area have not been investigated in Chinese population.

Unlocking the Recovery Potential: JMJD3 Inhibition-Mediated SAPK/JNK Signaling Inactivation Supports Endogenous Oligodendrocyte-Lineage Commitment Post Mammalian Spinal Cord Injury.

Spinal cord injury (SCI) induced catastrophic neurological disability is often incurable at present. The injury triggered immediately oligodendrocytes loss and overwhelming demyelination are regarded as an insurmountable barrier to SCI recovery. To date, effective strategy to promote the endogenous oligodendrocytes replacement post SCI remains elusive.

Decoding epigenetic codes: new frontiers in exploring recovery from spinal cord injury.

Spinal cord injury that results in severe neurological disability is often incurable. The poor clinical outcome of spinal cord injury is mainly caused by the failure to reconstruct the injured neural circuits. Several intrinsic and extrinsic determinants contribute to this inability to reconnect.

Catastrophic thoracolumbar spinal massive hematoma triggered by intraspinal anesthesia puncture: A CARE-compliant case report.

Rationale: Intraspinal anesthesia, the most common anesthesia type of orthopedic operation, is regarded as safe and simple. Despite of the rare incidence, puncture related complication of intraspinal anesthesia is catastrophic for spinal cord. Here we present an intradural hematoma case triggered by improper anesthesia puncture.

Thoracolumbar traumatic nucleus pulposus sequestration combined with a slight flexion distraction fracture: A rare case report and literature review.

Rationale: Traumatic nucleus pulposus sequestration (TNPS) usually occurs concurrently with severe destruction of bone. TNPS combined with a slight thoracolumbar flexion- distraction fracture, triggering a disastrous nerve injury, has rarely been reported. Due to the atypical radiologic manifestations, such a patient can easily be overlooked.

MSC-derived cytokines repair radiation-induced intra-villi microvascular injury.

Microvascular injury initiates the pathogenesis of radiation enteropathy. As previously demonstrated, the secretome from mesenchymal stem cells contains various angiogenic cytokines that exhibited therapeutic potential for ischemic lesions. As such, the present study aimed to investigate whether cytokines derived from mesenchymal stem cells can repair endothelial injuries from irradiated intestine.

Minocycline Attenuates Kidney Injury in a Rat Model of Streptozotocin-Induced Diabetic Nephropathy.

The effects of minocycline on the development of diabetic nephropathy (DN) in streptozotocin (STZ) induced diabetic rats were evaluated in this study. The diabetes rats with DN were induced by STZ (55 mg/kg) injection. The experiment included 5 groups 1) normal, 2) normal plus minocycline for 16 weeks, 3) DN plus vehicle, 4) DN plus minocycline 16 weeks and 5) DN plus minocycline for 8 weeks.

In vivo electroporation of adult mouse sensory neurons for studying peripheral axon regeneration.

Electroporation has been a widely used tool to introduce DNA plasmids or RNA oligos into cultured cells and recently in vivo into chick or mouse embryos. Here we report a rapid and efficient approach to transfect adult mouse dorsal root ganglion neurons in vivo with precise spatiotemporal control via electroporation. This approach will allow both gain- and loss-of-function experiments in vivo to study the function of adult sensory neurons, such as sensory axon regeneration.

Low back pain tied to spinal endometriosis.

Study Design: Case report.

Objective: We present a case of endometriosis of lumbar vertebrae. The literatures are reviewed with endometriosis of spine.

Akt-independent GSK3 inactivation downstream of PI3K signaling regulates mammalian axon regeneration.

Inactivation of glycogen synthase kinase 3 (GSK3) has been shown to mediate axon growth during development and regeneration. Phosphorylation of GSK3 by the kinase Akt is well known to be the major mechanism by which GSK3 is inactivated. However, whether such regulatory mechanism of GSK3 inactivation is used in neurons to control axon growth has not been directly studied.

Signaling pathways that regulate axon regeneration.

Neurons in the mammalian central nervous system (CNS) cannot regenerate axons after injury. in contrast, neurons in the mammalian peripheral nervous system and in some non-mammalian models, such as C. elegans and Drosophila, are able to regrow axons.

MicroRNA-138 and SIRT1 form a mutual negative feedback loop to regulate mammalian axon regeneration.

Regulated gene expression determines the intrinsic ability of neurons to extend axons, and loss of such ability is the major reason for the failed axon regeneration in the mature mammalian CNS. MicroRNAs and histone modifications are key epigenetic regulators of gene expression, but their roles in mammalian axon regeneration are not well explored. Here we report microRNA-138 (miR-138) as a novel suppressor of axon regeneration and show that SIRT1, the NAD-dependent histone deacetylase, is the functional target of miR-138.