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Background Spinal cord injury (SCI) is a severe central nervous system trauma. The present study aimed to evaluate the effect of HIF-1α on inflammation in spinal cord injury (SCI) to uncover the molecular mechanisms of anti-inflammation. Results HIF-1α was reduced in SCI model rats and HIF-1α activation reduced TNF-α, IL-1β, IL-6 and IL-18 levels in SCI model rats. Meanwhile, Circ 0001723 expression was down-regulated and miR-380-3p expression was up-regulated in SCI model rats. In vitro model, down-regulation of Circ 0001723 promoted TNF-α, IL-1β, IL-6 and IL-18 levels, compared with control negative group. However, over-expression of Circ 0001723 reduced TNF-α, IL-1β, IL-6 and IL-18 levels in vitro model. Down-regulation of Circ 0001723 suppressed HIF-1α protein expressions and induced NLRP3 and Caspase-1 protein expressions in vitro model by up-regulation of miR-380-3p. Next, inactivation of HIF-1α reduced the pro-inflammation effects of Circ 0001723 in vitro model. Then, si-NLRP3 also inhibited the pro-inflammation effects of Circ 0001723 in vitro model via promotion of autophagy. Conclusions We concluded that HIF-1α reduced inflammation in spinal cord injury via miR-380-3p/ NLRP3 by Circ 0001723.

Methylprednisolone exhibits anti-inflammatory antioxidant properties, and rosiglitazone acts as an anti-inflammatory and antioxidant by activating peroxisome proliferator-activated receptor-γ in the spinal cord. Methylprednisolone and rosiglitazone have been clinically used during the early stages of secondary spinal cord injury. Because of the complexity and diversity of the inflammatory process after spinal cord injury, a single drug cannot completely inhibit inflammation. Therefore, we assumed that a combination of methylprednisolone and rosiglitazone might promote recovery of neurological function after secondary spinal cord injury. In this study, rats were intraperitoneally injected with methylprednisolone (30 mg/kg) and rosiglitazone (2 mg/kg) at 1 hour after injury, and methylprednisolone (15 mg/kg) at 24 and 48 hours after injury. Rosiglitazone was then administered once every 12 hours for 7 consecutive days. Our results demonstrated that a combined treatment with methylprednisolone and rosiglitazone had a more pronounced effect on attenuation of inflammation and cell apoptosis, as well as increased functional recovery, compared with either single treatment alone, indicating that a combination better promoted recovery of neurological function after injury.

To investigate the role of miR-372/Beclin-1 on nerve cell apoptosis induced by spinal cord ischemia/reperfusion injury (SCII). We established in vivo and in vitro SCII model. MiR-372 and Beclin-1 expressions in spinal cord tissues of SCII rats and SCII nerve cells were measured. The cell apoptosis was detected by flow cytometry. MiR-372 inhibitor was used to reduce miR-372 expression. Dual luciferase reporter assay was used to confirm the interaction between miR-372 and Beclin-1. MiR-372 expression in spinal cord tissues of SCII rats and SCII nerve cells was increased, while Beclin-1 expression was decreased. Knockdown of miR-372 could inhibit SCII nerve cell apoptosis. In addition, MiR-372 could negatively regulate Beclin-1 expression. Autophagy inhibitor could inhibit autophagy to promote the apoptosis of SCII nerve cells through decreasing Beclin-1, while interference of miR-372 changed the effect of autophagy inhibitor. Interference of miR-372 could reduce nerve cell apoptosis in SCII via increasing autophagy by up-regulating Beclin-1.

Rationale Spontaneous spinal subdural hematoma (SSDH) without an underlying pathology is a very rare condition. The treatment protocol for SSDH is early diagnosis and treatment before irreversible damage to neural tissue. However, there is no agreement on the etiopathogenesis, as well as the need for surgery to treat spontaneous SSDH. Here, we report a rare case of spontaneous SSDH with progressive deterioration and symptoms of cauda equina syndrome after ineffective conservative treatment. Patient's concern A 38-year-old male patient presented with sudden lower back and bilateral leg pain. Diagnosis A magnetic resonance imaging (MRI) scan on the third day after the onset of symptoms revealed a subdural hematoma from L1 to S1, presenting as hyperintensities on T1 weighted sequences and hypointensities to isointensities on T2 weighted sequences. Intervention Laminectomy and subdural evacuation were performed immediately. Outcomes An abnormal ligamentum flavum was observed intraoperatively. A histological examination revealed extravasation of blood in the degenerated ligamentum flavum. Postoperatively, the lower limb pain improved immediately. At the 6-month follow-up, the pain and numbness of the lower limb disappeared, and the muscle strength of both legs recovered completely with normal gait. Lessons Spontaneous SSDH with ligamentum flavum hematoma was caused by a sudden increase of intravenous pressure, resulting from a marked surge in the intra-abdominal or intrathoracic pressure. Consecutive MRI scans provided valuable information, leading to a diagnosis of spontaneous SSDH. The treatment protocol for spontaneous SSDH should be determined based on the location and stage of the hematoma, as well as the subject's neurological status.

Recipients of solid organ transplantation are, because of immunosuppressive therapy, disposed to opportunistic infections including tuberculosis (TB). Spinal TB is a rare complication after transplantation but it is serious with high mortality. We report 3 cases of spinal TB in Chinese recipients of orthotopic liver transplant whose first complaint was back pain. These 3 cases were diagnosed by magnetic resonance imaging and percutaneous biopsy. After treatment with isoniazid, rifampicin, streptomycin, and ethambutol for >1 year, symptoms of 2 patients improved noticeably, but 1 patient died of liver failure and severe mixed pulmonary infection. Diagnosis and treatment regimens of spinal TB are discussed.

Kyphoplasty has been shown to provide symptomatic relief of vertebral compression fractures refractory to medical therapy. However, few reports have focused on refracture of cemented vertebrae after kyphoplasty. The presence of cemented vertebrae refracture concurrent with cement fragmentation is an extremely rare condition. We reported an 86-year-old man with a T12 osteoporotic compression fracture undergoing the kyphoplasty treatment. The patient postoperatively continued to have back pain at the same level. The solid lumped polymethylmethacrylate (PMMA) mass and inadequate use and insufficient filling of PMMA cement were observed in postoperative radiographs and magnetic resonance image (MRI) examination. He refused to receive the surgical intervention, but had not strict compliance with oral anti-osteoporotic medications. Ten months postoperatively, refracture of osteoporotic vertebral body concurrent with cement fragmentation occurred at the previously kyphoplasty-treated vertebral level. Bone mineral analysis showed severe osteoporosis with a T-score of -4.0. The patient finally obtained therapeutic benefit of pain relief and bony union of T12 vertebral body by consistently adhering to anti-osteoporotic medication treatment. This case illustrated that patients who underwent kyphoplasty to treat osteoporotic vertebral compression fractures with intravertebral fracture should be strictly followed up and supervised in their anti-osteoporotic medication treatment. The interdigitation injection pattern of PMMA and sufficient PMMA filling with trabeculae in the kyphoplasty procedure also might prevent refracture of the cemented vertebrae concurrent with PMMA fragmentation.

Brachial plexus injuries are generally rare and a double-superior-trunk injury of the brachial plexus has never been reported before. We report the first case of a brachial plexus injury in a 43-year-old Chinese male with a double superior trunk. This was observed incidentally during an operation 1 month after initial traction injury sustained in a car accident. The double superior trunk of the brachial plexus was formed by the double roots of C5 and C6, respectively. Six months after discharge, the patient reported the recovery of most of the function of his left arm except the muscles innervated by the radial nerve. Two years after discharge, he reported almost full functional recovery of his left arm. We discuss what is known about anatomical variations of the brachial plexus, and the possible association between this novel brachial plexus anatomy and the almost complete functional recovery of the arm.