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We reported a rare characteristic anomaly of the laminae of the axis with hypoplasia of the posterior arch of atlas. A multiplane reconstruction of the computed tomography images was very necessary for treatment of this case. Possible causes of this anomaly may be the failure of ossification or fusion of the embryological term, whereas invagination of the osteophyte may be associated with the traction of the dense fibrous band during growth and development. Surgical removal of the laminae could result in a satisfactory outcome.

Vertebral osteomyelitis caused by Aspergillus nidulans is rare and usually affects immunocompromised patients. This report presents a case of thoracic vertebral osteomyelitis with epidural abscesses due to A. nidulans in a 40-year-old immunocompetent female who presented with back pain, numbness and weakness of both lower limbs. Magnetic resonance imaging demonstrated osteomyelitis involving the thoracic (T)1-T3 vertebral bodies with epidural abscesses, resulting in spinal compression. The patient underwent a decompression laminectomy of T1-T3 and debridement of the thoracic epidural inflammatory granuloma. Histopathology revealed fungal granulomatous inflammation. The patient received 6 mg/kg voriconazole every 12 h (loading dose on day 1) followed by 4 mg/kg voriconazole twice daily for 1 month, administered intravenously. The patient returned with recurrent back pain 16 months after initial presentation. A. nidulans was identified by fungal culture and polymerase chain reaction. The patient showed no evidence of recurrence 1 year after a 6-month course of oral voriconazole. The key to the effective treatment of Aspergillus osteomyelitis is not to excise the abscess, but to administer systemic antifungal drug therapy.

Background: Glioblastoma has been seen as the most common malignancy of brain tumor. Emerging reports has claimed that SNHG29 (LRRC75A-AS1) was involved in several biological processes via modulation of signaling pathway, and served as an malignant facilitatorin osteosarcoma. However, the specific role of SNHG29 in glioblastoma remains unknown. Methods: RT-qPCR and microarray were operated to measure genes expression. Western blot was performed to examine protein expression. CCK-8 and colony formation assays were used to evaluate cell proliferation. Cell migration was tested by transwell assay. Nuclear-cytoplasmic fractionation was conducted to locate SNHG29. The binding capacity of miR-223-3p to SNHG29 or CTNND1 3′UTR was verified by RIP and luciferase reporter assay. Results: SNHG29 presented high expression in glioblastoma to boost cell proliferation, migration and EMT process. In addition, miR-223-3p was validated to bind with SNHG29 after prediction and screening. Furthermore, miR-223-3p was proved to be a negative regulator for its target CTNND1. Then, the inhibition on cell proliferation, migration and EMT process resulted from SNHG29 knockdown was recovered by CTNND1 overexpression. At last, the inhibitive impacts on cell proliferation, migration and EMT process of CTNND1 deficiency was abrogated by LiCl. Conclusions: In conclusion, SNHG29 regulates miR-223-3p/CTNND1 axis to promote glioblastoma progression via Wnt/β-catenin signaling pathway, offering a potential therapeutic point for glioblastoma patients.

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BackgroundLatest studies show that low-energy extracorporeal shock wave therapy (ESWT) can upregulate levels of vascular endothelial growth factor (VEGF). VEGF can ease nervous tissue harm after spinal cord injury (SCI). This study aims to explore whether low-energy ESWT can promote expression of VEGF, protect nervous tissue after SCI, and improve motor function.MethodsNinety adult female rats were divided into the following groups: Group A (simple laminectomy), Group B (laminectomy and low-energy ESWT), Group C (spinal cord injury), and Group D (spinal cord injury and low-energy ESWT). Impinger was used to cause thoracic spinal cord injury. Low-energy ESWT was applied as treatment after injury three times a week, for 3 weeks. After SCI, the Basso, Beattie, and Bresnahan (BBB) scale was used to evaluate motor function over a period of 42 days at different time points. Hematoxylin and eosin (HE) staining was used to evaluate nerve tissue injury. Neuronal nuclear antigen (NeuN) staining was also used to evaluate loss of neurons. Polymerase chain reaction was used to detect messenger RNA (mRNA) expression of VEGF and its receptor fms-like tyrosine kinase 1 (Flt-1). Immunostaining was used to evaluate VEGF protein expression level in myeloid tissue.ResultsBBB scores of Groups A and B showed no significant result related to dyskinesia. HE and NeuN staining indicated that only using low-energy ESWT could not cause damage of nervous tissue in Group B. Recovery of motor function at 7, 35, and 42 days after SCI in Group D was better than that in Group C (P<0.05). Compared with Group C, number of NeuN-positive cells at 42 days after SCI increased significantly (P<0.05). The mRNA levels of VEGF and Flt-1 and VEGF expression at 7 days after SCI in Group D were significantly higher than those in Group C (P<0.05).ConclusionLow-energy ESWT promotes expression of VEGF, decreases secondary damage of nerve tissue, and improves recovery of motor function. It can be regarded as one mode of clinical routine adjunctive therapy for spinal injury.