This study demonstrates that genetic variants in the promoter regions of the IL-6 and IL-10 genes are associated with lumbar disc herniation risk in this Northern Chinese Han population.

Rationale: Vocal fold paralysis and cauda equina syndrome are very rare neurologic deficits. This report describes the case of a patient who simultaneously developed both after uneventful spinal-epidural anesthesia with 0.5% hyperbaric bupivacaine. Patient concerns: We report the case of a 45-year-old female, who underwent surgery for bilateral hallux valgus developed cauda equina syndrome and unilateral vocal fold paralysis after uneventful spinal-epidural anesthesia was administered. There was no pain or paresthesia during needle placement or drug injection. Surgery was performed uneventfully. Diagnoses: Right vocal fold paralysis was diagnosed with flexible laryngoscopy. Interventions: Patient was started on the treatment with a surgery for bilateral hallux valgus, who developed cauda equina syndrome and unilateral vocal fold paralysis after uneventful spinal-epidural anesthesia was administered. Outcomes: Postoperatively, she had difficulty in urination and defecation. In addition, she developed unilateral vocal fold paralysis characterized by hoarseness, effortful voice production, and choking with liquids. Magnetic resonance imaging performed on the lumbosacral area and computed tomography of the neck, the chest, and the skull revealed entirely normal results. However, flexible laryngoscopy revealed a right vocal fold paralysis. Although cauda equina syndrome can occur due to neurotoxicity of local anesthetics, the exact etiology of vocal fold paralysis is uncertain. Lessons: The case highlights that 2 rare and serious complications of spinal-epidural anesthesia can even occur in the same patient after uneventful surgery and block performance.

Osteosarcoma (OS) is the most common type of malignant bone tumor in adults and children. Despite the great strides in biology and medicine, the survival rate of patients with metastatic disease remains very poor. This rate has been staggering with recurrence and metastasis. In the present study, we proposed Wnt/β-catenin pathway as a key biological target for the effective treatment in OS. Wnt signaling has been reported to play important roles in osteoblastogenesis. We hypothesized that docetaxel (DTX) will effectively arrest the osteosarcoma progression by suppressing the Wnt/β-catenin pathway in OS cells. Our results show that DTX significantly inhibited the cell proliferation of U2OS and SaOS-2 cancer cells in a time-dependent and dose-dependent manner. DTX inhibited the intrinsic transcriptional activity of β-catenin/Tcf in U2OS cancer cells and SaOS-2 cancer cells. GSK-3βinhibitor (SB216763) treatment remarkably increased the β-catenin/Tcf transcriptional activities. The transcriptional activities have been increased by around ~200% due to the decrease in the degradation of β-catenin mediated through GSK-3β. Summarizing, present study clearly showed that DTX inhibited Wnt/β-catenin signalling pathways and significantly reduced the matrix metallopeptodase 9 (MMP-9) protein expressions and its activity. Taken together, our findings provide novel insight on the effect of anticancer small molecules to improve the outcomes in osteosarcoma.

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