The High-Frequency Ultrasound Detection of Rat Sciatic Nerve in a Crushed Injury Model.

OBJECTIVE: This study aimed to visualize sciatic nerve injury in rats using ultrasound imaging in a crushed injury model. METHODS: Adult male Sprague-Dawley rats were subjected to a left sciatic nerve crush operation. Then, high-frequency ultrasound was used to image both sciatic nerves at 2 days and at 1, 2, 3, 4, and 6 weeks after surgery. RESULTS: Normal uninjured nerves have uniform thickness, display a smooth epineurium and inner adventitia, and are oblong in transverse sections. After the crush operation, nerve thickness increased, the inner echo signal decreased, the image of the epineurium became obscured and coarse before becoming smooth again, and transverse sections of the nerve fibers changed from being semicircular to oval in shape before becoming elliptical again. These observations were consistent with pathological changes associated with nerve injury. CONCLUSIONS: High-frequency ultrasound is capable of capturing dynamic changes in rat sciatic nerves in a crushed injury model. This can be used as an auxiliary method of evaluation in traditional peripheral nerve injury experiments.

Histone deacetylase HDAC4 promotes the proliferation and invasion of glioma cells.

Glioma is the most lethal type of primary brain tumor characterized by aggressiveness and a poor prognosis. Histone deacetylase 4 (HDAC4) is frequently dysregulated in human malignancies. However, its biological functions in the development of glioma are not fully understood. The present study aimed to evaluate HDAC4 expression in human glioma and to elucidate the mechanistic role of HDAC4 in glioma. The results suggested that HDAC4 was significantly upregulated in glioma tissues and a number of glioma cell lines compared with adjacent non-tumor tissues and the non-cancerous human glial cell line SVG p12, respectively (P<0.05). The proliferation, adenosine triphosphate (ATP) levels and invasion ability were substantially enhanced in U251 cells with HDAC4 overexpression, and suppressed in U251 cells with a knockdown of HDAC4 compared with that in U251 cells transfected with the negative control. Knockdown of HDAC4 resulted in cell cycle arrest at the G0/G1 phase and induced the increase of reactive oxygen species level in U251 cells. Furthermore, HDAC4 overexpression was revealed to substantially inhibit the expression of cyclin-dependent kinase (CDK) inhibitors p21 and p27, and the expression of E-cadherin and ß­catenin in glioma U251 cells. Knockdown of HDAC4 substantially promoted the expression of CDK1 and CDK2 and vimentin in glioma U251 cells. Mechanistically, the results of the present study demonstrated that HDAC4 displayed a significant upregulation in glioma, and promoted glioma cell proliferation and invasion mediated through the repression of p21, p27, E-cadherin and ß­catenin, and the potentiation of CDK1, CDK2 and vimentin. Altogether, the present study revealed that HDAC4 overexpression was central for the tumorigenesis of glioma, which may serve as a useful prognostic biomarker and potential therapeutic target for glioma.