RESUMO
Acellular nerve allografts conducted via chemical extraction have achieved satisfactory results in bridging whole facial nerve defects clinically, both in terms of branching a single trunk and in connecting multiple branches of an extratemporal segment. However, in the clinical treatment of facial nerve defects, allogeneic donors are limited. In this experiment, we exposed the left trunk and multiple branches of the extratemporal segment in six rhesus monkeys and dissected a gap of 25 mm to construct a monkey model of a whole left nerve defect. Six monkeys were randomly assigned to an autograft group or a xenogeneic acellular nerve graft group. In the autograft group, the 25-mm whole facial nerve defect was immediately bridged using an autogenous ipsilateral great auricular nerve, and in the xenogeneic acellular nerve graft group, this was done using a xenogeneic acellular nerve graft with trunk-branches. Examinations of facial symmetry, nerve-muscle electrophysiology, retrograde transport of labeled neuronal tracers, and morphology of the regenerated nerve and target muscle at 8 months postoperatively showed that the faces of the monkey appeared to be symmetrical in the static state and slightly asymmetrical during facial movement, and that they could actively close their eyelids completely. The degree of recovery from facial paralysis reached House-Brackmann grade II in both groups. Compound muscle action potentials were recorded and orbicularis oris muscles responded to electro-stimuli on the surgical side in each monkey. FluoroGold-labeled neurons could be detected in the facial nuclei on the injured side. Immunohistochemical staining showed abundant neurofilament-200-positive axons and soluble protein-100-positive Schwann cells in the regenerated nerves. A large number of mid-graft myelinated axons were observed via methylene blue staining and a transmission electron microscope. Taken together, our data indicate that xenogeneic acellular nerve grafts from minipigs are safe and effective for repairing whole facial nerve defects in rhesus monkeys, with an effect similar to that of autologous nerve transplantation. Thus, a xenogeneic acellular nerve graft may be a suitable choice for bridging a whole facial nerve defect if no other method is available. The study was approved by the Laboratory Animal Management Committee and the Ethics Review Committee of the Affiliated Wuxi No. 2 People's Hospital of Nanjing Medical University, China (approval No. 2018-D-1) on March 15, 2018.
RESUMO
OBJECTIVE: To investigate the effects of diabetes mellitus on amplitude of distortion product otoacoustic emissions ( DPOAE) and whether streptozotocin has ototoxicity or not. METHODS: Twenty-four SD rats were divided into diabetes mellitus group, insulin therapy group and control group. Diabetes was induced by streptozotocin. The blood glucose of insulin group was controlled by insulin. The amplitude of DPOAE was tested before streptozotocin injection and 3 months, 5 months after injection, respectively. RESULTS: The amplitude of DPOAE in diabetes rats was decreased in 3 months and there was statistical significance (P <0. 05) in 1038, 4126 and 5200 Hz, while obviously reduced in 5 months in all frequencies and there was also statistical significance (P <0. 01). The amplitude of DPOAE in all frequencies lacked of any significance between insulin therapy group and control group. CONCLUSIONS: Diabetes mellitus could induce the amplitude of DPOAE decreasing. Streptozotocin had not evident toxicity for inner ear.
