[Objective]To explore and analyze Professor GUO Weifeng's clinical experience in treating posterior circulation ischemic vertigo. [Methods] By learning with the teacher, collection of relevant information and medical records ,to expound Professor GUO Weifeng 's academic thoughts and clinical experience in posterior circulation ischemic vertigo, from aspects of etiology, pathogenesis, and syndrome differentiation and treatment variation, prescription medication, summarizing the characteristics of his prescriptions and ways of treatment as well as exemplifying them. [Results] Professor GUO Weifeng through many years of clinical practice proposes that the basic pathogenesis of this disease is liver with kidney deficiency and hyperactivity of liver-yang. Because of its more associated with obesity and high blood pressure, high blood lipids, diabetes, always mingle phlegm and stasis. The main treatment method is to nourish the Yin of liver-kidney, pacify liver and extinguish wind. Then, transform phlegm and disperse blood stasis. If pathogenic into collateral for a long time,we need using insect drug for treatment. Clinical treatment should be based on positive and evil of the partial ups and downs, the disease of both, flexible adjustment of medication, it is not limited by present method. [Conclusion] Professor GUO Weifeng 's clinical experience in treating posterior circulation ischemic vertigo is effective and worthy of wide application.

Objective:To investigate the effect of vagus nerve stimulation (VNS) on α7 nicotinic acetylcholine receptor (α7 nAChR) and inflammatory factor expressions and behavioristics in rats after traumatic brain injury (TBI).Methods:Seventy-two male Sprague-Dawley rats were randomly divided into sham-operated group, TBI group and VNS group ( n=24). The TBI models in the latter two groups were established by modified weight drop method; the dura mater in the sham-operated group was exposed without impingement. The VNS group received VNS treatment for 14 consecutive d (frequency: 30 Hz, pulse width: 100 μs, current: 0.8 mA, stimulation: 5 min, suspension: 5 min, repetition: 3 times). The neurological function was evaluated by Beam-Balance test and walking test 1, 3, 7, 14, 21, and 28 d after TBI; Morris Water Maze test was performed to observe the abilities of spatial learning and memory 24-28 d after TBI; the brain tissue sections were obtained for analyzing the volume of cerebral injury 28 d after TBI. Fourteen d after TBI, Nissel staining was used to observe the neuronal morphology and survival cell number of brain injured areas in each group, immunohistochemical staining was employed to detect the number of neuronalnuclear antigen (NeuN) positive neurons in the hippocampal dentate gyrus and CA3 area, and ELISA was used to detect the expressions of interleukin (IL)-1, IL-6, tumor necrosis factor (TNF)-α and nuclear factor (NF)-κB. Western blotting was used to detect the α7 nAChR protein expression levels 3, 7, 14 d after TBI. Results:As compared with the TBI group, the VNS group showed statistically longer beam-balance latency and shorter beam-walking time 7, 14, 21, and 28 d after TBI, significantly shortened escape latency and prolonged exploration time in the target quadrant 27 and 28 d after TBI ( P<0.05). The volume of cerebral injury in the VNS group was significantly smaller than that in TBI group 28 d after TBI ( P<0.05). As compared with those in the TBI group, the number of Nissel positive neurons around the brain injury area was significantly larger, the number of NeuN positive cells in the hippocampal dentate gyrus and CA3 areas was significantly larger, and the expression levels of IL-1β, IL-6, TNF-α and NF-κB were significantly decreased in the VNS group 14 d after TBI ( P<0.05). The α7 nAChR protein expression in the injury area of VNS group was significantly higher than that of the TBI group 7 and 14 d after TBI ( P<0.05). Conclusion:VNS treatment can improve the neurobehavioral outcome of TBI rats, which may be linked with the increased α7 nAChR protein expression, and the decreased release of inflammation cytokines IL-1β, IL-6, TNF-α and NF-κB.