Objective To reveal the distribution and effects of peripheral nerve axolemma ion channels in experimental allergic neuritis(EAN).Methods The alteration of Na+ and K+ channels on peripheral nerves(PNs) in the course of EAN was observed and the relationship between the channels and nerve conduction properties was analyzed by assessing histology and electrophysiology of PNs as well as clinical severity.Results Na+ and K+ channels obviously decreased on day 9 post immunization(p.i.),a time point of disease onset,and quickly became undetectable in next two weeks.Undergoing a slow and incomplete regeneration,neither of the channels regained the normal appearance on day 85 p.i.even if the clinical symptom disappeared several weeks before.Na+ and K+ channels had a synchronous development during disease course and remained a close correlation with the alteration of paranodal myelin.Electrophysiological abnormality kept consistent with the disturbance of PNs just in the acute period of EAN(9-23d p.i.) and the compound muscle action potential(CMAP) amplitude partly reflected the distribution of axolemma ion channels.Conclusion Loss of axolemma ion channels of PNs might be one of the reasons directly leading to the early symptoms of EAN.As a structural component,the channels were liable to damage and difficult to restore.The clustering and maintenance of the channels were closely related with the specialized paranodal myelin.

Objective To test the efficacy and safety of nicergoline in treatment of vascular dementia patients with mild or moderate cognitive impairment. Methods A multicenter,double blind,randomized,efficient drug controlled clinical trial was carried out All the subjects met the DSM-Ⅲ criteria for vascular dementia We used MMSE and WMS as main assessing items and ADL,CGI as secondary assessing items. Results 103 subjects were assessed MMSE were raised in both groups after the treatment and more obvious in nicergoline group than in anecetan group (1 62?2 33 and 2 88?2 85 respectively) WMS raised in nicergoline group (5 04?10 61),but not in anecetan group (1 98?9 49) ADL and CGI (SI) showed decreased scores in both groups Total efficiency of nicergoline was 80 0% and of anecetan was 56 6%. Conclusions Nicergoline was an effective drug in treatment of vascular dementia and more effective than anecetan Using nicergoline 60 mg per day was safe

Objective To investigate the pathological features of Lewy body disease. Methods An autopsy case of an 80 year old Chinese woman suffering from Lewy body disease was studied The patient had progressive dementia and myotonia for three years and was suspected with Alzheimer dementia clinically Brain tissue was analyzed neuropathologically by using HE staining and specific staining for nervous system, immunohistochemical staining for ubiquitin and by using ? synuclein and electronic microscopy. Results Neuropathological examination revealed the most characteristic features as follows: (1) The number of melanin pigmented neurons were markedly decreased in the substantia nigra and locus ceruleus, and some typical brain stem type Lewy bodies in the residual neurons with moderate gliosis were found (2) There appeared numerous cortical type Lewy bodies in deep layers of the cerebral cortex particularly in the cingulate gyrus, hippocampus, parahippocampal gyrus, transentorhinal contex, amygdala and insula (3) There were selective spongiform changes and many Lewy related neurites in positive ubiquitin immunohistochemical staining on the CA2/3 sectors, parahippocampal gyrus and transentorhinal cortex (4) A strong positive ? synuclein immunoreactivity was found in all Lewy bodies and Lewy related neurites (5) Alzheimer disease related changes such as senile plaques and neurofibrillary tangles were scarcely found only in hippocampus and parahippocampal gyrus. Conclusion Lewy body disease is a new group of degenerative disease of the central nervous system ? synuclein may play an important role in the degeneration of neurons and their neurites may be a major component of Lewy bodies in Lewy body disease It is considered that the present case should be a pure type of diffuse Lewy body disease

Objective To explore whether the 25 kD protein component was a specific decrease in skeletal muscles of the patients with myasthenia gravis (MG). Methods The muscular proteins were extracted from 21 cases of normal objects,18 cases of patients with myasthenia gravis and 20 cases of patients with other neuro-muscular disorders with Guba-Straub solution. The components of protein were analysed by SDS-PAGE in double blind. Components of glycoprotein were detected by using the ConA/HRP.Results SDS-PAGE patterns showed that the concentration of protein bands with mass of about 25 kD in the MG muscles was much lower than that of muscles in both normal and other neuro-musclular disorders. The value of density for 25 kD protein bands was 1.6?0.7 in the MG muscles,but was 3.4?1.5 and 3.7?1.5 in the muscles of normal and other neuro-musclular disorders,respectively. In addition,25 kD protein was found as a glycoprotein,but it was different from AChR in the molecular weight.Conclusion (1) It was suggested that the pathogeny or developing of MG could be associated with 25 kD protein of the skeletal muscle because of its specific decrease. (2) 25 kD protein was a glycoprotein which was unassociated with the AChR molecule.