Objective: To develop the norms of Chinese Words and Vocabulary Discerning Test (CWVDT). Methods: According to the principle of stratified proportional sampling,a total of 1605 adult subjects from 17 cities and their surrounding rural areas of China was measured by CWVDT. Results: ①There was significant difference in two dimensions scores and total score of CWVDT between city and countryside(P0.05). Conclusion: The nationwide norms of city and countryside with educated degrees on CWVDT have been developed and with a good representation.

Objective To investigate Guillain Barre syndrome (GBS) combined with demyelinating neuropathy in central nervous system(CNS), and explore the possible mechanism and the relationship between the two.Methods 3 cases GBS combined with demyelinating neuropathy in CNS were observed clinically and the datum of laboratory were analysed.Results Case 1, a 28 year old man had symptoms of general flaccid paralysis and coma.The result of blood gas analysis was normal. CSF showed an albuminocytological dissociation, delayed nerve conduction velocity and missed F waves. Brain MRI showed multifocal T 2 Wight Image high signs in white matter of bilateral brain and cervical spinal cord. The patient is getting recovery by treatment with plasma and immunoglobulin. Case 2 , a 5 year old girl with progressive weakness of her limbs and respiratory arrest, appeared confusion,dully light reflex and absent corneal reflex, at last she died because of rejecting treatment.Case 3,a 12 year old boy with progressive weakness of his limbs and the difficult of relieving the bowels.Brain MRI was normal.Spinal MRI showed multifocal T 2 weight imagine hight signs from T 5 to L 4.CSF showed an albuminocytological dissociation.EMG showed a delayed nerve conduction velocity.Conclusion GBS combined with disorders of consciousness are mostly severe, the pathological mechanism is unclear. It is suggested that auto immunoreaction caused by P 1 myelin basic protein can relate to around and CNS demyelination.

Objective To study the risk of recurrence after a first unprovoked seizure and analyze the potential predictors of recurrence. Methods 150 patients with one or more recently unprovoked seizures who attended our hospital from October, 1998 to June, 2000, which included 66 patients having a first unprovoked seizure, were followed up for 2 years. Recurrence rate was estimated by Kaplan-Meier curves. Univariate and multivariate analyses of the potential predictors of recurrence were performed for the first unprovoked seizure patients using the Cox proportional hazards model.Results All the 150 patients had 109 relapses in 2 years, Kaplan-Meier estimate of recurrence rate was 73%(?3.6%), while 66 first unprovoked seizure patients had 36 relapses, with the recurrence rate 54%(?6.1%). Cox Univariate and multivariate analyses showed that symptomatic etiology increased the risk of recurrence, and other predictors of recurrence included abnormal electroencephalogram, the occurrence of seizures during sleep and first seizure lasting longer than 10 minutes, whereas an age of 3 to 12 years decreased this risk.Conclusion The recurrence risk after the first unprovoked seizure is lower than those who have two or more recent seizures. Several factors enable us to predict the recurrence risk after a first unprovoked seizure.

Objective To observe the morphology of neuronal necrosis by kainic acid(KA) induced status epilepsy (SE) in rats, and to study the brain protective effect of Mg 2+.Methods 75 adult male Wistar rats were randomly divided into KA group, Mg 2+ group and normal saline group. SE was induced with KA for 3 hours, and the rats in Mg 2+ group were intraperitoneal injected magnesium sulfate before being injected KA. 72 hours later the rats were killed. We had all rat brain sections and observe the morphology of neuronal necrosis with microscope and electron microscope.Results In KA group, seizure was induced 16.1?4.7 min after injection of KA, but seizure delayed to 25.4?6.2 min in Mg 2+ group. There was a significant difference between two groups (P

Objective To observe the characteristics and onset time of seizures caused by kindling of bilateral amygdale, and to discuss its mechanism.Methods 40 adult Wistar rats were randomly assigned into bilateral amygdala kindling group and unilateral amygdala kindling group. The models were made according to Goddard's method. Results All the rats in bilateral amygdala kindling group developed stage Ⅴ convulsions after a mean of 20.9 stimulations.12 rats of which showed spontaneous seizure discharges. But in unilateral amygdala kindling group, the successful kindling rate was 60% after a mean of 8.9 stimulations. Comparing with unilateral kindling, bilateral amygdala kindling significantly increased the successful rate of kindling (P

OBJECTIVE: Epileptic attack can cause neuronal damage and increase the risk of potential seizure. Analysis of the possible mechanism of neuronal damage following epileptic seizure may provide evidences for implementing preventive measures against brain damage due to epileptic seizures.DATA SOURCES: A computer-based search of the related publications in PubMed database between June 1995 and June 2004 with different combinations of the key words of "epilepsy", "neuron damage", "necrosis"and "apoptosis", limiting the results to the language of English.STUDY SELECTION: The retrieved articles were examined at first to select reports of experimental study on human and animals related to epilepsy and the subsequent neuronal damages, and their full-text publications were obtained with the other unrelated articles excluded.DATA EXTRACTION: Eighteen articles documenting randomized controlled experiment immediately related to neuronal damage after epilepsy seizure, 4 reporting non-randomized controlled experiments related to central neuronal excitatory toxic damage, and 3 concerning neuronal damage were collected for this review.DATA SYNTHESIS: In the 14 randomized controlled experiments, chemical or electric methods were used to induce epilepsy in the animal models in which the ultrastructural changes of the neurons and cell organelles were observed and the expression of apoptosis-related factors determined.In the 4 non-randomized controlled experiments, central neuronal ischemic and hypoxic models were adopted for observing the expression of various apoptotic factors in the neurons due to different damages with the assistance of electron microscope, to provide direct evidences for the mechanism of central neuronal excitatory toxic damage. The other three related literatures introduced the pathways of neuronal damages and the expression of the related factors.CONCLUSION: Neuronal death after epileptic seizure is correlated with the severity of the damage and mitochondrial functional status, and the mitochondria constitute the control center for neuronal survival. The release of cytochrome C and the activation of caspases are the final common pathway of neuronal damage.

Epilepsy is one of the most common diseases of the central nervous system, affecting tens of millions of people around the world. Most of clinically used antiepileptic drugs are based on ion mechanism to antagonize epileptic seizures, targeted to various ion channels or ion channel receptors. However, with the in-depth research on the pathogenesis of epilepsy, the non-ionic antiepileptic mechanism has increasingly become the key to the control of various intractable epilepsy, and the relevant drugs have gradually achieved clinical transformation. In this paper, non-ionic antiepileptic mechanisms are classified to clinical and preclinical types according to whether clinical transformation has been achieved. The application of non-ionic antiepileptic drugs in refractory epilepsy was mainly introduced, including everolimus, cannabidiol, fenfluramine, padsevonil, medium chain triglyceride modified ketogenic diet, and anakinra. Additionally, some preclinical non-ionic antiepileptic mechanisms such as prostaglandin, adenosine, metabolic glutamate receptor and mitochondrial mechanism are briefly introduced. The authors believe that the current stage of ionic antiepileptic drugs research has reached the bottleneck of transformation and it is difficult to achieve a major breakthrough in the mechanism, but there are broader research prospects in non-ionic antiepileptic mechanisms because a large number of them have not yet been clinically transformed. From a deeper perspective, some non-ionic antiepileptic mechanisms may have been involved in the fundamental mechanism of epileptogenesis, and they may be the prospect for the future treatment of refractory epilepsy.

Objective To explore the effects of different doses of 5,2′,4′-trihydroxy-6,7,5′-trimethoxyflavone nanoparticles (TTF1-NP)on the apoptosis of human hepatoma cells and human normal hepatocytes,and to explore their mechanisms through endoplasmic reticulum stress (ERS)-meditated apoptosis pathway. Methods The human hepatoma cell lines (HepG2,Hep3B and PLC/PRF/5)and human hepatocytes (Chang Liver)were used as cell model, and divided into vehicle, 5-Fu and TTF1-NP treated groups with the concentrations of 50, 100 and 200 μmol·L-1 respectively. The inhibitory effects of TTF1-NP on the cell growth were assessed using MTT assay and the best inhibitory one (HepG-2)was selected as the main research cell lines.Flow cytometry was used to detect the TTF1-NP-induced apoptosis;Western blotting and immunocytochemistry were used to determine the expressions of ERS key proteins.Finally,the expressions of key proteins were detected by Western blotting after using the ERS inhibitor 4-PBA.Results Compared with vehicle group,the inhibitory rates of growth of 4 kinds of human hepatoma cells in different concentrations of TTF1-NP groups were increased (P <0.05 or P <0.01);moreover,the inhibitory effects of TTF1-NP were in a time-and dose-dependent manner.Compared with vehicle group,the apoptotic rates of the cells in TTF1-NP groups were increased in a dose-dependent manner (P <0.05 or P < 0.01 );the expression levels of ERS key proteins GRP78 and caspase-4 were increased with the increasing of the concentration of TTF1-NP (P < 0.05 or P < 0.01).The expression levels of ERS key proteins GRP78 and caspase-4 induced by TTF1-NP were inhibited by ERS inhibitor 4-PBA (P < 0.05 or P < 0.01 ). Conclusion TTF1-NP can induce the apoptosis of HepG2 cells;ERS pathway plays a central role in TTF1-NP-induced apoptosis of HepG-2 cells.

Objective To investigate the nursing of replantation methods of sea-water soaked rotated avulsion amputated fingers.Methods There were 8 cases (16 fingers) with sea-water soaked rotated avulsion amputated fingers.5 cases were replanted by synchronic replantation method,the other 3 cases were replanted by traditional replantation method.We adopted complete debridement and high quality vascular anastomosis during the operation,and give hyperbaric oxygen therapy and anticoagulant treatment post-operation.Results There were 15 survival fingers in 16 replanted fingers.The survival rate was 93.75％.After follow-up for three months to two years,the total good rate was 87.5％.No wound infection and nonunion of fracture occurred.The outline of the fingers was satisfying and patients felt well.The twopoint discrimination was 3～6 mm after 3～24 months follow-up.Conclusions The injury of sea-water soaked rotated avulsion amputated fingers is complicated and the replantation operation is difficult.but if we can adopt individual measure according to the actual circumstance,it is possible that the sea-water soaked rotated avulsion amputated fingers can survive.

Objective To study the role of gap junctions in epileptiform activity. Methods The epileptiform activity was induced by zero-Mg 2+ medium in cultured hippocampal neurons of newborn rats. Immunocytochemistry and real time RT-PCR were introduced to evaluate the expression of gap junction Cx32 and Cx43. Results The level of Cx32 mRNA increased quickly one hour after the neurons were treated with zero-Mg 2+ medium and was raised by 10 times 5 hours later, while Cx32 protein began to develop at the 2nd hour (21.80?1.74) and was raised by 5 times at the 8th hour (47.30?5.75). The expression of Cx43 mRNA went up obviously 5 hours later, and Cx43 protein developed visibly 8 hours later. Carbenoxolone depressed the expressions of Cx32 and Cx43. Conclusions The expression of Cx32 and Cx43 increases dramatically after epileptic discharges and carbenoxolone inhibits both the discharges and the expression of gap junctions, which indicates that gap junction could contribute to epileptogenesis.