Fifty-seven rabbits were used for the experimental study of blood-brain barrier (BBB)permeability quantitatively in early stage of brain injury by a designated drop- ping weight method.Animals were divided into three groups:(1) control;(2)brain injury group; (3)therapeutic group.The brain injured animals were treated with antisodamine.Three different sizes of colloidal gold (OG)particles in diameter 5,10 and 15mu were given intravenously as tracers for quantitative investigation of BBB changes with light and electron microscope,respectively.In addition,brain water contents were de4rmined,The preliminary data indicated that the increase of BBB permeability began at 0.5h after trauma showing a few of 5 and 10 mu CG particles present in the endocytic pits and endothelial microvilli.Augmentation of BBB per meability reached its peak 6h after injury.Many 5,10 and 15mu CG tracers were seen penetrating the BBB through the openings at the tight junctions of endothelial cells or by vesicular transportation.The variation of brain water contents was closely correlated to the above mentioned BBB changes.The use of antisodamine resulted in a remarkable attanuation of BBB permeability and seemed advantageous in the treat- meat of cerebral edema after brain injury.

Objective To investigate the effect and mechanism of p38 MAPK inhibition in reducing the damage to rat's hippocampal neurons caused by kainic acid (KA) and observe the three-dimensional morphological changes on the cell surface. Methods The rat's hippocampal neurons cultured primarily for 10 days were pretreated with SB203580 (0.2 ?mol/L, a p38 MAPK inhibitor). Thirty minutes later, the hippocampal neurons were administered with KA at concentrations of 0, 25 and 250 ?mol/L for action for 10 and 100 minutes respectively. The cellular membrane structure was scanned and examined at nano-level by using atomic force microscope. Results Normal neurons displayed smooth membrane surface with homogeneous and regular undulation. In contrast, the neurons treated with KA showed coarse membrane surface with holes. Furthermore, the degree changes increased with the action time and the KA concentrations in a dose-effect dependent fashion. The above-mentioned changes were obviously mitigated by means of pretreatment with SB203580 (200 nmol/L). Conclusions Inhibition of p38 MAPK may, in certain degrees, protect the neurons against the impairments on cytomembrane resulted from the toxic effect of KA.

Objective To establish a Alzheimer dementia(AD) model in mice. Methods The C57BL/6 mice were lesioned with ibotenic acid in Nucleus basalis of Meynert(NBM). Behavioral tests by eight-arm radial maze were conducted 8 weeks, and immunohistochemical staining of choline acetyltransferase(ChAT), serotonin(5-HT), GAD(GABA), amyloid-?protein (AP) was conducted 12 weeks after NBM lesioning. Results In NBM lesioned mice, the ChAT-positive neurons, serotonin-positive neurons, and GAD-positive neurons in right NBM reduced, and ChAT-positive neurons reduced most evidently. At the same time, the ChAT-positive fibers in prefrontal and parietal cortices decreased significantly, serotonin-positive axons slightly, accompanied by heavily AP co-expression. On the contrary, there was no change of GAD-positive neurons in cortex. The working memory error increased significantly.Conclusion Ibotenic acid lesioning in NBM can provide as a model of AD in that it produces deafferentation of cholinergic system and recent memory disruption.

As a kind of progenitor cells, the neural stem cells (NSC) possess the potential abilities of both proliferation and differentiation, from which some neurons or glias can be produced. Therefore, the neural stem cells show broad application prospects and clinic utility value. In this paper, the biological characteristics, distributions, main differentiation mechanisms, some experimental skills and application in neurosurgery of the neural stem cells were discussed.

To study the toxicity of monoamine in high concentrations to neurons. Neurons were treated in vitro with different doses of dopamine, norepinephrine and serotonin for various lengths of time. The toxicity of these reagents on neurons was observed. Apoptosis of neurons was analyzed by agar electrophoresis, in situ DNA end labeling technique and flow cytometry. The results showed that a high concentration of monoamine could induce apoptosis of the culturing neurons. At 24h after treatment with dopamine or norepinephrine (80, 160 and 320?mol/L) as well as with 320?mol/L serotonin, apoptotic rates of neurons were significantly higher than that of the controls, respectively ( P

Aiming at present situation and difficult position of clinical medical education,and based on the demand goal of modern medicine,this paper put forward constucting the mul-ti-dimensional optimization training pattern for five-year system clinical medicine inter-disciplinary talents by renewing the education idea,adopting the curriculum reform,the quality regulation,the educational reform,the innovation of teaching methods,and the construction of community medi-cal service practice base and so on,which is of great significance to train the high quality tal-ented person with adaptability to social development.

OBJECTIVE: A series of recent studies have demonstrated the mechanism of migration and nerve net of neural stem cells. These theories have further substantiated neural stem cell transplantation. In view of these new findings, this paper reviewed the mode of migration and information of network. The significance of these theories was discussed.DATA SOURCE: We search on Pubmed with the key words "neural stem cell", "migration", and "nerve net", limiting the language to English and publication date from 1970 to 2004. At the same time we searched on CNKI.STUDY SELECTION: We selected the randomized and non-randomized controlled studies related to migration and nerve net building of neural stem cells. Review articles and articles with repetitive studies were excluded.DATA EXTRACTION: Among 39 papers selected, 16 papers concerning the development of this topic were selected, and the others were excluded.DATA SYNTHESIS: For retrograde lesions and severe injury of nervous system, transplantation of nerve stem cells may replace aging degenerative and dead nerve cells and rebuild neural network for the recovery of cerebral function. Migration of nerve cell and network principle can solve the survival, differentiation, migration and creation of nerve network after transplantation of nerve stem cells so as to realize the recovery and reconstruction of cerebral function.CONCLUSION: Neural stem cells can migrate to intended places and can build nerve net under some conditions, which will be useful for medicine deyelopment.

This study was designed to explore the mechanism of signal transduction on BBB damage in brain injury. 75 male SD rats were randomly devided into 5 groups: control, sham operation, injury only, injury with Forskolin-treatment and H7 treatment.Evans blue permeation was observed qualitatively with an epifluo resence and mesured quantitatively with a spetrophotometer.The result shcwed that Evans blue significantly permeated in injuried group,and noticeably decereased in H7 treatment group and Forskolin treatment group. It indicated that Forskolin and H7 can effectively prevent BBB opening,and suggest that Forskoling and H7 may provide new ways on BBB protection.

Objective To investigate the distribution rule of NMDA receptor protein localizated on neuron membrane surface. Methods After the primary culture model of forebrain cortex neuron of rat had been set up,the NR1 subunit protein molecule of NMDA receptor has been combined with primary antibody IgG,and marked by Staphylococcus protein A-colloid gold particles (SPA-G). Then the neuron was observed with Field-emission SEM,and the content of AU element was calcalated by software. Results The cluster of NMDA receptor combined with SPA-G particulates was clearly observed as some globular being distributed mainly under some niches of lipid rafts,mainly localized at originating section of dendritic protuberance of neuron membrane surface. Conclusion NMDA receptor molecule protein was distributed on the membrane surface lipid rafts of originating section of dendritic protuberance of neuron. It was in accord with the distribution rule of postsynaptic membrane on neuron. The Field-emission SEM could distinguish single NMDA receptor melocule cluster after being marked with SPA-G molecule in neuron.

Objective To explore the effects of inflammatory mediator blocker AG490 on neurological deficits,apoptosis and expression of caspase-3 following cerebral ischemia-reperfusion(I/R) in rats.Methods The male SD rats were randomly divided into the groups sham-operation,I/R,saline and AG490;and the focal cerebral I/R models were made by middle cerebral artery thread embolism method.AG490(1 mg/kg) was intraperitoneal injection in AG490 group immediate and 12 h after ischemia-reperfusion respectively.The neurological deficits score was evaluated in 24 h after I/R in each group.The number of apoptosis in cerebral tissue was examined by d-utp nick end labeling staining(TUNEL).The expression of P-JAK2,P-STAT3,caspase-3 were detected by Western Blot.Results Compared with the groups I/R and saline,the neurological deficits score in AG490 group was significantly decreased(all P