Central nervous system(CNS) disease induces functional deficits in persons.Simultaneously,there appears axonal destruction and the formation of scar tissue,as well as cavity and physical gaps in the lesions.Olfactory ensheathing cells(OECs),acting as prime candidates for autologous transplantation,secrete neurotrophic factors for neuroprotection,angiogenesis and outgrowth of both intact and lesioned axons to different degrees,change the response status of endogenous glia after lesion,as well as remyelinate axons after a range of demyelinating insults.OECs transplantation has become an ongoing clinical therapeutic approach for human CNS disease in recent years.Thus,OECs transplantation can be used for cell-mediated repair following a variety of CNS lesions.Here,the paper reviews the current status of foundational research of OECs transplantation in treating CNS disease underlying the wide variation of results obtained in the field.

BACKGROUND: It is a researching tendency for tissue engineering to develop compound, bionic, biological-active and intelligent materials, which are characterized by biological activity and can promote proliferation and differentiation of stem cells and tissue regeneration. OBJECTIVE: To summarize the application and development of scaffold materials for nerve tissue engineering. RETRIEVAL STRATEGY: A computer-based online search was conducted in Pubmed and V6.32 database of VIP Information Resource System for English language publications containing the key words of "nerve tissue engineering, tissue engineering, neural, neural stem cells, Schwann cell, biomedical materials, scaffold" from January 2001 to June 2007. There were 123 literatures in total. Inclusion criteria: ① articles about nerve repair with tissue engineering; ② current published literatures in the same field or in authoritative journals. Exclusion criteria: duplicated researches. LITERATURE EVALUATION: Articles are mainly derived from basic researches on scaffold materials for nerve tissue engineering, including resource, physical and chemical properties and compatibility with neural stem cells and Schwann cells. Among 36 involved literatures, there were 6 reviews, statement and lectures, and the other articles are basic researches. DATA SYNTHESIS: ① Up to now, there are no significantly researching breakthroughs about regeneration and repair after nerve injury in clinic. With the discovery of adult neural stem cells and the development of material and cell culture techniques, tissue engineering brings prospect for the treatment of nerve injury. ② Scaffold imitates the structure and function of extracellular matrix (ECM) and plays a key role in replacing extracellular matrix. It is a core for tissue engineering to look for seed cells with strong regeneration capacity and biological materials adapted to cell survival. ③ Researches demonstrate that the resource of scaffold materials for nerve tissue engineering is plentiful. Gelatine, collogen, polylactic acid hybrid materials, chitosan and acellular extracellular matrix are all considered as biocompatibility, security and stable physical and chemical characteristics. Therefore, they have a greatly applied prospect for tissue engineering. ④ There are still many difficulties of scaffold for nerve tissue engineering. It is important significance to optimise tissue construction technique and accelerate clinical application and industrial development of tissue engineering technique via further exploring basic problems, systemically elucidating formation and maturity of tissue engineering and investigating basic scientific problems and internal mechanism during prognosis in vivo. While, tissue engineering will certainly become a hot topic in the future. CONCLUSION: Researches on scaffold for nerve tissue engineering have obtained some achievements, but there are still many difficulties.

BACKGROUND: Much research focuses on the link between β-amyloid peptide and neuron death, but there is little work about white matter alterations in the Alzheimer's disease.OBJECTIVE: To investigate the anterior commissure pathological alteration in the APP/PS1 transgenic mice which model brain amyloidosis of Alzheimer's disease.DESIGN, TIME AND SETTING: A grouping observational study based on the histology was performed in the Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology between September 2007 and September 2008.MATERIALS: Female transgenic APP/PS1 mice [Thy1 APP751 SL (Swedish mutation KM670/671NL, London mutation V7171 introduced in human sequence APP751) × human mutation gene PS1 M146L], control animals were amyloid-deposit free female PS1 mice. A total of 28 mice were divided into young group (2 months, 8 APP/PS1, 7 PS1) and old group (24 months, 6 APP/PS1, 7 PS1).METHODS: The slides of brain tissue were stained with Congo red and antibody against amyloid beta (4G8) to detect brain amyloidosis in Alzheimer's disease transgenic model. Myelin was stained with gold chloride and axon was stained with anti-neurofilament M antibody. The anterior commissure axonal density and myelination were quantitatively analyzed with the relative optical density value of staining with densitometry.MAIN OUTCOME MEASURES: ①The staining of intracellular and extracellular amyloid beta; ②the average area of anterior commissure in the coronal brain tissue sections; ④the relative optical density value of myelin and axon staining in the anterior commissure.RESULTS: A lot of Congo red positive amyloid beta plaques were observed in the cortex, hippocampus, thalamus, and anterior commissure of aged APP/PS1 mice, while intracellular amyloid beta was only present in the cortex of young APP/PS1 mice. A prominent increase in the surface area of the anterior commissure was observed in aged PS1 mice compared with young PS1 mice and aged APP/PS1 mice. The neurofilament staining remarkably decreased, both in aged APP/PS1 and aged PS1 mice; an increase trend of myelination in the anterior commissure was observed both the forementioned groups. Different phenotype analysis demonstrated that axonal density and myelination was comparative in the young APP/PS1 and young PS1 mice; axonal density of aged APP/PS1 mice decreased remarkably compared with aged PS1 control mice, while myelination of aged APP/PS1 mice had no significant difference with aged PS1 mice.CONCLUSION: There exists an axon loss in the anterior commissure in the aged APP/PS1 mice with a complete myelin sheath. The amyloid beta shows a direct toxicity on the axon.

BACKGROUND: Much research focuses on the link between ?-amyloid peptide and neuron death, but there is little work about white matter alterations in the Alzheimer’s disease. OBJECTIVE: To investigate the anterior commissure pathological alteration in the APP/PS1 transgenic mice which model brain amyloidosis of Alzheimer’s disease. DESIGN, TIME AND SETTING: A grouping observational study based on the histology was performed in the Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology between September 2007 and September 2008. MATERIALS: Female transgenic APP/PS1 mice [Thy1 APP751 SL (Swedish mutation KM670/671NL, London mutation V717I introduced in human sequence APP751) ? human mutation gene PS1 M146L], control animals were amyloid-deposit free female PS1 mice. A total of 28 mice were divided into young group (2 months, 8 APP/PS1, 7 PS1) and old group (24 months, 6 APP/PS1, 7 PS1). METHODS: The slides of brain tissue were stained with Congo red and antibody against amyloid beta (4G8) to detect brain amyloidosis in Alzheimer’s disease transgenic model. Myelin was stained with gold chloride and axon was stained with anti-neurofilament M antibody. The anterior commissure axonal density and myelination were quantitatively analyzed with the relative optical density value of staining with densitometry. MAIN OUTCOME MEASURES: The staining of intracellular and extracellular amyloid beta; ②the average area of anterior commissure in the coronal brain tissue sections; ③the relative optical density value of myelin and axon staining in the anterior commissure. RESULTS: A lot of Congo red positive amyloid beta plaques were observed in the cortex, hippocampus, thalamus, and anterior commissure of aged APP/PS1 mice, while intracellular amyloid beta was only present in the cortex of young APP/PS1 mice. A prominent increase in the surface area of the anterior commissure was observed in aged PS1 mice compared with young PS1 mice and aged APP/PS1 mice. The neurofilament staining remarkably decreased, both in aged APP/PS1 and aged PS1 mice; an increase trend of myelination in the anterior commissure was observed both the forementioned groups. Different phenotype analysis demonstrated that axonal density and myelination was comparative in the young APP/PS1 and young PS1 mice; axonal density of aged APP/PS1 mice decreased remarkably compared with aged PS1 control mice, while myelination of aged APP/PS1 mice had no significant difference with aged PS1 mice. CONCLUSION: There exists an axon loss in the anterior commissure in the aged APP/PS1 mice with a complete myelin sheath. The amyloid beta shows a direct toxicity on the axon.

Biological scaffolds imitate the structure and function of extracellular matrix,and so good biocompatibility is essential for it.The materials in neural tissue engineering mainly include natural biomaterial and artificial biodegradable materials presently.This article has reviewed the biological function of materials mostly used in neural tissue engineering.

Intracerebral hemorrhage is a neurological emergency with high disability and mortality. Studies have demonstrated that thrombin formation,erythrocytolysis and iron ions play important roles in the brain injury after intracerebral hemorrhage. This article reviews the mechanisms of thrombin and iron ions in intracerebral hemorrhage-mediated brain injury.

Objective To explore the effects of empowerment education on rehabilitation in patients with celebral hemorrhage . Methods Select 200 cases of patients with celebral hemorrhage cured rehabilitation medical center ,the patients were randomly and single-blindly divided into 2 groups (n=100 each) .Both the treatment group and the control group were given rehabilitation guid-ance on the day of discharge and 1st ,2nd ,4th ,7th ,9th ,12th weeks after discharge .Patients in control group were given compliance education philosophy ,and patients in treatment group were given empowerment education philosophy .Patients of both groups were used Barthel index (BI) to assess the activities of daily living (ADL)and motor assessment scale (MAS) to motor function in the day of discharge and 25th weeks after discharge from hospital .Results The BI [(44 .12 ± 8 .56) vs .(62 .16 ± 8 .77)]and MAS [(18 .70 ± 9 .47) vs .(28 .53 ± 8 .75)]of treatment group were apparently higher than those of the control group (P<0 .01) .The to-tal effective rate of the treatment group was higher than that of the control group(70% vs .85% ) Conclusion Empowerment educa-tion can obviously improve the ADL function and promote the recovery of motor function in patients with cerebral hemorrhage and improve the effect of family rehabilitation .

KCNK17 is a member of the acid-sensitive subfamily of tandem pore K(+) channels, which are open at all membrane potentials an red contribute to cellular resting membrane potential. Recent genome-wide study (GWA) has shown that variants within KCNK17 confer genetic susceptibility for increasing ischemic stroke. In an effort to discover additional polymorphism(s), we scrutinized the genetic polymorphisms in the KCNK17. By direct DNA sequencing in 32 individuals, we identified nine sequence variants within the 16 kb of whole KCNK17 gene: one in exon1, one in intron and seven in the promoter region. Haplotypes, their frequencies and linkage disequilibrium coefficients (D'), among polymorphisms were estimated. All the polymorphisms in the 5'-flanking region (SNP2-SNP7) being in complete (or nearly complete) association with each other in the promoter region maybe produce synergistic effect to regulate the expression of KCNK17 gene and then have an influence on the pathogenesis of cerebrovascular diseases. The common haplotypes were observed comprising 88.9% of the total haplotypes in the same block. Bioinformatic analysis predicted several potential transcriptional factors binding sites by SNP -95, -134, -596 and -846. However, these binding sites need to be experimentally verified. The information concerning genetic polymorphisms of KCNK17 gene might provide valuable information for future genetic studies of diseases.

BACKGROUND: Being a kind of regenerative and auto-transplanting cell, olfactory ensheathing cell (OEC) has been extensively concerned on transplantation treatment for spinal disease. Concerning to the transplantation in treatment of cerebral hemorrhage, it is expected a further accumulation of experimental results at present.OBJECTIVE: To observe the proliferation of neural progenitor cells in cerebral hemorrhagic rats after OEC transplantation and to evaluate the therapeutic effects of OEC transplantation on cerebral hemorrhage.DESIGN: Completely randomized controlled experiment.SETTING: Department of Neurology of Tongji Hospital affiliated to Tongji Medical College of Huazhong University of Science and Technology.MATERIALS: The experiment was performed in Research Center for Clinical Neurology , Tongji Medical College of Huazhong University of Science and Technology from March 2002 to March 2003. Thirty-two healthy male Wistar rats were employed and randomized into 2 groups, 16 rats in each. In OEC transplantation group, on the 3rd day of modeling hemorrhage of caudate nucleus, OEC suspension 10 μL was injected evenly in the brain of rat (1 μL/min). In the control group, physiological saline 10 μL was injected.METHODES: Neural function evaluation was done before transplantation,on the 3rd, 7th, 14th and 30th days after transplantation successively. On the first day after modeling, 1 rat was collected from each of two groups to prepare brain tissue section. Myelin sheath blue staining was used for observation of neuronal axonal myelin sheath. Never fiber argentophil staining was used for observation of never fiber. One rat was collected from each of two groups on the 3rd, 7th, 14th and 30th days after transplantation successively to prepare paraffin section. The survival and migration after OEC transplantation as well as proliferation of neural progenitor cell were observed.The count of neural progenitor cell was recorded.myelin sheath and nerve fiber after cerebral hemorrhage in rats of two function deficits on the 3rd, 7th, 14th and 30th days after cerebral hemorrhage in rats of two groups.around and in hematoma on the 30th day after cerebral hemorrhage: In transplantation group, myelinated amount and nerve fiber amount were cell after cerebral hemorrhage in rats of two groups: on the 7th, 14th and 30th days after cerebral hemorrhage, the amount of neural progenitor cell in OEC transplantation group was more remarkably than that in the control group [(41.1 ±2.4)pcs/vision field, (34.5 ±1.2)pcs/vision field; (43.6±1.2)pcs/vision rield, (37.2±2.0)pcs/vision field; (19.3±1.0)pcs/vision rield, ( 14.2±0.4)pcs/videficits after cerebral hemorrhage in rats of two groups: In OEC transplantation group, on the 14th and 30th days, the evaluation was lower remarkably than the 3rd day [(2.21 ±0.20)scores, (1.50±0.21)scores, (2.74±0.21)scores, (t=2.06, 3.27, P ＜ 0.05)]. In the control group, that on the 30th day after cerebral hemorrhage was lower than that on the 3rd day [(1.96±0.12)scores ,(2.76±0.20) scores, (t=2.47, P ＜ 0.05 )].tion of intracerebral nerve cell, re-myelination and building-up synaptic system so as to recover the motor function and accelerate repair of injured tissue.