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: 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.

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: 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.

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.

Neural stem cells were labeled with superparamagnetic iron oxide (SPIO) and tracked by MRI in vitro and in vivo after implantation. Rat neural stem cells were labeled with SPIO combined with PLL by the means of receptor-mediated endocytosis. Prussian blue staining and electron microscopy were conducted to identify the iron particles in these neural stem cells. SPIO-labeled cells were tracked by 4.7T MRI in vivo and in vitro after implantation. The subjects were divided into 5 groups, including 5 x 10(5) labeled cells cultured for one day after labeling, 5 x 10(5) same phase unlabeled cells, cell culture medium with 25 mug Fe/mL SPIO, cell culture medium without SPIO and distilled water. MRI scanning sequences included T(1)WI, T(2)WI and T(2)*WI. R(2) and R(2)* of labeled cells were calculated. The results showed: (1) Neural stem cells could be labeled with SPIO and labeling efficiency was 100%. Prussian blue staining showed numerous blue-stained iron particles in the cytoplasm; (2) The average percentage change of signal intensity of labeled cells on T(1)WI in 4.7T MRI was 24.06%, T2WI 50.66% and T(2)*WI 53.70% respectively; (3) T2 of labeled cells and unlabeled cells in 4.7T MRI was 516 ms and 77 ms respectively, R(2) was 1.94 s(-1) and 12.98 s(-1) respectively, and T(2)* was 109 ms and 22.9 ms, R(2)* was 9.17 s(-1) and 43.67 s(-1) respectively; (4) Remarkable low signal area on T(2)WI and T(2)*WI could exist for nearly 7 weeks and then disappeared gradually in the left brain transplanted with labeled cells, however no signal change in the right brain implanted with unlabeled cells. It was concluded that neural stem cells could be labeled effectively with SPIO. R2 and R(2)* of labeled cells were increased obviously. MRI can be used to track labeled cells in vitro and in vivo.