$524 Friday, November 11, 2005 Poster Abstracts

CD34+ 3.1 and mean white cell count 8.36. The trial is currently in the fifth of seven treatment blocks. Conclusions: The results will help inform the design of further trials including planning a large definitive trial assessing the safety and efficacy of G-CSF.

1672 Regulative mechanism of As~ocytes on Synaptie Plasticity in the CA1 region of rat Hippocampus

Tan, L 1, Guan, C 2, Sun, S 2, Duan, S 1, Wang, X 1. ZDepartment of Neurology, General Hospital, Wuhan University, Wuhan, PR China; 2Department of Neurology, Xiehe Hospital, Tonjing Medical College, Huazhong University of Science And Technology, Wuhan, PR China

Background: In vitro, astrocytes greatly influence the appearance and density of synapse. Previous studies do not provide information about whether the same rules happen in vivo, and the regulative mechanism of astrocytes on spine synoptic plasticity in the CA1 subfield of the hippocampus are required for further research. We investigated these issues to determine the effects of astrocytes on the spine synapric plasticity. Method: Male Sprague Dawley [10 new-born (<24h), 10 juvenile (28~30d) and 40 adult (90.~100d, equally divided into 4 groups: the adult, the ara-c, the mevastatin and the control)] rats were used. Three days after 30 of the adult rats were administered by continuous drug infusion with minipump to the intraventricuhis lateralis, the hippo- campi dissected out from the rat brains were studied with immuno- lfistochemAstry, electron mAcrophotography and high perfomtance liquid chromatography (HPLC). Results: No significant differences were observed among the density values of CA1 pyramidal cells of the rats. There are significant differences (p < 0.01) among the astrocytic density, CA value of glial fibrillary acidic protein (GFAP) staining (except those among the mevastatin, the control and the adult group), cholesterol content and the density values of spine synapses of the six groups except the four indexes between either the juvenicle and the ara-c or the adult and the control animals (p > 0.05). Conclusions: Astrocyte is required for the maintenance of normal spine synapse density in the CA1 region of the rat hippocampus, and neurons may rely on an import of cholesterol from astrocyte to form enough synapses in vivo.

1673 Mortality trend from Creutzfeldt-Jakob disease in Canada: 1998-2003

Hong-XSng Wu 1, Jun Wu ~, Robert Gervais ~, Gerard Jansen l, Elina Olsen 1, Zheng Wang ~, Antonio Giulivi ~. 1Blood Safety Surveillance arid Health Care Acquired Infections Division, Public Health Agency of Canada

Objective: To examine trends in mortality from Creutzfeldt-Jakob disease (CJD) in Canada during 1998-2003 through a comprehensive national surveillance program. Method: Case ascertairm~ent was based on notifications by neurolo- gists, neuropathologists, and laboratories. Mortality rates were calculated using all deaths from CJD from April 1 ~t, 1998 through December 31 ~t, 2003, on the basis of the 2001 census population. Descriptive epidemiology was employed to analyze the epidemiologic status of CJD. Results: A total of 182 deaths from definite or probable CJD were registered during the study period. The majority of cases were determined to be sporadic CJD (89.0%), with 4.4% GSS; 3.8% inherited; 2.2% iatrogenic; 0.6% variant CJD. Mortality rates ranged from approximately 0.80 in 1998 to 1.14 deaths per million in 2000. There was no gender difference in mortality after multivariate analysis (RR 1.04, 95% CI 0.77 to 1.41). Below 40 years of age, mortality rates were extremely low. Conversely, mortality rates increased substantially in the 50-59 year age group, reaching a peak of approximately 6 deaths

per million per year in the 70-79 year age group. Prion protein gene genotype at codon 129 was available in 86 definite or probable cases, with mettfionine homozygosity in 58.1%, valine homozygosity in 18.6%, and heterozygosity in 23.3%. Conclusion: The analysis of annual CJD mortality data would be an efficient tool for monitoring incidence trends. The intensive ongoing surveillance is important for assessing prospective events resulting from exposure to the bovine spongiforrn encephalopathy agent, or other new potential risk factors.

1674 Endothelin-1 induces Nitric Oxide release via Endothelin B receptors in cultured rat Cortical Neurons

Xu, A l, Tan, S ~, Di, j2, Zheng, S ~, Zeng, Z 3, Tan, Z ~, Song, X ~. ZDept. of Neurology, the First Affiliated Hospital, Yinan University Guangzhou, P.R. of China; 2Institute of Tissue transplantation arid bnmunology, Life Science and Technology College, ,,rinan University G-uangzhou, P.R. of China; 3Dept. of Pathology, Medical College, Jinan University Guangzhou, P.R. of China

Background: Exogenous endothelin-1 (ET-1) or activation of ET receptors can induce enhanced release of nitric oxide (NO) from nervous tissues, suggesting that ET-1 may promote the synthesis and release of NO in the central nervous system. The cellular source of NO, however, remains unclear. Method: Primary cortical neuron cultures were prepared from neonate SD rat brain and incubated for 7 days into confluence. Firstly, the cultures were stimulated with 10rmtol/L, 100rmtol/L ET-1, respec- tively. The medium was then collected at 0 man, 30 man, and 6h interval for detection of NO concentration using uitrate reductase method. Thereafter, in addition to 10 nM ET-I, BQI23 (a selective ETA receptor antagonist), BQ788 (a selective ETB receptor antago- nist) or PD145065 (a non-selective ET receptor antagonist) was simultaneously added into the cultures, respectively, and the medium was collected 6 h after the administration for NO concentration measurement. Result: After treated with 10 nM ET-1 and 100 nM ET-1 for 6 h, NO concentration in culture medium significant increased and was higher than that in control group (P - 0.029, 0.015, respectively). No significant difference of NO levels between 10 nM ET-1 and 100 nM ET-1 treated groups was found. BQ788 or PD 145065, but not BQ123, completely blocked the effect of ET-1 on NO release from cultured neurons, making the NO levels in medium unchanged as compared with control (P > 0.05, respectively). Conclusion: ET-I can directly stimulate cultured cortex neurons to release NO via ETB receptors.

1675 Diaphragm movement in Myotonic Dystrophy (MD1)

Yahara, O l, Kimura, T ~, Kuroda, K ~, Enomoto, H l, Fujiwara, K ~ , Saitou, T 1 , Aburakawa, y2, Sawada, J 2, Enomoto, N 2, Katayama, T 2, Aizawa, H 2. ZNational Hospital Organization Dohoku Hospital, Asahikawa, Japan; :Asahikawa Medical College, Asahikawa, Japan

Background: In myotonic dystrophy (MD1) patients, respiratory muscles, including diaphragm, weakness develops, contributes to lung infection and hypoventilation may occur. Some patients had respiratory insufficiency from early stage. Some studies showed that diaphragm showed reduced relaxation and myotonic discharges. To investigate the respiratory muscles weakness of MD patients clearly, we studied respiratory muscle movements, espedally diaphragm. Method: We evaluated diaphragm movements in MD patients and control by using the angiography equipment. On supine position, we measured the lateral and antero-posteeior diameter during maximal inspiration and expiration movement. Moreover, we drowned the shape of diaphragm between maximal respiration movements and,