Objective To investigate the mechanism of presynaptic protein (Munc18) antibody in inducing epilepsy on rat. Methods Munc18 antibody was continuously micro-injected into CA1 area of hippocampus in Sprague-Dawley (SD) rat (the injection times were nine). The potential epileptic seizure was evaluated according to both electroencephalogram (EEG) and behaviors. HE, Nissle and TUNEL staining were applied on rat brain sections as to detecting the cell damage and apoptosis after tenth week. Results Ten of twelve rats produced epileptic EEG, five cases among these ten rats maintained abnormal EEG after the sixth week since injections. Nine of the above twelve rats had epileptic seizure according to Racine grade one to four, four cases among these nine rats kept seizure after the sixth week since injections. The number of neurons decreased (155?20,P

Purpose:20 loci on chromosome 6 were examined to detect loss of heterozygosity(LOH)in 21 cases of glioblastoma(GBM) in order to locate the deletion areas probably harboring tumor suppressor genes.Methods:PCR based microsatellite polymorphism analyses were performed to detect LOH on chromosome 6, fluorescence labeled primers and Perkin Elmer 377 DNA Sequencer were applied.Results:47.6% informative cases of GBM displayed LOH on chromosome 6, 28.1% of informative loci showed LOH in our series, in which the most frequent LOH were observed at locus D6S281 (50%) on 6q tel and D6S287(50%) on 6q 16.3 ,the LOH frequency at locus D6S276 on 6p 21.1 21.3 is also high(35.3%).Conclusions:Loss of genetic material on chromosome 6 may be involved in the molecular genetic pathogenesis of GBM. The chromosomal regions at loci D6S281 on 6q tel ,D6S287 on 6q 16.3 and D6S276 on 6p 21.1 21.3 may harbor tumor suppressor genes associated with GBM. [

Objective To study the different patterns of hippocampal atrophy by MRI segmental analysis and to investigate the etiology and pathogenesis of temporal lobe epilepsy Methods GE 1 5 T Signa Horizon LX MRI scanner was used Oblique coronal T 1 weighted images perpendicular to the long axis of the hippocampus were obtained The mesial temporal structures were divided into four parts: the amygdala, hippocampal head, body and tail MRI patterns of atrophy in 50 patients with histologically confirmed hippocampal sclerosis were investigated by MRI volumetric measurement and segmental analysis, and the differences of clinical features and surgical outcome in different groups were compared Results Diffuse hippocampal atrophy was found in 22 of 50 patients (44%), 5 of the 50 patients (10%) showed diffuse atrophy involving both the amygdala and hippocampus 20 of the 50 patients (40%) had hippocampal focal atrophy and 8 of 50 patients (16%) had no obvious atrophy 38 of 50 (76%) hippocampal sclerosis had atrophy in the hippocampal body, 29 of 50 (58%) had hippocampal head atrophy, 24 of 50 (48%) had hippocampal tail atrophy, and the least involved part was the amygdala (16%, 8/50) 10 patients who had normal hippocampal volume showed focal hippocampal atrophy by segmental analysis Various patterns of hippocampal atrophy were found to be statistically related to the duration of epilepsy, the frequency of seizure and the outcome of surgery, respectively ( P 0 05) Conclusion MRI segmental analysis can improve the diagnostic sensitivity of temporal lobe epilepsy and help to investigate its etiology and pathogenesis

Purpose14 loci on chromosome 13 were examined to detect loss of heterozygosity(LOH) in 20 cases of glioblastoma (GBM) in order to locate the deletion areas probably harboring tumor suppressor genes(TSGs).MethodsPolymerase chain reaction (PCR) based microsatellite polymorphism analyses were performed to detect LOH on chromosome 13, fluorescence-labeled primers and Perkin Elmer 377 DNA Sequencer were applied.Results60 % informative cases of GBM displayed LOH on chromosme 13. 60 % of informative cases displayed LOH on 13q and 27% on 13p. 45.8% of informative loci showed LOH in our series, in which the higher frequent LOH were observed in the chromosomal regions from loci D13S217 to D13S263 on 13q12-14.2 and from D13S156 to D13S265 on 13q21.2-32 and at loci D13S153 on 13q14.1- 14.3 Conclusions Loss of genetic material on chromosome 13 may play an important role on the molecular pathogenesis of GBM. The chromosomal regions from loci D13S217 to D13S263 on 13q12-14.2 and from D13S156 to D13S265 on 13q21.2-32 and at loci D13S153 on 13q14.1-14.3 may harbor several TSGs associated with GBM, which may include novel TSGs apart from RB1.

Objective:To investigate the clinical efficacy of stereotactic radiation therapy combined with temozolomide on recurrent glioma.Methods:A total of 36 patients with recurrent glioma were retrospectively analyzed and divided into a control group (n=12),who received stereotactic radiation therapy,and an experimental group (n=24),who received stereotactic radiation therapy plus temozolomide.The clinical efficacy and adverse reactions for the 2 groups were compared.Results:Total effective rate and local control rate for clinical treatment were 66.67％ and 93.94％,respectively.Late adverse reaction was not observed.The effective rate and local control rate in the experimental group were 77.27％ and 95.45％,which were slight higher than those in the control group,with no statistical significance (P＞0.05).The 0.5-,1-,2-,3-year follow-up total survival rates were 90.91％,63.64％,42.42％,and 15.15％,respectively.The 0.5-,1-,2-,3-year follow-up survival rates in the experimental group were 95.45％,72.72％,54.54％ and 22.73％,respectively,while those in the control group were 81.82％,45.45％,18.18％,and 0％,respectively.Survival analysis showed the survival time for the experimental group was significantly longer than that of the control group (30.00 months vs 14.00 months,P=0.010).Conclusion:Stereotactic radiation therapy combined with temozolomide for recurrent glioma is effective,and it has positive effect on improving the clinical efficacy and survival rate for the patients.

OBJECTIVETo evaluate whether deletion of chromosome 14q is involved in the carcinogenesis of primary glioblastoma multiforme and to identify possibly common deletion regions. METHJODS: Fourteen fluorescent dye-labeled polymorphic markers were used and polymerase chain reaction-based microsatellite analysis was employed to investigate loss of heterozygosity (LOH) on chromosome 14q in 20 primary glioblastoma multiforme (GBM).

RESULTSTen of twenty (50%) GBM displayed LOH at one or more of the markers on chromosome 14q. Five tumors showed either LOH or non-informative on all markers tested. The most frequent LOH was observed at locus D14S65 (57.1%) on 14q32.1, and in the chromosomal region spanning from D14S63 (47.1%) to D14S74 (46.7%) on 14q23-31. None of the informative loci exhibited microsatellite instability.

CONCLUSIONSAllelic deletion on chromosome 14q plays an important role in the pathogenesis of GBM. Chromosomal regions at locus D14S65 on 14q32.1 and spanning from D14S63 to D14S74 on 14q23-31 may harbor multiple tumor suppressor genes associated with GBM.

Adult ; Aged ; Chromosomes, Human, Pair 14 ; Female ; Genes, Tumor Suppressor ; Glioblastoma ; genetics ; Humans ; Loss of Heterozygosity ; Male ; Microsatellite Repeats ; Middle Aged

OBJECTIVETo reveal the molecular genetic mechanisms for the pathogenesis of glioblastoma (GBM) and determine which chromosomes or chromosomal regions may play a role in the pathogenesis of GBM or may harbor tumor suppressor genes (TSGs) associated GBM.

METHODSAn allelotype study of 21 cases of GBM was performed by polymerase chain reaction and loss of heterozygosity (LOH) analysis. Three hundred and eighty-two microsatellite markers covering all 22 autosomes were used. The mean genetic distance between two flanking markers is about 10 cM. Fluorescent dye-labeled primers and Perkin Elmer 377 DNA Sequencer were applied.

RESULTSLOH was observed on all chromosomal arms examined in this study. The LOH frequencies of 10q, 10p, 13q, 17p and 9p were the highest (>50%), on which high LOH frequencies were detected at the regions resided by the known TSGs including PTEN, DMBT1, p16, p15, p53 and Rb. The following commonly deleted regions were detected: 9p22-23, 10p12.2-14, 10q21.3, 13q12.1-14.1, 13q14.3-31, 17p11.2-12, 17p13, 3q24-27, 11p12-13, 14q31-32.3, 14q21-24.1, 22q13.2-13.3, 4q35, 4q31.1-31.2, 6qtel, 6q16.3.

CONCLUSIONThis study demonstrated that the pathogenesis of GBM is very complicated and associated with various molecular genetic abnormalities on lots of chromosomes. The chromosomal arms most closely relevant to the pathogenesis of GBM are 10q, 10p, 9p, 17p and 13q. Besides the well-known TSGs, such as PTEN, DMBT1, p16, p15, p53 and Rb, multiple unknown TSGs associated with GBM may be present on the commonly deleted regions observed for the first time in this study.

Adult ; Aged ; Chromosomes, Human ; genetics ; DNA, Neoplasm ; genetics ; Female ; Glioblastoma ; genetics ; Humans ; Loss of Heterozygosity ; Male ; Microsatellite Repeats ; Middle Aged

OBJECTIVETo investigate the molecular genetic pathogenesis of primary glioblastoma multiforme (GBM) and identify which chromosomes or chromosomal regions of the entire genome may harbor tumor suppressor genes (TSGs) associated with GBM.

METHODSA high-resolution allelotype study of 21 cases of primary GBM was performed by PCR-based loss of heterozygosity (LOH) analysis. Three hundred and eighty-two fluorescent dye-labeled microsatellite markers covering all 22 autosomes were applied. The mean genetic distance between two flanking markers was about 10 cM.

RESULTSLOH was observed on all 39 nonacrocentric autosomal arms examined in this study. The LOH frequencies of 10q, 10p, 9p, 17p and 13q were the highest (> 50%). Furthermore, high LOH frequencies were detected in the regions containing known TSGs including PTEN, DMBT1, p16, p15, p53 and RB; the LOH frequencies on 14q, 3q, 22q, 11p, 9q, 19q were also high (> 40.5%). Our study observed the following commonly deleted regions: 9p22-23, 10p12.2-14, 10q21.3, 13q12.1-14.1, 13q14.3-31, 17p11.2-12, 17p13, 3q25.2-26.2, 11p12-13, 14q13-31, 14q32.1, 14q11.1-13, 22q13.3, 4q35, 4q31.1-31.2, 6q27 and 6q21-23.3.

CONCLUSIONSThe molecular pathogenesis of GBM is very complicated and associated with a variety of genetic abnormalities on many chromosomal arms. The most closely related chromosomal arms to the pathogenesis of GBM are 10q, 10p, 9p, 17p and 13q. Besides the well-known TSGs including PTEN, DMBT1, p16, p15, p53 and RB, multiple unknown TSGs associated with GBM may be present on the commonly deleted regions detected in the present study.

Adult ; Aged ; Alleles ; Chromosome Aberrations ; DNA ; isolation & purification ; Female ; Genome ; Glioblastoma ; genetics ; Humans ; Loss of Heterozygosity ; Male ; Microsatellite Repeats ; Middle Aged ; Polymerase Chain Reaction