Objective To study the influence of valproate sodium(VPA)on neuroprotective effects of topiramate(TPM).Methods For-ty-eight 3-4 week-old male Wistar rats were randomly divided into 4 groups of 12 rats each.Group A was negative control rats,and groups B-D were rat model of epilepsy,induced by pentylenetetrazol(PTZ).The rats in 2 experimental groups were adminstered intragastrically with TPM 40 mg/kg and TPM 40 mg/kg+ VPA 200 mg/kg;2 control groups(groups A and B)with the equal amount of distilled water administration.After 2-month administration,changes of the behavior,levels of serum neuron-specific enolase(NSE)and the pathological in hippocampus were examined.Results The level of NSE in the group of TPM were significantly lower than that in masculine group,but no difference between masculine group and the TPM plus VPA.The pathological change in hippocampus were abatement in the group of TPM.Conclusion TPM plus high dosage of VPA will impaire the neuroprotective effects of TPM.

Objective To determine the genetic diversity of germplasm resource in cultivated and wild Cistanche deserticola. Methods Fifty-eight samples from three populations of cultivated and wild C. deserticola were analyzed by amplified fragment length polymorphism (AFLP) DNA markers, and the gene- tic diversity was evaluated by PopGen32. Results The average percentage of polymorphic loci (PPL) of cultivated C. deserticola is 79.16%. The PPL of wild population is 89.53%. Average Neis gene diversity index (He) from four populations was 0.193 8, Shannons genetic diversity index (I) was 0.300 4, and genetic differentiation index (Gst) was 0.097 9. Conclusion The diversities of cultivated and wild C. deserticola are both higher and theres no differentiation between them. It shows that genetic diversity of inner-species is higher, which is not the reason for endangerment. Therefore, wild nursery and artificial cultivating are the best measures for the conservation and sustainable utilization in C.deserticola.

Objective To explore the effects of the neonatal handling and enriched environmental stimulation on brain damage in neonatal rats with hypoglycemia.Methods Thirty-six neonatal rats were randomly divided into the normal group,hypoglycemia intervention group and the hypoglycemia non-intervention group.Those rats in hypoglycemia intervention and hypoglycemia non-intervention groups were weaned for 12 h,then the blood sugar of both groups were monitored.After neonatal rat models with hyperglycemia were prepared,the rats in hypoglycemia intervention group received the neonatal handling for 14 d and then were kept in an enriched stimulation environment for another 14 d.Rats in normal group and hypoglycemia non-intervention group were fed in the routine way.Neonatal handling was done when the rats were born for 24 h.The rat was rubbed with the brush from head to tail softly.Rats in the hypoglycemia non-intervention group was not handled.The enriched environment stimulation was used after 15 d when the rats were born.Rats in the hypoglycemia intervention group was put into the enriched environment for 1 h per day until 28 d when the rats were born,and rats in the hypoglycemia non-intervention group was put into the normal environment.Then the body weight was scaled at 0 d,7 d,14 d,21 d and 28 d when the rats were born.Space learning and memory were tested with Morris earter at their third month's age.After that,changes of pathology was observed in their occipital cortex.Results The weight increase,the ability of space learning,memory and the number of survival pyramid neurons of occipital cortex in normal group were better than those in hypoglycemia intervention and hypoglycemia non-intervention group(Pa

Objective To explore protective effect of topiramate (TPM) and folic acid (FA) on mitochondrial damage in hippocampal CA3 neurons during pentylenetetrazol- induced kindling in immature rats.Methods Pentylenetetrazol (PTZ) - induced kindling in rats was used to establish rat models of epilepsy.Forty-eight 3-week-old male Wistar rats were randomly divided into 4 groups: two therapy groups with TPM 40 mg/(kg?d) or TPM 40 mg/(kg?d) and FA 5 mg/(kg?d) administration, 2 control groups (positive control group and negative control group) with the equal amount of distilled water administration. The seizure behaviors of rats were evaluated. Two months later, the rats were killed and the brain sections were made. The mitochondrial ultrastructures of neurons in hippocampal CA3 region were observed with transmission electron microscope.Results In the positive control group, the frequency of seizure was (48.4 ? 3.7)times, while in TPM group (44.3 ? 3.1)times and in TPM and FA group(40.8 ? 3 .7)times.The differences were significant among three groups (Pa

2 years),seizure frequency(≥1 time/month),persistence time(≥60 s),gene-ralized seizure were all associated with the incidence of the loss of neuron in ammonias.Multivariate Logistic regression analysis showed that the independent influencital factors for the loss of neuron in ammonias in children with temporal epilepsy included seizure frequency,persis-tence time and tape of seizure. Conclusions The loss of neuron in ammonias though 1H-MRS can be detected.The results of multivariate analysis verify that the development of the loss of neuron in ammonias may be associated with many factors including age of onset,course of di-sease,seizure frequency,persistence time and generalized seizure.In order to lower the incidence of the loss of neuron,early intervening treatment is very important.

Cold Temperature ; Dinoprost ; analogs & derivatives ; urine ; Dust ; Humans ; Interleukin-6 ; urine ; Thromboxane B2 ; analogs & derivatives ; urine ; Weather

Objective: To prepare a nanoprobe, anti-human melanoma ganglioside single chain variable fragment (GD/ScFvMEL) antibody conjugated with CdTe quantum dot, and to observe its ability to specifically bind human malignant melanoma cells. Methods: The GD/ScFvMEL gene was cloned into pET32a (+), and the plasmid was then transformed into E. coli BL21 (DE3) for GD/ScFvMEL protein antibody expression. The expressed GD/ScFvMEL antibody was purified by denaturing method and further refolded by modified dialysis method. The purified GD/ScFvMEL antibody was analyzed by SDS-PAGE. The GD/ScFvMEL-QDs nanoprobe was prepared by conjugating GD/ScFvMEL antibody with CdTe quantum dot, and its specificity was observed by incubating with MGC-803 cells and melanoma A375 cells. Results: The recombinant pET32a-GD/ScFvMEL was constructed and confirmed by PCR, restriction endonuclease analysis and DNA sequencing. The proportion of expressed GD/ScFvMEL antibody in total bacteria proteins was about 40% as detected by SDS-PAGE. The purified- and refolded-GD/ScFvMEL antibody was effectively conjugated with CdTe quantum dot, and the resulting GD/ScFvMEL-QDs nanoprobe was successfully prepared. The GD/ScFvMEL-QDs nanoprobe could specifically bind melanoma A375 cells, but could not bind stomach cancer MGC-803 cells. Conclusion: We have successfully prepared an anti-human melanoma ganglioside single-chain antibody-CdTe quantum dot nanoprobe, which can specifically bind melanoma cells.

OBJECTIVETo study the neuroprotective effects of topiramate (TPM) alone or together with folic acid (FA) on young rats with kindling-induced epilepsy.

METHODSRat models of epilepsy were prepared by pentylenetetrazol (PTZ)-induced kindling. Seventy-two 3-week-old male Wistar rats were randomly divided into 6 groups: four TPM-treated epilepsy groups (TPM 20, 40 or 80 mg/kg/d and TPM 40 mg/kg/d + FA 5 mg/kg/d), a positive control group (untreated epilepsy group) and a negative control group (normal control group). After two months of administration, behaviors of the rats were recorded; serum levels of neuron-specific enolase (NSE) were measured using ELISA; pathological changes in the hippocampus were observed.

RESULTSThe frequency of convulsion seizures in the 20, 40 and 80 mg TPM treatment and TPM+FA groups was 44.7 +/- 2.9, 44.3 +/- 3.1, 42.7 +/- 3.2, and 40.8 +/- 3.7 respectively, which were significantly lower than that in the positive control group (48.4 +/- 3.7) (P <0.01). Twenty, forty and eighty mg TPM treatment and TPM+FA treatment significantly reduced NSE levels from 35.71 +/- 5.97 microg/L of the control group to 27.40+/- 6.40, 24.79 +/- 6.22, 21.47 +/- 6.87 and 22.55 +/- 7.02 microg/L respectively (P <0.05). Neuronal apoptosis in the CA3 and CA1 regions were alleviated in the four TPM treatment groups compared with positive control. The number of necrotic neurons was progressively reduced with the increased dose of TPM. The 40 mg TPM+FA treatment group showed less necrotic neurons in the CA3 and CA1 regions than the 40 mg TPM alone treatment group.

CONCLUSIONSTPM has protective effects against epilepsy-induced neuronal damage. The effect is dose-dependent. A combination of TPM and FA can produce a synergistic effect.

Animals ; Dose-Response Relationship, Drug ; Enzyme-Linked Immunosorbent Assay ; Epilepsy ; drug therapy ; pathology ; Folic Acid ; pharmacology ; Fructose ; analogs & derivatives ; pharmacology ; Hippocampus ; pathology ; Kindling, Neurologic ; drug effects ; Male ; Neuroprotective Agents ; pharmacology ; Phosphopyruvate Hydratase ; blood ; Rats ; Rats, Wistar

OBJECTIVETo investigate the characteristics of gene mutations in unexplained infantile epileptic encephalopathy (EE).

METHODSA total of 47 infants with unexplained infantile EE were enrolled, and next-generation sequencing was used to analyze gene mutations in these infants and their parents.

RESULTSOf all 47 infants, 23 were found to have gene mutations, among whom 13 had de novo mutations and 10 had heterozygous mutations inherited from their father or mother. Among the 23 infants with gene mutations, 17 were found to have the gene mutations related to EE (among whom 14 had ion channel gene mutations), 2 had the gene mutations related to congenital inherited metabolic diseases, 2 had the gene mutations related to brain structural abnormality, and 2 had the gene mutations related to mental retardation.

CONCLUSIONSUnexplained infantile EE may have gene mutations, mainly ion channel gene mutations.