BACKGROUND:The stimulation parameters concern directly the antiepileptic effect and safety of vagus nerve stimulation in epileptic patients, and the optimal setting of these parameters is crucial to ensure safe and effective application for antiepileptic treatment.OBJECTIVE: To observe the effect of such parameters as output current,wave width, frequency, on/off time of intermittent stimulation in electric vagus nerve stimulation for antiepileptic therapy.DESIGN: Single-sample experiment.SETTING: Department of Neurobiology, School of Basic Medical Sciences, Capital University of Medical Sciences.MATERIALS: The experiment was carried out at Electrophysiological Laboratory of Department of Neurobiology, School of Basic Medical Sciences, Capital University of Medical Sciences between September 2000and September 2002, using totally 36 healthy adult Wistar rats.METHODS: Epileptic models were established in 36 healthy adult Wistar rats by cervical subcutaneous kainic acid injection, in which various settings of vagus nerve stimulation parameters were applied and their antiepileptic effects observed in terms of changes in the behaviors, electrocardiogram (ECG), electrocorticogram (ECoG), and hippocampal neuronal discharge to identify the optimal parameter setting.rameters.nerve stimulation produced antiepileptic effect mainly within 4 hours of with wave width of 2 ms, current intensity of 3-3.5 mA, frequency of 30-35 Hz, 1-minute on/2-minute off intermittent stimulation produced remarkable antiepileptic effect presented by obviously reduced seizure duration in ECoG and epileptic severity, with lowered frequency of bursting discharge in the epileptic rat CA1 neurons (P ＜ 0.05).CONCLUSION: With normal cardiac electric activity ensured, the minimum stimulation parameters sufficient for effective epilepsy control can be considered as the optimal parameter setting in electric vagus nerve stimulation, which has no adverse effect on the heart.

BACKGROUND: Vagus nerve stimulation (VNS) is a neurophysiological therapy (NPT) of refractory epilepsy, which can control the seizure by stimulating the vagus nerve stem in cervical part.OBJECTIVE: To study the effect of intermittent left-side VNS on seizure of epileptic animals, and provide theoretic basis for the interaction of somatic information and that of internal organs.DESIGN: Observation study.SETTING: Department of Neurobiology, Capital University of Medical Science.MATERIALS: The experiment was performed in the Laboratory of Electrophysiology in Department of Neurobiology, Capital University of Medical Science from March 2000 to September 2002. Thirty-four healthy adult SD rats and 8 rabbits, weighting (220-250) g and (2.2-2.5) kg respectively were selected.METHODS: ①Ten rats were intramuscularly injected with (150 000-160 000) U of penicillin (PCN). VNS effects on epileptiform activities of rats were studied by observing the changes in electrocorticogram (ECoG)and behavior of rats before and after VNS.②(0.24-0.48) mg of PCN was injected into the hippocampus of another 8 rabbits to induce epilepsy, and VNS effects on ECoG of epileptic rats were observed. ③Seizures of 16 rats were induced by Kainic acid, and changes in discharge activity of hippocampal neuron, ECoG and behavior of epileptic rats were observed after VNS. ④Seizures of 8 rabbits were induced by cortical injection of strychnine with microinjector, and VNS effects on ECoG of rabbits with epilepsy induced by acute cortical injury were observed.MAIN OUTCOME MEASURES: ①VNS effects on seizure of rats with epilepsy induced by PCN. ②VNS effects on seizure of rats with epilepsy induced by Kainic acid. ③VNS effects on epileptiform ECoG of rabbits with epilepsy induced by strychnine.RESULTS: A total of 34 rats and 8 rabbits were involved in the analysis of results. VNS could remarkably suppress the seizure of epileptic animals,and epileptiform ECoG, epileptiform discharges of hippocampal neuron and behavior significantly changed with the total effective rate greater than 50%. The total effective rate of VNS before seizure was greater than 80%.In epilepsy group indoeed by intramuscular injection of PCN, ECoG and behavior were markedlly aneliorated respectively for 40% and 50% of rats.In epilepsy group induced by injection of PCN in hippocampus, the ECoG was siguificantly ameliorated in 50% rats. In epileptic rabbit group induced by partial injection of strychnine via cerebral cortex, the epilepti form wave iu ECoG was controlled by VNS in 50 % of animals.CONCLUSION: VNS can effectively suppress seizure of epileptic animals. The antiepileptic effect of VNS is associated with cerebral cortical aud hippcampal neurons. Somatic epileptiform activity could be effectively inhibited by the integration of visceral afferent information in cortical and hippocampal parts.

Objective To explore initially the role of extracellular signal-regulated kinase (ERK1/2) in cerebral ischemic preconditioning. Methods Healthy adult SD rats were randomly divided into 5 groups: normal control group; sham group; ischemic preconditioning or ischemia tolerance group; bee venom group; peripheral noxious tolerance group. SDS-PAGE, Western blot and Gel Doc imagine systems were applied to determine the ERK1/2 phosphorylation and protein expression in somatosensory cortex and hippocampus of rats. Results The phosphorylation level of ERK1 in somatosensory cortex increased significantly (P<0.05) after ischemic preconditioning, while no significant changes in ERK2 and that of ERK1/2 in hippocampus. No significant changes in ERK1/2 protein expression were found both in somatosensory cortex and hippocampus after ischemic preconditioning. Conclusion The increased ERK1 phosphorylation level in somatosensory cortex may be involved in cerebral ischemic preconditioning.

Objective To explore initially the role of p38 mitogen activated protein kinases(p38 MAPK) in cerebral ischemic preconditioning.Methods Healthy adult SD rats were randomly divided into 5 groups: normal control group,sham-operated group,ischemia preconditioning or ischemia tolerance group,peripheral noxious control group,peripheral noxious tolerance group.SDS-PAGE,Western blot and Gel Doc imagine systems were applied to determine the p38 MAPK phosphorylation and protein expression in somatosensory cortex and hippocampus of rat.Results No significant changes of p38 MAPK in phosphorylation level and protein expression were found both in somatosensory cortex and hippocampus after ischemia preconditioning(P>0.05,n=6).Conclusion The development of cerebral ischemia preconditioning of rat might be not involved the phosphorylation and protein expression of p38 MAPK.

Objective To explore initially the role of c-Jun N-terminal protein kinases (JNK) in cerebral ischemia preconditioning.Methods Healthy adult SD rats were randomly divided into 5 groups: control group, sham-operated group, ischemic preconditioning or ischemic tolerance group, bee venom group, peripheral noxious tolerance group. SDS-PAGE, Western blot and Gel Doc imagine systems were applied to determine the JNK phosphorylation and protein expression in somatosensory cortex and hippocampus. Results The phosphorylation level of JNK46KD but not JNK54KD in somatosensory cortex increased significantly (P<0.05) after ischemia preconditioning, while no significant changes had been observed in that of JNK46KD and JNK54KD in hippocampus. In addition, the protein expression level of JNK46KD but not JNK54KD fell on control level in somatosensory cortex after ischemic preconditioning, while no significant changes in JNK46KD and JNK54KD protein expression were found in hippocampus. Conclusion The increased JNK46KD phosphorylation and fallen JNK46KD protein expression in somatosensory cortex may be involved in the development of cerebral ischemia preconditioning.

Objective To explore initially the roles of the 3 major signaling pathways of mitogen activated protein kinases (MAPK) in cerebral ischemia preconditioning. Methods Healthy adult SD rats were randomly divided into 3 groups: normal control group; sham-operated group and ischemic preconditioning or ischemic tolerance group (n=6). SDS-PAGE, Western blot and Gel Doc imagine systems were applied to determine the phosphorylation and protein expression of ERK, JNK and p38 in somatosensory cortex of rat. Results The phosphorylation level of ERK1 and JNK46KD in somatosensory cortex increased significantly (P<0.05) after ischemia preconditioning. Conclusion The increased ERK1 and JNK46KD phosphorylation in somatosensory cortex may be involved in the development of cerebral ischemia preconditioning and can not be ruled out in which the role of p38.

Objective To investigate whether the new mechanically-activated (MA) cation channel Piezo 1 protein can cause the apoptosis of human chondrocytes under compressive loading,using a Flexercell unit by activating MAPK/ERK5 signal pathway.Methods Primary human chondrocytes were isolated,cultured,and then subjected to the static compressive loading for 2 h,12 h,24.h and 48 h,respectively.The GsMTx4,which is the special inhibitor of the Piezo1 protein and the BIX02188,which is the inhibitor of the ERK5 served as the inhibitor group.The immunofluorescence was used to locate the expression of the Piezo 1 protein.The expressions of Piezo1 and ERK5 were assessed by reverse transcription-polymerase chain reaction (RT-PCR),as well as the apoptosis gene B cell lymphoma/leukemia-2 (Bcl-2),Bcl-associated X protein (Bax) and Bcl-associated death promoter (BAD).In addition,Piezo1 inhibitor,GsMTx4,was used to block the MA cation channel Piezo1,served as the inhibitor group.AVPI was used to detect the apoptosis of the OA chondrocytes.Results The location of the Piezo1 was expressed in nucleus and cytoplasm of chondrocytes.The expression of the Piezo1,ERK5,BAD,and Bax mRNA in the OA chondrocytes is weak.The 12 h stretch force group was significant increased,and the 24 h stretch force group was the highest expression.However,the expression of the 48 h group was decreasing.The expression of the Bcl-2 in the 12 h group was decreasing,and the 12 h stretch force group was the lowest expression while the 24 h stretch force group was increasing.In the GsMTx4 group,the expression of the Piezo1,ERK5,BAD,Bax was decreasing while the Bcl-2 was increasing.In the BIX02188 group,the expression of the ERKS,BAD,Bax was increasing while the Bcl-2 was decreasing,while the expression of the Piezo1 was not change.The result of AV-PI shown that the 2 h stretch force group increased early stage of apoptosis.The 12 h stretch force group increased late stage of apoptosis,and the 24 h stretch force group's apoptotic rate was the highest.However,the apoptotic rate of the 48 h group was lower than the 24 h stretch force group.The GsMTx4 could inhibit the late stage of apoptosis.Conclusion Piezo 1 plays an important role in the apoptosis of human chondrocyte through the MAPK/ERK5 signal pathway.

Objective To understand the present status of human parasitic infections and their characteristics in rural areas of the southern part of Jiangsu Province, to provide basis of making practical control measures.Methods Four thousand and eighty-two people were examined with stool tests and those people were distributed in 8 slected spots in the southern part of Jiangsu Province,according to the methods of national investigation scheme on human principal parasites. Results The avarage infection rate of parasites was 6.71%. The male and female infection rates of parasites were 4.77% and 8.42%,respectively. There were significant differences (P