Objective To establish a multi-drug resistant model of temporal lobe epilepsy,and then the sodium current of pyramidal neurons in CA1 areas of the hippocampus was used as as index to observe the effect of hippocampal stimulation on pharmacoresistant epileptic rats.Methods Eighty Wistar rats were selected to prepare an amygdaloid kindled model of epilepsy by chronic stimulation of amygaloid basal lateral nucleus.When the kindled model of epilepsy was prepared successfully,the pharmacoresistant epileptic rats were selected according their response to phenobabital and phenytoin.The selected pharmacoresistant epileptic rats were divided into a hippocampal stimulation group (HS group) and a pharmacoresistant control group (PR group).A low-frequency hippocampal stimulation was performed in the HS group,while the PR group received sham stimulation.The whole-cell recording technique by patch-clamp was used to observe the changes of sodium current of hippocampal pyramidal neurons after the hippocampal stimulation.Results Compared with the PR group,the pharmacoresistant epileptic rats in HS group underwent low-frequency stimulation for 2 weeks showed that the amygdale stimulus-induced seizures were decreased (2.32 ± 0.38 in HS group and 4.45 ± 0.42 in PR group,t =84.600,P =0.000) and the parameters of the after-discharges were improved significantly.In HS group,the peak current shifted towards depolarization,the sodium channels were difficult to activate,and were more susceptible to inactivation.Moreover,the recovery time after the sodium channel inactivation was slower in HS group ((17.9 ±0.6) s) than in PR group((16.3 +0.3) s,t =-25.420,P =0.000).Conclusions Hippocampal stimulation may inhibit the sodium channel current of pyramidal neurons in CA1 areas of hippocampus.The mechanism of hippocampal stimulation in the treatment of pharmacoresistant epilepsy might be achieved partly by inhibiting the sodium channel current so as to decrease the excitability of hippocampal neurons.

31 patients with cysticercosis of cerebral ventricles verified by operation or pathological investigation were reported. All patients were between 7 and 64 years of age and 14 were females. All had a single cyst. Since 29 patients (94%) were without a history of intestinal taeniasis, it was proposed that most patients of cysticercosis of cerebral ventricles were caused by hetero-infection and the entrance of Cysticercus into brain ventricle was through choroid plexus along the cerebro-spinal fluid. This is probably the reason why it occurs mostly in the 4th ventricle. The clinical manifestation of cysticercosis of cerebral ventricles were paroxysmal headache and vomiting caused by increased intracranial pressure. Ventricu-lography and CT scanning have considerable diagnostic value. Removal of Cysticercus by surgical operation is successful (Figs. 1 - 8).

Objective: To investigate the regulatory effects of interferon-stimulated gene Schlafen (SLFN) on hepatitis B virus (HBV) replication. Methods: Firstly, HepG2 cells were treated with IFN-α at different concentrations for 48 h or the same concentration for different periods of time. Expression of SLFN family genes was detected by quantitative real-time PCR (q-PCR). Secondly, the expression of SLFN gene family at mRNA level in HBV-infected tumor tissues and non-tumor tissues recorded in The Cancer Genome Atlas (TCGA) database was compared using t test. Furthermore, changes in the HBV DNA levels after the interference of small interfering RNA (siRNA)-mediated knockdown and overexpression of SLFN5 and SLFN11 genes were analyzed by q-PCR, Western blot and Southern blot. Results: Among the SLFN gene family, only SLFN5 expression was induced by IFN-α in a concentration-dependent manner. TCGA database analysis showed that the expression of both SLFN5 and SLFN11 in HBV-infected tumor tissues and non-tumor tissues was significantly different. In HepG2 cells, knocking down the expression of SLFN5 had no obvious effect on the levels of intracellular HBV DNA. It was observed that the level of intracellular HBV DNA increased 1.79 folds in Huh7 cells after knockdown of SLFN11 expression, while no significant change in HBc protein was detected. Conversely, overexpression of SLFN11 induced a 34.67% decrease in intracellular HBV DNA in HepG2 cells. Conclusions In HepG2 cells, SLFN5 expression was induced by IFN-α, but had no effect on HBV replication. However, SLFN11 could inhibit the HBV DNA replication in nucleocapsid.

Objective To investigate the regulatory role of host restriction factor Moloney leukemia virus 10 (MOV10) protein in HBV replication. Methods Firstly, a HBV replication-expression plasmid was transfected into Huh7 cells to investigate the effect of HBV replication on MOV10 expression. Secondly, HBV DNA was extracted and measured by quantitative PCR ( qPCR) after knocking down the expression of endogenous MOV10 or enhancing the expression of exogenous MOV10. Furthermore, MOV10 conserved do-mainⅡenzyme active mutants (D645A, E646Q and G648A) were constructed and analyzed regarding their antiviral activities. The HBV replication plasmid and MOV10 expression plasmid were co-transfected into hu-man renal epithelial cells (HEK293) to investigate whether MOV10 could bind to HBV mRNA using RNA binding protein immunoprecipitation ( RIP) . Results The expression of MOV10 was increased after trans-fection of HBV replication plasmid into Huh7 cells. After knocking down the expression of endogenous MOV10 by siRNA in Huh7 cells, HBV replication was increased about 1. 5 times compared with control group, while the viral DNA level was significantly decreased in Huh7 cells that overexpressed MOV10. MOV10 domain Ⅱ mutants also significantly inhibited HBV replication. MOV10 could bind to 3. 5 kb HBV RNA. Conclusion In liver cancer cells, the expression of the host restriction factor MOV10 was associated with HBV replication. Its inhibitory effect against HBV replication was independent of its helicase activity, but might be associated with its binding activity with 3. 5kb HBV RNA.