Central nervous system demyelination in children include acute disseminated encephalomyelitis (ADEM),multiple sclerosis (MS),optic neuritis(ON),transverse myelitis(TM),neuromyelitis optica(NMO).Most of these conditions are thought to be caused by immune -mediated demyelination triggered by an infectious agent in a ge-netically susceptible host.There are certain differences,including clinical features and imaging features,for these condi-tions.With the possible exception of the NMO -IgG autoantibody found in NMO,there are no disease -specific biomar-kers for these conditions,making it difficult to distinguish among them at the time of the initial presentation.However, certain clinical features,laboratory results,and imaging findings can usually lead to the correct diagnosis.MS is to a large extent still a diagnosis of exclusion,and therefore requires intense investigation for other conditions that might present in a similar manner.

Objective:To explore the change in virulence of Campylobacter jejuni (CJ) mutant after galE gene knock-out.Methods: Using Hep-2 cells, adherence and invasion assays were performed in the galE mutant and the parent strain, meanwhile, serum sensitivity assay and motility test were made in them. Results:The galE mutant showed a reduction in its ability to adhere to and invade Hep-2 cells. The ability of the galE mutant and parent strain to adhere to Hep-2 cells were 1.2 % and 8.3% respectively, and adherence ability of the former only was 14.5% of that of the latter. The difference was significant ( P

Convulsive status epilepticus (CSE) is an acute,life-threatening and neurologic emergency in children.The prognosis and the incidence of recurrent CSE depend upon the underlying etiology.It is very important to find related etiology and seek solution.The underlying etiology,classification and the diagnostic evaluation of the children with CSE will be outlined in this article.

Objective:To explore if galE knock-out mutant of Campylobacter jejuni(CJ) have a changed lipooligosaccharide(LOS) structure.Methods:Lipooligosaccharide from parental strains(CJ HB9313) and mutant strains were isolated and purified.The purified LOS preparations from parental and mutant strains were resolved by Tricine SDS polyacrylamide gel electrophoresis(PAGE),analyzed by silver staining and Western blot,tested for reaction with the ganglioside-binding ligands of cholera toxin(CT).Results:Silver staining showed that the parent strain expressed a LOS molecule of around 5 5 kD,whereas the galE mutant strain expressed a molecule of 4.5 kD.The Western blot showed that the LOS,expressed by galE mutant strain,no longer reacted with antiserum raised against CJ HB9313.Compared with parent strain,the mutant lost reactivity with CT.Conclusion:These results indicate that LOS molecule of galE mutants is truncated and removes epitopes that react with antiserum and ganglioside-like structures.The absence of these structures in the galE mutants may enable the development of a safe,live-vaccine without the possibility of inducing an immune response to host gangliosides.

Nonconvulsive status epilepticus (NCSE)is a peculiar kind of status epilepticus,which is not un-common in children,but it always be misdiagnosed due to its unnoticeable clinical signs.So far,there is no international unifying diagnose standard of NCSE.Therefore,electroencephalography(EEG)monitoring is recommended.Now,the progress in this field of clinical manifestation and EEG features of NCSE was reviewed.

0.05).The sera from animals immunized with parental strains had significant higher titer of IgG antibodies against GM1,GD1a and GT1b,at 14 and 28 day than before immunization(P

Persister cells are dormant or slowly grown variations in microbial populations .They are highly tolerant to antibiot-ics but the tolerance are not inherited as the genetic resistance , when persisters are inoculated to fresh medium , most bacteria are still susceptive to antibiotic , while only a small fractiont become persisters again .Persisters are believed to be closely related to clinic bio-film forming and the recurrence and recalcitrance of chronic infections .Different persisters have been found in Escherichia coli , Pseud-omonas aeruginosa , Staphyococcus aureus , Mycobacterium tuberculosis , Candida albicans and so on , and a few mechanisms about per-sisters formation have been studied .This article reviews the current progresses of research methods and achievements on persisters from different levels .

Objective To investigate the effect of cardiotrophin-1 (CT-1) mediated by recombinant adenovirus (Adv) on the neural differentiation of bone marrow mesenchymal stem cells (rBMSCs) of rats.Methods The rBMSCs were isolated and cultured by attachment method.The surface marker protein was identified by flow cytometry.The rBMSCs were divided into 4 groups:control group,AdV enhanced green fluorescence protein (Adv-EGFP) + induction group(empty virus group),CT-1 group and induction group.The cells were transfected by Adv in the corresponding multiplicity of infections.Each group was induced by neural induction medium except for control group.The cells morphological changes were observed by microscope and the expressions of Nestin,neuronal nuclei (NeuN) and glial fibrillary acidic protein(GFAP) were detected respectively by cellular immunofluorescence at 5 h,3 d and 7 d after induction.Results After induction treatment,neuron-like cells morphological changes were observed in all the groups except for control group,among which the most obvious change was found in CT-1 group.The positive rate of Nestin was the highest at 5 h after induction.Positive rate of CT-1 group[(86.31 ± 4.27)％] was higher than any other groups,the differences were statistically significant (all P ＜ 0.001);after which its positive rate gradually declined,the positive rate of CT-1 group changed more obviously than other groups,and the differences were statistically significant (all P ＜ 0.001).The difference in Nestin positive rate between the empty virus group and induction group was not statistically significant (all P ＞ 0.05) at various time points.The NeuN and GFAP could be observed in CT-1 group at 5 h after induction.Then the positive rate of NeuN and GFAP increased gradually,and climbed to the highest point [(64.41 ± 3.65)％,(47.14 ± 4.29)％] on 7 d after induction.Positive rate of NeuN and GFAP in CT-1 group at various time points were higher than that of other groups,and the differences were statistically significant (all P ＜0.001).The difference of NeuN and GFAP positive rate between the empty virus group and induction group was not statistically significant (all P ＞ 0.05).Conclusion CT-1 could promote the neural differentiation of rBMSCs.

AIM:To set up a glutamate-induced cell damage model in cultured hippocampal neurons, and to determine whether glutamate-induced neuronal apoptosis changes and whether this process is mediated by mitochondrial signal transduction pathways involving the release of cytochrome C. METHODS: Hippocampal neurons, isolated and cultured from new born Wistar rats, were exposed to various concentrations of glutamate. Extent of cell death was assessed by measuring the release of lactate dehydrogenase (LDH) in the culture media. Based on these data, an appropriate concentration of glutamate was selected, and all subsequent experiments were carried out under the concentration. Kinetics of glutamate-induced both apoptotic and necrotic cell death after exposure to glutamate for various times(3-24 h) were determined by flow cytometry and LDH release. The caspase-3 protein levels and cytochrome C release from mitochondria into cytosol in hippocampal neurons were determined by Western blotting. RESULTS: Glutamate treatment induced hippocampal neurons death in dose-dependent and time-dependent manners. A significant increase in LDH release (18.4%) was induced in the cells treated with 50 ?mol/L glutamate, compared to control untreated cells(P