巴蜀地区的“小神子”信仰及其文化谱系

从明朝初年开始,大批汉族移民跟随远征的军队从江浙一带进入到西南地区,随之带来的邪恶神灵(如五通神等)被当地原住民贬称为"小神子"。在不同的族群文化和民间宗教快速嬗变的过程中,小神子也逐渐演化成为一种无意识的集体信仰。据说其神性与一般的主神不同,虽然它能给主人家带来数不尽的财富,但若有人对之稍有不恭,它便行捉弄害人之事。因此普通村民对它都存有敬畏心理。在民间传说中人们又不断添加进去一些想象和诬蔑的成分,最终使得小神子被妖魔化成为地道的恶神。

Lipopolysaccharide-induced cerebral inflammatory damage and the therapeutic effect of platelet activating factor receptor antoganist

Objective To investigate lipopolysaccharide （LPS） induced acute cerebral inflammatory damage and the therapeutic effect of ginkgolide B （BN52021）. Methods Thirty Sprague-Dawley rats were randomly divided into 3 groups （n = 10 for each group）： Control group, Model group and Treatment group （treated with BN52021）. LPS were injected into the fourth ventricle of rat to make a neuroinflammatory murine model. Morris water maze was used to detect the learning and memory ability of rats; changes of synapse number and subcellular ultrastructures were observed under a transmission electron microscope; OX-42 positive microglia in the brain was detected by immunohistochemical method. Results The average escape latency in the Treatment group were significantly shortened than that in the Model group; and the percentage of swimming distance traveled in platform quadrant accounting for total distance increased markedly. The rough endoplasmic reticulum and polyribosomes in the Treatment group were more than that in the Model group, but the number of synapses seemed to have no obvious change. The number of OX-42 positive microglia in the Treatment group decreased markedly than that in the Model group, and the grey density of OX-42-positive cells increased significantly. Conclusion LPS can induce inflammatory damages to the brain, but the damage could be antagonized by BN52021. Platelet activating factor receptor antagonist may offer an effective therapy for neurodegeneration diseases.

The therapeutic mechanism of Shenyuan Gan in lipopolysaccharide-induced neuroinflammation in BV2 microglial cells

Objective To study the therapeutic effects of Shenyuan Gan(参远苷,SYG)on the inflammat-ory response in BV2 microglial cells induced by lipopolysaccharide(LPS).Methods The cytotoxicity of SYG to BV2 microglial cells was evaluated using a Cell Counting Kit-8(CCK-8)assay,and the effect of SYG concentrations on LPS-induced BV2 microglial cells was studied.The morphological changes were observed using an optical microscope.The nitric oxide(NO)concentration in cell culture supernatant was determined using Griess re-agent.The expression of cytokines and inflammatory mediators were also measured by an en-zyme-linked immunosorbent assay(ELISA).Western blot analysis was used to determine the levels of inducible NO synthase(iNOS),nuclear factor-kappa B(NF-κB)p65,alpha inhibitor of NF-κB(IκB-α),phosphorylation-IκB-α(p-IκB-α),NOD-like receptor 3(NLRP3),and cas-pase-1 expression.Moreover,the expression of iNOS,NLRP3,and ionized calcium binding adapter molecule 1(Iba1)was also observed using immunofluorescent staining.Results SYG had a low cytotoxic effect on BV2 microglial cells and could significantly decr-ease LPS-induced morphological changes of BV2 microglial cells(P<0.05).ELISA results showed that SYG significantly inhibited the LPS-induced increase in interleukin(IL)-1βand IL-6 in BV2 microglia cells(P<0.05),and Western blot analysis showed that the phosphoryla-tion levels of iNOS,NF-κB p65,and IκB-αas well as NLRP3 and caspase-1 expression were also significantly decreased,and IκB-αexpression was increased after SYG treatment(P<0.05,compared with the LPS-treated group).The immunofluorescence results were consist-ent with the Western blot results,and Iba1 staining indicated that the cell morphology tended to be resting.These results indicate that SYG has a certain inhibitory effect on LPS-induced inflammation in BV2 microglial cells.Conclusion SYG can inhibit LPS-induced release of inflammatory factors in BV2 microglial cells by affecting the phosphorylation levels of NF-κB p65 and IκB-α.SYG is a valuable candid-ate for treating neuroinflammation-related diseases.

MicroRNAs in neural cell development and brain diseases

MicroRNAs play important roles in post-transcriptional regulation of gene expression by inhibiting protein translation and/or promoting mRNA degradation.Importantly,biogenesis of microRNAs displays specific temporal and spatial profiles in distinct cell and tissue types and hence affects a broad spectrum of biological functions in normal cell growth and tumor development.Recent discoveries have revealed sophisticated mechanisms that control microRNA production and homeostasis in response to developmental and extracellular signals.Moreover,a link between dysregulation of microRNAs and human brain disorders has become increasingly evident.In this review,we focus on recent advances in understanding the regulation of microRNA biogenesis and function in neuronal and glial development in the mammalian brain,and dysregulation of the microRNA pathway in neurodevelopmental and neurodegenerative diseases.

Identification and functional annotation of novel microRNAs in the proximal sciatic nerve after sciatic nerve transection

The peripheral nervous system is able to regenerate after injury, and regeneration is associated with the expression of many genes and proteins. MicroRNAs are evolutionarily conserved, small, non-coding RNA molecules that regulate gene expression at the level of translation. In this paper, we focus on the identification and functional annotation of novel microRNAs in the proximal sciatic nerve after rat sciatic nerve transection. Using Solexa sequencing, computational analysis, and quantitative reverse transcription PCR verification, we identified 98 novel microRNAs expressed on days 0, 1, 4, 7, and 14 after nerve transection. Furthermore, we predicted the target genes of these microRNAs and analyzed the biological processes in which they were involved. The identified biological processes were consistent with the known time-frame of peripheral nerve injury and repair. Our data provide an important resource for further study of the role and regulation of microRNAs in peripheral nerve injury and regeneration.

Cross-reactivity of anti-programmed death ligand 2 polyclonal antibody in mouse tissues

The inhibitory co-receptor programmed death 1 （PD-1, encoded by pdcdl） and its two ligands PD-L1 and PD-L2 comprise an important immune inhibitory signaling pathway for defense against microbes and for self-tolerance. Unlike other members of the B7-CD28 family, expression of PD-L1 and PD-L2 is not limited to the immune system. In this study, we determined that a polyclonal antibody （pAb） （R＆D Systems） against extracellular domains of mouse PD-L2 （mPD-L2） could recognize anti- gen（s） in diverse mouse tissues, including the anterior and intermediate pituitary gland, olfactory bulbs and olfactory epitheli- um, tongue epithelium, keratinized epithelial ceils and skin and whisker hair follicles. These findings differed from previous reports of mPD-L2 localization. Reverse transcription PCR and Western blot analyses, however, were unable to detect any mPD-L2 transcripts or proteins of the 25-kD predicted molecular weight in RNA and protein extracts, respectively, from the above tissues, suggesting that the anti-mPD-L2 pAb cross-reacts with certain novel antigen（s）. Developmental studies revealed that the earliest expression of mPD-L2-1ike antigen was in the olfactory epithelium at embryonic day 12.5 （E12.5）. At E14.5, mPD-L2-1ike antigen was present in the skin, tongue and follicles of the skin and whiskers. The distribution patterns of mPD-L2-1ike antigen remained similar from E18.5 to adulthood. The results of bioinformatic analysis and other experiments suggested neural cell adhesion molecule and hemicentin-1 as candidate proteins with cross-reactivity to the anti-mPD-L2 pAb. These results demonstrate that care is required in interpreting staining patterns generated when anti-PD-L2 pAb is used to lo-cate PD-L2-expressing cells in the central nervous system and epithelial tissues, such as the olfactory epithelium. In addition, this anti-PD-L2 pAb may be used as an alternative antibody for labeling the olfactory epithelium during embryonic develop-ment in mice.