人乳头瘤病毒及宫颈癌疫苗的研究--解读2008年诺贝尔生理学或医学奖

德国科学家Harald zur Hausen因发现人乳头瘤病毒(HPV)导致子宫颈癌,与另外两位科学家共享了2008年的诺贝尔生理学或医学奖.HPV是一组小DNA病毒,目前已鉴定有118型.HPV感染人的上皮组织,诱发产生包括妇女宫颈癌和尖锐湿疣在内的多种良恶性增生性疾病,目前已有两种人乳头瘤病毒预防性疫苗上市.对病毒的生物学特性、致癌机制及相关的疫苗的研究进行综述.

Polypyrimidine Tract-Binding Protein Enhances Zika Virus Translation by Binding to the 5'UTR of Internal Ribosomal Entry Site

Objectives To identify the 5'untranslated region of Zika virus(ZIKV 5'UTR)RNA-binding proteins and to investigate the impact of the binding protein on the activity of internal ribosomal entry site(IRES)located in ZIKV 5'UTR and virus production.Methods Interacting proteins in U251 cells were captured using tRSA-tagged ZIKV 5'UTR RNA and tRSA-ZIKV 5'UTR RNA-binding proteins were visualized by SDS-PAGE silver staining,Subsequently,liquid chromatographytandem mass spectrometry(LC-MS/MS),bioinformatics analysis,and Western blot were used to identify the candidate proteins binding to ZIKV 5'UTR.Dicistronic expression assay and plaque forming assay were performed to analyze the effect of the binding protein on ZIKV IRES activity and ZIKV production,respecitvely.Results tRSA RNA pull-down assay,LC-MS/MS,and Western blot analysis showed that polypyrimidine tractbinding protein(PTB)bound to the ZIKV 5'UTR.Furthermore,dual luciferase reporter assay revealed that overexpression of PTB significantly enhanced the IRES activity of ZIKV(t=10.220,P<0.001),while PTB knockdown had the opposite effect(t=4.897,P<0.01).Additionally,virus plaque forming assay demonstrated that up-regulation of PTB expression significantly enhanced viral titer(t=6.400,P<0.01),whereas reducing PTB expression level weakened virus infectivity(t=5.055,P<0.01).Conclusion PTB positively interacts with the ZIKV 5'UTR and enhances IRES activity and virus production.

合理应用钙剂和钙通道阻滞药

介绍合理应用钙剂的必要性和基本原则,同时指出钙也是双刃剑。过度补钙和细胞内钙超载都会造成不良反应或危害。只有正确地认识和应用钙剂和钙阻滞药,才能更好地发挥其造福人类的效用。

Traditional Chinese Medicine(TCM)Domain Ontology:Current Status and Rethinking for the Future Development

The past twenty years have seen the increasingly important role of ontology in traditional Chinese medicine(TCM).However,the development of TCM ontology faces many challenges.Since the epistemologies dramatically differ between TCM and contemporary biomedicine,it is hard to apply the existing top-level ontology mechanically.“Data silos”are widely present in the currently available terminology standards,term sets,and ontologies.The formal representation of ontology needs to be further improved in TCM.Therefore,we propose a unified basic semantic framework of TCM based on in-depth theoretical research on the existing top・level ontology and a re-study of important concepts in TCM.Under such a framework,ontologies in TCM subdomains should be built collaboratively and be represented formally in a common format.Besides,extensive cooperation should be encouraged by establishing ontology research communities to promote ontology peer review and reuse.

The mechanism of galanthamine regulating IL-1β/IL-1RA ratio to ameliorate inflammatory microenvironment

In the present study,we aimed to evaluate the anti-inflammatory mechanism of galanthamine,a classic therapeutic drug for Alzheimer s disease(AD).The co-culture system of hippocampal nerve cell line HT-22 and microglial cell line BV-2 was established to observe the effect of galanthamine on the expressions of inflammatory factors induced by lipopolysaccharide(LP S).MTT method was used to observe the protective effect of galanthamine on neurons.ELISA and qPCR methods were used to detect the expressions of interleukin-β(IL-1β) and IL-1 receptor antagonist(IL-1 RA) at the protein and mRNA levels,respectively.IL-1β and IL-1 RA were evaluated by the ELISA method after pretreating with galanthamine and α7 nAChR blockerα-bungarotoxin(α-bun),mAChR blocker atropine(Atr),PI3 K inhibitor LY294002,IKKβ inhibitor SC514,or MEK inhibitor PD98059,respectively.The results showed that galanthamine significantly inhibited LPS-induced increased IL-1β and IL-1 RA expressions and maintained the ratio of IL-1β/IL-1 RA.α-Bun could block the regulatory effect of galanthamine on IL-1β and IL-1 RA.As PI3 K and NF-κB pathways were blocked,the regulatory effect of galanthamine on the IL-1β expression was significantly inhibited.Blocking PI3 K and MEK pathways could significantly inhibit the regulation of galanthamine on IL-1 RA expression.In summary,galanthamine regulated the inflammatory activity of the IL-1 subfamily to play an anti-inflammatory role mediated by α7 nAChR and PI3 K/NF-κB/MAPK pathways,which probably provided a new strategy for AD treatment.