简介：AbstractBird infections with highly pathogenic avian influenza A(H5N6) viruses have been identified since 2014. With very limited occasion, the virus could sporadically spilled over to infect humans. It has been recognized that all human infections were within southern region of Mainland China until the case reported here in Beijing in Aug. 2019. This was the first human case infected with highly pathogenic avian influenza A(H5N6) virus in northern China. The infection was confirmed by real-time RT-PCR assay. The whole genome sequences were obtained from clinical sample. Genetic characteristics of the virus were identified similar to those of previous avian influenza A(H5N6) viruses, retaining the main features of the avian influenza virus.

简介：Oncolysate,adebrisoftumorcells,hasbeenproventobeeffectiveintumoractiveimmunotherapy,itwasreportedthatthevacciniavirus,especiallyrecombinantvacciniavirusesencodinghumanIL-2(rVV-IL-2),enhancedtheimmunogenicityoftransfectedtumorcells.Inthisexperiment,themurinemelanomacellB16-F10oncolysatestransfectedbyrVV-IL-2(IL-2VBO)wereusedasvaccine.TheIL-2VBOorTK-VBOwaspreparedbyincubatingB16-F10cellswithrVV-IL-2orrVV-TKat

简介：2009H1N1流行性感冒流行表明了对人的全球健康威胁的意义。尽管流行H1N1疫苗很快被开发了，被动serotherapy可以在孩子对感染提供优异立即的保护，老、妥协免疫者的病人在流行性感冒期间流行。这里，我们基于使不朽的Epstein-Barr病毒(EBV)使用了新奇策略从个人屏蔽高病毒的抵销monoclonal抗体(MAbs)的外部血记忆B房间与2009流行H1N1疫苗的PANFLU.1种牛痘。通过13090使不朽的记忆B房间的一幅巨大的屏幕，从三的克隆选择了vaccinees，七MAbs与两个高病毒的抵销能力和红血球凝聚抑制(HAI)被识别对2009个流行H1N1病毒的活动。这些MAbs可以与严重呼吸症候群为感染的病人的被动serotherapy治疗有重要临床的含意，特别孩子，老并且immunodeficient个人。我们为从使EBV不朽的外部血记忆B房间产生高亲密关系的MAbs的成功的策略可能也对另外的传染或自体免疫的疾病适用。

简介：LearningfromthepainfullessonsoftheWorldWarII,humanrightstheoryrediscoveredthevalueofhumandignity,andmadetheprotectionofhumandignitythebasisandpurposeofhumanrightsprotection.Anyabuseofhumanrightsisaninfringementonhumandignity.Howhumandignityisrespectedandvaluedisameasureofasociety’shumanrightssituation.Humanrightswill

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简介：AbstractEbola virus (EBOV) is one of the most pathogenic viruses in humans which can cause a lethal hemorrhagic fever. Understanding the cellular entry mechanisms of EBOV can promote the development of new therapeutic strategies to control virus replication and spread. It has been known that EBOV virions bind to factors expressed at the host cell surface. Subsequently, the virions are internalized by a macropinocytosis-like process, followed by being trafficked through early and late endosomes. Recent researches indicate that the entry of EBOV into cells requires integrated and functional lipid rafts. Whilst lipid rafts have been hypothesized to play a role in virus entry, there is a current lack of supporting data. One major technical hurdle is the lack of effective approaches for observing viral entry. To provide evidence on the involvement of lipid rafts in the entry process of EBOV, we generated the fluorescently labeled Ebola virus like particles (VLPs), and utilized single-particle tracking (SPT) to visualize the entry of fluorescent Ebola VLPs in live cells and the interaction of Ebola VLPs with lipid rafts. In this study, we demonstrate the compartmentalization of Ebola VLPs in lipid rafts during entry process, and inform the essential function of lipid rafts for the entry of Ebola virus. As such, our study provides evidence to show that the raft integrity is critical for Ebola virus pathogenesis and that lipid rafts can serve as potential targets for the development of novel therapeutic strategies.

简介：Whitespotsyndromevirus(WSSV)isoneofthemajorshrimppathogenscausinglargeeconomiclossestoshrimpfarming.Inanattempttoidentifytheenvelopeproteinsinvolvedinthevirusinfection,purifiedWSSVvirionsweremixedwiththreeantiseraagainstWSSVenvelopeproteins(VP39,VP124andVP187),individually.Andthentheywereinjectedintramuscularlyintocrayfish(Procambarusclarkii)toconductinvivoneutralizationassays.TheresultsshowedthatforgroupsinjectedwithvirionsonlyandgroupsinjectedwiththemixtureofvirionsandantiserumagainstVP124,thecrayfishmortalitieswere100%and60%onthe8thdaypostinfection,individually.ThevirusinfectioncouldbedelayedorneutralizedbyantibodyagainsttheenvelopeproteinVP124.QuantitativePCRwasusedtofurtherinvestigatetheinfluenceofthreeantiseradescribedaboveonthevirusinfection.TheresultsshowedthattheantiserumagainstVP124couldrestrainthepropagationofWSSVincrayfish.AlloftheresultssuggestedthattheviralenvelopeproteinVP124playedaroleinWSSVinfection.

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简介：AbstractBackground:Acinetobacter baumannii (A. baumannii) has become one of the most important opportunistic pathogens inducing nosocomial pneumonia and increasing mortality in critically ill patients recently. The interaction between A. baumannii infection and immune response can influence the prognosis of A. baumannii related pneumonia. The target of the present study was to investigate the role of immunodeficiency in A. baumannii induced pneumonia.Methods:Male BALB/c mice were randomly divided into the normal immunity control (NIC) group, normal immunity infection (NIA) group, immune compromised control (CIC) group, and immune compromised infection (CIA) group (n = 15 for each group). Intraperitoneal injection of cyclophosphamide and intranasal instillation of A. baumannii solution were used to induce compromised immunity and murine pneumonia, respectively. The mice were sacrificed at 6 and 24 h later and the specimens were collected for further tests. Seven-day mortality of mice was also assessed.Results:After A. baumannii stimulation, the recruitment of neutrophils in mice with normal immunity increased sharply (P = 0.030 at 6 h), while there was no significant raise of neutrophil counts in mice with compromised immune condition (P = 0.092 at 6 h, P = 0.772 at 24 h). The Th cell polarization presented with pulmonary interleukin (IL)-4 and interferon (IFN)-γ level in response to the A. baumannii in CIA group were significantly depressed in comparison with in NIA group (IFN-γ: P = 0.003 at 6 h; P = 0.001 at 24 h; IL-4: P < 0.001 at 6 h; P < 0.001 at 24 h). The pulmonary conventional dendritic cell accumulation was even found to be inhibited after A. baumannii infection in immunocompromised mice (P= 0.033). Correspondingly, A. baumannii associated pneumonia in mice with compromised immunity caused more early stage death, more severe histopathological impairment in lung.Conclusion:A. baumannii could frustrate the immune response in immunocompromised conditions, and this reduced immune response is related to more severe lung injury and worse outcome in A. baumannii induced pneumonia.

简介：Inhisgovernmentworkreporttothe3rdSessionofthe11thNationalPeople’sCongress(NPC)onMarch5,2010,ChinesePremierWenJiabaosaid:"Everythingwedoistomakethepeoplelivehappierandmoredignified,makethesocietymorejustandmoreharmonious."Thisisheldupbythemediaasthe

简介：AbstractFoot-and-mouth disease virus (FMDV), swine vesicular disease virus (SVDV) and classical swine fever virus (CSFV) all cause important animal diseases. FMDV affects many different cloven-hoofed animals, whereas SVDV and CSFV are restricted to domestic and feral pigs together with wild boar. Europe is normally free of these diseases, but occasionally outbreaks happen, which can cause huge economic losses. Handling of these viruses, in particular FMDV and CSFV, is only allowed within high containment laboratories and stables. Periodically such facilities need to be decommissioned for repair or closing down, which is done by cleaning and chemical disinfection, followed by fumigation due to residual risk from virus on surfaces in inaccessible places. However, building materials in older laboratories or stables that have housed infected animals may not be well-suited for fumigation. Heat treatment is another way of inactivating viruses. In this study, we have determined the survival of infectivity in air-dried virus samples on glass and plastic surfaces incubated at room temperature or heated to 70 °C for 1, 2, 3, 5 and 7 days. Each of the tested viruses was inactivated to below the limit of detection after 24 h or 48 h of incubation at 70 °C; in contrast, some of these viruses were still infectious after 7 days of incubation at room temperature. This study provides important information that can be used in relation to decontamination of buildings and in risk-assessments.

简介：继去年9月的‘樱花’病毒之后前些日子又有一个叫“正版骗子”的病毒在网络上流传开采．和“樱花”病毒相同．该病毒也是拿反病毒厂商的杀毒软件开涮．不但会终止这几款杀毒软件．还会弹出具有迷惑性语言的对话框，给国内杀毒软件的正版用户开了一个大大的玩笑。

简介：在xenotropic之间的潜在的协会鼠科的白血球过多症自从2006，病毒相关的gammaretrovirus(XMRV)和前列腺癌症(PCa)被记录了。查明这个协会是否是原因的，为推进我们PCa的生物机制的理解是重要的。总结可得到的信息在上流行病学并且协会的实验室调查结果，我们进行了PubMed电子数据库的文学搜索(从2006年3月到2011年2月)那检验了在XMRV和PCa之间的协会识别相关出版研究。尽管几研究显示出在XMRV和PCa之间的积极协会，更最近的研究没支持这个结论。积极调查结果可能由于人的样品的污染。进一步的研究被需要澄清这个协会。

简介：AbstractBackground:Endothelial cells play a key role in the cytokine storm caused by influenza A virus. MicroRNA-155 (miR-155) is an important regulator in inflammation. Its role in the inflammatory response to influenza A infection, however, has yet to be elucidated. In this study, we explored the role as well as the underlying mechanism of miR-155 in the cytokine production in influenza A-infected endothelial cells.Methods:Human pulmonary microvascular endothelial cells (HPMECs) were infected with the influenza A virus strain H1N1. The efficiency of H1N1 infection was confirmed by immunofluorescence. The expression levels of proinflammatory cytokines and miR-155 were determined using real-time polymerase chain reaction. A dual-luciferase reporter assay characterized the interaction between miR-155 and sphingosine-1-phosphate receptor 1 (S1PR1). Changes in the target protein levels were determined using Western blot analysis.Results:MiR-155 was elevated in response to the H1N1 infection in HPMECs (24 h post-infection vs. 0 h post-infection, 3.875 ± 0.062 vs. 1.043 ± 0.013, P = 0.001). Over-expression of miR-155 enhanced inflammatory cytokine production (miR-155 mimic vs. negative control, all P < 0.05 in regard of cytokine levels) and activation of nuclear factor kappa B in infected HPMECs (miR-155 mimic vs. negative control, P = 0.004), and down-regulation of miR-155 had the opposite effect. In addition, S1PR1 was a direct target of miR-155 in the HPMECs. Inhibition of miR-155 enhanced the expression of the S1PR1 protein. Down-regulation of S1PR1 decreased the inhibitory effect of the miR-155 blockade on H1N1-induced cytokine production and nuclear factor kappa B activation in HPMECs.Conclusion:MiR-155 maybe modulate influenza A-induced inflammatory response by targeting S1PR1.

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简介：Securityofsmarttechnologieslikesmartgridsandcrowdenergysystemscannotrelyonlyontechnicalsolutions,humansplayasignificantroleinfailure,securityculture,informationsecurity,cybersecurity,trustandsharing,andperceptionsandconcern.Thispaperinvestigatessecurityissuesinsmarttechnologiesandtherelatedroleofhumanfailure,whetheritisintentionalorunintentional.Methodsthathelpreducingthisfailurearediscussed.Ahumanorientedframeworkforfailurereductionispresentedinordertoenhancesecurity.IndexTermsCrowdenergy,humanrole,intentionalfailure,security,smartgrids,unintentionalfailure.1.IntroductionManystateofthearttechnologiesaretaggedwiththe'smart'label.Ingeneralunderstandingthismeansinterconnectedness,interactivityand4.0automation,i.e.theapplicationofsensorsandinformationandcommunicationtechnology(SICT)andprocessinganever-changingandexpandingdata/knowledgebase.Fromahigherpointofview'smart'standsbutformorethanjusttheabove-mentionedtechnicalaspects;alsoandinparticularsocial,political,economicandecologicalaspectswillbeaddressed.Thismeansthat'smartmeetschallengestoimprovesustainablewelfare'[1].Inthissense,forexample,thetermsmartgridaddressesnotonlythecommunicativeinterconnectionandcontroloftheentitiesofapowersystem,i.e.technology,butpreciselyalsosustainability,conservationofresources,renewability,andefficiency.Securityhasbeenveryimportantfornewtechnologiesandsystemslikeelectricalgridsandpowerplants.Theseneedtobesecuredcarefullybecauseweaknessesinthesecuritymightleadtopartialdamageandreductionofserviceinseveralways.Inextremecasesdestructioncanhap-

简介：Launchedin2002,theHumanRightsmagazineoperatesundertheauspicesoftheChinaSocietyforHumanRightsStudies,anon-governmentalorganizationinSPECIALconsultativestatuswiththeEconomicandSocialCounciloftheUnitedNations.ThemagazineisthefirstofitskindeverpublishedinChina.Whiledevotedtotheoreticalstudiesofhumanrightsandhumanrightseducation,itprovidesaforumfordialoguebetweenChinaandforeigncountriesonhumanrights-relatedissues.

简介：Launchedin2002.theHumanRightsmagazineoperatesundertheauspicesoftheChinaSocietyforHumanRightsStudies,anon-governmentalorganizationinSPECIALconsultativestatuswiththeEconomic

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