简介：TheAmericanHeartAssociationandtheEuropeanResuscitationCouncilrecentlyrecommendedthatvasopressincanbeusedforcardiopulmonaryresuscitation,insteadofepinephrine.However,theguidelinesdonotdiscusstheeffectsofvasopressinduringcerebralresuscitation.Inthisstudy,weintraperitoneallyinjectedepinephrineand/orvasopressinduringcardiopulmonaryresuscitationinaratmodelofasphyxialcardiacarrest.Theresultsdemonstratedthat,comparedwithepinephrinealone,thepathologicaldamagetonervecellswaslessened,andthelevelsofc-JunN-terminalkinaseandp38expressionweresignificantlydecreasedinthehippocampusaftertreatmentwithvasopressinaloneorthevasopressinandepinephrinecombination.Nosignificantdifferenceinresuscitationeffectswasdetectedbetweenvasopressinaloneandthevasopressinandepinephrinecombination.Theseresultssuggestthatvasopressinaloneorthevasopressinandepinephrinecombinationsuppresstheactivationofmitogen-activatedproteinkinaseandc-JunN-terminalkinasesignalingpathwaysandreduceneuronalapoptosisduringcardiopulmonaryresuscitation.

简介：像成纤维细胞的synoviocytes(FLS)在风湿性关节炎(RA)贡献synovial增生。Smoothened(Smo)是发信号的声音的刺猬(嘘)的一个关键部件并且贡献肿瘤房间增长。这研究的目的是在RAsynoviocyte增长调查Smo的角色。FLS从RAsynovium被孤立。发信号的嘘用一个Smo对手(GDC-0449)和在FLS指向Smo基因的小介入RNA(siRNA)被学习。房间增长被使用kit-8试金和房间周期分发确定，apoptosis被流动cytometry评估。房间周期相关的基因和蛋白质被即时PCR和西方的污点检测。与GDC-0449或Smo-siRNA对待的FLS与控制相比显示出显著地减少的增长(P<；0.05)。有GDC-0449的孵化或有Smo-siRNA的transfection与控制相比导致了G1阶段房间的重要增加(P<；0.05)。房间周期拘捕被cyclinD1和E1mRNA表示的重要增加验证，在在Smo-siRNAtransfected房间的cyclin依赖的kinasep21mRNA表示的减少(P<；0.05)。cyclinD1的蛋白质表示也是在Smo基因以后的downregulated击倒(P<；0.05)。结果建议发信号的嘘以一种Smo依赖的方式在RA-FLSs增长起一个重要作用并且可以贡献synovial增生。指向嘘发信号可以帮助与RA在病人控制联合损坏。

简介：AbstractBackground:Degree of mucosal recovery is an important indicator for evaluating the therapeutic effects of drugs in treatment of inflammatory bowel disease (IBD). Increasing evidences has proved that tight junction (TJ) barrier dysfunction is one of the pathological mechanisms of IBD. The aim of this study was to observe whether enhancement of TJ can decrease colitis recurrence.Methods:Eighty C57BL/6 mice were randomly divided into four groups including normal group, colitis group, sulfasalazine (SASP) treated group, and traditional Chinese drug salvianolic acid B (Sal B) treated group. Colitis was established in mice by free drinking water containing dextran sulfate sodium, after treatments by SASP and Sal B, recombinant human interleukin-1β (IL-1β) was injected intraperitoneally to induce colitis recurrence.Results:Compared with sham control, cell apoptosis in colitis group was increased from 100.85 ± 3.46% to 162.89 ± 11.45% (P = 0.0038), and TJ dysfunction marker myosin light chain kinase (MLCK) was also significantly increased from 99.70 ± 9.29% to 296.23 ± 30.78% (P = 0.0025). The increased cell apoptosis was reversed by both SASP (125.99 ± 8.45% vs. 162.89 ± 11.45%, P = 0.0059) and Sal B (104.27 ± 6.09% vs. 162.89 ± 11.45%, P = 0.0044). High MLCK expression in colitis group was reversed by Sal B (182.44 ± 89.42% vs. 296.23 ± 30.78%, P = 0.0028) but not influenced by SASP (285.23 ± 41.04% vs. 296.23 ± 30.78%, P > 0.05). The recurrence rate induced by recombinant human IL-1β in Sal B-treated group was significantly lower than that in SASP-treated group.Conclusions:These results suggested a link between intestinal mucosal barrier dysfunction, especially TJ barrier dysfunction, and colitis recurrence. The TJ barrier dysfunction in remission stage of colitis increased the colitis recurrence. This study might provide potential treatment strategies for IBD recurrence.

简介：无

简介：Salmeterol是长行动的β；激活adenylatecyclase的2收缩筋，引起长持续的bronchodilation并且被用于许多年到控制气喘。然而，很少信息都不关于salmeterol的immunoregulatory效果是可得到的。我们发现salmeterol减少在表示了肿瘤坏死factor-alpha，interleukin-1和interleukin-6的质问变应原的老鼠的一个模型的支持inflammatorycytokines的生产。树枝状的房间(DC)是介绍抗原的房间并且在航线充当哨兵。我们发现了那salmeterol(10−5mol/l)减少了lipopolysaccharide引起的发炎(0.1µ；g/ml)在激活的鼠科的骨头导出髓的DC。而且，西方的污点证明这保护的效果被禁止通过原子factor-kappaB发信号部分调停(NF-κ；B)，激活mitogen的蛋白质kinase(MAPK)小径和津贴的戏剧性地减少的层次。我们建议salmeterol由modulatingDC调整导致变应原的气喘的发炎。在结论，我们提供DC是为对气喘的salmeterol的行动负责的目标免疫者房间的证据。

简介：AbstractObjective:The impact of dairy fat on inflammatory bowel disease remained inconclusive. We aimed to compare the effects of whole-milk and skimmed-milk consumption on the risk of inflammatory bowel disease using a Mendelian randomization analysis.Methods:We conducted a genome-wide association study of the preference for whole versus skimmed milk using data for 20,200 whole-milk consumers and 67,847 skimmed-milk consumers from the UK Biobank. The lead single nucleotide polymorphisms in the associated loci were identified at the genome-wide significance level, and were further employed as instrumental variables for whole-milk preference. We conducted a two-sample Mendelian randomization analysis with whole-milk preference as the exposure and inflammatory bowel disease as the outcome. The pleiotropic effects and heterogeneity of the instrumental variables were estimated using Mendelian randomization-Egger regression and Cochran Q test, respectively. This study was conducted using the UKB resources under the application "53536" . The UK Biobank was approved by the North West Multi-center Research Ethics Committee, the National Information Governance Board for Health and Social Care in England and Wales, and the Community Health Index Advisory Group in Scotland.Results:The genome-wide association study identified five lead nucleotide polymorphisms associated with whole-milk preference. Mendelian randomization indicated that whole-milk preference significantly decreased the risk of inflammatory bowel disease (β=-1.735, P=0.048). Of the two subtypes, whole-milk preference was associated with a lower risk of Crohn disease (β=-2.549, P=0.032), but had no significant effect on the risk of ulcerative colitis (β=-1.002, P=0.44).Conclusion:Consumption of whole-milk fat may protect against Crohn disease, compared with skimmed milk. This conclusion was based on causal inference in a cohort study, and further validation in randomized controlled trials is warranted.

简介：AIM:ToinvestigatethemechanismsbywhichCskbindingprotein(CBP)inhibitstumorprogressioninesophagealcarcinoma.METHODS:ACBPoverexpressingesophagealcarcinomacellline(TE-1)wasestablished.Thegrowth,invasion,andmigrationofCBP-TE-1cells,aswellastheexpressionofSrcwerethendeterminedandcomparedwiththoseinnormalTE-1cells.RESULTS:TheexpressionofSrcwasdecreasedbytheoverexpressionofCBPinTE-1cells.Thegrowth,invasion,andmigrationofTE-1cellsweredecreasedbytheoverexpressionofCBP.CONCLUSION:ThisstudyindicatesthatCBPmaydecreasethemetastasisofesophagealcarcinomabyinhibitingtheactivationofSrc.CBPmaybeapotentialtumorsuppressorandtargetingtheCBPgenemaybeanalternativestrategyforthedevelopmentoftherapiesforesophagealcarcinoma.

简介：MicroRNAs(miRNAs)是小非编码的规章的RNA的一个班，并且在miRNAs的变化涉及肿瘤起源和前进。研究证明了miR-20a是在人的卵巢的癌症纸巾的overexpressed并且这miRNA提高长期的细胞的增长和侵略能力。在这研究，在浆液miR-20a表示和卵巢的癌症舞台之间的积极关联被观察。我们发现miR-20a直接绑，导致它的降级并且减少它MICA/BmRNA的-untranslated区域在血浆膜上铺平的蛋白质3′；。膜界限MICA/B蛋白质的减小，是2成员D(NKG2D)受体在生来的杀手(NK)上发现了房间的生来的迷人的组的ligands，γ；δ；+T房间和CD8+T房间，允许肿瘤房间躲避调停免疫者的杀死。尤其是，反对miR-20a行动提高了在vitro并且在肿瘤的vivo模型的在两个的肿瘤房间的调停NKG2D的杀死。一起拿，我们的数据显示在肿瘤房间的miR-20a的增加的层次可以间接地由downregulatingMICA/B压制NK房间cytotoxicity表达式。这些数据提供在转移能力和NK房间的肿瘤房间的有免疫力的逃跑之间的一个潜在的连接。