简介：AbstractThe chemokine-like factor (CKLF)-like MARVEL transmembrane domain-containing family (CMTM) is widely expressed in the immune system. Abnormal expression of CMTM is associated with the development of various diseases. This article summarizes the relevant research on the role of the CMTM family in immune disorders. This information will increase our understanding of pathogenesis and identify promising targets for the diagnosis and treatment of autoimmune diseases. The CMTM family is highly expressed in peripheral blood mononuclear cells. CKLF1 may be involved in the development of arthritis through its interaction with C-C chemokine receptor 4. CKLF1 is associated with the pathogenesis of lupus nephritis and psoriasis. Both CMTM4 and CMTM5 are associated with the pathogenesis of systemic lupus erythematosus. CMTM1, CMTM2, CMTM3, and CMTM6 play a role in rheumatoid arthritis, systemic sclerosis, Sjögren syndrome, and anti-phospholipid syndrome, respectively. The CMTM family has been implicated in various autoimmune diseases. Further research on the mechanism of the action of CMTM family members may lead to the development of new treatment strategies for autoimmune diseases.

简介：AbstractSchnitzler syndrome is a rare disease of adult-onset with main features including chronic urticarial rash, recurrent fever, arthralgia or arthritis, monoclonal gammopathy of undetermined significance (MGUS), and marked systemic inflammation. Schnitzler syndrome is often underdiagnosed. Patients with Schnitzler syndrome may present to dermatologists and allergists for urticaria, hematologists for MGUS, or rheumatologists for arthritis. It is important to recognize Schnitzler syndrome for its remarkable response to interleukin (IL)-1 blockade. Besides, many cases of Schnitzler-like syndromes do not meet the diagnostic criteria of classical Schnitzler syndrome but display excellent response to IL-1 inhibitors. The overly produced IL-1 is the result of a somatic mosaic gain of function mutation of NLRP3 (nucleotide-binding oligomerization domain [NOD]-like receptor [NLR] family pyrin domain containing 3) gene in some patients with Schnitzler-like syndromes. Inflammasome activation is evident in patients with classical Schnitzler syndrome although no NLRP3 gene mutation is identified. Collectively, Schnitzler syndrome and Schnitzler-like syndromes represent a spectrum of IL-1 mediated adult-onset autoinflammatory diseases.

简介：AbstractAntiphospholipid syndrome (APS) is a systemic autoimmune disease defined by thrombotic or obstetrical events and persistent antiphospholipid antibodies (aPLs). Chemokine-like factor-like MARVEL transmembrane domain-containing family (CMTM) is widely expressed in the immune system and may closely related to APS. This review aimed to systematically summarize the possible effects of CMTM on APS. Publications were collected from PubMed and Web of Science databases up to August 2020. CKLF, CKLFSF, CMTM, antiphospholipid syndrome, immune cells, and immune molecules were used as search criteria. Immune cells, including neutrophil, dendritic cells (DCs), T-cells, B-cells, and inflammatory cytokines, play an important role in the development of APS. Chemokine-like factor 1 (CKLF1) has a chemotactic effect on many cells and can affect the expression of inflammatory cytokines and adhesion molecules through the nuclear factor-kB (NF-kB) pathway or mitogen-activated protein kinase (MARK) pathway. CKLF1 can participate in the maturation of DCs, T lymphocyte activation, and the activation of neutrophils through the MAPK pathway. CMTM1 may act on Annexin A2 by regulating Ca2+ signaling. CMTM2 and CMTM6 are up-regulated in neutrophils of APS patients. Some CMTM family members influence the activation and accumulation of platelets. CMTM3 and CMTM7 are binding partners of B-cell linker protein (BLNK), thereby linking B cell receptor (BCR) and activating BLNK-mediated signal transduction in B cells. Moreover, CMTM3 and CMTM7 can act on DCs and B-1a cell development, respectively. CMTM may have potential effects on the development of APS by acting on immune cells and immune molecules. Thus, CMTM may act as a novel prognostic factor or immunomodulatory treatment option of APS.

简介：Inthepresentstudywehavefoundthatproto-oncogenec-fosproteincanexpressinthenoradrenergicneuronsofrathindbrainfollowingperipheralelectricalstimulation.Ratsweregivenperipheralelectricalstimulationviathinstainlesssteelpinsinsertedintothepointsnearkneejoint(S36)andanklejoint(Sp6)whichmimicthemanipulationofelectroacupuncture(EA)performedinhumans.Animalswereperfusedfordoublestainingimmunohistochemistry2haftertheterminationofEA.InratssubjectedtoEAstimulationFos-likeproteinwasfoundinthetyrosinehydroxylase(TH)-likeimmunoreactiveneuronsinrathindbrain.TheFosandTHcoex-istingneuronsweredistributedinthelocuscoeruleus,solitarytractnucleus,ventrolateralmedul-la,periaqeductalgray,aswellassuperiorcolliculus.ThepercentageofthecoexistingneuronscomparedwiththetotalnumberofneuronscontainingFos-likeproteininthesenucleirangedfrom6%to32%.Theresultssuggestthatthenoradrenergicneuronsintheseregionsmaybeac-tivtedbyacupuncturestimulation.

简介：TheSOD-likeactivityoffiveCu(Ⅱ)complexes[Cu(HSal)_2·EtOH,Cu(Gly)_2,Cu(Lys)_2,Cu(His)_2,Cu(Try)_2]havebeenstudiedbyusingcytochromeCmethod,aswellaschemilumine-scenceandESRtechnique.Thefoursurfactants(CTAB,SDS,TritonX-100andTween20)werepurifiedandtheircriticalmiceileconcentration(CMC)inphosphatebuffer(pH=7.4)wasmea-sured.TheeffectsoffoursurfactantsonO_2~-havebeeninvestigated.Theco-operativeeffectsof

简介：象天生一样B房间(ILB)是有性质的天生的察觉到并且反应的异乎寻常的B房间的异构的人口。在老鼠的ILB由B1房间，边缘的地区(MZ)B房间和另外的相关B房间组成。ILB以稳定的状态维持自然IgM层次，并且在天生的激活以后，他们能很快通过自然IgM和IL-10的分泌物获得有免疫力的规章的活动。因此，ILB组成IL-10-producing规章的B房间(Bregs)的重要来源，它被显示了在autoimmunity，发炎和感染起关键作用。现在的评论在他们的规章的功能上的ILB和焦点的地里加亮最近的进展。理解ILB和他们的内在的机制的规章的活动能在操作他们的功能在打开新大街煽动性，传染并且另外的相关疾病。

简介：Theconceptsofstemcellsbeingresistanttotherapy,stem-likecellsexistinginbraintumors,andthesetumorsinitiallyrespondingto

简介：Objective:Toestablishananimalmodeloflike-auditoryneuropathyinneonatalrat.MethodsTheani-malswereinjectedwithphenylhydrazinehydrochlorideorsalineat7-dayofage.ABRandDPOAEwereperformedtoassesstheauditoryfunction.Thecochleabasilarmembranestretchedpreparationandcochlearfrozensectionswerepreparedforimmunohistochemicalstainingtoexaminethemorphologicalchangeofhaircellsandspiralganglioncells(SGNs).ResultsAt7-dayagetheABRwaveI,III,V,latenciesandI-III,I-VIWIsintheexperimentalgroupweresignificantlyprolongedcomparedwiththoseinthecontrolgroup.TheABRthresholdswerealsoelevatedintheexperimentalgroup.Wefoundthereisnosignificantdiffer-enceinDPOAEinphenylhydrazinehydrochlorideexposuregroupcomparetocontrolgroup.Thecochlearhaircellsshowednosignsoflossinbothgroup,butthetotalnumberofneurofilamentspositivecellsinSGNsweresignificantlyreducedinthephenylhydrazinetreatedanimals.ConclusionOurstudysuggeststhatphenylhydrazinehydrochloridecanchangetheauditoryfunctionandinduceperipheralnervepathologybytargetedmainlytheSGNsinneonatalrat.

简介：摘要错配修复系统功能缺失与结直肠癌的发生相关。有部分结直肠癌出现了错配修复缺陷，不仅检测不到MLH1启动子甲基化，也检测不出错配修复基因的胚系突变，因这部分群体表现与Lynch综合征非常相像而得名Lynch-like综合征。Lynch-like综合征具有一定的遗传特性，但发病机制还未得到足够的认识，不能将其简单的划为散发性结直肠癌或者Lynch综合征，也缺乏对该类型患者的遗传学认知及监测标准。文章将对Lynch-like综合征的研究进展进行综述。

简介：TheSOD-likeactivitiesofcoppersalicylateencapsulatedinneutralpositivelyandnegativelychargedliposomeswerestudiedwithcytochromecmethod.TheresultsshowedthattheSOD-likeactivityofcoppersalicylateencapsulatedinneutralliposomeswasenhancedover3timesmorethanthatofcoppersalicylateinaqueoussolution.However,theactivitydecreasedforcoppersalicylateencapsulatedinpositivelyandnegativelychargedliposomes.Itwasalsofoundthatatexperimentalconcentrationstherewasnoregularityforthechangeofactivityofcoppersalicylateencapsulatedinnegativelychargedliposomes,andcoppersalicylateencapsulatedinliposomeswithmorenegativechargescouldpromotethedismutationofsuperoxideanionfreeradicals,however,socouldcoppersalicylateencapsulatedinliposomeswithfewernegativechargesonlyinlowerconcentrations.

简介：ＥＦＦＥＣＴＳＯＦＡＰＡＴＩＴＥＣＥＲＡＭＩＣＳＯＮＣＥＬＬＧＲＯＷＴＨＳＡＮＤＤＮＡＳＹＮＴＨＥＳＥＳＩＮＨＵＭＡＮＯＳＴＥＯＢＬＡＳＴＬＩＫＥＣＥＬＬＥＦＦＥＣＴＳＯＦＡＰＡＴＩＴＥＣＥＲＡＭＩＣＳＯＮＣＥＬＬＧＲＯＷＴＨＳＡＮＤＤＮＡＳＹＮＴＨ...

简介：Parthenogeneticembryonicstemcellshavepluripotentdifferentiationpotentials,akintofertilizedembryo-derivedembryonicstemcells.Theaimofthisstudywastocomparetheneuronaldifferentiationpotentialofparthenogeneticandfertilizedembryo-derivedembryonicstemcells.Beforedifferentiation,karyotypeanalysiswasperformed,withnormalkaryotypesdetectedinbothparthenogeneticandfertilizedembryo-derivedembryonicstemcells.SexchromosomeswereidentifiedasXX.Immunocytochemistryandquantitativereal-timePCRdetectedhighexpressionofthepluripotentgene,Oct4,atboththemRNAandproteinlevels,indicatingpluripotentdifferentiationpotentialofthetwoembryonicstemcellsubtypes.Embryonicstemcellswereinducedwithretinoicacidtoformembryoidbodies,andthendispersedintosinglecells.SinglecellsweredifferentiatedinN2differentiationmediumfor9days.Immunocytochemistryshowedparthenogeneticandfertilizedembryo-derivedembryonicstemcellsbothexpresstheneuronalcellmarkersnestin,βIII-tubulinandmyelinbasicprotein.Quantitativereal-timePCRfoundexpressionofneurogenesisrelatedgenes(Sox-1,Nestin,GABA,Pax6,Zic5andPitx1)inbothtypesofembryonicstemcells,andOct4expressionwassignificantlydecreased.NestinandPax6expressioninparthenogeneticembryonicstemcellswassignificantlyhigherthanthatinfertilizedembryo-derivedembryonicstemcells.Thus,ourexperimentalfindingsindicatethatparthenogeneticembryonicstemcellshavestrongerneuronaldifferentiationpotentialthanfertilizedembryo-derivedembryonicstemcells.

简介：实验表明给小鼠五灵脂提取液，小鼠血液ＳＯＤ活性增强。测定五灵脂有类ＳＯＤ活性，在ｐＨ４５～８５，温度２５～１００℃条件下活性稳定

简介：Invitrocellloadingexperimentsareusedtoinvestigatestimulationofstraintocellularproliferation.Astheflowingconditionsofculturefluidinloadingsystemshasbeenlittleknown,strictlypeoplecannotdetecttheinfluenceofstraintocellularproliferationexactlybecauseshearflowcanenhancecellproliferationeither.Basedontheworkingprincipleandcyclicloadingparameters,wesimplifyNavier-Stokesequationtodescribetheflowofculturefluidonsubstratesofuniaxialandequi-biaxialfiattensileloadingsystemsandfourpointbendingsystem.Withapproximatesolutions,thedistributionsofvelocityfieldandwallshearflowtocellsaregained.Resultsshow:shearflowsarezerointhemiddle(orfixedpointorline)ofsubstrateforallsystems,andtheygetlargerproportionallytodistancefrommiddleandsubstrateelongate;theshearflowonthesubstrateoffourpointbendingsystemismuchgreaterthanthoseofothers.Thisshearflowinfourpointbendingsystem,confirmedbyOwan,I.,etalwithOPNmRNAincreaseintheirexperiment,couldcausemoreinfluencetoosteoblast-likecellsthanthatcausedbystrain.WeestimatetheaveragemagnitudeofshearstressinOwan'sdevice,theresultsareconsistentwithotherexperimentaldataaboutshearflow.Inconclusionourstudymakesitpossibletodifferentiatetheinfluenceofstrainoncellularproliferationtothatofshearflowinloadingexperimentswiththedevicesmentionedabovequantitatively.

简介：AIM:Toinvestigateifanimmuneimbalancemayaccountforthedevelopmentandprogressionofchronicradiationenteritis.WeanalyzedtheTh1/Th2immuneresponseprofileearlyand6moafterfractionatedcolorectalirradiation.METHODS:Aratmodeloffractionatedcolorectalγ-irradiation(4-Gyfractions,3fractionsperweek)wasdesignedtoinvestigatetheeffectsofcumulativedoseoninflammatorymediators(cytokinesandchemo-kines)andimmuneresponse(Th1/Th2profileandim-munosuppressivemediatorIL-10)duringacute(early)responseand6moaftertheendoffractionatedirradia-tion(chronicresponse).Analyseswereperformed1dafterthecumulativedosesof16Gyand36Gyand1d,3d,and26wkafterthecumulativedoseof52Gy.RESULTS:Withoutcausinghistologicaldamage,fractionatedradiationinducedelevatedexpressionofIL-1β,TNFα,MCP-1,andiNOSindistalcolonicmucosaduringtheearlypost-irradiationphase.Atthattime,aTh2profilewasconfirmedbyexpressionofboththeTh2-specifictranscriptionfactorGATA-3andthechemokinereceptorCCR4andbysuppressionoftheTh1cytokineIFNγ/IP-10throughouttheirradiationprotocol.After6mo,despitethe2-foldreductionofiNOSandMCP-1levels,theTh2profilepersisted,asshownbya50%reductionintheexpressionoftheTh1transcriptionfactorT-bet,thechemokinereceptorCCXCR3,andtheIFNγ/STAT1pathway.Atthesametime-point,theimmuno-suppressiveIL-10/STAT3pathway,knowntoregulatetheTh1/Th2balance,wasexpressed,inirradiatedrats,atapproximatelyhalfitslevelascomparedtocontrols.ThissuppressionwasassociatedwithanoverexpressionofSOCS3,whichinhibitsthefeedbackoftheTh1polarizationandregulatesIL-10production.CONCLUSION:ColorectalirradiationinducesTh2polarization,defectiveIL-10/STAT3pathwayactivationandSOCS3overexpression.Thesechanges,inturn,maintainaimmunologicalimbalancethatpersistsinthelongterm.

简介：

简介：AbstractBackground:Epithelial to mesenchymal transition (EMT) is a key process in determining distant metastasis and intra-hepatic dissemination of hepatocellular carcinoma (HCC). Follistatin (FST) family members are considered to be an attractive therapeutic targets and prognostic indicators in cancers. As a derivative of FST, Follistatin Like 5 (FSTL5) may play a similar role in HCC cells. This study aimed to investigate the expression and function of FSTL5 in HCC and its role in EMT.Methods:FSTL5, E-cadherin and vimentin in HCC, and paracancerous tissues were detected by immunohistochemistry. Correlation of FSTL5 expression with overall survival was assessed. The proliferation and invasion of HCC cell lines SK-Hep1 and MHCC-LM3 were analyzed by cell counting kit-8 and Transwell assays. The expression of FSTL5, E-cadherin, and vimentin in HCC cells was examined by polymerase chain reaction and Western blot analysis. T-test was used to analyze the difference in proliferation and invasion ability between groups. The Spearman rank correlation test was used to detect the correlation between the expression of FSTL5 and E-cadherin or vimentin.Results:The expression of FSTL5 in HCC was lower than that in paracancerous tissues (9.97% vs. 82.55%, χ2 = 340.15, P < 0.001). Patients with high FSTL5 expression had a better prognosis (χ2= 8.22, P= 0.004) and smaller tumor diameter (χ2 = 45.52, P < 0.001), less lymph node metastasis (χ2 = 5.58, P= 0.02), earlier tumor node metastasis stage (χ2 = 11.29, P= 0.001), a reduced number of tumors (χ2 = 5.05, P= 0.02), lower alpha-fetoprotein value (χ2 = 24.36, P < 0.001), more probability of hepatitis carrying (χ2 = 40.9, P < 0.001), and better liver function grade (χ2 = 5.21, P = 0.02). Immunohistochemistry showed that FSTL5 expression in HCC tissues was positively correlated with E-cadherin expression (r = 0.38, P < 0.001) and negatively correlated with vimentin expression (r = -0.385, P < 0.001). Furthermore, over-expression of FSTL5 up-regulated the expression of E-cadherin and down-regulated the expression of vimentin in SK-Hep1 (negative control [NC] vs. FSTL5-interfering group [Lv-FSTL5]: E-cadherin [t= 45.03, P < 0.001], vimentin [t= 67, P < 0.001]) and MHCC-LM3 (NC vs. Lv-FSTL5: E-cadherin [t = 50, P < 0.001], vimentin [t = 72.75, P < 0.001]) cells at mRNA level. The same as protein level. In addition, the over-expression of FSTL5 inhibited the proliferation (NC vs. Lv-FSTL5: SK-Hep1, 3 d [t = 7.324, P = 0.018], 4 d [t = 6.23, P = 0.021], 5 d [t= 10.21, P= 0.003]; MHCC-LM3, 3 d [t= 4.32, P= 0.037], 4 d [t= 7.49, P= 0.012], 5 d [t= 9.3661, P = 0.009]) and invasion (NC vs. Lv-FSTL5: SK-Hep1, t= 21.57, P < 0.001; MHCC-LM3, t= 18.04, P < 0.001) of HCC cells.Conclusions:Down-regulation of FSTL5 may contribute to EMT of HCC, and FSTL5 is a potential target in the treatment of HCC.

简介：我们从人的树枝状的房间识别了新奇象ubiquitin一样分子DULP。DULP包含与ubiquitin分享26%身份和34%类似的一个领域，并且它拥有恐水病的补丁由mono-ubiquitin或poly-ubiquitin过去常与一个ubiquitin相互作用主题(UIM)或联系ubiquitin的领域(UBA)交往的相应Ile-44。相应于6ubiquitin的离氨酸残余，涉及能绑proteasomal子单元Rpn10/S5a的multi-ubiquitin链的形成，也在它的ubiquitin相同领域被保存。然而，DULP不拥有Gly-Gly为要求让polyubiquitin链的形成为降级指向底层的ubiquitin变化形式或Lys-48要求的高度保存的C终点，建议它可能是新奇ubiquitin域蛋白质(UDP)。DULP被发现广泛地在许多房间表示了，ubiquitin相同领域没被劈开。我们也证实那DULP表情在原子核和在cytosol更弱的大部分被充实。而且，我们发现在293T房间的DULP的overexpression导致了apoptosis，它可能没与mitochondrial或proteasome小径被联系，与特定的机制遗体不清楚。进一步的调查被需要识别DULP的精确生物功能。

简介：AbstractThe maternal-fetal interface is a key barrier to protect the fetus from infection. Toll-like receptors (TLRs) at the maternal-fetal interface are involved in antiviral responses. TLRs are expressed in both maternal decidua and fetal trophoblasts. Virus-induced activation of TLR signaling pathways triggers the release of interferon-related antiviral molecules and other inflammatory cytokines and/or chemokines by the host innate immune system, which may disrupt immune tolerance at the maternal-fetal interface and lead to pregnancy complications. In this review, we summarize the state of knowledge on the most common viral infections during pregnancy, antiviral TLR responses at the maternal-fetal interface, and TLR-associated pregnancy complications.

简介：AbstractObjective:Despite the fact that adenomyosis is a fairly common gynecological disorder, its pathogenesis remains elusive. Several theories on the pathogenesis of adenomyosis have been proposed, but none of them has been proven experimentally. So far, the most used one is the neonatal feeding of tamoxifen (TAM) in Institute of Cancer Research/cryopreserved (ICR/CD-1) mouse. However, its underlying mechanism of action is unknown. To further delineate the mechanism of TAM-induced adenomyosis in ICR/CD-1 mouse with regard to specific estrogen receptor (ER), we conducted an experiment that neonatal mice were fed with either TAM, or 4,4′,4″-(4-propyl-[1H]-pyrazole-1,3,5-triyl) trisphenol (PPT; an ERα agonist), or 2,3-bis(4-hydroxyphenyl)-propionitrile (DPN; an ERβ agonist), or G-1 (a G-protein coupled receptor 30 agonist), or just vehicle, in an attempt to tease out which specific receptor plays a dominant role in the genesis of adenomyosis induced by neonatal feeding of TAM.Methods:Forty female neonatal mice were randomly divided into 5 equal-sized groups: CTL (control), TAM, PPT, DPN, and G-1. Three months later, all mice were sacrificed and their uterine horns were harvested, weighed, and processed for histological evaluation.Results:All mice in the TAM group developed adenomyosis, so did 4 mice (50%) in the DPN group, a result that should be considered significant given that mice in the CTL group would not develop adenomyosis. No mouse in the PPT or G-1 group developed adenomyosis. Remarkably, all lesions in the DPN group were seen exclusively near the uterine serosa, which are dramatically different from that of TAM mice and reminiscent of extrinsic or external adenomyosis in humans.Conclusions:Neonatal feeding of DPN induces adenomyosis, but the adenomyotic lesions appear to be different from those induced by TAM. Thus, the cause of TAM-induced adenomyosis in ICR/CD-1 mouse cannot be attributable to one specific ER alone. This suggests that the extrinsic/external adenomyosis may have a pathogenesis that is different from other sub-types of adenomyosis.