简介：Themechanismswhichcontrolsthefixationand/orreleaseofPinsedimentofanextremelyacidiclake(pH=2.0to3.0)anditsresponsetotheinfluenceofeutrophicurbanwastewaterwereinvestigated.Theresults,inthechemicalcomposition,inthemineralogyofthesedimentandinthematerialasobtainedfromsedimenttraps,showthatthelakesedimentsaremainlyvolcanicmaterialreflectingvolcanicfeaturesofthebasin.Thesedimentationratecalculatedforthelake(2.5×10~(-2)mgm~(-2)day~(-1))washigherthanthatobservedinothersimilarglaciallakesinbothAndeanPatagoniaandalsoelsewhereintheworld.TheTotalPhosphorusconcentrationinsedimentswashigherthanfiguresreportedbyotherauthorsforminingacidlakes,andthemainfractionofPwasfoundassociatedwithorganicmatter.TherewasnocontrolbyFeorAlonP,becausebothareinsolutionatpH<3.0.Itwasconcludedthatchangesinthenaturalinputofnutrients(derivativesofCopahuevolcanofluid,thedischargeofsewage,orbasinrun-off)areresponsibleforahighconcentrationofSRPandN-NH_4~+inthelake.LaboratoryexperimentsshowedthatsedimentshavenoabilitytoretainphosphorusandacontinuousreleaseofPfromthesedimentsintothewatercolumnwasobserved.TheassayswherethepHwasartificiallyincreasedshowedthatthePstillremainsinsolutionuntilatleastpH7.0.Itwasconcludedthatchangesinthenaturalinputofnutrientsdueto:1)thevolcanicfluids,2)theincreaseinsewagecharges,or3)surfacerunoffupstream,maintainahightrophicstatewithhighconcentrationsofdissolvedPandN-NH_4~+,althoughthethresholdofneutralpHinthelakeisexceeded.Thisstudywillenableabetterunderstandingaboutofthemechanismofrelease/fixationofphosphorusinacidicsedimentsinordertoassistinmakingdecisionsregardingtheconservationandmanagementofthisnaturalenvironment.

简介：Citricandmalicacidsatconcentrationsof0.1,1.0,10,and100mmol/LwereaddedtothreeUltisolsandoneOxisol,TheamountofPinsolutionincreasedwithincreasingorganicacidconcentrations,whiletheamountofFe-andAl-boundPdecreased.ThisresultsuggestedthatnaturallyoccurringproductsoforganicmatterdecompositioncouldincreasethePavailabilitytoplantsinsoilswherethereisarelativelylargepoolofFe-andAl-boundP.Theinteractionsbetweencitricandmalicacidsattheaboveconcentrations,andpaddedatratesof10,20,40,and80mg/kgweredetermined.Atzerolevelsoforganicacids,alladdedPbecameeitherlabileorbound,andgreaterproportionsremainedsolubleastheconcentrationoforgaicacidsincreased,whichsuggestedthatorganicacidsreducedfixationofdissolvedPinFe-andAL-richsoils.AgriculturalpracticeswhichincreaseorganicmatterinputonP-deficientacidsoildcoulddecreasePdeficiency,Thiswouldbeimportantinmanytropicalandsubtropicalregionswherethesesoilsarecommon,andwherethecostsoffertilizersandlimearerelativelyhigh.

简介：Inthispaperweshallgivethecharacteristicdifferencemethodsfortwophasedisplacemeatprobleminnaturallyfracturedreservoirs.Weshallprovetheexistence,uniquenessoftheapproximatesolutionandaprioridiscreteL2-errorestimates.

简介：Transientratedeclinecurveanalysisforconstantpressureproductionispresentedinthispaperforanaturallyfracturedreservoir.Thisapproachisbasedonexponentialandconstantbottom-holepressuresolution.Basedonthismethod,whenln(flowrate)isplottedversustime,twostraightlinesareobtainedwhichcanbeusedforestimatingdifferentparametersofanaturallyfracturedreservoir.Parameterssuchasstoragecapacityratio(ω),reservoirdrainagearea(A),reservoirshapefactor(C_A),fracturepermeability(k_f),interporosityflowparameter(λ)andtheotherparameterscanbedeterminedbythisapproach.TheequationsarebasedonamodeloriginallypresentedbyWarrenandRootandextendedbyDaPratetal.andMavorandCinco-Ley.Theproposedmethodhasbeendevelopedtobeusedfornaturallyfracturedreservoirswithdifferentgeometries.Thismethoddoesnotinvolvetheuseofanychartandbyusingthepseudosteadystateflowregime,theinfluenceofwellborestorageonthevalueoftheparametersobtainedfromthistechniqueisnegligible.Inthistechnique,alltheparameterscanbeobtaineddirectlywhileinconventionalapproachesliketypecurvematchingmethod,parameterssuchasωandλshouldbeobtainedbyothermethodslikebuild-uptestanalysisandthisisoneofthemostimportantadvantagesofthismethodthatcouldsavetimeduringreservoiranalyses.Differentsimulatedandfieldexampleswereusedfortestingtheproposedtechnique.Comparisonbetweentheobtainedresultsbythisapproachandtheresultsoftypecurvematchingmethodshowsahighperformanceofdeclinecurvesinwelltesting.

简介：ＴＷＯ－ＰＨＡＳＥＦＬＯＷＦＯＲＡＨＯＲＩＺＯＮＴＡＬＷＥＬＬＰＥＮＥＴＲＡＴＩＮＧＡＮＡＴＵＲＡＬＬＹＦＲＡＣＴＵＲＥＤＲＥＳＥＲＶＯＩＲＷＩＴＨＥＤＧＥＷＡＴＥＲＩＮＪＥＣＴＩＯＮＧｕｏＤａｌｉ（郭大立）ＬｉｕＣｉｑｕｎ（刘慈群）（Ｒｅｃｅｉｖｅ...

简介：ImpactsongrowthofyoungtreesofPinusKoraiensisof6environmentalfactorsofintensityofsunlight,directsunlight,thicknessofsoilhumus,neighboringtrees,uppercanopyspecies,herbsandshrubswereinvestigatedonyoungtreeofPinusKoraiensisand4neighboringtreeswhichareconsideredthestructuralunitofthemicroenvironment.Resultsindicatedthatthe6environmentalfactorsunderinvestigationhadeffects,tovariousextents,ongrowthoftheyoungtrees.Basedonthefindings,suitablegrowingconditionsforregeneratedyoungtreeofPinusKoraiensisunderforestwereidentifiedandcorrespondingsilviculturalmeasureswereproposedforoperationalpractice.

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简介：自然地发生的产生胸腺的CD4+CD25+规章的T(Treg)房间被认为在自我忍耐起一个中央作用。支持Treg房间的开发的精确信号留下逃犯，却可观证据建议T房间在胸腺在遇到抗原的costimulatory分子，cytokines，TCR的性质和壁龛或上下文起重要作用。从Treg房间的TCR的分析证明了这张人口的一个大比例从CD4+CD25-房间与TCR比较有更高的热望到自我抗原，那外部抗原为他们的发展，维护，或扩大被要求。Treg房间被显示了在圆周经历扩大，多半由自我抗原的存在调整了。许多研究证明了在忍耐正式就职的Treg房间的参与是抗原特定的，与甚至错配MHC在移植/接枝对主人疾病(GVHD)，autoimmunity，癌症，和怀孕。论文研究在身体正直的维护为自我反应的Treg房间结束了一个重要角色。基于那些研究，我们假设自我反应的Treg细胞在所有健康个人之中被分享并且认出一样的自我抗原和他们的TCR，这为定义健康自我的每个器官的很少主导的抗原编码。这些主导的自我抗原能被认为是“通用有免疫力的代码”。

简介：尽管有CD4+CD25+规章的T房间(Tregs)在过去的十年期间，在他们的临床的翻译以后的进步仍然保持停滞。增长证据建议那自然地发生的CD8+CD122+T房间也是有能力的Tregs禁止T房间回答并且象alloimmunity一样压制autoimmunity。事实上，他们是像记忆的Tregs类似于一个中央记忆T房间(T厘米)显型。位于他们的抑制下面的机制仍然不好被理解，尽管他们可以包括IL-10生产。我们最近证明了那个规划death-1(PD-1)表达式区分在之间规章并且存储器CD8+CD122+T房间和那CD8+CD122+Tregs经历更快的homeostatic增长并且比常规CD4+CD25+Tregs。这些调查结果可以为在诊所加速有效Treg治疗打开调查的一根新线。在这评论，我们在CD8+CD122+Treg在诊所研究并且讨论他们的显型，在autoimmunity和alloimmunity的镇压角色，功能的要求，行动的机制和潜在的应用。

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简介：AbstractBackground:Emerging evidence indicates that the sineoculis homeobox homolog 1-eyes absent homolog 1 (SIX1-EYA1) transcriptional complex significantly contributes to the pathogenesis of multiple cancers by mediating the expression of genes involved in different biological processes, such as cell-cycle progression and metastasis. However, the roles of the SIX1-EYA1 transcriptional complex and its targets in colorectal cancer (CRC) are still being investigated. This study aimed to investigate the roles of SIX1-EYA1 in the pathogenesis of CRC, to screen inhibitors disrupting the SIX1-EYA1 interaction and to evaluate the efficiency of small molecules in the inhibition of CRC cell growth.Methods:Real-time quantitative polymerase chain reaction and western blotting were performed to examine gene and protein levels in CRC cells and clinical tissues (collected from CRC patients who underwent surgery in the Department of Integrated Traditional and Western Medicine, West China Hospital of Sichuan University, between 2016 and 2018, n = 24). In vivo immunoprecipitation and in vitro pulldown assays were carried out to determine SIX1-EYA1 interaction. Cell proliferation, cell survival, and cell invasion were determined using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, clonogenic assay, and Boyden chamber assay, respectively. The Amplified Luminescent Proximity Homogeneous Assay Screen (AlphaScreen) method was used to obtain small molecules that specifically disrupted SIX1-EYA1 interaction. CRC cells harboring different levels of SIX1/EYA1 were injected into nude mice to establish tumor xenografts, and small molecules were also injected into mice to evaluate their efficiency to inhibit tumor growth.Results:Both SIX1 and EYA1 were overexpressed in CRC cancerous tissues (for SIX1, 7.47 ± 3.54 vs.1.88 ± 0.35, t = 4.92, P = 0.008; for EYA1, 7.61 ± 2.03 vs. 2.22 ± 0.45, t = 6.73, P = 0.005). The SIX1/EYA1 complex could mediate the expression of two important genes including cyclin A1 (CCNA1) and transforming growth factor beta 1 (TGFB1) by binding to the myocyte enhancer factor 3 consensus. Knockdown of both SIX1 and EYA1 could decrease cell proliferation, cell invasion, tumor growth, and in vivo tumor growth (all P < 0.01). Two small molecules, NSC0191 and NSC0933, were obtained using AlphaScreen and they could significantly inhibit the SIX1-EYA1 interaction with a half-maximal inhibitory concentration (IC50) of 12.60 ± 1.15 μmol/L and 83.43 ± 7.24 μmol/L, respectively. Administration of these two compounds could significantly repress the expression of CCNA1 and TGFB1 and inhibit the growth of CRC cells in vitro and in vivo.Conclusions:Overexpression of the SIX1/EYA1 complex transactivated the expression of CCNA1 and TGFB1, causing the pathogenesis of CRC. Pharmacological inhibition of the SIX1-EYA1 interaction with NSC0191 and NSC0933 significantly inhibited CRC cell growth by affecting cell-cycle progression and metastasis.