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简介：Thispapersummarizesthelatestdevelopments,futureprospects,andproposedcountermeasuresofreservoirsedimentationandchannelscourdownstreamoftheThreeGorgesReservoir(TGR)ontheYangtzeRiverinChina.Threekeyresultshavebeenfound.(1)TheincomingsedimentloadtotheTGRhasbeensignificantlylowerthanexpected.(2)TheaccumulatedvolumeofsedimentdepositionintheTGRissmallerthanexpectedbecausetheoverallsedimentdeliveryratioisrelativelylow,andthedepositioninthenear-damareaoftheTGRisstilldeveloping.(3)RiverbedscourintheriverreachesdownstreamoftheGezhoubaDamisstilloccurringandchannelscourhasextendedtoreachesasfardownstreamastheHukoureach.Significantly,sedimentationoftheTGRislessproblematicthanexpectedsincethestartofoperationoftheTGRontheonehand;ontheotherhand,thepossibleincreasesinsedimentrisksfromdependenceonupstreamsedimentcontrol,depositioninthereservoir,andscouralongmiddleYangtzeRivershouldbepaidmoreattention.(1)SedimenttrappedbydamsbuiltalongtheupperYangtzeRiverandbilliontonsofloosematerialsonunstableslopesproducedbytheWenchuanEarthquakecouldbenewsedimentsourcesfortheupperYangtzeRiver.Moreseriously,possiblereleaseofthissedimentintotheupperYangtzeRiverduetonewearthquakesorextremeclimateeventscouldoverwhelmtheriversystem,andproducecatastrophicconsequences.(2)IncreasingsedimentdepositionintheTGRisharmfultothesafetyandefficiencyofprojectoperationandnavigation.(3)ThedrasticscouralongthemiddleYangtzeRiverhasintensifiedthedown-cuttingoftheriverbedanderosionofrevetment,ithasalreadyledtoincreasingrisktofloodcontrolstructuresandecologicalsafety.ItissuggestedtocontinuetheFieldObservationProgram,toinitiateresearchprogramsandtofocusonrisksofsedimentation.

简介：在从流量的1960～2012个文件趋势的上面的Qingjiang河里的水文学数据由在降雨设计工程和长期的变化的水力发出的电力引起了。年度流量与年度降水强烈相关，但是是显著地与更早的价值相比在水库建设以后减少了。比较强烈，构造前和构造以后的降雨事件建议Chebahe和Dalongtan水库工程分别地抓紧洪水山峰和延期流量交货的大小。

简介：ＡＮＵＭＥＲＩＣＡＬＥＸＰＥＲＩＭＥＮＴＯＮＴＨＥＩＮＦＬＵＥＮＣＥＳＯＦＴＨＥＱＩＮＧＨＡＩ－ＸＩＺＡＮＧＰＬＡＴＥＡＵＯＮＴＨＥＵＰＳＴＲＥＡＭＢＬＯＣＫＩＮＧＥＶＥＮＴＺｈｅｎｇＱｉｎｇｌｉｎ（郑庆林），ＧｕＹｕ（古瑜），ＳｏｎｇＱｉｎｇｌｉ（...

简介：ExistingEthernetPassiveOpticalNetwork(EPON)DynamicBandwidthAllocation(DBA)algorithmssufferfromthedisadvantageofidletimeloss,whichlowertheupstreambandwidthutili-zation.Thisletterproposesanimprovedupstreamtransmissionschemewithidle-timeeliminatingmechanism.Theoreticalanalysisandnumericalcalculationprovethattheimprovedschemecanef-fectivelyeliminatetheidletimeandenhancetheefficiencyofupstreamlinkutilization.Simulationresultshaveshownthatthebandwidthutilizationcanberaisedupto15%inheavy-loadscenarioswhilethetimedelayperformanceofAssuredForwarding(AF)andBestEffort(BE)servicesareimprovedsimultaneously.

简介：Thispaperstudiesatwostagesupplychainwithadominantupstreampartner.ManufactureristhedominantpartnerandoperatesinaJust-in-Timeenvironment.Productionisdoneinasinglemanufacturinglinecapableofproducingtwoproductswithoutstoppingtheproductionforswitchingfromoneproducttotheother.Themanufacturerimposesconstraintsonthedistributorbyadheringtohisfavorableproductionschedulewhichminimizeshismanufacturingcost.Distributorontheotherhandcaterstoretailers'orderswithoutincurringanyshortagesandisresponsibleformanagingtheinventoryoffinishedgoods.Adheringtomanufacturer'sschedulemayleadtohighinventorycarryingcostsforthedistributor.Distributor'sproblem,whichistofindanoptimaldistributionsequencewhichminimizesthedistributor'sinventorycostundertheconstraintimposedbythemanufacturerisprovedNP-HardbyManojetal.(2008).Therefore,solvinglargesizeproblemsrequireefficientheuristics.Wedevelopalgorithmsforthedistributionproblembyexploitingitsstructuralproperties.Weproposetwoheuristicsandusetheirsolutionsintheinitialpopulationofageneticalgorithmtoarriveatsolutionswithanaveragedeviationoflessthan3.5%fromtheoptimalsolutionforpracticalsizeproblems.

简介：我们试验性地表明并且分析10Gbit/s完整的双波长部门multiplexing被动光网络(WDM-PON)系统。non-return-to-zero调音的微分阶段移动(NRZ-DPSK)调整技术首先为downlink方向被利用，然后downlink信号每隧道与10Gbit/s的数据率用调音的开关(OOK)的紧张调整技术为uplink方向被重新调制。一个有效无色WDM-PON完整的双传播系统与低力量惩罚在25km的距离上与60GHz的隧道间距每隧道为10Gbit/s的数据率被完成。

简介：Toinvestigatethemutationsintheupstreamregulatoryregion(URR)ofhumanpapillomavirustype16(HPV-16)fromthecervicalcancerbiopsiesinXinjiangUygurwomenanditsrelationshiptothehighincidenceofcervicalcancerinthesouthernXinjiang,thetissueDNAwasextractedfromthecervicalcancerbiopsies,andtheURRsegmentofHPV-16DNAwasamplified,sequencedandanalyzed.Thereafter,thepolymorphismofURRinHPV-16wasthenanalyzed.ItwasdemonstratedthatthepositiveratedetectedforthepresenceofURRinHPV-16was89.47%(17/19).ComparedwiththepreviouslypublishedsequenceinURRofprototypeHPV-16,somemutationsweredetectedinthesequenceofURR.Themutationsin17URRfragmentsofHPV-16couldbedividedinto11patterns(XJU-1toXJU-11)atnucleicacidlevel,inwhicheachofXJU-1andXJU-4accountedfor23.53%(4/17),andotherpatternsofmutationaccountedfor5.88%(1/17).IncomparisonwiththeURRofprototypeHPV-16,theDNAidentityofthesepatternswas98.50%-99.68%.Inthese17URRfragments,twopointmutationsoccurredatposition7192(GtoT)andposition7520(GtoA)andtheyappearedtobeconstantinXinjiangarea.ThesetwomutationswereubiquitousintheAsia-Americantypeandconferredstronginfectionactivityandcarcinogenicityofthisvirus.Inaddition,themutationsatposition7729(AtoC),position7843(AtoG)andposition7792(CtoT)couldenhanceitstranscriptionactivityconsiderably.ItisconcludedthatsomemutationsoccurinURRgeneofHPV-16inthecervicalcancerbiopsiestakenfromUygurwomeninXinjiangarea,suggestingthatcertainrelationshipexistsamongthemutationsinURRofHPV-16,thephylogenyofHPV-16andthehighincidenceofcervicalcancerinsouthernpartofXinjiangarea.

简介：TounderstandtheDNA-methylationmediatedgenesilencingmechanisms,weanalyzedincellcultureofthepromoterfunctionoftheMAGE-A1gene,whichisfrequentlydemethylatedandover-expressedinhumanhepatocellularcarcinoma.WehaveestablishedthecorrelationoftheDNAmethylationofthepromoterCpGislandwithexpressionstatusofthisgeneinapaneloftheestablishedlivercancercelllines.ThecrucialCpGdinucleotide(s)withintheminimalpromotersubjectedtothecontrolmediatedbyDNAmethylationwithprofoundbiologicalfunctionswasalsodelineated.Furthermore,anovelsequence-specificDNA-proteininteractionatthe-30CpGdinucleotideupstreamofthegenewasfoundhavingavitalparttoplayintheDNAmethylationmediatedtranscriptionsilencingoftheMAGE-A1gene.OurresultswouldnotonlyprovidenewinsightsintotheDNAmethylationmediatedmechanismsovertranscriptionoftheMAGE-A1gene,butalsopavethewayforfurtherdefiningthecross-talkamongDNAmethylation,histonemodificationandchromatinremodelingindetail.

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简介：AbstractBackground:Pancreatic cancer (PC) is a highly deadly malignancy with few effective therapies. We aimed to unmask the role that long non-coding RNA small nucleolar RNA host gene 6 (SNHG6) plays in PC cells by targeting far upstream element binding protein 1 (FUBP1) via microRNA-26a-5p (miR-26a-5p).Methods:SNHG6 expression was predicted by bioinformatics, followed by verification via reverse transcription quantitative polymerase chain reaction. Then, the interactions among SNHG6, miR-26a-5p, and FUBP1 were detected through online software analysis, dual luciferase reporter assay and RNA pull-down. After that, cells were treated with different small interfering RNAs and/or mimic to determine the interactions among SNHG6, miR-26a-5p, and FUBP1 and their roles in PC cells. Finally, the role of SNHG6 in tumor growth in vivo was evaluated by measuring the growth and weight of transplanted tumors in nude mice. A t-test, one-way and two-way analysis of variance were used for data analysis.Results:Compared with that in normal tissues, SNHG6 was highly expressed in PC tissues (1.00 ± 0.05 vs. 1.56 ± 0.06, t= 16.03, P < 0.001). Compared with that in human pancreatic duct epithelial cells (HPDE6-C7), SNHG6 showed the highest expression in PANC-1 cells (1.00 ± 0.06 vs. 3.87 ± 0.13, t= 34.72, P < 0.001) and the lowest expression in human pancreatic cancer cells (MIAPaCa-2) (1.00 ± 0.06 vs. 1.41 ± 0.07, t= 7.70, P= 0.0015). Compared with the levels in the si-negative control group, SNHG6 (0.97 ± 0.05 vs. 0.21 ± 0.06, t = 16.85, P < 0.001), N-cadherin (0.74 ± 0.05 vs. 0.41 ± 0.04, t= 8.93, P < 0.001), Vimentin (0.55 ± 0.04 vs. 0.25 ± 0.03, t= 10.39, P < 0.001), and β-catenin (0.62 ± 0.05 vs . 0.32 ± 0.03, t= 8.91, P < 0.001) were decreased, while E-cadherin (0.65 ± 0.06 vs. 1.36 ± 0.07, t= 13.34, P < 0.001) was increased after SNHG6 knockdown or miR-26a-5p overexpression, accompanied by inhibited cell proliferation, migration, and invasion. SNHG6 overexpression exerted the opposite effects. SNHG6 upregulated FUBP1 expression by sponging miR-26a-5p. Silencing SNHG6 blocked the growth of PC in vivo.Conclusion:Silencing SNHG6 might ameliorate PC through inhibition of FUBP1 by sponging miR-26a-5p, thus providing further supporting evidence for its use in PC treatment.