简介：InthispaperwegiveapartialaffrmativeanswertoaconjectureofGreene-WuandYau.Amongotherthings,weprovethatacompletenoncompactKhlersurfacewithpositiveandboundedsectionalcurvatureandwithfiniteanalyticChernnumberc1(M)2isbiholomorphictoC2.

简介：ThegeneclustercfaABCED′ofenterotoxigenicEscherichiacoli,encodingthefimbriaewhichiscalledcolonizationfactorantigenⅠ(CFA/Ⅰ),locatedonaplasmid.ItispositivelyregulatedbycfaR,amemberoftheAraCfamily,andthecfaD′generegion,whichislocateddownstreamofcfaEandishomologoustocfaR,hadbeendescribedasatruncatedcrypticgene.InthepresentstudyweobservedthattheCFA/Ⅰfimbriaesubunit,cfaB,wasexpressedinloweramountbythecfoABCED′clonepNTP513inhostE.coliHB101.TheexpressionofCFA/ⅠdiminishedbydeletionofcfaD′generegionfrompNTP513,andwasrestoredbyacquisitionofcfaD′intrans.Furthermore,CFA/ⅠexpressionbycfaD′deletionmutant,thecfaABCEclone,wasremarkablyincreasedbythepresenceofCFA/ⅠintransinatopoisomeraseAdeficientstrainofE.coliDM800.ThesedatasuggestthatcfaD′regionisafunctionalregionofgene,thatregulatestheCFA/ⅠexpressionwithcfaRbyunknownmechanism.

简介：Itisbelievedthathumanancestorsevolvedtheabilitytorunbipedallyapproximately2millionyearsago.Thisformoflocomotionmayhavebeenimportanttooursurvivalandlikelyhasinfluencedtheevolutionofourbodyform.Asourbodieshaveadaptedtorun,itseemsunusualthatupto79%ofmoderndayrunnersareinjuredannually.Theetiologyoftheseinjuriesisclearlymultifactorial.However,1aspectofrunningthathassignificantlychangedoverthepast50yearsisthefootwearweuse.Modernrunningshoeshavebecomeincreasinglycushionedandsupportive,andhavechangedthewaywerun.Inparticular,theyhavealteredourfootstrikepatternfromapredominantlyforefootstrike(FFS)landingtoapredominantlyrearfootstrike(RFS)landing.Thischangealtersthewayinwhichthebodyisloadedandmaybecontributingtothehighrateofinjuriesrunnersexperiencewhileengagedinanactivityforwhichtheywereadapted.Inthispaper,wewillexaminethebenefitsofbarefootrunning(typicallyanFFSpattern),andcomparethelowerextremitymechanicsbetweenFFSandRFS.Theimplicationsofthesemechanicaldifferences,intermsofinjury,willbediscussed.WewillthenprovideevidencetosupportourcontentionthatFFSprovidesanoptimalmechanicalenvironmentforspecificfootandanklestructures,suchastheheelpad,theplantarfascia,andtheAchillestendon.Theimportanceoffootwearwillthenbeaddressed,highlightingitsinteractionwithstrikepatternonmechanics.Thisanalysiswillunderscorewhyfootwearmatterswhenassessingmechanics.Finally,properpreparationandsafetransitiontoanFFSpatterninminimalshoeswillbeemphasized.Throughthediscussionofthecurrentliterature,wewilldevelopajustificationforreturningtorunninginthewayforwhichwewereadaptedtoreducerunning-relatedinjuries.

简介：Let{Xi；i≥1}beastrictlystationarysequenceofassociatedrandomvariableswithmeanzeroandletσ^2=EX1^2+2∑j=2^∞EX1Xjwith0

简介：白手起家的断然控告了nanofiltration(NF)膜被用来对待纺织品染料自河为影响象操作压力那样的nanofiltration过程的复用，和因素产生水，喂fl嗷并且膜清洗被调查。与1.0MPa和40L/h的feedflow的一个应用压力，这NF膜在完成100%的浓度移动的TDS，咸度和电导率为CODcr和约51.0%的减小有93.3%的移动。通过这膜获得的permeate对再循环合适。而且，膜能在与1%NaOH答案被清洗以后被再使用。

简介：Carbonsurfacewithlargeoxygenandcarbonratio(O/C)indicatedanoutstandingelectro-catalyticactivitytowardL-ascorbicacidoxidation,comparedtoplatinumgroupmetals.However,interrelationofsurfacefunctionalgroupsanditselectro-catalyticactivityisstillunclear.Inthispaper,weprepareddifferentlevelsofoxidizedcarbonsbyasimpleacidtreatmentandinvestigatedthecorrelationbetweenthesurfaceoxygenfunctionalgroupsofacid-treatedcarbonandelectro-catalyticactivityinanelectrooxidationofL-ascorbicacid.Positivelychargedcarbonwasdemonstratedbylonepairelectronofoxygenfromvalencebandspectrastudy.Itwasrevealedthatthepositivelychargedcarbon,especiallyinvolvedincarbonyl,showedenhancedtheelectro-catalyticactivitythroughbothbetteradsorptionofnegativelychargedreactantsandloweredLUMObyelectronegativityofoxygen.

简介：Usingasimpletwo-parameterwavefunction,wecalculatevariationallythebindingenergyofpositivelyandnegativelychargedexcitonsinGaAs/AlxGa1-xAsquantumwellsforwellwidthsfrom10to300A.Weconsidertheeffectofeffectivemass,dielectricconstantmismatchinthetwomaterials,andthewholecorrelationamongtheparticles.Theresultsarediscussedandcomparedindetailwithpreviousexperimentalandtheoreticalresults,whichshowfairagreementwiththem.

简介：AbstractBackground:Osteoarthritis (ΟΑ) is characterized by cartilage breakdown and subchondral sclerosis. Micro-fractures of the calcified tissues have been, also, detected, but their exact role has not been elucidated yet. This study was to examine the frequency of cracks during OA progression and to correlate them with the underlying cellular modifications and matrix metalloproteinase-2 (MMP-2) expression using histological/immunohistological methods.Methods:Overall, 20 patients and 3 controls (9 specimens per patient), aged 60-89 years, diagnosed with hip/knee OA were included. The development of cracks was examined in 138 sections, whereas the expression of MMP-2 was examined in 69 additional sections.Results:Based on Mankin score, three groups of OA severity were analyzed: Group I (mild) was constituted of sections with score 1-5 while Groups II (moderate) and III (severe) with score 6-7 and greater or equal to 8, respectively. Demographic characteristics did not reveal any association between the number of microdefects and age or body mass index (BMI). Cartilage micro-cracks were increased during moderate and severe OA, while bone cracks were increased during mild and severe OA. In knee OA, cartilage cracks were not correlated with Mankin score, whereas in hip OA they appeared association with severity score. Bone cracks were positively correlated with matrix apoptotic osteocytes and osteoblastic cells, but not with osteoclasts. MMP-2 immunostaining was increasing by OA severity in the osteochondral unit. Similarly, MMP-2 was expressed on the microcracks’ wall mainly in Group III.Conclusion:Our data displayed that bone cracks during primary OA stages, represent an early adaptative mechanism aiming to maintain cartilage integrity. Accumulation of bone defects and concomitant increase of apoptotic osteocytes activated an abnormal remodeling due to osteoblastic activity, in which MMP-2 played a pivotal role, leading to subchondral sclerosis promoting further osteochondral deformities.

简介：AbstractBackground:Gastric cancer (GC) is one of the most common malignancies, and intestinal-type GC is the main histopathologic type of GC in China. We previously reported that casein kinase 2 interacting protein 1 (CKIP-1) acts as a candidate tumor suppressor in intestinal-type GC. CKIP-1 participates in the regulation of multiple signaling pathways, including the Wnt/β-catenin pathway, of which caudal-related homeobox 1 (CDX1) may be a downstream target gene. The purpose of this study was to investigate the relationship between CKIP-1 and CDX1 in intestinal-type GC.Methods:Sixty-seven gastroscopy biopsy specimens and surgically resected gastric specimens were divided into four groups: gastric mucosa group, intestinal metaplasia (IM) group, dysplasia group, and intestinal-type GC group. The expression levels of CKIP-1 and CDX1 were detected in these groups and GC cell lines, and the correlations between these expression levels were analyzed. SGC7901 and BGC823 cells were divided into CKIP-1 shRNA groups and CKIP-1 over-expression groups, and CDX1 expression was detected. β-Catenin expression was detected in intestinal-type GC tissue samples and CKIP-1 shRNA and CKIP-1 over-expression SGC7901 cells, and its correlation with CKIP-1 expression in intestinal-type GC tissue was analyzed. The Wnt/β-catenin pathway inhibitor DKK-1 and activator LiCl were incubated with SGC7901 cells, BGC823 cells, and CKIP-1 shRNA and CKIP-1 over-expression SGC7901 and BGC823 cells, following which CDX1 and Ki-67 expression were detected.Results:The expression levels of CKIP-1 and CDX1 were lower in patients with intestinal-type GC than in patients with IM and dysplasia (both P < 0.05). CKIP-1 and CDX1 expression levels were positively correlated in IM, dysplasia, and intestinal-type GC tissue and cell lines (r = 0.771, P < 0.01; r = 0.597, P < 0.01; r = 0.654, P < 0.01; r = 0.811, P < 0.01, respectively). CDX1 expression was decreased in the CKIP-1 shRNA groups and increased in the CKIP-1 over-expression groups of SGC7901 and BGC823 cells compared to that in the corresponding control groups (both P < 0.05). CKIP-1 expression was negatively correlated with β-catenin expression in intestinal-type GC patients (r = -0.458, P < 0.01). Compared to the control group, β-catenin expression was increased in the CKIP-1 shRNA SGC7901 cell group and decreased in the CKIP-1 over-expression SGC7901 cell group (P < 0.05). CDX1 expression was increased in SGC7901 and BGC823 cells treated with DKK-1, DKK-1 increased CDX1 expression and decreased Ki-67 expression in the CKIP-1 shRNA group; the opposite result was observed in SGC7901 and BGC823 cells treated with LiCl, and LiCl decreased CDX1 expression and increased Ki-67 expression in the CKIP-1 over-expression group (both P < 0.05).Conclusions:Through the Wnt/β-catenin signaling pathway, CKIP-1 may positively regulate CDX1 in intestinal-type GC.

简介：像使用费的受体(TLR)是主人防卫系统的哨兵，它认出很多微生物引起的病原体。主机防卫系统可能是低效的或如果由TLR和随后的被触发TLR的cytokine生产的微生物引起的识别是deregulated，煽动性的疾病可以发展。激活抄写因素4(ATF4)，ATF/CREB抄写因素家庭的一个成员，是参予几个pathophysiological过程的一个重要因素。在这份报告，我们发现ATF4也涉及调停TLR的天生的有免疫力的反应，它参予TLR4信号transduction并且调停许多cytokines的分泌物。我们观察到ATF4被激活并且translocates到经由TLR4-MyD88-dependent小径跟随lipopolysaccharide(LPS)刺激的原子核。另外，cytokine数组试金证明某关键煽动性的cytokines例如IL-6，IL-8和RANTES，被ATF4断然调整。我们也证明c6月直接绑在ATF4，从而支持煽动性的cytokines的分泌物。一起拿，这些结果显示ATF4在被触发TLR4的cytokine充当一个积极管理者生产。