W13-How_to_deal_with_nuclear_NK
有关核武器的英语作文
有关核武器的英语作文The Complexities of Nuclear Weapons.The topic of nuclear weapons evokes a range of emotions and perspectives, ranging from fear and alarm to strategic calculations and geopolitical analysis. These weapons, with their immense destructive power, have loomed large in international relations and global security discussions for decades. Their existence and potential for use have shaped international law, security policies, and strategic doctrines around the world.The Origins and Evolution of Nuclear Weapons.The development of nuclear weapons can be traced back to the early years of the 20th century, when scientists began to experiment with atomic reactions and nuclear fission. The race to develop these weapons was a激烈的竞争between the United States and the Soviet Union during the Cold War. By the mid-20th century, both superpowers hadstockpiled enough nuclear arms to destroy civilization several times over.Since then, nuclear weapons technology has evolved, becoming more sophisticated and diverse. Today, nuclear arsenals are not just limited to a few select countries; several other nations, including China, France, the United Kingdom, India, Pakistan, and North Korea, also possess nuclear capabilities.The Global Impact of Nuclear Weapons.The mere existence of nuclear weapons has had profound global impacts. Firstly, it has altered the nature of warfare. The potential for mass destruction has made conventional wars between nuclear-armed states increasingly unlikely, leading to a situation where conflicts are often resolved through diplomatic channels and proxy wars.Secondly, nuclear weapons have shaped international law and security norms. The Non-Proliferation Treaty (NPT), for instance, aims to prevent the spread of nuclear weapons andweapons technology, while promoting the peaceful use of nuclear energy. The Treaty on the Prohibition of Nuclear Weapons (TPNW) is a more recent effort to outlaw nuclear weapons altogether.The Moral and Ethical Dilemma.The moral and ethical implications of nuclear weapons are complex. On one hand, they are seen as a deterrent against aggression and a guarantee of national security. On the other hand, the potential for catastrophic harm and the risk of accidental or unauthorized use raise seriousethical concerns.The argument for nuclear deterrence rests on the premise that possession of nuclear weapons dissuades potential aggressors from attacking, knowing that a nuclear retaliation would be devastating. However, this logic also assumes a state of perpetual alert and readiness, which can lead to a situation where the risk of miscalculation or accidental conflict becomes dangerously high.The Future of Nuclear Weapons.The future of nuclear weapons remains uncertain. While the threat of nuclear war may have decreased in recent decades, the proliferation of nuclear technology and the emergence of new security challenges pose new risks. The need for global cooperation and disarmament efforts is paramount.Efforts towards nuclear disarmament and non-proliferation, such as the NPT and the TPNW, are steps in the right direction. However, achieving a world without nuclear weapons will require sustained diplomatic efforts, technological advancements, and a collective commitment to global security and peace.In conclusion, nuclear weapons are a complex and multifaceted issue that requires a nuanced understanding and a balanced approach. It is crucial to recognize the security concerns that underlie their existence while also acknowledging their devastating potential. Only throughcollective action and continuous dialogue can we hope to move towards a safer, more secure world.。
小学上册第13次英语第二单元暑期作业
小学上册英语第二单元暑期作业英语试题一、综合题(本题有100小题，每小题1分，共100分.每小题不选、错误，均不给分)1.The periodic table organizes elements by their ______.2.The dog is ________ around the yard.3. A __________ (酸) tastes sour and can be found in lemons.4.Some flowers bloom at _______ times of the year.5.What do you call the part of the plant that absorbs water and nutrients?A. LeafB. StemC. RootD. Flower6.I enjoy going to the farmer's market to buy __________.7.What do you call a person who repairs buildings?A. EngineerB. ArchitectC. BuilderD. CarpenterD8.Which fruit is red and often mistaken for a vegetable?A. TomatoB. StrawberryC. RaspberryD. CherryA9.ts are sensitive to ______ (光线) changes. Some pla10.She is a historian, ______ (她是一名历史学家), who loves ancient cultures.11.local food movement) emphasizes regional produce. The ____12.What do we call the tool we use to write on paper?A. BrushB. PenC. RulerD. ScissorsB13.The flowers smell ________.14.What is the main ingredient in pancakes?A. FlourB. SugarC. MilkD. Eggs15.When it snows, I like to stay ______ (温暖).16.How many legs do spiders have?A. 6B. 8C. 10D. 12B17.My favorite season is _____ (winter/summer).18.I enjoy showing my friends my newest ____. (玩具名称)19.What do you call the person who repairs cars?A. BakerB. MechanicC. TeacherD. Doctor20.The sun is _______ (shining) on the water.21.The _____ (soil) needs to be rich for healthy plants.22.The _____ (holly) bush is festive in winter.23.I have a ______ (相机) to take pictures of my friends and family. It helps me capture ______ (回忆).24.What is the term for a baby cow?A. CalfB. LambC. FoalD. KidA Calf25.__________ (化学挑战) encourage innovative solutions to global issues.26.How many planets are in our solar system?A. 7B. 8C. 9D. 1027.training session) builds capacity. The ____28.What do we call the act of improving relationships?A. ReconciliationB. HealingC. MendingD. All of the AboveD29.The chemical formula for ethylene is _______.30.The squirrel collects _______ (坚果) in the fall.31.My favorite pet is a ______ (狗) that loves to cuddle.32.What do we call the study of fungi?A. MycologyB. BotanyC. ZoologyD. EcologyA33.What is the fastest land animal?A. LionB. CheetahC. HorseD. Deer34.I found a __ in the garden. (bug)35.My aunt is a great __________ (演讲者).36.I can _______ my own breakfast.37.What is the main purpose of the lungs?A. To pump bloodB. To breatheC. To digest foodD. To moveB To breathe38.The _____ (温度) must be right for seeds to germinate.39.The __________ of a substance can affect its chemical properties.40.What is the name of the place where you go to see paintings?A. LibraryB. GalleryC. ParkD. TheaterB41.What is the capital city of the United Kingdom?A. ParisB. LondonC. BerlinD. RomeB42.Many plants have ______ (防御机制) against herbivores.43.The cat scratches its _____ post.44.My favorite part of the day is after school when I can play with my ____. (玩具名称)45.The __________ is the highest waterfall in the world. (安赫尔瀑布)46.The _______ (小鸟) sings beautifully.47.What do we call a large body of saltwater?A. LakeB. OceanC. RiverD. Stream48.The ________ (cake) looks delicious.49.The __________ (灌溉) system helps water the crops.50.The _____ (营养) in soil is vital for growth.51.The seahorse is known for its unique _______ (外形).52.Butterflies love to visit ______.53.Chemical properties describe how a substance _____ with other substances.54.What is the capital of Micronesia?A. PalikirB. PohnpeiC. YapD. ChuukA55.What is 1 + 1?A. 1B. 2C. 3D. 456.What do you call a person who plays the piano?A. PianistB. SingerC. ComposerD. MusicianA57.We have a ______ (丰富的) schedule filled with activities.58.What do we call the process of changing from a liquid to a solid?A. MeltingB. FreezingC. BoilingD. Evaporating59.The ______ (植物的特性) often dictate their growth patterns.60.The ____ is an animal that loves to dig.61. A solid has a ______ shape.62.Bacteria can be helpful or ______ to humans.63.I can ___ (swim) in the pool.64.What is the name of the ancient city buried by volcanic ash?A. AthensB. PompeiiC. RomeD. Carthage65.She has a ________ (plan) for her career.66.The chemical symbol for rhodium is ____.67.The train is _____ (fast/slow).68.The __________ is a region known for its biodiversity.69. A __________ (温室) is a good place for plants.70.What do we call the largest living structure on Earth?A. Great Barrier ReefB. Amazon RainforestC. SerengetiD. Himalayan MountainsA71.The _______ (骆驼) can survive in the desert.72.Having a variety of ________ (玩具名) allows me to be more ________ (形容词) in play.73.What do we call a person who studies insects?A. EntomologistB. BiologistC. EcologistD. BotanistA74.The first emperor of China was _____.75.The nurse provides care and support in _____ (医院).76.My birthday is in ______ (七月). I want to have a big ______ (派对) with cake and ______ (气球).77.How many planets are in our solar system?A. 8B. 9C. 10D. 1178. A dwarf planet is a celestial body that is not a ______ planet.79.What do we call a large body of saltwater?A. OceanB. LakeC. RiverD. PondA80.What is the opposite of "big"?A. LargeB. HugeC. SmallD. TallC81.I want to _____ (cook) dinner tonight.82.Herbs are often used in __________ (烹饪).83.The ______ contributes to the ecosystem.84.Metals are typically good conductors of _____.85.I have a toy _______ that rolls and spins everywhere I go.86.The __________ is known for its stunning architecture.87.I saw a _______ (蝴蝶) land on a flower.88.Carbon dioxide is produced when we ______.89.My _______ (狗) barks at everyone who passes by.90.What do you call the sound that a cat makes?A. BarkB. MeowC. RoarD. ChirpB91.The process of dissolving a solute in a solvent is called _____.92.Heat makes molecules move ______.93.What is the name of the famous scientist known for his work on radioactivity?A. Marie CurieB. Albert EinsteinC. Isaac NewtonD. Charles DarwinA94.What is the name of the famous landmark in Italy?A. ColosseumB. Tower of PisaC. Vatican CityD. Leaning Tower of PisaD Leaning Tower of Pisa95.小鸟) builds its nest in spring. The ___96.The goat loves to _______ (吃) grass on the hill.97.How many planets are in our solar system?A. 7B. 8C. 9D. 1098.I like to drink ______ (牛奶) every morning.99.I have a collection of ________ (漫画书) that I read during my free time. They are so ________ (有趣).100.I love eating ______ with my family.。
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Links between Tumor Suppressors p53 Is Required for TGFβ Gene Responses by Cooperating with Smads
Cell,Vol.113,301–314,May 2,2003,Copyright 2003by Cell PressLinks between Tumor Suppressors:p53Is Required for TGF-Gene Responses by Cooperating with Smadsphosphorylation and activation of the Smad family of signal transducers.Two different Smad signaling branches have been described:TGF--like signals,including TGF-Michelangelo Cordenonsi,1Sirio Dupont,1Silvia Maretto,1Alessandra Insinga,2Carol Imbriano,3and Stefano Piccolo 1,*s,Activin,and Nodal,are transduced by Smad2or 1Department of Histology,Microbiology,and Smad3,whereas BMPs are transduced by Smad1(Mas-Medical Biotechnologiessague ´,2000).Section of Histology and Embryology Once activated,the Smads translocate into the nu-University of Padua cleus where they control gene expression in association viale Colombo 3with Smad4and partner transcriptional regulators (Mas-35121Padua sague ´,2000).How the Smads recognize and properly Italy activate a specific promoter is not fully understood.In 2Department of Experimental Oncology part,specificity depends on the differential expression European Institute of Oncology of distinct Smad partners in distinct cell types;however,via Ripamonti 435several inputs can profoundly modify both the percep-20141Milan tion of the TGF-signal and its biological output (Mas-Italy sague ´,2000).Understanding how this transcriptional 3Department of Biologyplasticity is attained is central for embryonic develop-University of Modena and Reggio Emilia ment and cancer.For example,most carcinomas have via Campi 213selectively lost the growth arrest response and gained 41100Modena metastatic abilities in response to TGF-(Wakefield and ItalyRoberts,2002).Importantly,this change can occur with-out acquiring genetic defects in known components of the TGF-pathway,indicating that alterations in other Summaryregulatory molecules can have a profound influence on the cellular responsivenss to TGF-.Some of these reg-The p53tumor suppressor belongs to a family of pro-ulators appear to act in parallel to the Smad signal trans-teins that sense multiple cellular inputs to regulate cell duction cascade,namely converging at the level of tar-proliferation,apoptosis,and differentiation.Whether get gene expression (Lehmann et al.,2000).and how these functions of p53intersect with the ac-To further understand the molecular mechanisms that tivity of extracellular growth factors is not understood.control of TGF-gene responses,we performed an un-Here,we report that key cellular responses to TGF-biased screen for TGF-modulators.Here,we report the signals rely on p53family members.During Xenopus unexpected identification of p53as an in vivo relevant embryonic development,p53promotes the activation partner of Smad2in the activation of multiple TGF-of multiple TGF-target genes.Moreover,mesoderm target genes.p53is a key tumor suppressor in mammals differentiation is inhibited in p53-depleted embryos.In as it is mutated,or inactive,in the majority of human mammalian cells,the full transcriptional activation of tumors (Vogelstein et al.,2000).p53belongs to a family the CDK inhibitor p21WAF1by TGF-requires p53.p53-of proteins,including p63and p73,that have evolved deficient cells display an impaired cytostatic response pleiotropic—and perhaps overlapping—cellular func-to TGF-signals.Smad and p53protein complexes tions (Yang and McKeon,2000).converge on separate cis binding elements on a target We find that several TGF-target genes are under promoter and synergistically activate TGF-induced joint control of p53and Smads.p53binds to Smads in transcription.p53can physically interact in vivo with vivo and strongly cooperates transcriptionally with the Smad2in a TGF--dependent fashion.The results un-activated Smad complex.In Xenopus embryos and hu-veil a previously unrecognized link between two pri-man cells,TGF-requires the assistance of p53to medi-mary tumor suppressor pathways in vertebrates.ate the activation of key TGF-target genes and to carry out some of its biological ing the Mix.2Introductionpromoter as a paradigm,we find that p53adjusts TGF--induced transcription by interacting directly with a Members of the TGF-growth factor family are promi-cognate binding site on promoter DNA.However,differ-nent signals regulating cellular fates in a variety of physi-ent from other Smad partners,this p53binding element ological contexts,from embryonic development to adult is located in a separate position from the Activin/TGF-tissue homeostasis (Massague ´,2000).The loss of this responsive element.We argue that these findings unveil control leads to aberrant cell behaviors contributing to a convergence of the p53and the Smad signaling net-the development of cancer and inborn defects (Wake-works to regulate development and tissue homeostasis.field and Roberts,2002).In recent years,tremendous progress has been made Resultsin the elucidation of how cells sense and transduce TGF-signals.TGF-ligands bind to cognate serine/Cloning of an Alternatively Spliced Isoform of p53threonine kinase receptors leading,intracellularly,to(p53AS)in a Screen for Activators of TGF-Signaling To identify molecules that modulate TGF-/Activin/Nodal signaling during development,we performed an*Correspondence:piccolo@civ.bio.unipd.itCell302unbiased functional screen for genes whose expression nally modified p53isoform has not been described in promoted the differentiation of embryonic cells into en-human or frog cells that express regular p53(p53R) doderm and mesoderm,as this is the hallmark of TGF-(Wolkowicz et al.,1995).Xenopus and mammalian p53 signaling in early vertebrate embryos(Whitman,2001).proteins share similar functional properties and regula-We generated a mouse gastrula(embryonic day[E]6.5)tory mechanisms(Cox et al.,1994).To assay for func-cDNA library constructed in an RNA expression plasmid.tional conservation,we compared the ability of mouse Synthetic mRNA was prepared from pools of100bacte-p53AS,human p53R,and Xenopus p53(Xp53)to induce rial colonies and injected into the animal hemispheremesoendoderm differentiation in animal cap assays. of2-cell Xenopus embryos.At the blastula stage,the Figure1C shows that the inducing activities of mp53AS ectoderm was explanted and cultivated until siblingsand Xp53are similar.hp53R can also stimulate expres-reached the gastrula stage.The injected animal caps sion of the same marker genes but at5-to10-fold lower were then assayed by RT-PCR to identify pools able toefficiency than mp53AS,perhaps revealing a partial in-activate the expression of Mixer(endoderm)and Xbra hibitory role for p53C terminus in these activation pro-(mesoderm).Of five positive pools,two of the activecesses.Of note,injection of higher doses(above400 cDNAs isolated after sib selection corresponded to pg for all mRNAs)was detrimental for survival(data not Smad2(Baker and Harland,1996)and,unexpectedly,shown).three corresponded to p53AS,a natural variant of p53p53may stimulate TGF-gene responses acting in generated by alternative splicing at the C terminus(Wol-partnership with endogenous Smads or,alternatively, kowicz et al.,1995).p53AS shares with commonly operating in an independent pathway.To discriminate spliced p53(p53R)the N-terminal transactivation do-between these two possibilities,we tested whether a main,the central DNA binding and oligomerization do-blockade of Smad function had an effect on p53-medi-mains,but lacks the most C-terminal26amino acids ofated gene expression.As shown in Figure1D,coinjec-p53R.tion of p53AS and dominant-negative Smad2(Candia A wealth of data indicates that the TGF-and p53et al.,1997)mRNAs downregulated all the TGF--like signaling networks operate independently as powerful inductions triggered by p53AS.We conclude that ex-tumor suppressors in mammalian cells;yet,the cloningpression of p53activates the transcription of TGF-of a p53isoform in a TGF-screen unveiled the possibil-target genes in a Smad-dependent fashion.ity of a previously unrecognized partnership betweenTo explore the possibility that p53and Smad may these two types of molecules.We initially addressed jointly control the TGF-output,we tested whether rai-this issue by characterizing the p53AS effects in moresing the levels of p53may correspond to an enhanced detail.Different doses of p53AS mRNA were injected in responsiveness to TGF-.Figure1E shows that in animal the animal pole of each blastomere at the2-cell stagecaps explants,coinjection of suboptimal levels of activin and tested for the induction of several tissue-specific and p53AS mRNAs cooperated in the induction of endo-markers in animal cap cells explanted from these em-dermal and mesodermal markers,whereas each compo-bryos(Figure1A).At lower doses of injected mRNA,nent alone was weak or inactive.In contrast,the BMP4 p53AS induced first mesodermal(Xbra,Eomes)and thentarget Vent-1was neither induced by p53AS alone nor mesendodermal(VegT,Mix.2)genes;at a higher con-in combination with BMP4(see Supplemental Figure centration,mainly endodermal markers were turned onS1A online at /cgi/content/full/113/ (Sox17,Mixer,Xnr6)(Figure1A,lanes1–5).This pattern3/301/DC1).of gene expression is typical of the ectopic activationWe further tested whether p53-mediated effects are of TGF-/Activin/Nodal/Smad2signaling in animal caps direct by assaying the biological activities of p53and (Figure1A,lanes6and7)(Harland and Gerhart,1997).Smad2in the presence of cycloheximide,a protein syn-However,other genes activated by Activin/Smad2such thesis inhibitor.Transcription of Xbra,Mix.2,and Eomes as goosecoid,XWnt8,and Xnr-1were not induced inis initiated as immediate response to Activin/Smad2 p53AS-injected cells(Figure1A,bottom).This suggests stimulation in Xenopus animal caps(Harland and Ger-that p53AS specifically activates a subset of TGF-tar-hart,1997)and,as shown in Supplemental Figure S1B, get genes.p53directly promotes transcription of the same genes We tested the biological activity of p53mRNA in thein the absence of de novo protein synthesis.In keeping context of the whole embryo.When microinjected into with this notion,injection of p53alleles bearing inactivat-a single ventral blastomere at the4-cell stage,p53ASing mutations in the DNA binding(R273H)or transactiva-mRNA induced the formation of ectopic trunk-tail struc-tion domain(22-23)failed to induce any mesoendoder-tures(nϭ155,77%),phenocopying the biological ef-mal marker(Figure1F).This suggests that p53relies fects triggered by low doses of Smad2mRNA(Figure1B)entirely on its properties as sequence-specific transcrip-(Baker and Harland,1996).Histological analysis showedtion factor in these inductive events.that these secondary structures contained muscle,neu-p53is biochemically a latent transcriptional regulator ral tissue,and in several cases an ectopic gut,but allthat becomes active in response to a variety of stimuli lacked notochord(data not shown).(Vogelstein et al.,2000).Little is known on the activation We conclude from these experiments that ectopicstatus of Xp53in early embryos.This can be visualized expression of p53stimulates multiple gene responses by monitoring p53-dependent transcription.To this end, and long-term phenotypic effects typically mediated bywe injected at the1-cell stage a luciferase reporter for activation of the TGF-signaling cascade in embryonic p53signaling whose transcription is driven by multimer-cells(Harland and Gerhart,1997).ized p53binding elements(PG13)(Kern et al.,1992).We Alternative spliced p53AS represents up to30%of compared PG13transcription with MG13,in which the total p53in rodent cells but,curiously,a similar C termi-p53binding elements are disrupted.Intriguingly,weConvergence of p53and Smads303Figure1.p53Promotes Mesoderm and En-doderm Formation in Xenopus Embryos(A)RT-PCR for mesoderm(Mes)and endo-derm(Endo)markers activated in animal capsexpressing the indicated ne1:lacZ mRNA(200pg).Lanes2–5:p53AS mRNA(3,10,30,150pg,respectively).Lane6:ac-tivin mRNA(30pg).Lane7:Smad2mRNA(200pg).Lane8:eFGF(50pg).Lanes9and10:whole embryo total RNA without(ϪRT)and with reverse transcriptase.(B)Injection of p53AS mRNA(50pg;nϭ155,77%)mimicks the long-term effects of Smad2mRNA overexpression(100pg;nϭ12,100%).Side view of stage28embryos.Dot-ted lines indicate the induced secondarytrunk-tail structures.(C)RT-PCR of animal caps expressing thefollowing mRNAs:hp53R(20pg and200pg),mp53AS(20pg),and Xp53(30pg).(D)TGF--like activities promoted by p53ASmRNA(50pg)are inhibited by dominant-neg-ative Smad2(DNS2:1ng)mRNA.(E)Lane2:inductions by activin mRNA at ahigh dose(35pg)but lower amounts of p53ASor activin mRNA(1pg,each)were effectiveonly in combination(Lanes3–5).Lanes6–8,synergism of p53AS with activin,both usedat5pg of mRNA.(F)RT-PCR on animal caps expressing theindicated mRNAs(200pg each).Lane2:hp53(WT).Lane3:p53L22E-W23S bears an inac-tive transactivation ne4:p53R273H is unable to bind DNA.(G)Detection of p53transcriptional activity inearly embryos.PG13-lux and MG13-lux(40pg per embryo)were injected at the2-cellstage in each blastomere and luciferase ac-tivity was measured on extracts from gastru-lae(nϭ40each).found that Xenopus embryos have considerable endog-protein levels for-catenin(Figure2A)or actin(data notshown).enous p53transcriptional activity(Figure1G).We examined the effect of p53knockdown on mes-oendoderm differentiation mediated by Activin protein p53Is Required for TGF-/Activin/Nodal-Mediated in animal caps(Figure2B).p53MO and control MO were Gene Responses in Xenopus Embryos injected into the animal hemispheres at the2-cell stage, We sought to establish to what extent p53is required animal caps were removed at blastula and treated in for TGF-/Activin/Nodal signaling in vivo.To this end,Activin-containing medium(50pM).As shown in Figure we reduced the endogenous p53protein level with an2B,Activin-mediated inductions of mesodermal(Xbra anti-p53morpholino oligonucleotide(p53MO)covering and Eomes)or endodermal(Mix.2and Mixer)markers the initial codons of Xp53mRNA.As specificity control,were inhibited in p53-depleted caps(Figure2B,com-we used a mutant morpholino oligonucleotide(control pare lanes3and4).Three evidences indicate that this MO).p53MO specifically blocked Xp53mRNA transla-interference is specific.First,the control MO has no tion initiation in vivo,leading to effective knockdown of effect on Activin signaling.Second,normal Activin-the endogenous levels of p53protein,without affectingmediated gene responses can be restored by coinjec-Cell304Figure2.In Vivo Requirement of p53in TGF-Gene Responses(A)p53morpholino oligonucleotides(MO,20ng)specifically knockdown the translation ofboth endogenous(left)and overexpressed(right)Xp53mRNA(100pg)in animal halvesexplanted at gastrula stage.-catenin proteinserves as specificity control.(B)Animal caps,injected with the indicatedMO,were explanted and treated with Activinprotein(50pM).Lane4:p53MO selectivelyblocks Activin inductions of Mixer,Mix.2,Eomes,and Xbra,but not of goosecoid(Gsc).Lane5:mp53AS mRNA injection rescues Ac-tivin inductions in p53MO injected animalcaps.(C)Whole-mount in situ hybridizations oncontrol-and p53morphant embryos showingsevere phenotypes.Control MO or p53MO(10ng each),together with lacZ mRNA(200pg),were injected at the4-cell stage in a sin-gle blastomere.Embryos shown in the upperpanels were collected at gastrula,stained for-gal activity(red staining),and processedfor in situ hybridization.Embryos shown inthe lower panels were radially injected(20ngper embryo)and collected at stage13.Notethat upon p53knockdown,staining forChordin,Xbra,and XmyoD,but not for Vent-1,is reduced.(D and E)Phenotypes of p53-depleted em-bryos.Embryos were injected as in(C)andcultured until siblings reached the tailbudstage.(F–I)Embryos were injected on the right sideat the2-cell stage with15ng of control MO(F)or p53MO either alone(G)or in combina-tion with mp53AS mRNA([H],30pg;[I],100pg).Embryos were collected at stage26andprocessed for in situ hybridization with theXmyoD probe.tion of mouse p53AS,whose translation is not antago-of the pan-mesodermal marker Xbra in early gastrulae;incontrast,expression of Vent-1was not affected(see nized by the p53MO(Figure2B,lane5).Third,Activin-mediated induction of goosecoid is p53independent closer images in Supplemental Figure S2online at http:// (Figure2B,lane4).Collectively,these findings indicate/cgi/content/full/113/3/301/DC1).In a critical role of p53for the activation of a subset of embryos injected in all blastomeres with p53MO,the TGF-/Activin targets.development of dorsal mesoderm derivatives was as-We next asked whether p53function was also re-sayed molecularly using probes for Chordin and XmyoD,whose expression at the neurula stage marks axial quired in the whole embryo.Several findings have dem-onstrated that Nodals and Derriere,a group of TGF-mesoderm and prospective skeletal muscle,respec--related ligands,induce and pattern the mesoderm intively.As shown in Figure2C,p53MO,but not control vertebrates(Whitman,2001;Sun et al.,1999).If p53MO,severely downregulated Chordin and XmyoD ex-plays a role in endogenous TGF-signaling,p53knock-pression.In monolateral injection experiments(right down should attenuate these inductions in embryos.We side in Figures2F–2I),coinjection of p53MO with in-creasing levels of p53AS mRNA rescues this phenotype. injected p53MO in a single dorsal or ventral blastomereat the4-cell stage and assayed the resulting phenotype At the tailbud stage,major developmental changes oc-using molecular markers by in situ hybridization.Ascurred in p53-depleted embryos compared to control shown in Figure2C,p53MO,but not control MO,attenu-MO injected embryos(Figures2D and2E).Part of the ated the expression of the organizer marker Chordin andp53morphants(23%)failed to gastrulate properly dueConvergence of p53and Smads305to defective blastopore formation.Among the p53mor-activity,although a weaker,p53-independent p21WAF1 phants that survived after gastrulation and neurulation,induction can be observed after hours of Activin sig-several(nϭ76,54%)lacked tail structures and devel-naling.oped a reduced trunk,indicative of defective mesodermOf note,activation of p21WAF1by TGF-has been formation.These phenotypes recapitulate aspects of shown to be p53independent in some tumorigenic orimmortalized epithelial cell types(Datto et al.,1995). embryonic TGF-deficiencies,such as embryos in-jected with low doses of Cerberus-short,a secreted This indicates,perhaps not surprisingly,that different antagonist of Nodal,or with an inhibitory construct forgenetic programs may be at work in distinct cells(Mas-derriere,both leading to defective trunk development sague´,2000);additionally,it also leaves open the possi-(Piccolo et al.,1999;Sun et al.,1999).bility that p63of p73may be able to compensate for Together,these loss-of-function experiments suggest p53loss-of-function in some contexts.HaCaT cells are that depletion of p53leads to impaired edogenous TGF-a point in case,as this cell line of immortalized keratino-/Activin/Nodal gene responses resulting in defective cytes is p53mutant,but highly TGF-responsive(Dattoet al.,1995).However,these cells express high levels embryonic development.of p63(Hall et al.,2000),whose reduction by anti-p63siRNA led to a concomitant reduction in of p21WAF1induc-p53Is Required for Full TGF-Gene Responsesibility by TGF-1(see Supplemental Figure S3online at and TGF--Mediated Growth Arrest/cgi/content/full/113/3/301/DC1). in Mammalian CellsThese results suggest that p53and p63may have par-Having established the biological activities of p53in thetially overlapping roles in modulating the expression of frog embryo,we wished to determine to what extentat least one key gene in the TGF-cytostatic program p53is required for TGF--mediated gene responses inin keratinocytes.human cells.We monitored the expression of a groupGiven the gene expression changes observed in the of genes playing key roles in different aspects of theresponse to Activin after ablation of p53in HepG2cells, cellular response to TGF-signaling in mammals,suchwe assayed for their biological importance in the context as p21WAF1,plasminogen activator inhibitor-1(PAI-1),of the TGF-cytostatic program.For this purpose,bro-matrix metalloprotease-2(MMP2),and TGF-induciblemodeoxyuridine(BrdU)incorporation was analyzed as early gene(TIEG).p21WAF1is a Cyclin-dependent kinasean indication of DNA synthesis and S phase entry of (CDK)inhibitor and a central mediator of the cellularcontrol and p53-depleted cells(Figure3D).As expected, growth arrest program(Deng et al.,1995).PAI-1andActivin inhibited cell-cycle progression of control HepG2 MMP2are secreted proteins required for extracellularcells.Strikingly however,Activin had limited effect on matrix remodeling and epithelial-mesenchymal transfor-the BrdU incorporation after siRNA-mediated ablation mation,whereas TIEG is thought to be important in TGF-of p53,indicating that p53knockdown is sufficient to -mediated apoptosis.overcome the growth arrest imposed by TGF-sig-We analyzed the relevance of p53in the activation ofnaling.these TGF-targets.For this purpose,we reduced theLack of sensitivity to TGF-growth-suppressing ef-endogenous levels of p53using the small interferingfects is a landmark of most cancers.Given that a high RNA(siRNA)technique in the HepG2model system(Fig-proportion of human cancers carry mutations in p53, ure3A),as this hepatoma cell line is highly TGF-/Activinour data at least suggest that inactivation of p53may responsive and expresses wild-type p53,but not p63be one of the possible mechanisms for the selective or p73.Figure3B shows RT-PCR analyses in which allloss of TGF-tumor-suppressing effects in cancer cells. the markers were clearly upregulated in HepG2cells asWe explored this hypothesis trying to restore the anti-an early response to Activin treatment.In the presenceproliferative effects of TGF-in cancer cell lines lacking of anti-p53siRNA,these inductions were reduced forp53.SAOS-2is a p53null osteosarcoma cell line,not p21WAF1,MMP2,and PAI-1.Notably,induction of TIEGexpressing p63or p73,that is insensitive to growth ar-was p53independent,implicating that p53knockdownrest mediated by TGF-treatment or overexpressed has no effect,per se,on the overall TGF-respon-Smad2(Figure3E,lane2,and data not shown)(Prunier siveness.This further suggests that knockdown of p53et al.,2001).Strikingly,however,coexpression of Smad2 affects a significant proportion,but not all the TGF-and low amounts of p53AS,by themselves unable to target genes,as previously noted in the TGF-differenti-trigger any effect,resulted in a marked inhibition of cell ation program of the frog embryo.growth as measured by BrdU incorporation(compare The CDK inhibitor p21WAF1is a critical determinant oflane5and6).Thus,reintroduction of p53activity in p53-growth arrest in response to a variety of stimuli;thesedeficient cancer cells may restore part of the TGF-activate p21WAF1expression p53dependently,such ascontrol over the cell cycle.DNA damage,or p53independently,such as terminaldifferentiation and senescence(Macleod et al.,1995).As our data argued that Activin/TGF-signaling and p53p53Is Required for TGF-1-Mediated Growth elevate in concert p21WAF1expression in HepG2cells,Arrest in Mouse Embryonic Fibroblastswe examined in more detail the effect of p53depletion and Hematopoietic Progenitorson the induction of p21WAF1by Activin at the protein level.Since transient siRNA ablation of p53had a strong im-Mock and anti-p53siRNA transfected HepG2cells were pact on the TGF-response of HepG2cells,we next stimulated for different times with Activin and then ana-asked whether the genetic inactivation of p53was also lyzed by Western blotting.As shown in Figure3C,the relevant for some biological responses to TGF-in nor-elevation of p21WAF1as response to Activin requires p53mal cell types.One complicating issue in the interpreta-Cell306Figure3.p53Activity Is Required for Full TGF-Responsiveness in Human Cells(A)Effectiveness of siRNA-mediated depletion of p53in HepG2cells controlled by Western blotting.(B)Control and p53-depleted HepG2cells were treated with Activin(1nM)for2hr and subjected to RT-PCR analyses for endogenous targets of Activin/TGF-.(C)Time course of p21WAF1induction by Activin(1nM)in mock and p53-depleted HepG2cells.(D)p53is required for Activin-mediated growth inhibition in HepG2cells treated with increasing doses of Activin for24hr.Columns show the effects of Activin expressed as percentage of inhibition of BrdU incorporation relative to unstimulated cultures.(E)p53rescues Smad2growth suppressing activity in p53null SAOS-2cells.Cells were transfected with the indicated plasmids and then plated onto coverslips for BrdU incorporation assay.Transfection of p53AS expression vector at high doses(lane3,750ng)blocked cell growth,but less than10-fold lower doses of p53AS had no effect(lane4,150ng;lane5,30ng).Cotransfection of of p53AS and Smad2(lane 6,30ng and1g,respectively)inhibited BrdU incorporation(up to87%inhibition).Arrows indicate the comparable amounts of p53AS.tion of genetic analyses is that the three p53family as judged by the decreased number of cells in S phase, members are coexpressed in most tissues in vivo(Yangthe concomitant increase in the G1phase and blockade and McKeon,2000).Nonetheless,recent data by Flores of BrdU incorporation.In contrast,p53Ϫ/ϪMEFs were et al.(2002)unveiled that induction of p21WAF1by DNAlargerly insensitive to TGF-1antiproliferative proper-damage relies on p53and is independent from p63and ties.As a control,we verified that the TGF-signalingcascade itself was effective in p53-deficient cells.For p73in mouse embryonic fibroblasts(MEFs).Thus,p53may be the main member of its family regulating p53-this purpose,we monitored the TGF-1-dependent tran-dependent growth arrest in this cell type.This simpli-scription of two synthetic reporters for Smad activation, fying finding provided us with a window of opportunity ARE3-lux and CAGA12-lux(Dennler et al.,1998;Huang to test a genetic requirement of p53for TGF-mediatedet al.,1995)and found that their inducibility was indistin-growth suppression.Primary wild-type and p53Ϫ/ϪMEFs guishable in wild-type and mutant cells(Figure4E).We were seeded at low density and treated with differentconclude that p53is a significant player in the antiprolif-doses of TGF-1;the distribution of the cell population erative effects mediated by TGF-in embryonic fibro-in the G1and S phases of the cell cycle was analyzedblasts.by flow cytometry after TGF-1treatment and the per-We next aimed to extend these findings to an addi-centage of cells in active DNA synthesis was assayedtional experimental system reflecting a role of TGF-in by BrdU incorporation.As shown in Figures4A–4D,wild-vivo.TGF-signaling has been shown to restrain the type MEFs were efficiently growth arrested by TGF-1,proliferative potential of hematopoietic progenitors。
放射医学专业外语翻译
UIA在1895年德国物理学家伦琴发现了一种新的射线，它从一个气体放线管发射出来的，它能够使位于密闭容器中的感光胶片感光，他在1895年12月分的时候，第一次宣称自己发现了这种射线，并将它命名为X线，X是代表了未知。
在一次公开的讲座当中，他为了阐述X射线的性质，伦琴就请求以为瑞士的著名解剖学家科勒尔，让他把手放到X射线流当中这样产生了世界上第一张X光片子。
关于X线用于医疗方面，它的第一次报道是在1896年1月23号的柳叶刀杂志，在这篇报道当中人们利用X射线，对一名喝醉了的水手后背上插着的一把刀进行定位，当人们将刀移除了之后，这位水手就不再瘫痪了。
这项新技术很快就在欧美开展开了诊断放射生物学就这样诞生了。
关于是谁第一次将X射线用于治疗存在着一些争论，但是在1897年有一个叫弗洛伊德的德国外科医生在维也纳的医学研究会表演了他成功的利用X射线使一个毛痣消失。
亨利贝克勒尔在1898年的时候发现了放射线的活性，在同一年居里夫妇发现了镭。
放射生物学界第一个有记录的实验是由贝克勒尔偶然的将镭放到自己的内衣口袋里，很快的就他发现了他的皮肤上起了红斑，并且于两周之后红斑变成了溃疡，溃疡面需要好几个星期才能愈合。
据传说皮埃尔居里在1901年的时候重复了这一实验，他是把一个镭故意的放在他的前臂，重复这些早期的开始。
从上世纪初，这些关于放射生物学的研究才刚刚开始。
α粒子是由罗斯福和罗伊这两个人发现的。
他们发现α粒子是由一个氦核组成的，这个氦核是由两个质子和两个中子组成的。
这四个粒子如此紧密的结合在一起使它在很多情况下表现得就仿佛是一个基本粒子。
一个阿尔法粒子的原子量是4U，它带有两个单位的正电荷。
β射线是由起源于原子核的高速电子所组成，这些核电子与核外电子拥有同样的特性，它们都有1840分之一U的原子质量，并且携带着一个单位的负电荷。
另一种β射线在1932年被安德森所发现。
这些射线所包含的粒子与负β粒子有着相同的原子质量，但是含有着一单位的正电荷，它被我们命名为正电子辐射。
接触到核物理英语作文
接触到核物理英语作文Title: Exploring the Depths of Nuclear Physics。
Nuclear physics stands as one of the most fascinating and complex branches of science, delving into the inner workings of atomic nuclei, their interactions, and the immense energy they possess. In this essay, we embark on a journey to explore the intricacies of nuclear physics, from its fundamental principles to its diverse applications in various fields.At its core, nuclear physics examines the structure and behavior of atomic nuclei, which are composed of protons and neutrons bound together by the strong nuclear force. Understanding the forces that govern these tiny yet powerful entities is essential for comprehending the nature of matter and energy on a fundamental level.One of the key concepts in nuclear physics is nuclear reactions, wherein nuclei undergo transformations, leadingto the release or absorption of energy. These reactions can take various forms, including fusion and fission. Fusion involves the merging of lighter nuclei to form heavier ones, releasing vast amounts of energy in the process, as exemplified by the reactions occurring in the core of stars. On the other hand, fission entails the splitting of heavy nuclei into smaller fragments, accompanied by the releaseof energy, as witnessed in nuclear power plants and atomic bombs.The study of nuclear physics has far-reaching implications across multiple disciplines. In astrophysics, nuclear processes govern the behavior of stars, dictating their lifespan, energy output, and eventual fate. Understanding these processes enables scientists to unravel the mysteries of the cosmos and comprehend phenomena suchas supernovae and black holes.In the realm of medicine, nuclear physics plays acrucial role in diagnostic imaging techniques such as positron emission tomography (PET) and single-photon emission computed tomography (SPECT). These imagingmodalities rely on the detection of radioactive tracers injected into the body, allowing physicians to visualize and diagnose various conditions, including cancer and neurological disorders, with remarkable precision.Furthermore, nuclear physics finds applications in energy production, with nuclear power serving as a viable alternative to fossil fuels. Nuclear reactors harness the energy released from fission reactions to generate electricity, offering a reliable and relatively low-carbon source of power. However, the proliferation of nuclear technology also raises concerns about safety, waste management, and the potential for nuclear proliferation, highlighting the importance of stringent regulations and international cooperation in this field.In particle physics, nuclear collisions provideinsights into the fundamental forces and constituents of matter, allowing scientists to probe the building blocks of the universe at the smallest scales. Accelerators such as the Large Hadron Collider (LHC) facilitate experiments that recreate conditions akin to those in the early universe,shedding light on phenomena such as the Higgs boson and dark matter.In conclusion, nuclear physics stands as a cornerstone of scientific inquiry, offering profound insights into the nature of matter, energy, and the universe itself. From unraveling the mysteries of the cosmos to powering our cities and healing the sick, its applications are as diverse as they are impactful. As we continue to push the boundaries of knowledge, the principles of nuclear physics will undoubtedly remain at the forefront of scientific exploration and innovation.。
Global Study of Nuclear Structure Functions
S. A. Kulagin∗ Institute for Nuclear Research, 117312 Moscow, Russia R. Petti† CERN, CH-1211 Gen´ eve 23, Switzerland
arXiv:hep-ph/0412425v3 22 Oct 2005
Abstract
We present the results of a phenomenological study of unpolarized nuclear structure functions for a wide kinematical region of x and Q2 . As a basis of our phenomenology we develop a model which takes into account a number of different nuclear effects including nuclear shadowing, Fermi motion and binding, nuclear pion excess and off-shell correction to bound nucleon structure functions. Within this approach we perform a statistical analysis of available data on the ratio of the nuclear structure functions F2 for different nuclei in the range from the deuteron to the lead. We express the off-shell effect and the effective scattering amplitude describing nuclear shadowing in terms of few parameters which are common to all nuclei and have a clear physical interpretation. The parameters are then extracted from statistical analysis of data. As a result, we obtain an excellent overall agreement between our calculations and data in the entire kinematical region of x and Q2 . We discuss a number of applications of our model which include the calculation of the deuteron structure functions, nuclear valence and sea quark distributions and nuclear structure functions for neutrino charged-current scattering.
细胞练习题及答案
二、是非判断1．蛋白核定位信号(nuclear localization signal)富含碱性氨基酸。
2．有亮氨酸拉链模式的Jun和Fos蛋白质是以二聚体或四聚体的形式结合DNA的。
3．端粒酶以端粒DNA为模板复制出更多的端粒重复单元，以保证染色体末端的稳定性。
4．核纤层蛋白B受体(1amln B receptor，LBR)是内核膜上特有蛋白之一。
5．现在认为gp210的作用主要是将核孔复合体锚区定在孔膜6．由RNA聚合酶I转录的rRNA分子是在胞质中与核糖体蛋白结合成RNP颗粒的，rRNA的转运需要能量。
7．核内有丝分裂指核内DNA多次复制而细胞不分裂，产生的子染色体并行排列，且体细胞内的同源染色体配对，紧密结合在一起成为体积很大的多线染色体。
8．已有的研究表明，组蛋白去乙酰化伴随着对染色质转录的抑制，与活性X染色体相比，雌性哺乳动物失活的X染色体及其组蛋白没有乙酰化修饰。
9．gp210是结构性跨膜蛋白，位于核膜的孔膜区，具有介导核孔复合体与核被膜的连接、将核孔复合体锚定在“孔膜区”的功能。
从而为核孔复合体装配提供一个起始位点。
10．p62是核膜上的功能性核孔复合体蛋白，在脊椎动物中具有两个功能结构域，其c端区可能在核孔复合体功能活动中直接参与核质交换。
11．第一个被确定的NLS来自猴肾病毒(SV40)的T抗原，由7个氨基酸残基构成。
12．常染色质在间期核内折叠压缩程度低，处于伸展状态(典型包装率750倍)，包含单一序列DNA 和中度重复序列DNA(如组蛋白基因和tRNA基因)。
13．异染色质化可能是关闭基因活性的一种途径。
14．T带是C带的反带，显示染色体的末端区。
15．染色质的区间性是通过基因座位控制区( locus control region，LCR)和隔离子(insulator)等顺式作用元件维持的。
三、填空1．细胞核外核膜表面常常附着有颗粒，与相连通。
2．核孔复合体是特殊的跨膜运输蛋白复合体，在经过核孔复合体的主动运输中，核孔复合体具有严格的选择性。
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Group Discussion
3
1993: NK announces that NK will withdraw from
Nuclear Nonproliferation Treaty 1994: Geneva Agreed Framework
NK pledges to freeze and eventually dismantle nuclear weapons program US offers the building of two power-producing reactors South Korea and Japan would provide oil to NK.
Defensive, rather than offensive military doctrines
All three factors are missing in NK Therefore, considerable chance of NK’s preemptive/preventive
6
Containment
Hawk Engagement (Victor Cha)
Preemption Preventive action
Dove (Full-blown) Engagement (David Kang)
7
Containment Isolation policy Key features: no communication, coercion, threats, and intimidation Hawk Engagement Containment plus Engagement or Conditional Engagement If you do x (dismantling of nuclear program), I will do y (withdrawal of economic sanction or signing of nonaggression pact) Maintaining necessary deterrent measures is precondition for this. Dove (Full-blown) Engagement Unilateral Engagement Give NK what it want first, then see what NK does (i.e., sunshine policy) Maintaining superior military and economic capabilities is precondition for this.
Week 13 International Relations of East Asia
1
Issues Knowledge
Historical Background of North Korea Nuclear Crisis
(major chronology) Nature of NK’s Nuclear Program
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April 2003 April ~ Nov 2006: Five rounds of Six Party Talks Jan 2006: NK says it won’t return to the Talks unless US lifts financial
restrictions imposed for its alleged currency counterfeiting Oct 9 2006: NK says it has conducted its first-ever nuclear test Feb 2007: Sixth round of Six Party Talks opens. In a last minute deal, NK agrees to close its main nuclear reactor in exchange for fuel aids Dec 2008: NK says it will slow down dismantlement process due to delays in fuel aids from US May 2009: NK argues that it has successfully carried out its second, underground nuclear test Dec 2011: Kim Jong-il died April 2012: NK launches a rocket-mounted satellite but fails. Observers argue that it is a long-range missile test of the sort.
July 2000: NK threatens to restart nuclear program due to delays in
building nuclear power plants 2001: US President Bush’s axis of evil speech and condemnation of NK Oct 2002: NK tells US that it has a second covert nuclear weapons program Nov 2002: US, South Korea, and Japan halt oil supplies to NK promised in 1994 deal
1995 violation of the armistice by intruding the Joint Security Area
1998 ballistic missile testing over the sea of Japan
2012 Yeonpyong-do Bombing
5
North Korea: Regime security
Economic difficulty
US alleged aggression and threat (BoP turned against it) South Korea: Non-proliferation, avoidance of hostage
Dove Engagement Too dangerous in the sense that US may end up giving everything to NK while failing to dismantle NK nuclear program
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Why? No reason to be afraid of full-blown engagement with NK Defensive and deterrent nature
strike How to prevent NK’s strike-first policy? Hawk Engagement!
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Hawk Engagement is the only realistic option Conditional engagement; if you do x, I will do y Underlying assumption: We can’t believe NK Deceptive and Veiled NK (Several skirmish examples)
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Preemption It occurs when a state perceives aggression by another as imminent and acts first to forestall the impeding attack Preventive action It occurs when a state is motivated to attack first, or otherwise suffer increasing inferiority in capabilities vis-à-vis the opponent over time Similarity and Difference Both preemption and preventive action (striking first) occurs out of fear and anticipation, not anchored in what is happening to a state Difference b/w them is time horizon (imminent or over time) Possible Options for inferior NK toward superior SK
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Why? Possibilities of NK’s preemptive and/or preventive strike Three mitigating factors:
liberal democracy பைடு நூலகம் Concern with reputational cost of being branded as an aggressor
9
Exclusion of Containment Policy Containment is likely to reinforce NK’s “double-ornothing” logic by increasing NK’s fear of being wiped out in international relations ….can lead to NK’s suicidal attack Containment policy only exacerbates NK’s security fears (Kang) Engagements, how to do it? Hawk vs. Dove