生物学英语与论文写作有没有翻译
好的，而且我不喜欢真核的东西。。。
不诚恳没诚意100分你还不如给5分，反正都没人干
对不起 基本上不懂英语
系统学 磷虾命令的所有成员是虾象甲壳动物的总目 Eucarida的动物。 他们的护胸甲单位或者thoracomers，加入与甲壳。 这些thoracomers的短的长度在甲壳的每边使鳃南极磷虾可看见对肉眼。 腿不形成下颌结构，区分这顺序从螃蟹、龙虾和虾。 (也参见Euphausia superba在Wikispecies。) 生命周期 南极磷虾主要产卵季节是从一月通过三月，在大陆架之上并且在深海海洋区域的上部区域。 在所有euphausiaceans典型的方式，男性附有一个精液包裹女性的生殖开头。 为此，第一腹肢 (腿附加腹部)男性被修建作为联接的工具。 女性一次下6，000-10，000个鸡蛋。 他们被施肥，当他们通过在生殖开头外面从由男性的精囊解放的精液[RQ86]附有了。 根据Marr [Marr62]古典假说，获得从著名英国调查船RRS发现的远征的结果，蛋发展然后进行如下： 原肠形成(鸡蛋的发展到胚胎里)在架子设置在6 mm鸡蛋的下降期间在底部，在海洋区域深度在2，000-3，000 附近。 从时间鸡蛋 舱口盖，第1 无节幼体 (即，幼虫阶段)起动移居往表面在它的三个对的帮助下腿; 所谓的发展上升。 下二个幼虫阶段，被命名第2 无节幼体 和meta无节幼体 ，仍然不吃，而是由剩余的卵黄质养育。 在三个星期以后，小的磷虾完成了上升。 生长更大，另外的幼虫阶段跟随(第2和第3 calyptopis，第1到第6 带叉幼体)。 他们描绘的是为增加另外的腿、复眼和刺毛的发展。 在15 mm，少年磷虾类似成人的习惯。 磷虾伸手可及的距离成熟在二到三年以后。 象所有甲壳纲，磷虾必须蜕变为了增长。 大约每13到20天磷虾流洒了他们的甲壳质皮肤并且留下它后边作为exuvia。有些自翻译不过来啊！不过已经努力了，希望对你有帮助！
与生物有关的专业英语论文含翻译
Congenital kidney maldevelopment and molecular biology research The abstract kidney maldevelopment is the kidney has theunusual clinical consequence， its typical histo-pathologycharacteristic is appears originally Beginning kidney pellet and 肾小管， 软骨样 metaplasia andso In recent years through application molecular technology and soon target gene and home position clone Has the molecular regulation mechanism research to the normalmammal kidney， has to the congenital kidney maldevelopmentpathogenesis More This article will make a discussion to thecongenital kidney maldevelopment molecular biology research recentsituation， and will be right Including the growth factor several kind of gene mutation，copies the regulative barrier and the expression change and the kidneysends the good relations Carries on the The kidney maldevelopment is the kidney has not been able to carry onthe congenital disease which the normal growth growth forms， in thepast arose to it The mechanism understanding are really few， along with themember biological technology development and the application， expoundsthe kidney occurrence from the member study mechanism Had a more thorough understanding from the molecular biologylevel to the kidney maldevelopment This article onshort-term regarding this question The research progress makes an 1 kidney occurs with the kidney maldevelopment Before the normal mammalia kidney is located between liesbetween 中胚层， 中胚层 the differentiation forms the kidneydrive pipe， after further tempts Leads forms 中肾 the drive pipe to the ureter bud， under theureter bud induction， end the embrionic body two sides fresh reninssplits up into after The kidney 胚基， the kidney embryonic development isprecisely completes by the ureter bud and the latter kidney 胚基 twoparts， former gradually grows Becomes 肾盂， 肾盏 and 集合管， latter grows肾小管and the kidney pellet， finally 肾小管and集合管docking， Constitutes normally 肾单位 If the ureter bud and thelatter kidney 胚基 two parts cannot grow according to the normaldegree and implement rightly Meets namely creates the kidney The kidneymaldevelopment may be partial， also may be Most types The kidney maldevelopment partner has the cyst， prompts themaldevelopment each kind of form to have machine-made together in On clinical common congenital kidney maldevelopment including multi-pouches， obstruction kidney maldevelopment as well as with gene The related kidney growth is The histo-pathologyimportant characteristic appears primitive 肾小管and the Complete list The side kidney maldevelopment， may display for does not havethe In most maldevelopment case of illness， the kidney flawis the double side， prompts Gene mutation in normal kidney growth vital Shan Cexingdisease then possibly is one kind of obtaining damage is the resultof， This damage destroyed the gene normal expression， thenaffected maturely had the vital significance to the kidney the 2 kidneys maldevelopment common type 1 congenital multi- pouches kidneys maldevelopment The multi- pouches kidney maldevelopment (multiple cystichypoplastic) is one common completeness The kidney maldevelopment， are many for the single sidepathological change (14-20% for double side nature)， contracts thekidney to lose the normal shape， irregular The size cyst replaces， the kidney function loses and oftenthe partner has the ureter obstruction， is newborn abdomen Bao Kuaizuicommon One of The multi- pouches maldevelopment kidney outlook assumes thekidney-shaped structure， the most case of illness partner has a 闭锁 Pregnancy The early polycystic kidney includes the normal growth to havethe ingredient， loses the urine including the induction after kidney胚基 island and the branch The tube drive pipe， may distinguish the pouch change in thisstage 肾单位 each Duan Yijun [ 1 ] After lives the multi- pouchesmaldevelopment kidney The histo-pathology variation including the primitive肾小管pouch change， expands also the disarrangement of thestructure， has around the obvious tube Response nature， textile fiber myo- link formation， cartilageingredient as symbol organization transformation and so 2 congenital obstructions kidneys maldevelopment The congenital urine road obstruction in dissects in theposition often to occur to the ureter and urinary bladder 连接处，after congenitalness The urethra valve is the babies and infants uninary systemobstruction important Congenital obstruction kidney histologycharacteristic and multi- pouches The kidney maldevelopment is similar， including 肾单位 eachDuan Rushen the pellet pouch transformation， the nature expands alsothe disarrangement of the structure， the marrow The nature and the straight small blood vessel remarkablehypoplasia， has around the tube the textile fiber myo- link， the manykinds of forms kidney pellet and the growth kidney Unit each Is same with the multi- pouches kidneymaldevelopment， the congenital obstruction kidney performance is aseries of diseases， its degree and The embryonic period urine 流阻 related fills the time whichoccurs [ 2 ] The table partner has the kidney to grow the unusual syndrome ------------------------------------------------------ Syndrome chromosome heredity form ------------------------------------------------------ The tip and refers to (foot) to be abnormal (Apert ' s)常染色体 the dominance Sends chest gallery malnutrition 常染色体 recessivenesswhich suffocates Obese， reproduction hypofunction and so on 常染色体recessiveness Gill - ear - kidney 常染色体 dominance Campomelic growth exceptionally 常染色体 recessiveness Brain - liver - kidney (Passarge ' s) 常染色体recessiveness Fryns ' s 常染色体 recessiveness Goemine ' s X- connection Goldston (hereditary blood capillary expands) 常染色体recessiveness? Hall-Pallster ' s sending out Ivemark ' s 常染色体 recessiveness Marden-Walker ' s 常染色体 recessiveness Mecket-Gruber 常染色体 recessiveness Miranda ' s 常染色体 recessiveness Senlor-Loken ' s 常染色体 recessiveness? Three bodies chromosomes 16-18 (Edwards) Three bodies chromosomes 13-15 (Patau) Three bodies chromosomes 21 (Down) 结节性 hardened 常染色体 dominance Von Hippel-Lindau 常染色体 dominance ------------------------------------------------------ 3 kidneys maldevelopment syndrome The kidney maldevelopment syndrome is includes kidney abnormalthe and so on pouch maldevelopment hereditary indication group (seesthe table ) Presently expounds a part of syndromes its special gene andthe protein The maldevelopment phenotype apparent rate assumes Presently a band， prompts has other gene influence kidneysfinally 表型 The maldevelopment usually all contains the many kindsof organs， Explained the flaw the gene involves the normal organogenesisthe The histo-pathology discovered that， this kind ofsyndrome light is possible Appears the great pouch to form (for example 结节性hardening)， heavy possibly appears the pouch growth exceptionally withthe renal failure (Meckel- Gruber syndrome) 3 kidneys maldevelopment molecular biology The present research discovery has the many kinds of genes andthe kidney maldevelopment related， like WT-1， Pax-2， GDNF， B Gene and so on F-2， BMP-7， PDGF， Wnt-4 in after kidney 胚基 Pax-2， c-ret， BMP-7， alpha 3 beta 1 and so on in ureter bud When these genes lack ordestroys， the kidney cannot normally occur with the growth [ 3 ] Sonnenberg and so on [ 4 ] 补体 RNA and the DNA probeconducts the research with the specificity immune body and theemission mark， the determination Multi- peptides growth factor， heparin structure growth factorand their acceptor， extracellular matrix member and cell surfaceentire Gathers gene and so on element in the kidney growth specificexpression For example liver cell growth factor mainly inafter kidney embryo gene Expression， but its acceptor c-met in ureter plumule This kind of peptides and its the acceptor are thin in twokind of types On butcher's expression explanation ureter drive pipe formsthe induction to the after 肾间 archery Schuchardt and so on[ 5 ] passes Using the gene recombination and the preparation 纯合子invalid sudden change mouse， discovers some influence kidney growththe gene and the multi- peptides， like The shift growth factor - beta， the liver cell growth factor，the insulin type growth factor - II， according to saw finally shows The inference specific gene has the function in the Tyrosine activating enzyme body acceptor c-ret leads in thebranch ureter The tube as well as matches in the nerve nutrition factorwhich the body - neuroglia grows to When the mouse c-ret geneis destroyed， leads Sends the entire kidney Copies the factor genecode protein to be able with the DNA union， moreover has regulatesother gene tables Reaches In the mammal kidney growth， Wilms ' tumorgene WT-1 and Pax2 code copies the factor， Its expression form influence kidney cell differentiation [ 6，7 ] The gene syndrome and the kidney form exceptionally related， inthe table arranges in order Leaves the disease， some syndromes have the heredity， somewhathas located the specific gene flaw with the home position clonetechnology [ 8 ] These syndromes are being sick the family members to beable to have the remarkable 表型 This kind of situationand in 纯合子 is invalid The sudden change mouse sees the variation is similar， namelythe kidney finally 表型 is decided by the experimental mouse's The kidney maldevelopment occurrence is several kind of differentgenes flaws， perhaps meets in the embryo development period sends 畸the factor And so on many kinds of genes regulation barrier 肾间 the nature - epidermis transforms process as well asureter branch and growth Is complex and the huge gene system guides by， some genes arethe kidney specificity， some rights and wrongs are special Certain growth factor genes， although they have the timeexpression in the kidney to be active， but when they are destroyedcertainly not shade The loud kidney normal growth， this meant the growth kidneynormal expression each kind of gene has in the function overlaps [ 9] Another one Plants the possibility is this kind of normal expression formdestruction in the kidney maldevelopment occurrence development thecertain function， or Is the kidney maldevelopment The latter 肾间 nature flaw may cause the kidney Moreover， the gene ill should is the dislocation expression， possiblyto kidney The maldevelopment plays the certain On clinical hasthe isolation the multi- pouches kidney maldevelopment and theobstruction kidney maldevelopment two Parallel existence case of Congenitalness and theexperimental nature single gene mutation may cause the pouch kidneygrowth to be unusual， these genes The sudden change may change mutually Theoreticallyspeaking， the sudden change may affect: (1) 胚基 proliferation andsplit up ureter drive pipe minute An institute must peptide and matrix protein expression; (2)Ureter drive pipe to after kidney 胚基 signal reaction capacity; (3)Loses After the ureter drive pipe expression starts and maintainsthe kidney 胚基 epidermis induction to need the protein the ability;(4) Latter kidney 胚基 to these letters The number carries on the response the ability; (5) Ureterbud and latter kidney 胚基 cell to signal reaction capacity [ 10 ] Recently already separated the phosphoric acid glucose phaseomanniteglycoprotein gene， was called the GPC3 The GPC3 flaw and aremany Pouch kidney maldevelopment related [ 11 ] Although thesingle gene may finally cause the kidney maldevelopment with themulti- genes flaw， but Its 表型 possibly decided to receives the gene regulationwhich affects to be out of balance or the expression change at first，like congenital obstruction and pouch Kidney maldevelopment [ 12， 13 ] The multi- pouchesmaldevelopment kidney， and in the nature has the growth factor gene inthe pouch epidermis C In the mouse obstruction growth kidney， the bloodvessel tense element and the shift growth factor assumes excessivelyexpresses [ 14 ] Grinds Investigates the proof， in the after kidney growth unusualarea， promotes the acorn tube epidermis to appear the pouch changefactor Pax2 and Bcl-2 same Assumes excessively expresses [ 15， 16 ] This researchpossibly can provide the important line to each kind of form kidneymaldevelopment pathogenesis R 先天性肾发育不良与分子生物学的研究 摘要 肾发育不良是肾发生异常的临床后果，其典型病理组织学特征是出现原始肾小球和肾小管、软骨样化生等。近年来通过应用靶基因和原位克隆等分子技术对正常哺乳动物肾脏发生分子调控机制的研究，对先天性肾发育不良的发病机理有了更多的了解。本文将对先天性肾发育不良的分子生物学研究近况作一讨论，并对包括生长因子在内的几种基因突变、转录调控障碍及表达变化与肾发良不良的关系进行探讨。 肾发育不良是肾脏未能进行正常生长发育形成的先天性疾病，过去对其发病机理了解甚少，随着分子生物技术的发展和应用，从分子学机理来阐明肾脏的发生，从分子生物学水平对肾发育不良的发生有了较深入的认识。本文就近期对此问题的研究进展作一介绍。1 肾发生与肾发育不良 正常哺乳类肾脏位于间介中胚层，中胚层分化形成前肾导管，经进一步诱导形成中肾导管至输尿管芽，在输尿管芽诱导下，胚体尾端两侧的生肾素分化为后肾胚基，肾脏的胚胎发育正是由输尿管芽和后肾胚基二部分完成的，前者逐步发育成肾盂、肾盏和集合管，后者发育成肾小管和肾小球，最后肾小管和集合管对接，构成正常的肾单位。如果输尿管芽和后肾胚基二部分不能按正常程度发育和实行对接即造成肾发育不良。肾发育不良可以是部分性的，也可以是完全性的。多数类型的肾发育不良伴有囊肿，提示发育不良的各种形式在形成中有共同机制。 临床上常见的先天性肾发育不良包括多囊性、梗阻性肾发育不良以及与基因有关的肾发育异常。病理组织学重要特征是出现原始肾小管和化生软骨。完全性单侧肾发育不良，可表现为无症状。多数发育不良病例中，肾缺陷是双侧性的，提示基因突变在正常肾发育中起重要作用。单侧性疾病则可能是一种获得性损伤所致，该损伤破坏了基因的正常表达，进而影响了对肾成熟有重要意义的蛋白质的产生。2 肾发育不良常见类型1 先天多囊性肾发育不良 多囊性肾发育不良（multiple cystic hypoplastic）是一种常见的完全性肾发育不良，多为单侧病变（14-20%为双侧性），患肾失去正常形态，被不规则的大小囊肿所代替，肾脏功能丧失并常伴有输尿管梗阻，是新生儿腹部包块最常见的原因之一。 多囊性发育不良肾外型呈肾形结构，多数病例伴有一个闭锁的输尿管。妊娠早期的多囊肾含有正常发育所必须的成份，包括未诱导的后肾胚基岛和分支的输尿管导管，在此阶段肾单位各段已均可鉴别出囊性改变[1]。生后多囊性发育不良肾的病理组织学变异包括原始肾小管的囊性改变、膨大且结构破坏、具有明显管周围反应的间质、纤维肌环的形成、软骨成分为标志的组织转化等。2 先天梗阻性肾发育不良 先天性尿路梗阻在解剖位置上常发生于输尿管和膀胱的连接处，先天性后尿道瓣膜是婴幼儿泌尿系统梗阻的重要原因。先天梗阻性肾的组织学特征与多囊性肾发育不良相似，包括肾单位各段如肾小球的囊性转化、间质膨大且结构破坏、髓质和直小血管显著发育不全、发生管周围纤维肌环、多种形式的肾小球和发育的肾单位各段。与多囊性肾发育不良一样，先天梗阻性肾表现为一系列疾病，其程度与胚胎期尿流阻塞发生的时间有关[2]。表 伴有肾发育异常的综合症------------------------------------------------------综合症 染色体遗传形式------------------------------------------------------尖头并指（趾）畸形（Apert’s） 常染色体显性 致窒息的胸廓营养不良 常染色体隐性 肥胖、生殖机能减退等 常染色体隐性 鳃-耳-肾 常染色体显性 Campomelic发育异常 常染色体隐性 脑-肝-肾（Passarge’s） 常染色体隐性 Fryns’s 常染色体隐性 Goemine’s X-连接的 Goldston(遗传性毛细血管扩张) 常染色体隐性？ Hall-Pallster’s 散发的 Ivemark’s 常染色体隐性 Marden-Walker’s 常染色体隐性 Mecket-Gruber 常染色体隐性 Miranda’s 常染色体隐性 Senlor-Loken’s 常染色体隐性？ 三体染色体16-18（Edwards） 三体染色体13-15（Patau） 三体染色体21（Down） 结节性硬化 常染色体显性 Von Hippel-Lindau 常染色体显性------------------------------------------------------ 3 肾发育不良综合症 肾发育不良综合症是包括囊性发育不良等肾畸形在内的遗传性征候群（见表）。现阐明一部分综合症其特异的基因和蛋白质缺陷。发育不良表现型的外显率呈现一个谱带，提示有其他基因影响肾的最终表型。发育不良通常都包含多种器官，说明缺陷的基因涉及正常器官发生的基础。病理组织学发现，此类综合症轻者可能出现巨囊形成（如结节性硬化），重者可能出现囊性发育异常和肾衰竭（Meckel-Gruber综合症）。3 肾发育不良分子生物学 目前的研究发现有多种基因与肾发育不良有关，如WT-1、Pax-2、GDNF、BF-2、BMP-7、PDGF、Wnt-4等基因在后肾胚基表达。Pax-2、c-ret、BMP-7、α3β1等在输尿管芽表达。当这些基因缺乏或被破坏时，肾脏不能正常地发生与发育[3]。Sonnenberg等[4]用特异性抗体与放射标记的补体RNA和DNA探针进行研究，确定了多肽生长因子、肝素结构生长因子及它们的受体、细胞外基质分子和细胞表面整合素等基因在肾发育中的特定表达位置。例如肝细胞生长因子主要在后肾胚基因内表达，而其受体c-met则在输尿管胚芽上皮表达。这种多肽及其受体在两种类型细胞上的表达说明输尿管导管对后肾间质的形成起诱导作用。Schuchardt等[5]通过应用基因重组与制备纯合子无效突变小鼠，发现一些影响肾发育的基因和多肽，如转移生长因子-β、肝细胞生长因子、胰岛素样生长因子-Ⅱ，根据所见到的最终表型推断特定基因在正常肾发生中的作用。酪氨酸激酶体受体c-ret在分支输尿管导管以及配体-神经胶质衍生的神经营养因子上表达。当小鼠c-ret基因被破坏时，导致全肾发育不良。转录因子基因编码蛋白能与DNA结合，而且具备调控其它基因表达的功能。在哺乳动物肾发育中，Wilms’肿瘤基因WT-1及Pax2均编码转录因子，其表达形式影响肾细胞的分化[6，7]。基因性综合症与肾形成异常有关，表中所列出的疾病，有些综合症有遗传性，有些用原位克隆技术已定位出特定的基因缺陷[8]。这些综合症在患病家族成员能发生显著的表型变异。这种情况与在纯合子无效突变小鼠所见的变异相似，即肾的最终表型取决于实验小鼠的基因背景。 肾发育不良的发生是几种不同的基因缺陷，或是在胚胎发育期遇到致畸因子等多种基因调控障碍的最终结果。肾间质-上皮转化的过程以及输尿管分支和生长，是由一个复杂而庞大的基因体系来导向，有些基因是肾特异性的，有些是非特异的。某些生长因子基因，尽管它们在肾发生期表达活跃，但当它们被破坏时并不影响肾的正常发育，这意味着发育肾正常表达的各种基因在功能上有重叠[9]。另一种可能性是这种正常表达形式的破坏在肾发育不良的发生发展中起一定作用，或者就是肾发育不良的起因。 后肾间质缺陷可导致肾发育不良。另外，基因不适应和错位表达，可能对肾发育不良起一定作用。临床上有孤立的多囊性肾发育不良和梗阻性肾发育不良两者并行存在的病例。先天性和实验性单基因突变均可导致囊性肾发育异常，这些基因突变可改变相互联系。从理论上讲，突变可影响：①胚基增生和分化输尿管导管分支所必需的肽和基质蛋白的表达；②输尿管导管对后肾胚基信号的反应能力；③输尿管导管表达启动和维持后肾胚基上皮诱导所需蛋白的能力；④后肾胚基对这些信号进行反应的能力；⑤输尿管芽和后肾胚基细胞对信号的反应能力[10]。 最近已经分离出磷酸葡萄糖肌醇糖蛋白基因，简称GPC3基因。GPC3缺失与多囊性肾发育不良有关[11]。虽然单基因与多基因缺陷均可最终导致肾发育不良，但其表型可能决定于最初受影响的基因调控失调或表达改变，如先天性梗阻性和囊性肾发育不良[12，13]。多囊性发育不良肾，在囊性上皮和间质中均有生长因子基因的改变。在小鼠梗阻性发育肾中，血管紧张素和转移生长因子呈过度表达[14]。研究证明，在后肾发育异常区，促进小管上皮出现囊性改变的因子Pax2和Bcl-2同样呈过度表达[15，16]。此研究可能会对各种形式肾发育不良的发病机制提供重要线索。
Deoxypentose核酸分子结构 而生物特性，提出了deoxypentose核酸分子结构复杂、x射线衍射含有伟大的研究表明了基本的分子结构具有巨大的简单。这种交流的目的是描述方法，进行了初步的实验证据，为polynucleotide链结构中存在的螺旋，是本表格时，在自然状态。更大的工作将发表。 deoxypentose核酸的结构是一样的所有物种(虽然氮基率大幅改变)，或在核蛋白细胞，在净化核。同样的线性群polynucleotide链可以装在一起平行或paracrystalline材料在所有情况下，x -射线衍射相是由两个区域，很大程度上决定了常规间距的核苷酸道旁的锁链上，和其他的长链结构的影响。不同氮基础的顺序道旁的锁链上不可见。 paracrystalline deoxypentose以核酸(“B”结构在接下来的通信由富兰克林，傻帽)提供了一种纤维图显示在图1(4)。Astbury暗示强烈的4 ~ flexion相对应的internucleotide沿着纤维轴的重复。layer线的~ 34A，然而，并不是由于重复的polynucleotide组成，但对链条结构重复，导致强烈的衍射的核苷酸链有更高的密度比水的空隙。没有reflexions附近的经络立即提出了螺旋结构与轴平行的纤维长度。 图1。deoxypentose纤维图核酸免受Bli。光纤轴垂直
甲基化模式与继承 密集铯甲基化是在所有观察到的序列修改由RIP和MIP，有相关的甲基化信号似乎是一个改变序列组成[19]或配对DNA片段的长度超过400个基点[17 · ·]。虽然大多数存在于植物中的甲基化对称的重心和CNG核苷酸组（n常务委员会对阿，克，C或T），甲基化的非对称铯被观察到包括外国序列（转基因及污水附加费）和（[10]总结）内源性基因。此外，沉重的非对称发生甲基化铯周围的转录起始位点和最对单一弱epialleles转录区域内源性基因复制超人[20日]指示这种甲基化模式并不需要大量的的DNA - DNA的配对或一个容易辨认外源DNA序列，如TE或一个明显的重复长度。超人基因确实，但是，包含50 bp的核苷酸ç的[A / T]的运行，它包括转录起始位点。这个简短的微卫星可能吸引甲基化的表达下降。 该Ascobolus甲基转移酶（转移酶）基因，Masc1，负责为去甲基化过程中的所有按揭保险计划在配对的DNA区域铯，编码一种酶，不像已知的真核生物MTases [17 · ·]，其中优先因此，修改hemimethylated DNA和执行主要维护甲基化的作用。维护甲基化是不扰动masc1突变体，因此第二部小说的延续甲基化转移酶非对称铯还必须在Ascobolus [16]提出。进一步表征三种类型的MTases迄今发现，以确定是否有必要MTases类似的活动和底物特异性在植物中[10] 关于转基因表达的位置效应 在酵母和果蝇中，沉默的立场造成的影响可能发生在端粒和着丝粒，而在果蝇[21，22]异色。这些沉默现象是不相同的：端粒位置效应花斑（PEV）不敏感，抑制果蝇和着丝粒PEV [23]增强。除了着丝粒和端粒，大多数高等植物基因组含有大量的闰异和重复的DNA，可作为标志性建筑使用评估与转基因沉默相关的区域。位置效应涉及一个或多个基因位点可进行研究（图1）的各种方法。
楼主，文献检索也是必备技能啊，pubMed上随便搜一搜就有了啊。
有关生物的英语论文带翻译
在生物学实验室中的数位影像Terry Moxon1， Gaynor WightmanDoncaster1 和伊莉莎白中学皇后、 Gainsborough 的， 英国生物学教育 (2005)39(4)179 的日记较廉宜的 SLR 数码相机的来到和联合的软件已经允许数位影像的迅速创造。 我们解释允许显微像的世代的三简单的技术。 较进一步的技术被描述那允许来自显微镜滑的一个完整区段的图像的生产。 显微像的班级组非常提高实际的会议前或后的任何的讨论。xxx字: 显微镜使用; 数码相机; 显微像介绍显微镜使用已经担任生物学的教育的一个被减少的角色在过去的十年内。理由被改变但是落下预算已经意谓给显微镜的班级组的资金已经变得贵。 第二，国立课程的要求已经减少显微镜使用在学校的角色。 然而学生，尤其在主要阶段 3 ，多源自快乐在非常使用显微镜和显微镜使用方面富足那理论上的教学和学问规划程序。 然而，和一个 30 班级一起使用显微镜不没有问题: 显微镜的稀少使用需要检查学生显微镜调整的额外的老师参与 大的班级放限制在老师有效上帮助藉由个别学生的问题 老师有的一点控制什么学生实际上见到。 较年长的学生已经被知道承认当尝试的时候为了要观察苏格兰的植物学家 Robert Brown 的运动， 他们已经度过时间看他们自己的睫毛! 学生有关他们应该见到的也是比较不自信。 这洞察力， 哪些老师已经以经验发展，仍然有被学生获得。在现阶段，学生有整体而言的样品的小空间赏识。大部份这些问题可能被藉由提供完全图像或挑选重要区域的显微像给学生克服。 然而，在 photomicroscopy 的电影的使用意谓了相当多的投资及时，技术和努力是在～手边生产甚至可通行的图像老师需要。 那数传摄影的来到而且处理已经允许那显微像的创造描绘，那能被当作教学帮助使用。图像可能是可用来使用各种不同的团体或者准备了个体的塑料保护的班级床单。 虽然费用是下滑， 但是，主要的设备会仍然方面被视为贵的一个生物学部门编入预算。 在这里，我们描述一个让图像与只有一个谦逊有定价的数码相机一起产生的方法。教学意志的显微镜使用的比较一般使用希望在中学 导致较棒的信心和超过， 哪里这些技术仍然有棒的价值。
Nucleic acids and proteins such biological molecules life is the material base， the origin of life key lies in the origin of these life substances， the original in no life on the earth because of natural causes， and through inanimate matter produce various chemical action， organic matter and biological Therefore， the origin of life problem is first primitive of the origin and early evolution of organic The role of chemical evolution is a kind of chemical materials， these chemical material composition amino acids， sugar etc universal "structural unit"， nucleic acids and proteins such life from this knot "material is the combination of structural element" In 1922， biochemists Mr Bahrain's first proposed can be used to verify that the hypothesis， the original earth in some of the inorganic， from lightning， sunlight， under the action of the energy into the first batch of organic After the 1953 after 31 years， American chemist miller's first test card in bahrain that He die like original earth with atmospheric composition， hydrogen， methane and ammonia and water vapor， through the heating and spark discharge， synthetic organic molecular amino Following the miller， many through simulation experiment of original earth And the other for the synthesis of the important biological organisms molecules， such as DNA and its set， adenine， deoxyribose nucleoside and nucleotide，， fatty acid， porphyrins and lipid， In 1965 and 1981， our country and in the world's first synthetic insulin and yeast alanine transfer RNA Protein and nucleic acid is formed by the turning point to a lifeless The above two kinds of biological molecules of synthetic success， started by artificial synthetic life substances to study the new era of the origin of Generally speaking， life chemical evolution process including four stages: small molecules generated from inorganic small organic molecules; Small organic molecules from formation organic macromolecular; From organic macromolecular composition can sustain itself the stability and development of many molecular system; Evolution of molecular system from more primitive 核酸和蛋白质等生物分子是生命的物质基础，生命的起源关键就在于这些生命物质的起源，即在没有生命的原始地球上，由于自然的原因，非生命物质通过化学作用，产生出多种有机物和生物分子。因此，生命起源问题首先是原始有机物的起源与早期演化。化学进化的作用是造就一类化学材料，这些化学材料构成氨基酸，糖等通用的“结构单元”，核酸和蛋白质等生命物质就来自这结“结构单元”的组合。 1922年，生物化学家奥巴林第一个提出了一种可以验证的假说，认为原始地球上的某些无机物，在来自闪电，太阳光的能量的作用下，变成了第一批有机分子。时隔31年之后的1953年，美国化学家米勒首次实验证了奥巴林的这一假说。他模似原始地球上的大气成分，用氢、甲烷、氨和水蒸气等，通过加热和火花放电，合成了有机分子氨基酸。继米勒之后，许多通过模拟原始地球条件的实验。又合成出了其他组成生命体的重要的生物分子，如嘌呤、嘧定、核糖、脱氧核糖、核苷、核苷酸、脂肪酸、卟啉和脂质等。1965年和1981年，我国又在世界上首次人工合成胰岛素和酵母丙氨酸转移核糖核酸。蛋白质和核酸的形成是由无生命到有生命的转折点。上述两种生物分子的人工合成成功，开始了通过人工合成生命物质去研究生命起源的新时代。一般说来，生命的化学进化过程包括四个阶段：从无机小分子生成有机小分子；从有机小分子形成有机大分子；从有机大分子组成能自我维持稳定和发展的多分子体系；从多分子体系演变为原始生命。
Congenital kidney maldevelopment and molecular biology research The abstract kidney maldevelopment is the kidney has theunusual clinical consequence， its typical histo-pathologycharacteristic is appears originally Beginning kidney pellet and 肾小管， 软骨样 metaplasia andso In recent years through application molecular technology and soon target gene and home position clone Has the molecular regulation mechanism research to the normalmammal kidney， has to the congenital kidney maldevelopmentpathogenesis More This article will make a discussion to thecongenital kidney maldevelopment molecular biology research recentsituation， and will be right Including the growth factor several kind of gene mutation，copies the regulative barrier and the expression change and the kidneysends the good relations Carries on the The kidney maldevelopment is the kidney has not been able to carry onthe congenital disease which the normal growth growth forms， in thepast arose to it The mechanism understanding are really few， along with themember biological technology development and the application， expoundsthe kidney occurrence from the member study mechanism Had a more thorough understanding from the molecular biologylevel to the kidney maldevelopment This article onshort-term regarding this question The research progress makes an 1 kidney occurs with the kidney maldevelopment Before the normal mammalia kidney is located between liesbetween 中胚层， 中胚层 the differentiation forms the kidneydrive pipe， after further tempts Leads forms 中肾 the drive pipe to the ureter bud， under theureter bud induction， end the embrionic body two sides fresh reninssplits up into after The kidney 胚基， the kidney embryonic development isprecisely completes by the ureter bud and the latter kidney 胚基 twoparts， former gradually grows Becomes 肾盂， 肾盏 and 集合管， latter grows肾小管and the kidney pellet， finally 肾小管and集合管docking， Constitutes normally 肾单位 If the ureter bud and thelatter kidney 胚基 two parts cannot grow according to the normaldegree and implement rightly Meets namely creates the kidney The kidneymaldevelopment may be partial， also may be Most types The kidney maldevelopment partner has the cyst， prompts themaldevelopment each kind of form to have machine-made together in On clinical common congenital kidney maldevelopment including multi-pouches， obstruction kidney maldevelopment as well as with gene The related kidney growth is The histo-pathologyimportant characteristic appears primitive 肾小管and the Complete list The side kidney maldevelopment， may display for does not havethe In most maldevelopment case of illness， the kidney flawis the double side， prompts Gene mutation in normal kidney growth vital Shan Cexingdisease then possibly is one kind of obtaining damage is the resultof， This damage destroyed the gene normal expression， thenaffected maturely had the vital significance to the kidney the 2 kidneys maldevelopment common type 1 congenital multi- pouches kidneys maldevelopment The multi- pouches kidney maldevelopment (multiple cystichypoplastic) is one common completeness The kidney maldevelopment， are many for the single sidepathological change (14-20% for double side nature)， contracts thekidney to lose the normal shape， irregular The size cyst replaces， the kidney function loses and oftenthe partner has the ureter obstruction， is newborn abdomen Bao Kuaizuicommon One of The multi- pouches maldevelopment kidney outlook assumes thekidney-shaped structure， the most case of illness partner has a 闭锁 Pregnancy The early polycystic kidney includes the normal growth to havethe ingredient， loses the urine including the induction after kidney胚基 island and the branch The tube drive pipe， may distinguish the pouch change in thisstage 肾单位 each Duan Yijun [ 1 ] After lives the multi- pouchesmaldevelopment kidney The histo-pathology variation including the primitive肾小管pouch change， expands also the disarrangement of thestructure， has around the obvious tube Response nature， textile fiber myo- link formation， cartilageingredient as symbol organization transformation and so 2 congenital obstructions kidneys maldevelopment The congenital urine road obstruction in dissects in theposition often to occur to the ureter and urinary bladder 连接处，after congenitalness The urethra valve is the babies and infants uninary systemobstruction important Congenital obstruction kidney histologycharacteristic and multi- pouches The kidney maldevelopment is similar， including 肾单位 eachDuan Rushen the pellet pouch transformation， the nature expands alsothe disarrangement of the structure， the marrow The nature and the straight small blood vessel remarkablehypoplasia， has around the tube the textile fiber myo- link， the manykinds of forms kidney pellet and the growth kidney Unit each Is same with the multi- pouches kidneymaldevelopment， the congenital obstruction kidney performance is aseries of diseases， its degree and The embryonic period urine 流阻 related fills the time whichoccurs [ 2 ] The table partner has the kidney to grow the unusual syndrome ------------------------------------------------------ Syndrome chromosome heredity form ------------------------------------------------------ The tip and refers to (foot) to be abnormal (Apert ' s)常染色体 the dominance Sends chest gallery malnutrition 常染色体 recessivenesswhich suffocates Obese， reproduction hypofunction and so on 常染色体recessiveness Gill - ear - kidney 常染色体 dominance Campomelic growth exceptionally 常染色体 recessiveness Brain - liver - kidney (Passarge ' s) 常染色体recessiveness Fryns ' s 常染色体 recessiveness Goemine ' s X- connection Goldston (hereditary blood capillary expands) 常染色体recessiveness? Hall-Pallster ' s sending out Ivemark ' s 常染色体 recessiveness Marden-Walker ' s 常染色体 recessiveness Mecket-Gruber 常染色体 recessiveness Miranda ' s 常染色体 recessiveness Senlor-Loken ' s 常染色体 recessiveness? Three bodies chromosomes 16-18 (Edwards) Three bodies chromosomes 13-15 (Patau) Three bodies chromosomes 21 (Down) 结节性 hardened 常染色体 dominance Von Hippel-Lindau 常染色体 dominance ------------------------------------------------------ 3 kidneys maldevelopment syndrome The kidney maldevelopment syndrome is includes kidney abnormalthe and so on pouch maldevelopment hereditary indication group (seesthe table ) Presently expounds a part of syndromes its special gene andthe protein The maldevelopment phenotype apparent rate assumes Presently a band， prompts has other gene influence kidneysfinally 表型 The maldevelopment usually all contains the many kindsof organs， Explained the flaw the gene involves the normal organogenesisthe The histo-pathology discovered that， this kind ofsyndrome light is possible Appears the great pouch to form (for example 结节性hardening)， heavy possibly appears the pouch growth exceptionally withthe renal failure (Meckel- Gruber syndrome) 3 kidneys maldevelopment molecular biology The present research discovery has the many kinds of genes andthe kidney maldevelopment related， like WT-1， Pax-2， GDNF， B Gene and so on F-2， BMP-7， PDGF， Wnt-4 in after kidney 胚基 Pax-2， c-ret， BMP-7， alpha 3 beta 1 and so on in ureter bud When these genes lack ordestroys， the kidney cannot normally occur with the growth [ 3 ] Sonnenberg and so on [ 4 ] 补体 RNA and the DNA probeconducts the research with the specificity immune body and theemission mark， the determination Multi- peptides growth factor， heparin structure growth factorand their acceptor， extracellular matrix member and cell surfaceentire Gathers gene and so on element in the kidney growth specificexpression For example liver cell growth factor mainly inafter kidney embryo gene Expression， but its acceptor c-met in ureter plumule This kind of peptides and its the acceptor are thin in twokind of types On butcher's expression explanation ureter drive pipe formsthe induction to the after 肾间 archery Schuchardt and so on[ 5 ] passes Using the gene recombination and the preparation 纯合子invalid sudden change mouse， discovers some influence kidney growththe gene and the multi- peptides， like The shift growth factor - beta， the liver cell growth factor，the insulin type growth factor - II， according to saw finally shows The inference specific gene has the function in the Tyrosine activating enzyme body acceptor c-ret leads in thebranch ureter The tube as well as matches in the nerve nutrition factorwhich the body - neuroglia grows to When the mouse c-ret geneis destroyed， leads Sends the entire kidney Copies the factor genecode protein to be able with the DNA union， moreover has regulatesother gene tables Reaches In the mammal kidney growth， Wilms ' tumorgene WT-1 and Pax2 code copies the factor， Its expression form influence kidney cell differentiation [ 6，7 ] The gene syndrome and the kidney form exceptionally related， inthe table arranges in order Leaves the disease， some syndromes have the heredity， somewhathas located the specific gene flaw with the home position clonetechnology [ 8 ] These syndromes are being sick the family members to beable to have the remarkable 表型 This kind of situationand in 纯合子 is invalid The sudden change mouse sees the variation is similar， namelythe kidney finally 表型 is decided by the experimental mouse's The kidney maldevelopment occurrence is several kind of differentgenes flaws， perhaps meets in the embryo development period sends 畸the factor And so on many kinds of genes regulation barrier 肾间 the nature - epidermis transforms process as well asureter branch and growth Is complex and the huge gene system guides by， some genes arethe kidney specificity， some rights and wrongs are special Certain growth factor genes， although they have the timeexpression in the kidney to be active， but when they are destroyedcertainly not shade The loud kidney normal growth， this meant the growth kidneynormal expression each kind of gene has in the function overlaps [ 9] Another one Plants the possibility is this kind of normal expression formdestruction in the kidney maldevelopment occurrence development thecertain function， or Is the kidney maldevelopment The latter 肾间 nature flaw may cause the kidney Moreover， the gene ill should is the dislocation expression， possiblyto kidney The maldevelopment plays the certain On clinical hasthe isolation the multi- pouches kidney maldevelopment and theobstruction kidney maldevelopment two Parallel existence case of Congenitalness and theexperimental nature single gene mutation may cause the pouch kidneygrowth to be unusual， these genes The sudden change may change mutually Theoreticallyspeaking， the sudden change may affect: (1) 胚基 proliferation andsplit up ureter drive pipe minute An institute must peptide and matrix protein expression; (2)Ureter drive pipe to after kidney 胚基 signal reaction capacity; (3)Loses After the ureter drive pipe expression starts and maintainsthe kidney 胚基 epidermis induction to need the protein the ability;(4) Latter kidney 胚基 to these letters The number carries on the response the ability; (5) Ureterbud and latter kidney 胚基 cell to signal reaction capacity [ 10 ] Recently already separated the phosphoric acid glucose phaseomanniteglycoprotein gene， was called the GPC3 The GPC3 flaw and aremany Pouch kidney maldevelopment related [ 11 ] Although thesingle gene may finally cause the kidney maldevelopment with themulti- genes flaw， but Its 表型 possibly decided to receives the gene regulationwhich affects to be out of balance or the expression change at first，like congenital obstruction and pouch Kidney maldevelopment [ 12， 13 ] The multi- pouchesmaldevelopment kidney， and in the nature has the growth factor gene inthe pouch epidermis C In the mouse obstruction growth kidney， the bloodvessel tense element and the shift growth factor assumes excessivelyexpresses [ 14 ] Grinds Investigates the proof， in the after kidney growth unusualarea， promotes the acorn tube epidermis to appear the pouch changefactor Pax2 and Bcl-2 same Assumes excessively expresses [ 15， 16 ] This researchpossibly can provide the important line to each kind of form kidneymaldevelopment pathogenesis R 先天性肾发育不良与分子生物学的研究 摘要 肾发育不良是肾发生异常的临床后果，其典型病理组织学特征是出现原始肾小球和肾小管、软骨样化生等。近年来通过应用靶基因和原位克隆等分子技术对正常哺乳动物肾脏发生分子调控机制的研究，对先天性肾发育不良的发病机理有了更多的了解。本文将对先天性肾发育不良的分子生物学研究近况作一讨论，并对包括生长因子在内的几种基因突变、转录调控障碍及表达变化与肾发良不良的关系进行探讨。 肾发育不良是肾脏未能进行正常生长发育形成的先天性疾病，过去对其发病机理了解甚少，随着分子生物技术的发展和应用，从分子学机理来阐明肾脏的发生，从分子生物学水平对肾发育不良的发生有了较深入的认识。本文就近期对此问题的研究进展作一介绍。1 肾发生与肾发育不良 正常哺乳类肾脏位于间介中胚层，中胚层分化形成前肾导管，经进一步诱导形成中肾导管至输尿管芽，在输尿管芽诱导下，胚体尾端两侧的生肾素分化为后肾胚基，肾脏的胚胎发育正是由输尿管芽和后肾胚基二部分完成的，前者逐步发育成肾盂、肾盏和集合管，后者发育成肾小管和肾小球，最后肾小管和集合管对接，构成正常的肾单位。如果输尿管芽和后肾胚基二部分不能按正常程度发育和实行对接即造成肾发育不良。肾发育不良可以是部分性的，也可以是完全性的。多数类型的肾发育不良伴有囊肿，提示发育不良的各种形式在形成中有共同机制。 临床上常见的先天性肾发育不良包括多囊性、梗阻性肾发育不良以及与基因有关的肾发育异常。病理组织学重要特征是出现原始肾小管和化生软骨。完全性单侧肾发育不良，可表现为无症状。多数发育不良病例中，肾缺陷是双侧性的，提示基因突变在正常肾发育中起重要作用。单侧性疾病则可能是一种获得性损伤所致，该损伤破坏了基因的正常表达，进而影响了对肾成熟有重要意义的蛋白质的产生。2 肾发育不良常见类型1 先天多囊性肾发育不良 多囊性肾发育不良（multiple cystic hypoplastic）是一种常见的完全性肾发育不良，多为单侧病变（14-20%为双侧性），患肾失去正常形态，被不规则的大小囊肿所代替，肾脏功能丧失并常伴有输尿管梗阻，是新生儿腹部包块最常见的原因之一。 多囊性发育不良肾外型呈肾形结构，多数病例伴有一个闭锁的输尿管。妊娠早期的多囊肾含有正常发育所必须的成份，包括未诱导的后肾胚基岛和分支的输尿管导管，在此阶段肾单位各段已均可鉴别出囊性改变[1]。生后多囊性发育不良肾的病理组织学变异包括原始肾小管的囊性改变、膨大且结构破坏、具有明显管周围反应的间质、纤维肌环的形成、软骨成分为标志的组织转化等。2 先天梗阻性肾发育不良 先天性尿路梗阻在解剖位置上常发生于输尿管和膀胱的连接处，先天性后尿道瓣膜是婴幼儿泌尿系统梗阻的重要原因。先天梗阻性肾的组织学特征与多囊性肾发育不良相似，包括肾单位各段如肾小球的囊性转化、间质膨大且结构破坏、髓质和直小血管显著发育不全、发生管周围纤维肌环、多种形式的肾小球和发育的肾单位各段。与多囊性肾发育不良一样，先天梗阻性肾表现为一系列疾病，其程度与胚胎期尿流阻塞发生的时间有关[2]。表 伴有肾发育异常的综合症------------------------------------------------------综合症 染色体遗传形式------------------------------------------------------尖头并指（趾）畸形（Apert’s） 常染色体显性 致窒息的胸廓营养不良 常染色体隐性 肥胖、生殖机能减退等 常染色体隐性 鳃-耳-肾 常染色体显性 Campomelic发育异常 常染色体隐性 脑-肝-肾（Passarge’s） 常染色体隐性 Fryns’s 常染色体隐性 Goemine’s X-连接的 Goldston(遗传性毛细血管扩张) 常染色体隐性？ Hall-Pallster’s 散发的 Ivemark’s 常染色体隐性 Marden-Walker’s 常染色体隐性 Mecket-Gruber 常染色体隐性 Miranda’s 常染色体隐性 Senlor-Loken’s 常染色体隐性？ 三体染色体16-18（Edwards） 三体染色体13-15（Patau） 三体染色体21（Down） 结节性硬化 常染色体显性 Von Hippel-Lindau 常染色体显性------------------------------------------------------ 3 肾发育不良综合症 肾发育不良综合症是包括囊性发育不良等肾畸形在内的遗传性征候群（见表）。现阐明一部分综合症其特异的基因和蛋白质缺陷。发育不良表现型的外显率呈现一个谱带，提示有其他基因影响肾的最终表型。发育不良通常都包含多种器官，说明缺陷的基因涉及正常器官发生的基础。病理组织学发现，此类综合症轻者可能出现巨囊形成（如结节性硬化），重者可能出现囊性发育异常和肾衰竭（Meckel-Gruber综合症）。3 肾发育不良分子生物学 目前的研究发现有多种基因与肾发育不良有关，如WT-1、Pax-2、GDNF、BF-2、BMP-7、PDGF、Wnt-4等基因在后肾胚基表达。Pax-2、c-ret、BMP-7、α3β1等在输尿管芽表达。当这些基因缺乏或被破坏时，肾脏不能正常地发生与发育[3]。Sonnenberg等[4]用特异性抗体与放射标记的补体RNA和DNA探针进行研究，确定了多肽生长因子、肝素结构生长因子及它们的受体、细胞外基质分子和细胞表面整合素等基因在肾发育中的特定表达位置。例如肝细胞生长因子主要在后肾胚基因内表达，而其受体c-met则在输尿管胚芽上皮表达。这种多肽及其受体在两种类型细胞上的表达说明输尿管导管对后肾间质的形成起诱导作用。Schuchardt等[5]通过应用基因重组与制备纯合子无效突变小鼠，发现一些影响肾发育的基因和多肽，如转移生长因子-β、肝细胞生长因子、胰岛素样生长因子-Ⅱ，根据所见到的最终表型推断特定基因在正常肾发生中的作用。酪氨酸激酶体受体c-ret在分支输尿管导管以及配体-神经胶质衍生的神经营养因子上表达。当小鼠c-ret基因被破坏时，导致全肾发育不良。转录因子基因编码蛋白能与DNA结合，而且具备调控其它基因表达的功能。在哺乳动物肾发育中，Wilms’肿瘤基因WT-1及Pax2均编码转录因子，其表达形式影响肾细胞的分化[6，7]。基因性综合症与肾形成异常有关，表中所列出的疾病，有些综合症有遗传性，有些用原位克隆技术已定位出特定的基因缺陷[8]。这些综合症在患病家族成员能发生显著的表型变异。这种情况与在纯合子无效突变小鼠所见的变异相似，即肾的最终表型取决于实验小鼠的基因背景。 肾发育不良的发生是几种不同的基因缺陷，或是在胚胎发育期遇到致畸因子等多种基因调控障碍的最终结果。肾间质-上皮转化的过程以及输尿管分支和生长，是由一个复杂而庞大的基因体系来导向，有些基因是肾特异性的，有些是非特异的。某些生长因子基因，尽管它们在肾发生期表达活跃，但当它们被破坏时并不影响肾的正常发育，这意味着发育肾正常表达的各种基因在功能上有重叠[9]。另一种可能性是这种正常表达形式的破坏在肾发育不良的发生发展中起一定作用，或者就是肾发育不良的起因。 后肾间质缺陷可导致肾发育不良。另外，基因不适应和错位表达，可能对肾发育不良起一定作用。临床上有孤立的多囊性肾发育不良和梗阻性肾发育不良两者并行存在的病例。先天性和实验性单基因突变均可导致囊性肾发育异常，这些基因突变可改变相互联系。从理论上讲，突变可影响：①胚基增生和分化输尿管导管分支所必需的肽和基质蛋白的表达；②输尿管导管对后肾胚基信号的反应能力；③输尿管导管表达启动和维持后肾胚基上皮诱导所需蛋白的能力；④后肾胚基对这些信号进行反应的能力；⑤输尿管芽和后肾胚基细胞对信号的反应能力[10]。 最近已经分离出磷酸葡萄糖肌醇糖蛋白基因，简称GPC3基因。GPC3缺失与多囊性肾发育不良有关[11]。虽然单基因与多基因缺陷均可最终导致肾发育不良，但其表型可能决定于最初受影响的基因调控失调或表达改变，如先天性梗阻性和囊性肾发育不良[12，13]。多囊性发育不良肾，在囊性上皮和间质中均有生长因子基因的改变。在小鼠梗阻性发育肾中，血管紧张素和转移生长因子呈过度表达[14]。研究证明，在后肾发育异常区，促进小管上皮出现囊性改变的因子Pax2和Bcl-2同样呈过度表达[15，16]。此研究可能会对各种形式肾发育不良的发病机制提供重要线索。
有没有翻译英语论文的软件啊
论文翻译软件比较多，比如百度、谷歌、有道等等，软件其实大同小异吧。
你下的已经够全的了！我知道的有，有道翻译，灵格斯（Lingoes，我看了不少介绍翻译软件的网站都推荐灵格斯，有个什么五大翻译软件的排名，他好像排第二呢，反正是广受好评），金山（这个也不错，我姐是英语老师，她们老师也常用这个），谷歌翻译（这个一般，不太稳定，有时候翻译的很准，有时候简直不是人话，跟抽风一样），韦氏词典（这个很专业！我原来不知道这个，但是后来好几个人向我推荐，说是这个的释义最专业！备考GRE的人常用它），必应（这个在线翻译据说也很不错，但是在中国不太普及，在国外很常用，既然是美赛那就很有用了），这些足够了。。。。。。。
谷歌浏览器翻译和有道翻译，有道翻译可以直接提供文档翻译，译文也还不错。谷歌浏览器翻译 优点可以pdf直接翻译，准确率高。
回答 百度翻译适合在外出旅游时，通过拍照翻译英文路牌可以更好的了解方向。有道则更擅长于全文翻译功能。这两款翻译软件基本能满足用户日常翻译需求。 1、有道翻译官有道翻译官是网易有道公司出品的翻译应用，支持中英、中日、中韩和中法等多语种离线翻译，在没有网络的情况下也能顺畅使用。同时配备强大的摄像头取词和短信翻译功能，无需手动输入便可快速获取翻译结果。2、百度翻译百度翻译是一款集翻译、词典、情景例句于一身的翻译应用。免费提供高质量中英和中日互译的翻译服务，同时整合离线翻译、语音翻译和摄像头翻译功能，能够随时随地便捷的满足用户的翻译需求，是您生活、旅游、学习不可或缺的最佳帮手。3、谷歌翻译Google 翻译是谷歌公司提供一项免费的翻译服务，可提供 80 种语言之间的即时翻译，支持任意两种语言之间的字词、句子和网页翻译。可分析的人工翻译文档越多，译文的质量就会越高。对于大多数语言，您可以读出短语，然后便可听到相应的语音翻译。 希望回答对您有帮助，给个赞！谢谢 更多1条
有没有英语论文免费翻译网站
1：彩云小译适用场景：长篇文献很简洁干净的界面，让人看起来一目了然，直接将文档上传到网站，就可完成翻译。彩云小译翻译的结果有一个很大的特点：翻译结果直接嵌在英文下方！阅读非常方便！2：搜狗翻译适用场景：长篇文献这是搜狗出品的翻译工具。翻译结果可实现左右两边同步中英对照。惊喜的是，可直接下载Word格式的翻译结果，而且免费！意味着不满意的地方可以二次修改~还能选择输出格式，既可以是pdf格式也可以是word格式。3：百度翻译适用场景：长 / 短文献其实百度翻译的翻译结果还是很不错的，在做数学建模美赛的时候感觉这里的翻译还是很不错的，很多英文文献需要快速阅读就来这里翻译翻译。4：谷歌翻译谷歌翻译类似于百度翻译，都是很不错的翻译软件5：网页翻译适用场景：网页端英文翻译搜英文文献时网页全是英文，看着是不是很头疼？其实很多浏览器自带翻译功能，比如谷歌浏览器。只要点击网页右上角的「翻译此页」，立马就能得到中文页面~
google在线翻译 在百度中找即可
本人6年国内外个人/企业/图书翻译经验(笔译/口译)，英语专八，认真负责，客户不用花时间审核，随时在线。也有个团队，能翻译其他语种，韩日德法等。 为人认真负责，讲诚信。感兴趣的，可以搜索“韭莲翻译工作室”
（爱词霸英语）这个翻译网站挺好。