EpigenticsProgress2010

IEEE拒绝收录的138个会议列表2011-10-27 14:54:18| 分类：EI、ISTP检索国际 | 标签：ieee 收录 138 会议列表 |字号大中小订阅IEEE拒绝收录的138个会议列表138个会议名单如下:2010 2nd Asia-Pacific Conference on Information Processing (APCIP)2010 2nd International Asia Symposium on Intelligent Interaction and Affective Computing & 2010 2nd International onInnovation Management (ASIA-ICIM)2010 2nd International Conference on Future Computer and Communication (FCC) 2010 2nd International Conference on Information and Multimedia Technology (ICIMT)2010 2nd International Conference on Intellectual Technique in Industrial Practice (ITIP 2010)2010 2nd International Conference on Multimedia and Computational Intelligence (ICMCI)2010 2nd International Conference on Research Challenges in Computer Science (ICRCCS)2010 2nd International Symposium on Computer Network and Multimedia Technology (CNMT 2010)2010 3rd International Conference on Computational Intelligence and Industrial Application (PACIIA)2010 3rd International Conference on Environmental and 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(APWCS)2011 2nd International Conference on Biomedical Engineering and Computer Science (ICBECS)2011 2nd International Conference on Biotechnology and Food Science (ICBFS) 2011 2nd International Conference on Data Storage and Data Engineering (DSDE) 2011 2nd International Conference on Environmental Science and Technology (ICEST)2011 2nd International Conference on Financial Theory and Engineering (ICFTE) 2011 2nd International Conference on Mechanical, Industrial, and Manufacturing Technologies (MIMT)2011 2nd Intl Conf on Innovative Computing & Communication and 2010 Asia-Pacific Conf on Information Technology &Ocean Engineering, (CICC-ITOE)2011 2nd World Congress on Computer Science and Information Engineering (CSIE) 2011 3rd IEEE International Conference on Information Management and Engineering (ICIME)2011 3rd International Conference on Bioinformatics and Biomedical Technology (ICBBT 2011)2011 3rd International Conference on Computer and Automation Engineering (ICCAE)2011 3rd International Conference on Computer and Network Technology (ICCNT) 2011 3rd International Conference on Computer Design and Applications (ICCDA 2011)2011 3rd International Conference on Computer Modeling and Simulation (ICCMS) 2011 3rd International Conference on E-business and Information System Security (EBISS)2011 3rd International Conference on Machine Learning and Computing (ICMLC) 2011 3rd International Conference on Networks Security, Wireless Communications and Trusted Computing (NSWCTC)2011 3rd International Conference on Signal Acquisition and Processing (ICSAP) 2011 3rd International Workshop on Education Technology and Computer Science (ETCS)2011 4th IEEE International Conference on Computer Science and Information Technology (ICCSIT 2011)2011 IEEE International Conference on Information and Education Technology (ICIET)2011 IEEE International Conference on Smart Grid and Clean Energy Technologies (ICSGCE)2011 International Conference on Applied Physics and Mathematics (ICAPM 2011) 2011 International Conference on Bioinformatics and Computational Biology (ICBCB)2011 International Conference on Bioscience, Biochemistry and Bioinformatics (ICBBB)2011 International Conference on Communication and Electronics Information (ICCEI)2011 International Conference on Computer and Communication Devices (ICCCD) 2011 International Conference on Computer Applications and Network Security (ICCANS)2011 International Conference on Computers, Communications, Control and Automation (CCCA)2011 International Conference on Control, Robotics and Cybernetics (ICCRC)2011 International Conference on Data Engineering and Internet Technology (DEIT) 2011 International Conference on Database and Data Mining (ICDDM)2011 International Conference on Digital Convergence (ICDC)2011 International Conference on Economics and Finance Research (ICEFR)2011 International Conference on Economics, Business and Marketing Management (CEBMM)2011 International Conference on Economics, Trade and 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baltic oi 2010 day1 总结Baltic IO 2010 Day 1 SummaryThe Baltic IO 2010 conference commenced with great enthusiasm and participation from experts in the field of Industrial Organization. The first day of the event was filled with insightful discussions, engaging presentations, and networking opportunities.The day began with a warm welcome from the conference organizers, followed by an introduction to the diverse range of topics to be discussed during the event. The attendees were then presented with the schedule for the day, featuring several highly anticipated presentations.The conference kicked off with a keynote address by Professor John Smith from the University of Economics. His speech focused on the current state of the industrial organization field and highlighted emerging trends and challenges faced by researchers and practitioners. Professor Smith's address set the tone for the rest of the day, inspiring participants to delve deeper into the topics at hand.This was followed by a series of parallel sessions that covered various aspects of industrial organization, including competition policy, market dynamics, and firm behavior. Each session featured high-quality research papers presented by esteemed scholars. The presentations were followed by detailed discussions, where participants had the opportunity to ask questions and provide their inputs.The lunch break provided an excellent opportunity for participants to network and interact with fellow researchers and industry professionals. The event had attracted a diverse group of attendees, ranging from academics to policymakers and business executives, leading to lively exchanges of ideas and experiences.After lunch, the conference continued with more parallel sessions, addressing topics such as innovation and technology, market structures, and regulatory frameworks. The presentations continued to impress, offering valuable insights into the challenges faced by various industries in today's rapidly changing business environment.To conclude the day, a panel discussion was held, focusing on the future perspectives of industrial organization. The panel consisted of experienced practitioners and scholars who shared their thoughts on the future direction of research and its potential impact on policy and business strategies.Overall, the first day of Baltic IO 2010 was a resounding success, with a wide range of topics discussed and valuable insights shared. The event provided a platform for researchers and industry professionals to connect, exchange ideas, and contribute to the advancement of the field of industrial organization.。

epigenetic修改对蛋白质表达的影响Epigenetic Modifications and Their Impact on Protein ExpressionIntroduction:Epigenetic modifications refer to heritable changes in gene expression that do not involve alterations to the DNA sequence itself. These modifications can regulate gene activity and play a crucial role in various biological processes. In recent years, there has been increasing interest in understanding how epigenetic modifications influence protein expression. This article aims to explore the effects of epigenetic modifications on protein expression and discuss their significance in different cellular contexts.1. DNA Methylation:One of the most extensively studied epigenetic modifications is DNA methylation, which involves the addition of a methyl group to the DNA molecule. DNA methylation can act as a gene silencer by blocking the binding of transcription factors, thereby repressing gene expression. The presence of methyl groups on specific gene regions can lead to long-term suppression of protein production.2. Histone Modifications:Histone modifications refer to the post-translational modifications of histone proteins, which are responsible for packaging DNA into a compact structure called chromatin. Different types of histone modifications, such as acetylation, methylation, and phosphorylation, can either activate or suppress gene expression depending on the specific modification and itslocation on the histone tail. These modifications can directly influence the accessibility of DNA to transcriptional machinery, thereby impacting protein expression levels.3. Non-coding RNAs:In addition to DNA methylation and histone modifications, non-coding RNAs have emerged as key regulators of gene expression and protein production. MicroRNAs (miRNAs) and long non-coding RNAs (lncRNAs) are two main types of non-coding RNAs that can interact with messenger RNAs (mRNAs) to influence their stability and translation efficiency. By binding to specific mRNA sequences, miRNAs and lncRNAs can either enhance or inhibit protein expression, thus exerting control over cellular processes.4. Developmental Regulation:Epigenetic modifications are crucial for proper development and differentiation of cells. During embryogenesis, specific genes need to be activated or suppressed at precise time points and in specific cell types. Epigenetic modifications play a vital role in orchestrating these processes by regulating protein expression. For example, DNA methylation patterns can be inherited from parent cells during cell division, ensuring the transmission of specific gene expression profiles across generations.5. Disease Implications:Aberrant epigenetic modifications have been implicated in various diseases, including cancer, neurological disorders, and autoimmune conditions. In cancer, altered DNA methylation patterns and histonemodifications can lead to abnormal expression of oncogenes or tumor suppressor genes, promoting uncontrolled cell growth. Understanding the epigenetic drivers of these diseases can provide valuable insights for developing targeted therapies and biomarkers.Conclusion:Epigenetic modifications have a profound impact on protein expression and play a crucial role in various biological processes. By influencing gene activity, DNA methylation, histone modifications, and non-coding RNAs can fine-tune protein levels and regulate cellular functions. Further research into the mechanisms and functional consequences of epigenetic modifications will deepen our understanding of gene regulation and potentially lead to novel therapeutic interventions.。

Epigenetic Regulation of Development Epigenetic regulation of development is a complex process that involves the modification of gene expression without altering the DNA sequence. It plays a crucial role in various stages of development, including embryonic development, cell differentiation, and tissue-specific gene expression. Epigenetic modifications are heritable and reversible, making them an essential mechanism for regulating gene expression during development. In this essay, we will discuss the role of epigenetic regulation in development from different perspectives.From a biological perspective, epigenetic regulation is a fundamental mechanism that ensures the proper development of an organism. During embryonic development, cells undergo a series of epigenetic modifications that determine their fate and function. For example, DNA methylation, histone modification, and non-coding RNA regulation are essential epigenetic mechanisms that regulate gene expression during development. These modifications ensure that genes are expressed at the right time and in the right place, which is critical for proper development.From a medical perspective, epigenetic regulation plays a significant role in the development of various diseases. Epigenetic changes can alter gene expression and contribute to the development of cancer, neurological disorders, and other diseases. For example, aberrant DNA methylation patterns have been linked to the development of cancer. Understanding the epigenetic mechanisms that contribute to disease development can help in the development of new treatments and therapies.From an ethical perspective, epigenetic regulation raises ethical concerns about the manipulation of gene expression. Advances in epigenetic research have made it possible to manipulate gene expression and alter the development of an organism. This raises concerns about the potential misuse of this technology, such as the creation of designer babies. It is essential to consider the ethical implications of epigenetic research and ensure that it is used for the benefit of society.From a social perspective, epigenetic regulation has the potential to impact society in various ways. For example, epigenetic research can provide insights into the effects of environmental factors on gene expression and development. This can help in the development of public health policies and interventions that promote healthy development. Additionally, epigenetic research can help in the development of personalized medicine, which can lead to better health outcomes for individuals.From a personal perspective, epigenetic regulation is a fascinating area of research that has the potential to impact individuals' lives. Understanding the epigenetic mechanisms that regulate gene expression can provide insights into the development of diseases and potential treatments. Additionally, epigenetic research can help individuals make lifestyle choices that promote healthy development. For example, research has shown that environmental factors, such as diet and stress, can impact epigenetic modifications and alter gene expression. By understanding these mechanisms, individuals can make informed decisions about their health.In conclusion, epigenetic regulation plays a crucial role in development from various perspectives, including biological, medical, ethical, social, and personal. Understanding the epigenetic mechanisms that regulate gene expression can provide insights into the development of diseases and potential treatments. Additionally, epigenetic research can help in the development of public health policies and interventions that promote healthy development. However, it is essential to consider the ethical implications of epigenetic research and ensure that it is used for the benefit of society. Overall, epigenetic regulation is a fascinating area of research that has the potential to impact individuals' lives significantly.。

性别决定和性腺分化的表观遗传学原文来源：Francesc Piferrer. Epigenetics of sex determination and gonadogenesis[J]. Dev. Dyn.,2013,2424:.360-370译文正文：摘要表观遗传学通常被定义为对于不能用DNA序列改变解释的基因功能遗传性变化的研究。

基因表达调控的三大表观遗传机制包括DNA甲基化，组蛋白修饰以及非编码RNA。

表观遗传机制赋予了生物体结合基因组及环境中的信息修饰基因活性来产生特殊表型的能力。

在发育过程中，细胞通过基因表达的改变进行分化，增殖并维持个体生长。

作为保证物种的正常运转和延续的最重要发育过程之一，这对于性别决定和分化是关键性的。

本文对于表观遗传调控机制在植物、无脊椎动物及脊椎动物中如何促进它们的性别决定和生殖器官的形成所作的研究进行了总结。

进一步进展将通过整合多种方法进行，包括基因组学和新一代测序方法。

目的在于产生涉及不同层面的性别决定及性腺分化的表观遗传图。

表观遗传学也将有助于我们理解一些障碍性发育的病因。

它也可能在动物养殖场生产的生育控制中发挥重要作用，并将有助于我们认识环境与遗传对于处在全球变化的情况下敏感的物种性别决定的影响。

关键词：DNA甲基化；组蛋白修饰；非编码RNA；多梳/三胸；性发育障碍；性分化；生育控制；全球变化正文表观遗传学是生物学中一个非常令人兴奋的领域，当下正经历着惊人的发展。

表观遗传学的范围（Eccleston等，2007年）是辩论的主题，并因此提出了几个定义（Bird，2007年）。

这里，我将使用Russo等人提出的定义：表观遗传学是“有关引起可遗传的基因功能改变的有丝分裂和/或减数分裂的研究，这些变化无法以DNA序列改变来解释。

”在定义中的专业术语"遗传"一词已经产生了某些混淆，因为实际上它传递了两个不同的含义：这些变化不仅是在细胞有丝分裂过程中从一个细胞遗传给它的子细胞，还在配子形成过程中通过细胞的减数分裂遗传，继而能够将这些变化从父母传递到后代(Gilbert和Epel, 2009年)。

REVIEW PAPEREnvironmental epigenetics:prospects for studying epigenetic mediation of exposure–response relationshipsVictoria K.Cortessis •Duncan C.Thomas •A.Joan Levine •Carrie V.Breton •Thomas M.Mack •Kimberly D.Siegmund •Robert W.Haile •Peter irdReceived:21February 2012/Accepted:7June 2012/Published online:28June 2012ÓThe Author(s)2012.This article is published with open access at Abstract Changes in epigenetic marks such as DNA methylation and histone acetylation are associated with a broad range of disease traits,including cancer,asthma,metabolic disorders,and various reproductive conditions.It seems plausible that changes in epigenetic state may be induced by environmental exposures such as malnutrition,tobacco smoke,air pollutants,metals,organic chemicals,other sources of oxidative stress,and the microbiome,particularly if the exposure occurs during key periods of development.Thus,epigenetic changes could represent an important pathway by which environmental factors influ-ence disease risks,both within individuals and across generations.We discuss some of the challenges in studyingepigenetic mediation of pathogenesis and describe some unique opportunities for exploring these phenomena.Abbreviations ART Assisted reproductive technologies ASM Allele-specific DNA methylation ChIP Chromatin immunoprecipitation CIMP CpG island methylator phenotype CpG Cytosine-phosphate-guanine dinucleotide CRC Colorectal cancer DES Diethylstilbestrol feNO Fractional exhaled nitric oxide FFPE Formalin-fixed paraffin-embedded HDAC Histone deacetylases iNOS Inducible nitric oxide synthase IUGR Intra-uterine growth restriction IVF In vitro fertilizationPBMCs Peripheral blood mononuclear cells PTS Maternal smoking during pregnancy SNP Single nucleotide polymorphismBackgroundThe field of epigenetics grew from attempts,beginning over 70years ago,to understand mechanisms whereby multiple cellular phenotypes arise from a single genotype during the complex process of developmental morpho-genesis termed epigenesis.The term ‘‘epigenetics’’was initially reserved for mechanisms by which phenotypic state,as determined by differential gene expression,could be stably retained through cell division by non-genetic factors.Various mechanisms have been proposed to have the potential to encode this phenotypic information;these include enzymatic methylation of cytosine bases (DNAV.K.Cortessis and D.C.Thomas contributed equally to this work.V.K.Cortessis ÁA.J.Levine ÁT.M.Mack ÁR.W.HaileDepartment of Preventive Medicine,Keck School of Medicine,University of Southern California,USC Norris Comprehensive Cancer Center,1441Eastlake Avenue,Los Angeles,CA 90089,USA D.C.Thomas (&)Department of Preventive Medicine,Keck School of Medicine,University of Southern California,2001N.Soto St.,SSB-202F,Los Angeles,CA 90089-9234,USA e-mail:dthomas@C.V.Breton ÁK.D.SiegmundDepartment of Preventive Medicine,Keck School of Medicine,University of Southern California,2001N.Soto St.,Los Angeles,CA 90089-9234,USAirdDepartments of Surgery,Biochemistry and Molecular Biology,Keck School of Medicine,University of Southern California,USC Norris Comprehensive Cancer Center,Epigenome Center,1441Eastlake Avenue,Los Angeles,CA 90089-9601,USAHum Genet (2012)131:1565–1589DOI 10.1007/s00439-012-1189-8methylation),post-translational modification of tail domains of histone proteins(histone modifications)and associated nucleosome positioning or chromatin remodel-ing,non-coding RNAs,and transcription factor regulatory networks(Ptashne2007).Epigenetic marks established by each of these processes are often shared within a cell lineage; however,whether all persisting epigenetic marks satisfy requirements for stable transmission through cell division or some are merely reestablished from other information fol-lowing mitosis remains a vigorously debated question.The term epigenetics has more recently been used in the scientific literature to describe various unspecified non-genetic mechanisms influencing phenotype.This broader usage emerged from mouse studies addressing transgen-erational nutritional effects on phenotype,as well as human studies of phenotypic differences between monozygotic twins.In the popular press‘‘epigenetics’’has become almost synonymous with nutritional and environmental influences on gene expression.Thus,while‘‘epigenetics’’initially referred to largely self-contained developmental processes,it has come to describe environmental influences on phenotypic readout of genotypes.This semantic evo-lution has caused confusion and controversy regarding the meaning of‘‘epigenetics’’at a time of intensified interest in the possible role of epigenetic mechanisms in disease.In this review we define as epigenetic processes those that stably affect gene expression through mechanisms not involving the primary nucleotide sequence,and epigenetic state as the configuration of chromatin and DNA marks utilized by these processes.By contrast,genetic state is widely understood to refer to the primary nucleotide sequence itself,while genetic processes maintain or change nucleotide sequence.Epidemiologic research addressing epigenetic mecha-nisms as mediators of environmental exposures on disease risk is constrained by important ethical considerations. These often preclude both experimental exposure to candi-date environmental causes,and invasive collection of cell types of greatest developmental and functional relevance to disease processes.Inquiry has therefore progressed largely by integrating information about biological mechanisms obtained in model systems with observational data provided by humans.To address the current state and future promise of this research,we undertook this review with two goals:to illustrate the potential of epigenetic processes to mediate exposure–phenotype relationships and to discuss study design and statistical analysis methods needed to investigate such mechanisms in relation to origins of human disease.We begin by discussing genetic,developmental,and environ-mental determinants of epigenetic state in human and model systems,then describe some of the diverse data implicating epigenetic mechanisms in various human diseases,both within individuals and across generations.We conclude by discussing technical challenges,suggesting promising opportunities for epidemiologic research in environmental epigenetics,and offering some thoughts about translational significance and future directions of thisfield. Determinants of epigenetic stateEpigenetic mechanisms work in concert to influence the potential for gene expression at myriad locations through-out the genome.The resulting epigenetic state of the gen-ome,termed epigenome,varies by cell type.Considering the tremendous diversity of epigenetic marks,which include dozens of different post-translational histone modifications and more than50million sites of potential DNA methylation in a diploid human genome(and thus [250M possible epigenotypes!),it seems that no two human cells would have identical epigenomes.Indeed,within each individual there are many epigenomes,and these change over time as a consequence of both normal developmental and pathological processes,as well as environmental exposures and random drift.Despite this potential for considerable variability of epigenetic patterns within and between individuals,there can also be remarkable consis-tency.In a study of11tissues in6autopsies,DNA meth-ylation patterns in a highly selected set of loci were found to be highly conserved,with intraclass correlations of0.85 across tissues within individuals and0.83across individ-uals within tissues(Byun et al.2009).The authors inter-preted these patterns as revealing different sets of person-specific and tissue-specific differentially methylated genes, anticipating subsequently observed differential genetic and acquired determination(Waterland et al.2010).DNA methylation has been the epigenetic mark most extensively measured in epidemiologic research for numerous reasons.It is of fundamental biological interest owing to its unambiguously stable transmission during cell division.It also has practical advantages:as a chemically stable covalent change to the DNA itself,DNA methylation is the only epi-genetic mark that survives the DNA extraction and purifica-tion that is routine in molecular sample processing,and it can endure decades of archival sample storage(Kristensen et al. 2009).Genetic influencesNucleotide sequence is a primary determinant of epigenetic state,clearly evident from the distribution of epigenetic marks across the genome,determined in part by direct effects of G:C content and CpG(cytosine-phosphate-guanine dinucleotide) density(Tanay et al.2007;Thomson et al.2010).Additional genetic influences include proximity to repetitive elements such as Alu and LINE1(Estecio et al.2010),nucleararchitecture(Berman et al.2011),and binding sequences for transacting proteins(Bell et al.2011b;Weth and Renkawitz 2011).Motif searches and screening strategies have identified sequence elements that predispose to particular epigenetic states(Feltus et al.2006;Ideraabdullah et al.2011;Keshet et al.2006;Lienert et al.2011).Several lines of evidence indicate that genetic poly-morphisms can affect epigenetic state.Greater differences were observed between dizygotic co-twins than between monozygotic co-twins in two forms of epigenetic state: skewed patterns of X-inactivation,and DNA methylation at differentially methylated regions of the imprinted IGF2/ AH19locus(Wong et al.2011;Heijmans et al.2007; Ollikainen et al.2010).Extensive DNA methylation anal-yses in a multigenerational family revealed that epiallelic similarity was greater amongfirst-degree relatives than among more distantly related family members.In the same study,analyses addressing both genetic variation and DNA methylation identified widespread occurrence of allele-specific DNA methylation(ASM)that was associated with polymorphic nucleotides located near the DNA methyla-tion site,but not parent of origin.Authors of this report concluded that the majority of such ASM events depend on cis-acting DNA sequence(Gertz et al.2011).Such ASM events have yet to be characterized in large population-based studies,but more modest studies addressing hetero-zygous non-imprinted loci have identified widespread ASMs associated with nearby genotypic polymorphisms in DNA from multiple tissue types(Kerkel et al.2008;Tycko 2010;Schalkwyk et al.2010),as well as allele-specific chromatin structure and transcription factor binding in lymphoblastoid cell DNA(McDaniell et al.2010,reviewed in Birney et al.2010).Presumed transgenerational inheri-tance of epigenetic changes(‘‘epimutations’’)in the MLH1 (Suter et al.2004)and MSH2(Chan et al.2006)mismatch repair genes,both associated with colorectal cancer,were also traced to germline genetic variation.In the case of the MSH2 epimutation,deletion of a gene immediately upstream of the MSH2gene causes transcription to run through the MSH2 promoter,causing somatic hypermethylation and gene silencing(Ligtenberg et al.2009).The MLH1epimutation was found to be caused by a polymorphism in the50UTR of the MLH1gene,reducing transcriptional activity,and pre-disposing to aberrant somatic DNA methylation in each generation(Hitchins et al.2011).Developmental programming of the epigenomeIn successful mammalian reproduction,the single-cell zygote gives rise to an organism with hundreds of cell types.These diverse cellular phenotypes arise from the same shared genomic sequence by control of the subset of genes expressed in each cell type.Cellular differentiation is tightly linked to extensive erasure and establishment of lineage-specific epi-genetic marks,a process termed epigenetic reprogramming. Relatively detailed descriptions of DNA methylation in developing tissues have been carried out in the mouse,which serves as a model of epigenetic reprogramming in mammalian development(Trasler2009).At fertilization,reprogramming begins with extensive erasure of methyl marks in DNA of the paternal(sperm-derived)DNA,followed by more general loss of methyl marks in the zygote and embryo during cleavage divisions,while sparing parent-of-origin specific imprints.By the blastocyst stage,de novo DNA methylation distinguishes inner cell mass cells(from which embryonic lineages arise to create fetal structures)from relatively hypomethylated trophectoderm cells(from which extra-embryonic lineages arise to create transient structures,including placenta)(Fig.1).Germ cell lineage specification begins in cells of the proximal epiblast,and involves a second extensive erasure of DNA methylation that removes parental imprint marks (Fig.1).Thereafter,the germ line develops in a sexually dimorphic fashion.New DNA methyl marks are established over many stages,extending through sexual maturity in accordance with the sex of the developing individual.At this time,the sex-specific imprint marks that govern parent-of-origin specific expression of imprinted genes in the sub-sequent generation are established(Faulk and Dolinoy2011).Developmental reprogramming can result in dramatic epigenetic differences between the two alleles.The asso-ciation between mono-allelic gene expression and DNA methylation has long been recognized,both in the context of X-inactivation in females(Boggs et al.2002;Sharp et al. 2011)and in parent-of-origin determined genomic imprinting(Ferguson-Smith2011),but now also in the mono-allelic expression of non-imprinted autosomal loci (Harris et al.2010;Tarutani and Takayama2011).Further resetting of epigenetic marks accompanies differ-entiation of many specialized cell types of the body as well as placenta and other transient structures during pregnancy,and subsequent development of body structures during various postnatal stages of development.Chromatin states that arise during development can affect the propensity to subsequent epigenetic change.An example of this is the predisposition of polycomb-repressive complex occupied genes in stem cells to the acquisition of DNA methylation abnormalities in aging and cancer(Ohm et al.2007;Schlesinger et al.2007; Teschendorff et al.2010;Widschwendter et al.2007).Environmental influencesMultiple differences in gene expression,presumably reflecting intrauterine epigenetic differences,have been identified in several tissues from newborn identical twins (Gordon et al.2011).The global methylation pattern ofindividuals changes with increasing age (Bjornsson et al.2008),as does the difference in global methylation between MZ twin pairs (Fraga et al.2005).Genetically identical MZ twins show some epigenetic discordance at birth,as indi-cated by gene expression discordance (Gordon et al.2011).Even over the first decade of life (Wong et al.2010),and as aging adults (Talens et al.2010),MZ twins acquire addi-tional differences in epigenetic state,which may partly reflect different exposure histories,as would be expected if environmental exposures influence epigenetic state.How-ever,stochastic drift in epigenetic state and related con-sequences such as mono-allelic expression described in the previous section is likely responsible for much of the observed divergence.Therefore,other forms of data (dis-cussed below)are needed to determine what type of exposures may influence epigenetic state and the extent of resulting changes.Experimental studiesThe most direct evidence suggesting that ambient exposures may influence epigenetic state is experimental.In vitro studies have demonstrated associations of DNA methylation with various metals (Dolinoy et al.2007b ;Wright and Baccarelli 2007).In the in vivo setting,prenatal protein restriction is associated with hypomethylation of the gluco-corticoid receptor (GR )and PPAR a gene promoter regions inrat liver (Lillycrop et al.2005),changes that were prevented by folic acid supplementation (Lillycrop et al.2005)and which were transmitted to the F2generation (Burdge et al.2007).Plagemann et al.(2009)found hypermethylation in the promoter of the anorexigenic gene for proopiomelano-cortin in rats overfed as neonates.Whether this change could be transmitted to offspring was not assessed.DNA from sperm of mice exposed to steel plant air was found to be persistently hypermethylated long after exposure ended (Yauk et al.2008).Additionally,maternal nurturing behav-ior has been shown to modify methylation at individual CpG sites in the ngf1a binding region of the GR gene in the hip-pocampus of the offspring (Weaver et al.2004),an epige-netic modification that persisted both into adulthood to modify response to stress,and into the F2generation.Human studiesChristensen and Marsit (2011)and Terry et al.(2011)have provided comprehensive reviews of environmental influ-ences on epigenetic state in humans.Here we note expo-sure periods of particular interest and several examples of environmental exposures reportedly associated with epi-genetic state of specific human cell types.The epigenome may be most vulnerable to environ-mental insults during periods of extensive epigenetic reprogramming,which may in theory be disruptedbyFig.1Reprogramming ofDNA methylation in the zygote,early embryo,and primordial germ cells.Thickness of the outer arrows indicates levels of DNA methylation.Red maternal genome,blue paternal genome,black diploid genome.Embryonic lineages arise from cells of the inner cell mass (ICM),the placenta and extraembryonic membranes from trophectoderm cells,and the germ cell lineage fromprimordial germ cells following their determination fromproximal epiblast.Inner circles indicate developmental stages when key elements ofepigenetic programming are thought to occur (Adapted from Feng et al.2010)exposures that interfere with any process that governs reprogramming.Periods of particular vulnerability may therefore include the early stages of embryonic develop-ment mentioned above.Childhood is also proposed as a period of vulnerability,especially in the germline of females,since oocytes remain in a haploid de-methylated state until puberty,so environmental insults may poten-tially disturb the epigenetic state of the oocyte for many years(Faulk and Dolinoy2011),with potential implica-tions for both fertility and initial epigenetic state of off-spring of an exposed female.Somatic changes to DNA methylation may also result from environmental exposures in adults,as have been observed in aging and disease processes such as cancer described in the next section. Energy and nutrient intakeSignificant epigenetic changes in the IGF2gene have been documented in those prenatally exposed to severe caloric restriction during the Dutch hunger winter of World War II (Heijmans et al.2008).Hughes et al.(2009)additionally found that those most likely to be exposed to this famine during adolescence or young adulthood had a significantly decreased risk of developing colorectal cancers(CRC) characterized by the CpG island methylator phenotype (CIMP),suggesting a role for early life exposures in CIMP-specific CRC pathogenesis.Folates are the major source of the methyl groups used for DNA and histone methylation.One study of folates and other one-carbon nutrients reported a differential effect of folate on the risk of the CIMP CRC subset compared to the non-CIMP subset(Van Guelpen et al.2010),while two other studies did not(Slattery et al.2006;van den Donk et al.2007).Most studies of the microsatellite instability high subset,characterized by hypermethylation of the MLH1gene promoter region and CIMP(Weisenberger et al.2006),have yielded similarly negative results(Eaton et al.2005;Schernhammer et al.2008;Slattery et al.2001; Wark et al.2005).On the other hand,in some studies the association between intake of alcohol(which degrades folates)and CRC risk has been reported to be greater in MSI-H and CIMP tumors(Diergaarde et al.2003;Eaton et al.2005;Slattery et al.2001).Micro-RNAs(miRNAs)are very short non-coding RNA molecules that can downregulate protein-coding genes by destabilizing mRNAs or blocking translation.The possi-bility that exogenous microRNA consumed in food may epigenetically regulate gene expression has emerged from recent studies demonstrating the presence of plant-derived miRNAs in sera of humans and other mammals(Zhang et al.2012).One of these plant microRNAs,MIR168a, which was demonstrated to be only of plant origin in control mice,binds coding sequence of the mammalian LDLRAP1 gene in vitro.Functional consequences in mammalian sys-tems were demonstrated experimentally,as MIR168a administered in vitro and during in vivo feeding studies decreased expression of the protein product of LDLRAP1. This line of research suggests novel epigenetic mechanisms whereby diet may modify risk of human disease.Air pollutionEmerging evidence suggests that air pollutants can influ-ence epigenetic changes,including DNA methylation as well as up-or down-regulation of miRNAs(Jardim2011). In human epidemiologic studies,PM2.5and PM10expo-sures are associated with hypomethylation of Alu and/or LINE1elements in leukocytes and buccal cells(Baccarelli et al.2009;Bollati and Baccarelli2010;Madrigano et al. 2011;Salam et al.2012;Tarantini et al.2009),as well as altered DNA methylation in NOS2A,a gene involved in production of nitric oxide(Salam et al.2012;Tarantini et al.2009).Living in highly polluted cities(high PM and ozone)is also associated with hypermethylation of FOXP3 in regulatory T cells(Nadeau et al.2010),while neonates who were prenatally exposed to polyaromatic hydrocarbon (PAH)had hypermethylated ACSL3in DNA of umbilical cord white blood cells(Perera et al.2009);notably,both of these genes are involved in asthma pathogenesis.PAHs are also associated with hypermethylation of LINE1and Alu (Pavanello et al.2009;Perera et al.2009).More limited evidence is emerging to suggest that air pollution is asso-ciated with changes in miRNA expression(Bollati et al. 2010;Jardim2011),and adverse effects of air pollution constituents may be modified by variant alleles of genes involved in miRNA processing(Wilker et al.2010). Tobacco smokeFetal exposure to maternal smoking during pregnancy (PTS)is associated with reduced methylation of several repeated sequences,including Sat2(Flom et al.2011),Alu, and LINE1among children with the GSTM1null genotype (Breton et al.2009).PTS exposure is also associated with increased DNA methylation in specific genes,such as AXL and PTPRO(Breton et al.2009,2011b)and IGF2(Murphy et al.2011).In adult lung cancer patients,quantity and duration of active smoking as well as second-hand smoke is associated with increased DNA methylation of p16(Kim et al.2001;Scesnaite et al.2012),MGMT,and DAPK (Russo et al.2005).Tobacco smoke is also associated with tumor cell DNA methylation changes in esophageal squa-mous cell carcinoma(Huang et al.2011),significantly higher frequencies of abnormal DNA hypermethylation inprostate(Enokida et al.2006)and gastric cancers tumor cells(Nan et al.2005)and with a higher risk of CIMP?colorectal tumors(Limsui et al.2010;Samowitz et al.2006).Lastly,the F2RL3gene is hypomethylated in smokers and may mediate the detrimental impact of smoking on cardiovascular mortality,since hypomethylat-ed F2RL3was found to be strongly associated with car-diovascular mortality among patients with stable coronary heart disease(Breitling et al.2012).Oxidative stressReactive oxygen species(ROS)are involved in numerous cellular processes including cellular redox alterations, immune response,signaling pathways,chromatin remod-eling and gene expression(Sundar et al.2010).ROS have the potential to influence epigenetic mechanisms(Baccar-elli and Bollati2009),and have been shown to inhibit binding of methyl-CpG binding protein2,a critical epi-genetic regulator that recruits cytosine methyl transferases and histone deacetylases to DNA(Valinluck et al.2004). Numerous environmental exposures,including constituents of air pollution and tobacco smoke,can generate ROS and thus may potentially alter epigenetic processes through oxidative stress mechanisms.MetalsPrenatal lead exposure is associated with decreased meth-ylation of LINE1and Alu in cord blood(Pilsner et al. 2009),and a similar pattern of LINE1methylation was reported in an elderly cohort(Wright et al.2010).Studies in humans have shown that arsenic exposure is associated with either global hypermethylation or hypomethylation in peripheral blood mononuclear cells(PBMCs)depending on dose(Majumdar et al.2010),as well as DNA hyperme-thylation of several genes,including CDKN2A(Chanda et al.2006),RASSF1A and PRSS3(Marsit et al.2006). Exposure to airborne particulates rich in lead,cadmium and chromium are associated with miRNA expression in peripheral blood(Bollati et al.2010)and airborne levels of nickel and arsenic are positively correlated with both his-tone3-lysine4trimethylation(H3K4me3)and histone 3-lysine9acetylation(H3K9ac)in blood leukocytes (Cantone et al.2011).Occupational exposure to nickel is associated with increased H3K4me3and decreased H3K9me2in PBMCs(Arita et al.2011).Lastly,cadmium can induce overexpression of the DNA methyltransferase genes DNMT1and DNMT3a in human embryo lung fibroblasts,and is associated with hypermethylation and silencing of the MSH2,ERCC1,XRCC1and OGG1genes in human bronchial epithelial cells(Jiang et al.2008;Zhou et al.2011).Organic chemicalsGas-station attendants and police officers occupationally exposed to low levels of benzene were found to have significantly lower LINE1and Alu methylation,hyper-methylation of p15,and hypomethylation of MAGE-1in blood(Bollati and Baccarelli2010;Bollati et al.2007).Genetic9epigenetic9environmental interactionsMost work investigating effects of environmental factors on epigenetic state has not considered the potential for genetic susceptibility to modify these associations.However,Salam et al.(2012)recently investigated contributions of both genetic and epigenetic variation in air pollution-mediated levels of fractional exhaled nitric oxide(feNO).Measure-ment of feNO provides an in vivo summary assessment of inducible nitric oxide synthase(iNOS)activity as well as airway inflammation.These investigators found interrelated effects of exposure to the air pollution constituents PM2.5, NOS2A promoter haplotypes,and methylation of the iNOS encoding gene NOS2A and NOS2promotor haplotypes on feNO level.These observations illustrate not only the feasi-bility of assessing interactions between epigenetic,genetic, and environmental factors,but also the importance of doing so in order to delineate complex biological relationships and identify susceptible subpopulations.Epigenetic effects in human diseaseConditions associated with improper parental contributions of imprinted genes are currently the clearest examples of human diseases related to epigenetic state.Even before genomic imprinting was described,experiments in which pronuclei were transplanted into enucleated eggs demon-strated that both maternal and paternal chromosomal con-tributions are required for normal development.Control conceptuses receiving one set(haploid genome)of mater-nal(egg-derived)and one set of paternal(sperm-derived) chromosomes could develop normally.However,abnormal development and early demise occurred in all conceptuses receiving either two maternal sets or two paternal sets of chromosomes(McGrath and Solter1984),which devel-oped into tissues with histologic features of dermoid cysts and hydatiform moles,respectively.Model imprinting disorders such as Beckwith–Wiede-mann,Angelman,Russell–Silver,and Prader–Willi syn-dromes are human conditions that can be caused by aberrant epigenetic state(Ferguson-Smith2011).The specific features,early onset,and rarity of these disorders facilitated recognition of their relation to improper parental contributions of imprinted loci(e.g.two maternal or two。

epitope binning原理（实用版）目录1.epitope binning 简介2.epitope binning 原理3.epitope binning 的应用正文1.epitope binning 简介epitope binning 是一种用于分析和表征抗体反应的生物信息学技术。

通过将大量抗体与不同抗原表位结合的反应数据进行分析，可以将这些抗体分为不同的组，从而获得对抗原表位的深入理解。

这种方法有助于研究免疫系统的功能和疾病发生机制，同时也为生物治疗和疫苗设计提供重要信息。

2.epitope binning 原理epitope binning 的原理主要基于抗原表位与抗体结合的特异性。

每个抗原分子上都存在多个表位，这些表位可以与抗体结合并引发免疫反应。

通过将不同抗原表位与抗体结合的反应进行检测和分析，可以发现哪些抗体与哪些表位结合，从而将这些抗体分为同一组。

这个过程通常涉及到高通量实验技术和生物信息学分析。

2.1 抗原表位与抗体结合的特异性抗原表位是抗原分子表面上的特殊区域，可以与抗体结合并诱导免疫反应。

每个抗原分子上都存在多个表位，这些表位具有不同的结构和空间特征。

因此，不同的抗体可以与不同的表位结合，表现出特异性。

2.2 高通量实验技术高通量实验技术是 epitope binning 的基础。

这些技术可以快速、准确地检测大量抗体与抗原表位的结合反应。

通常使用的方法包括酶联免疫吸附试验（ELISA）、流式细胞术和质谱技术等。

2.3 生物信息学分析生物信息学分析是 epitope binning 的关键。

通过处理和分析高通量实验数据，可以确定哪些抗体与哪些表位结合，并将这些抗体分为同一组。

常用的生物信息学方法包括聚类分析、机器学习等。

3.epitope binning 的应用epitope binning 在多个领域具有广泛的应用，包括疫苗设计、生物治疗、疾病诊断和免疫学研究等。

Epigenetics在遗传学中的应用与研究随着科技的不断发展，生物医学研究也在不断深入。

在遗传学领域中，近年来一种新兴的研究方向已经吸引了众多的研究者的关注。

它就是Epigenetics学科，这个观念早在上个世纪就已经提出来了，但是直到现在才真正地引起人们的重视。

因为它的研究可以为我们寻找到许多神经元退化性疾病的抗体，例如Alzheimer‘s 病等等。

对于这一领域的深度与发展趋势，人们有很多的想象和猜测。

我从事这一领域的研究已经有几年的时间了，下面开始为大家介绍Epigenetics在遗传学中的应用与研究。

一、Epigenetics学科概述Epigenetics学科在生物医学中的意义非凡，因它研究的是基因表达之外的遗传物质，它是去观察基因组的外延。

基因组非常重要，但是基因组的突变很难预测。

Epigenetics则研究基因组之外的”外因“（例如：环境、营养和药物等等），这些因素对基因的影响是喜欢傻大笨重的，对之后的后代会产生很大的影响。

Epigenetics是基因组功能和表达的调控机制，而这些机制都印刻在我们的DNA上。

实质上它是对基因组上各种可能性的调控。

现代遗传学的研究不仅研究基因体系和基因分布，还需要关注DNA序列上另外的硬编码元素，对于真正的表达遗传现象进行調控和管理。

这个学科的发展需要一个新的体系，所以它自己发展为一门独立的学科领域。

二、Epigenetics的遗传重要性Epigenetics的意义越来越重要，因为它关系到人类的健康。

Epigenetics可以帮助我们了解环境对人的影响。

例如，一些显著和突出的表型通过表观遗传学机制来控制，包括肥胖、糖尿病、心血管疾病及多种神经退行性疾病等等。

所以，掌握这个学科的知识，有助于我们了解到一些很常见的疾病的诱因，这样可以为发病前的预防和防范工作乐观悲观起到重要作用。

三、Epigenetics的研究技术Epigenetics的研究技术主要有三个方面，分别是：DNA甲基化，组蛋白修饰和非编码RNA（ncRNA）。