网站公告：&公司简介广州达晋生物科技有限公司是于2008年成立的一家专注于生物医学学领域的学术英语语言编辑服务公司，同时也是中国医学科研与学术推广的开拓者。经过长时间运作，我们聚集了国内外众多社会资源，网罗了上百位具有欧美国医学作家协会(American Medical Writers Association)的认证资格之专业医学专家编辑团队，拥有雄厚的学术背景。此外，实验研究和学术推广方面，我们正积极与国内外各大医学实验室、研究所和科研机... &编辑专业背景Jean AndrewsUniversity of South Florida: M.A., Library and Information Science. Beta Phi Mu and Phi Kappa Phi honor societies.University of Massachusetts, Amherst: B.S., magna cum laude, and graduate courses Major: NaturalDr.RobertsonDr Robertson曾从事动物学和比较动物生理学研究，博士研究课题是蛇的消化酶。曾在开普敦大学执教动物学4年，后在南非罗德斯大学药学系获得终生学术职位。曾为药学专业学生和体育教育专业学生讲授人体生理学课程，目前，为四年级药学专业学生讲授选修课程“营养学与老年医学”，为动物学专业学生讲授选修课程“爬虫动物学”。发表了数篇关于蛇毒的研究论文，还编写了一些普通科学教科书。Gail Schofield我在英国布里斯托大学()攻读的是动物学。在此期间，我参加了希腊的海龟研究。另外还参加了希腊和英国的野生生物保护工作。大学毕业后，我继续从事保护和咨询工作，主要业务领域为海洋和沿海生态学（1996-至今）Jones,MichelleI earned a PhD in Cellular and Molecular Medicine from the Johns Hopkins University School of Medicine, where I studied interactions between prostate cancer cells and
including abstracts Bauman, NormanMedical news and feature stories for an audience of physicians, based on journal articles, phone interviews and meeting coverage. Clinical specialties include oncology, urology, ophthalmology, general surgery, Dr.MarchDr March是癌症生物学家，主要研究领域是细胞信号传导和肠道肿瘤学。博士课题内容是研究MAP激酶通路对AP- 1蛋白的调节。目前任英国剑桥大学肿瘤研究所高级博士后研究员，工作重点是应用新模型来判定和表征大肠癌的新驱动基因。此前在英国Babraham研究所做博士后研究，工作内容是与UCB制药公司合作，研究癫痫药物的作用模式。另外还曾在生物技术行业工作。Larson,JodyAuthor-friendly, well-seasoned editor and nonfiction writing specialist. Developmental work, writing, and copyediting in college-level biology, A/P, botany, genetics, ecology, environment, astronomy, physics, aElgin Yile专业背景是医学细胞生物，重点是儿科研究。她的博士研究重点是各种激素对胎儿生长的迟缓作用。从2000年到2003年，被授予美国心脏协会佛罗里达州联盟博士后奖学金。出色的写作技巧、丰富的写作经历和非英语母语作者稿件的编辑经验。现任新西兰奥克兰大学生理学系讲师兼研究员。目前正在研究胎儿心脑血管对窒息的适应机制，并研究围产期治疗方案。客户反馈我已通过贵公司的邀请函，成功报名。...
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Reprod Dom Anim 46, 338–343 (2011); doi: 10.1111/j.10.01672.xISSN Review ArticleTelegony, the Sire Effect and non-Mendelian Inheritance Mediated by Spermatozoa:A Historical Overview and Modern Mechanistic SpeculationsYS LiuHenan Institute of Science and Technology, Xinxiang, ChinaContentsTelegony is the belief that the sire first mated to a female willhave an influence upon some of that female’s later offspring byanother male. Although the reality of telegony was acknowledgedby such authorities as Darwin, Spencer, Romanes andmany experienced breeders, it has been met with scepticismbecause of Weismann’s unfavourable comments and negativeresults obtained in several test experiments. In this article,alleged cases of telegony are provided. A search of theliterature of cell biology and biochemistry reveals severalplausible mechanisms that may form the basis for telegony.These involve the penetration of spermatozoa into the somatictissues of the female genital tract, the incorporation of theDNA released by spermatozoa into maternal somatic cells, thepresence of foetal DNA in maternal blood, as well as spermRNA-mediated non-Mendelian inheritance of epigeneticchanges.IntroductionThe subject of telegony is an exceptional, allegedphenomenon that enjoyed a remarkable career in thenineteenth century (Burkhardt 1979). Its principle is thatfemales are impregnated by the first males to which theyare mated, so that some of their subsequent offspring,regardless of their actual father, will show influence of thefirst male (Rabaud 1914). In modern parlance, the term‘sire effect’ would cover such a phenomenon. Althoughthe story of the son who resembles his mother’s formerhusband has circulated among the people in China forgenerations, Charles Darwin was the first to summarizethis phenomenon in biological science. In Chapter 11 ofhis book The Variation of Animals and Plants underDomestication, Darwin (1868) collected many allegedexamples of ‘the direct action of the male element on thefemale form’. He mentioned the case of Lord Morton’sfamous hybrid, from a chestnut mare and a male quagga.Not only the hybrid but also the offspring subsequentlyproduced by the mare when mated to a black Arabian sirewas more plainly barred across the legs than even thepure quagga. Darwin concluded that ‘there can be nodoubt that the quagga affected the character of theoffspring subsequently begot by the black Arabianhorse’. He considered it to be of special importance forunderstanding the mechanisms of heredity and developmentand advanced this case as one of several in supportof his hypothesis of Pangenesis – a developmental theoryof heredity (Darwin 1868; Liu 2008).It is a historical fact that in the nineteenth century, thephenomenon of telegony commanded considerablerespect, guided the practice of many animal breedersand played an important role in pre-1900 discussions ofheredity. The reality of Morton’s mare was acknowledgedby such authorities as Louis Agassiz, ClaudeBernard, Herbert Spencer, George John Romanes,Francis Galton, William Bernard Tegetmeier and manyexperienced breeders (Thomson 1908; Burkhardt 1979).Spencer (1893) regarded it as a major weapon in hisdebate with August Weismann over the reality of theinheritance of acquired characters. Scientists who madeany pretence of understanding reproduction and hereditymanaged to find ways of explaining it. Unfortunately,modern biology has no place for it. Althoughxenia (pollen effects on seeds and fruits) has been wellrecognized by most plant biologists and is more alivethan ever, telegony, a different case of the same generalphenomenon in animals, has been met with scepticism(Burkhardt 1979).A search of the literature of cell biology andbiochemistry reveals several plausible mechanisms thatmay form the basis for telegony. Over the past severaldecades, convincing evidence has accumulated for thepenetration of somatic cells by spermatozoa. Thesuccessful achievements in mammalian cell transfectionby foreign DNA and the new findings of foetal DNA inmaternal blood and sperm RNA-mediated non-Mendelianinheritance of epigenetic changes furnish a basis fortelegony. Thus, it is timely to reconsider the case oftelegony.Reasons Why Telegony has been met withScepticismIt was August Weismann who coined the term ‘telegony’.Weismann (1912) was confident that if telegonywas a genuine phenomenon, he could explain it withoutsacrificing his theory of the germ plasm. He suggestedthe possibility that ‘spermatozoa had reached the ovaryafter the first sexual union had occurred and hadpenetrated into certain ova which were still immature.’When these ova mature, amphimixis might occur andcoincide in time with the second coitus to which thesubsequent offspring would be ascribed. But were thisthe explanation, one should sometimes find that offspringwere produced without any second sire at all. Nosuch phenomenon is known among higher animals.Thus, he was sceptical that the phenomenon was real. Inhis book The Germ-Plasm, he placed telegony under theheading ‘doubtful phenomena of heredity’. He thoughtthat the recorded instances of telegony were based on a‘misconception’ and suggested that experiments beconducted to test this question (Weismann 1912). Wenow know that some animals have sperm that live foryears and the classic example is attine ants. But for mostanimals, the sperm has a relatively short life in thefemale genital tract. It is admitted that the life ofthe spermatozoa is limited to a few hours or days at thelongest, and that their powers of fertilizing exist onlyduring their life. None could possibly live to fertilize anegg secreted 1 or 10 years later. Thus, most people thinkthat there is not a theoretical basis for telegony.Realizing that ‘no problem … claims wider attentionat the present time than what is now generally known astelegony’, Ewart (1899) conducted a series of experimentsthat were designed ‘to repeat as exactly aspossible Lord Morton’s experiment’. He had no illusionsthat his work constituted a formal disproof oftelegony but concluded that the striping of Morton’shybrid was best explained as a case of reversion. Inaddition, Daniel (1959) carried out a controlled breedingexperiment with rats and with Drosophila to re-determinethe validity of telegony. No evidence was obtainedto support the view that previous matings can have anygenetic effect on the offspring of later matings.
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Possible Data in Respect of the Existence ofTelegonyMany people thought that Morton’s mare was acoincidence and not a causal connection. As a matterof fact, Darwin (1868) cited nine sources beside LordMorton with respect to the idea of the influence of aprevious sire on the offspring of a female’s later matings.He gave a number of references to other cases, not onlyin horses but also in pigs, dogs and sheep. For example,a sow of Lord Western’s black and white Essex breedwas mated with a wild boar of a and the ‘pigs produced partook in appearance of bothboar and sow, but in some the chestnut colour of theboar strongly prevailed.’ After the boar had long beendead, the sow was mated to a boar of her own black andwhite breed – a kind that is well known to breed verytrue and never to show any chestnut colour – yet fromthis union the sow produced some young pigs that wereplainly marked with the same chestnut tint as in the firstlitter. After Darwin’s death, there appeared otherexamples of telegony in dogs, sheep, birds and human(see Table 1). It should be noted that some dog andsheep breeders, as a rule, still adhere to the idea, andseveral sheep breeders’ associations even refuse toregister lambs whose mother were ever ‘impregnated’by mating with a common ram (Rabaud 1914; Mole2006). Zhelnin (1964) observed the phenomenon oftelegony in rabbits and argued that telegony did notoccur rarely as was previously thought.
Interestingly, a telegony phenomenon, or sire effect,has also been observed in the immune system of mice.When normal females that had borne at least three littersto males made tolerant neonatally were subsequentlymated to normal, non-immune males, the offspringshowed a hyporesponsive phenotype that did not differfrom that of the progeny of fathers made tolerantneonatally. The response of this offspring was significantlylower than the response of mice born to normalfemales mated only to normal mates (Gorczynski et al.1983). This type of observation has also been reportedby Cooper-Willis et al. (1985). In addition, Sobey andConolly (1986) demonstrated that male domestic rabbits,mating after recovering from myxomatosis, maytransmit immunity to progeny born to the female in thenext 7 months, including progeny sired by other maleslacking immunity. This has been confirmed by laterresearches (Williams andMoore 1991; Parer et al. 1995).Although always largely an animal breeders’ issue,telegony is also invoked in ideas about human inheritance(Bynum 2002). A remarkable illustration oftelegony in humans has been observed and recoded byLingard (1884), in which a hypospadian, whose fatherand paternal grandfather were similarly malformed,contracted a marriage with a woman not related to him,who bore him three sons, hypospadians. He died a fewyears after the birth of his three sons. His widow within18 months after his death contracted a second marriage,the husband in this instance not being a hypospadianand having no history of any such deformity in hisfamily. By this marriage, she had four sons, all hypospadians.Sedgwick (1896) believed that this case mighthelp to overcome some of the objections that have beenurged against the influence of a previous marriage on thesubsequent offspring by a second or even by a thirdhusband. Thomson (1908) cited the case of a womanmarried to a deaf-mute, by whom she had one deaf-mutechild. By a second normal husband, she had a deaf-mutechild and then others who were normal. There is alsoevidence for telegony in modern China. For example,two Chinese women gave birth to children after theymarried their second husband. Interestingly, the appearancesof their children closely resemble their firsthusband (Hui 1989; Mei 2000).
Table 1. Cases of telegony in animals and humansSpecies ReferencesHorse Morton (1821); Darwin (1868); Finn (1893)Pig Giles (1821); Darwin (1868); Finn (1893)Sheep Darwin (1868); Cornevin (1891); Finn (1893)Dog Darwin (1868); Cornevin (1891); Spencer (1893); Mole (2006)Bird Darwin (1868); Finn (1893)Human Lingard (1884); Flint (1888); Cornevin (1891); Hui (1989);Redfield (1903); Mei (2000)Mice Gorczynski et al. (1983); Cooper-Willis et al. (1985)Rabbit Zhelnin (1964); Sobey and Conolly (1986); Parer et al. (1995);Williams and Moore (1991)It should be mentioned that to confirm the existenceof telegony, Romanes (1893) pursued investigations onthree different lines: (i) He raised discussions on thesubject in the principal breeders’ and fanciers’ journal ofEngland and America. (ii) He entered into privatecorrespondence with contributors of the largest experienceand also with professional and amateur breedersand fanciers who addressed him directly on the subject.(iii) He started experiments with different animals. Heconcluded that ‘my evidence is enough to prove the factof a previous sire asserting his influence on a subsequentprogeny, although this fact is one of comparatively rareoccurrence.’Previous Explanations for TelegonyTo explain telegony, xenia, reversion, regeneration,prepotency (Mendelian inheritance), graft hybridization,sex-limited inheritance, the effect of use and disuse, theinheritance of acquired characters and many other factspertaining to inheritance, variation and development,Darwin (1868) elaborated his ‘provisional hypothesis ofPangenesis.’ Darwin’s Pangenesis had two basic postulates:first, that the cells of the body throw off gemmules(the embryonic form of our modern genes), which‘circulate freely throughout the system’; and second,that these gemmules are not only self-replicating andcorpuscular but also able to penetrate other nascent cellsand modify their subsequent development. Darwin(1868) maintained: ‘it is certain that [the mother’s]ovaria are sometimes affected by a previous impregnation,so that the ovules subsequently fertilized by adistinct male are plainly influenced in character’. Hebelieved that in case of Morton’s mare it was ‘thediffusion, retention, and action of the gemmulesincluded within the spermatozoa of the [first] male’ thatleft the mare with a ‘quagga taint’ that continued tomanifest itself in her later offspring. Darwin was notvery explicit about this, but he did say more regardingthe effect of pollen on the tissues of the mother plant.Darwin explained that in the case of xenia, ‘thegemmules derived from the foreign pollen do notbecome developed merely in contact with pre-existingcells, but actually penetrate the nascent cells of themother plant’ (Darwin 1868).
In addition to Darwin’s Pangenesis, there is anotherexplanation, which is that the mother is influencedthrough the foetus during pregnancy and that theinfluence manifests on subsequent offspring. That is tosay, the first sire impresses his own offspring with certainof his the offspring of this sireimpresses the mother through the blood- themother, in turn, transmits the peculiarities of the firstsire to her subsequent progeny by means of the bloodelement she has received from her first offspring (Bell1896).n the mucosal cells of the uterus and uterine tube in themouse, rabbit and bat. He maintained that modificationof the mucosal cells could mediate a paternal influenceupon the embryo, and he suggested that this influence,persisting from one pregnancy to the next, could be themechanism of telegony (Kohlbrugge ). Itshould be mentioned that Austin et al. examined sectionsof uteri of the Great Horseshoe bat and the CommonPipistrelle, and their observations strongly suggest thatspermatozoa do in fact enter the mucous membrane ofthe uterine tube in these animals. These observationsare compatible with the possibility that the mucosa ofthe uterine-tube isthmus may be altered in some way byinvading spermatozoa. They concluded that this couldconceivably be brought about by transfer of geneticinformation in a manner analogous to that of bacterialtransformation (Austin ; Austin and Bishop1959). Since the first light-microscopic observationsof the presence of numerous spermatozoa within theuterine mucosal cells, there have been numerous reportsdescribing the penetration of spermatozoa into tissues,both maternal and embryonic (see Table 2). Recently,Brodsky and Ivanov (2009) proposed that spermatozoidsmay penetrate somatic cells in vivo, forming viablechimeric cells, which may survive in the body for a longtime.
The incorporation of exogenous DNA into somatic cellsDarwin (1868) supposed that the gemmules derivedfrom the spermatozoa actually penetrate the nascentcells of the mother animal. It has been suggestedDarwin’s so-called gemmules could include RNAs(particularly mRNA and small RNAs), circulatingDNA, mobile elements, prions or as yet unknownmolecules (Steele et al. 1998; Liu 2005). In our modernlanguage, DNA/RNA may penetrate the somatic tissuesof female animals. Interestingly, Watson et al. (1983)found that within 24–48 h after artificial inseminationwith spermatozoa, in which the DNA had been labelledwith tritiated thymidine, a minimum of 9% of theradioactivity was transported across the uterine walls. Insperm-treated animals, the ovaries, the adrenals and amesenteric lymph node exhibited strikingly large accumulationsof radioactivity. They concluded that thelymphatic system could serve as a route for thedissemination of radioactivity originally associated withspermatozoa deposited in the uterus to maternal tissues.Ledoux and Charles (1972) demonstrated that if miceare killed 1 or 2 h after an I.V. injection of labelledDNA, this DNA can be recovered in the follicle cells ofthe ovary, in the vagina, embryos and tumour cells. Theexogenous labelled DNA has therefore been transportedby the blood and has become absorbed by cells ofdifferent tissues of the organism, without importantdestruction.Table 2. Penetration of spermatozoa into somatic tissues and cells of the female genital tract (incomplete statistics)Species Results ReferencesBat Penetration of spermatozoa into uterine mucosa, fallopian-tube mucosaand oviducal epithelial cellsKohlbrugge (); Austin (1959);Austin and Bishop (1959);Uchida et al. (1984) ; Rasweiler (1987)Mouse Penetration of spermatozoa into uterine mucosa, fallopian-tube mucosa and L cells Kohlbrugge (); Lau (1975)Rabbit Penetration of spermatozoa into uterine mucosa and cervical mucosa Kohlbrugge (); Austin (1960);Sievers-Altermann and Engelbrecht (1990)Rat Penetration of spermatozoa into uterine mucosa Stein-Werblowsky (1973)Hamster Penetration of spermatozoa into fibroblast cells and ovary cells Bendich et al. (1974); Lau (1979)Dog Penetration of spermatozoa into uterine tube and uterine glands Doak et al. (1967); England and Pacey (1998);Rijsselaere et al. (2004)
It has been known for years that naked DNA can bedelivered to cells in vivo and result in gene expression,although the efficiency of gene transfer into skeletal orcardiac muscle is relatively low and variable (Wolff et al.1990). In recent years, it has been demonstrated thatnaked plasmid DNA can be delivered efficiently into cellsin vivo via electroporation, intravascular delivery and tailvein DNA injection (Herweijer andWolff 2003). Bendichet al. (1974) demonstrated that penetration of somaticmammalian cells by spermatozoa occurred after simpleadmixture in culture. With sperm labelled in vivo,autoradiography revealed incorporation of DNA intonuclei of recipient cells, indicating release of DNA afterentrance by sperm. Reid and Blackwell (1967) demonstratedthat the pattern of saline elution of DNAprepared from cultured sheep macrophage cells ischanged after these cells have been exposed to rat sperm.They believed that this altered pattern is because of theincorporation of intact sperm DNA by the macrophage.Holmgren et al. (1999) raised the question whetherDNA can be transferred from one cell to another via thephagocytosis of apoptotic bodies. They demonstratedthat genomic DNA from apoptotic bodies is transferredto the nuclear compartment of phagocytosing cells andthat this transferred DNA is stable over time. Thus, it ispossible that apoptotic bodies, derived from spermatozoa,might be taken up by phagocytosing cells of thematernal tissues. It is now a well-established notion thatmature spermatozoa act as vectors of genetic material,not only for their own genome but also for exogenousDNA molecules. This is called sperm-mediated genetransfer (Spadafora 2007). Although the sperms of thefirst sire cannot be supposed to persist and fertilize ovadischarged long afterwards, it is conceivable that theDNA released by these sperms may persist and influencethe ovaries and the ova, which does not amount tofertilization. During coition, millions of DNA-containingspermatozoa are deposited in the body of the femaleand those not used in fertilization are absorbed by it. Ifthis foreign DNA could incorporate into somatic cellsand influence ova, then later offspring might show thisinfluence in their genetic constitution and therebyfurnish a basis for telegony. Generally speaking, thetransfection efficiency is low in nature. This mightexplain the rare occurrence of telegony.
Presence of foetal cells and foetal DNA in maternal bloodCirculating nucleic acids occur ubiquitously and arebioactive in living organisms. Two sources of circulatingnucleic acids have been considered and discussed in theliterature: dying cell, whether necrotic or apoptotic, andactive nucleic acids release (Stroun et al. 2001; Gahan2008). There is also increasing evidence that bothcirculating cells and free foetal DNA persist inthe maternal circulation after delivery of the foetus(Lissauer et al. 2007). It has been demonstrated thatfoetal cells circulate in the bloodstream of mostpregnant women and may persist for many years, andeven decades, postpartum (Bianchi et al. 1996). Interestingly,male cells have also been identified in femaleswith no history of male children or miscarriage. Onepossibility is the transfer of cells from the women’spartner through sexual intercourse (Lissauer et al.2007). Lo et al. (1997) demonstrated foetal DNA inplasma and serum from healthy pregnant women. Usingquantitative real-time PCR, a surprisingly high meanconcentration (6.2% of total plasma DNA) of foetalDNA was found in maternal plasma. Generally, gestationalage correlates positively with amount of foetalDNA in plasma. Lo et al. (1998) reported foetal DNAconcentrations to be low in the first trimester, rising inthe second and third trimester. During the last 8 weeksof pregnancy, there is a sharp increase in foetal DNA inmaternal plasma. It has been proposed that circulatingfoetal DNA is released from foetal and / or placental cellsundergoing apoptosis (Bischoff et al. 2005). Invernizziet al. (2002) found that cell-free foetal DNA could bepresent in maternal plasma decades after pregnancy.The discovery of circulating foetal DNA in maternalblood not only has disclosed new strategies to performnon-invasive testing for prenatal diagnosis but also shedsa new light on the influence of hybrid embryo on itsmother. We may suppose that the circulating DNAreleased by the hybrid embryo is transferred into themother’s body by circulation and later is incorporatedinto the mother’s subsequent hybrid embryo by anothermale, thus being able to influence the characteristics ofthe subsequent offspring. There is also possibility thatduring pregnancy, whilst the embryo is developing andcontinuously releasing DNA into the maternal bloodstream, the ovaries, and hence the primary oocytes, willstand a good chance of receiving this foetal DNA and sobeing transfected. This can be reinforced by thesubsequent continued flow of foetal DNA in the maternalsystem after the foetus has been delivered (Gahan2008). Hence, there is the possibility of transfectedoocytes being fertilized at a later date by a second male.
Sperm RNA-mediated non-Mendelian inheritanceRecently, Krawetz et al. studied sperm from 10 fertilemen and found that they contained some 3000 differentkinds of mRNA. Some of them coded for proteinsneeded for earl others werepreviously unknown (Ostermeier et al. 2004; Ainsworth2005). Rassoulzadegan et al. (2006) demonstrated thatthe genotypically wild-type (Kit+/+) offspring of heterozygousKit(tm1 Alf) parents displayed the white spotscharacteristic of Kit-mutant animals. The modifiedphenotype was associated with decreased Kit mRNAlevels and accumulation of non-polyadenylated RNAmolecules. The sustained transcriptional activity at thepost-meiotic stages resulted in the accumulation ofRNA in spermatozoa. They were able to reproduce thephenotype by microinjection into fertilized eggs of eithertotal RNA from Kit(tm1 Alf) heterozygotes or Kit-specificmicroRNAs, both of which induced a heritable whitetailphenotype. This study of spotted mice suggestedthat as well as contributing their usual cargoes of DNA,mammalian sperm and eggs might also transmit heritablegenetic information in the form of RNA. It has beensuggested that under certain conditions, spermatozoacan translate their mRNAs de novo and that spermatozoaRNA can potentially affect phenotypic traits inoffspring (Miller 2007).Thirty years ago, Steele presented a modern molecularview of Darwin’s Pangenesis in his ‘somatic selection’hypothesis, which states that mutant somatic information,if selected sufficiently for expression, will betransmitted to the germline in the form of RNAcaptured by endogenous retroviral vectors. Once in thegermline, the RNA will be transcribed to DNA byreverse transcriptase and become integrated into thegermline DNA (Steele 1979; Steele et al. 1998).Recently, it has been fully confirmed that RNA canact as a template for DNA synthesis in the reversetranscription of retroviruses and retrotransposons andguide genome rearrangement (Storici et al. 2007;Nowacki et al. 2008). More recently, Spadafora (2008)described the phenomenon of sperm-mediated ‘reverse’gene transfer (SMRGT) and believed that such amechanism would lead to the generation and non-Mendelian propagation of new genetic information bymature spermatozoa, independent from the informationcarried in the genome. Thus, plausible mechanisms nowexist to explain the sire effects claimed to occur in thepast under the phenomenon of telegony. Spermatozoaappear able to penetrate somatic tissues and could intheory deliver RNA to somatic cells where it could haveregulatory and genetic effects. Further, retroviruses orretrotransposons may facilitate the transfection andreverse transcription of mRNA into cDNA leading totheir integration into the female ovum genome and thusexpression in the progeny.
我还是去找个翻译器吧
ConclusionTelegony is the belief that the sire first mated to afemale will have an influence upon some of thatfemale’s later offspring by another male. AlthoughDarwin and many famous nineteenth-century biologistsheld strong belief in telegony, it has been met withscepticism because of Weismann’s unfavourable commentsand negative results obtained in several testexperiments. There are some data which raise thepossible existence of telegony, although at present,there is no good experimental evidence. There are alsopossible molecular explanations which could be arguedfor this phenomenon that has not definitively beenproven. The time has come when further progress inour understanding of heredity requires that we reconsiderthe case of telegony.AcknowledgementsI am deeply indebted to Dr Edward J. Steele for providing me withvaluable research materials and for his enthusiastically encouragement.I am also very grateful to the referees and editors for their valuablecomments and suggestions.Conflict of interestNone of the authors have any conflict of interest to declare.Author contributionsYongsheng Liu has written the manuscript and has participated in allphases.ReferencesAinsworth C, 2005: The secret life of sperm. Nature 436, 770–771.Austin CR, 1959: Entry of spermatozoa into the fallopian-tubemucosa. Nature 183, 908–909.Austin CR, 1960: Fate of spermatozoa in the female genitaltrack. J Reprod Fertil 1, 151–156.Austin CR, Bishop MWH, 1959: Presence of spermatozoa inthe uterine-tube mucosa of bats. J Endocrinol 18, R7–R8.Bell AL, 1896: The influence of a previous sire. J Anat Physiol30, 259–274.Bendich A, Borenfreund E, Sternberg SS, 1974: Penetration ofsomatic mammalian cells by sperm. Science 183, 857–859.Bianchi DW, Zickwolf GK, Weil GJ, Sylvester S, DeMariaMA, 1996: Male fetal progenitor cells persist in maternalblood for as long as 27 years postpartum. Proc Natl AcadSci USA 93, 705–708.Bischoff FZ, Lewis DE, Simpson JL, 2005: Cell-free fetal DNAin maternal blood: kinetics, source and structure. HumReprod Update 11, 59–67.Brodsky SV, Ivanov I, 2009: Spermatozoa-somatic cell fusion– A mechanism for micro-chimerism formation. J TheorBiol 259, 190–192.Burkhardt RW, 1979: Closing the door on Lord Morton’sMare: the rise and fall of telegony. Stud Hist Biol 3, 1–21.Bynum B, 2002: Discarded diagnoses – telegony. Lancet 359,1256.Cooper-Willis CA, Olson JC, Brewer ME, Leslie GA, 1985:Influence of paternal immunity on idiotype expression inoffspring. Immunogenetics 21, 1–10.Cornevin CH, 1891: Traite de Zootechnie Generale. Bailliere,Paris.Daniel JC, 1959: Telegony retested. J Hered 50, 274–298.Darwin C, 1868: The Variation of Animals and Plants underDomestication. John Murray, LondonDoak RL, Hall A, Dale HE, 1967: Longevity of spermatozoa in
the reproductive tract of the bitch. J Reprod Fertil 13, 51–58.England GCW, Pacey AA, 1998: Transportation and interactionof dog spermatozoa within the reproductive tract of thebirch: comparative aspects. Centre Reprod Biol 3, 57–84.Ewart JC, 1899: Experimental investigation on telegony.Nature 60, 330–333.Finn F, 1893: Some facts of telegony. Nat Sci 3, 436–446.Flint A, 1888: A Text-Book of Human Physiology. D.Appleton & Co, New York, p. 797Gahan PB, 2008: Circulating nucleic acids in plasma andserum: roles in diagnosis and prognosis in diabetes andcancer. Infect Disord Drug Targets 8, 100–108.Giles D, 1821: Particulars of fact, nearly similar to that relatedby Lord Morton. Philos Transact R Soc 111, 23–24.Gorczynski RM, Kennedy M, Macrae S, Ciampi A, 1983:A possible maternal effect in the abnormal hyporesponsivenessto specific alloantigens in offspring born to neonatallytolerant fathers. J Immunol 131, .Herweijer H, Wolff JA, 2003: Progress and prospects: nakedDNA gene transfer and therapy. Gene Ther 10, 453–458.Holmgren L, Szeles A, Rajnavolgyi E, Folkman J, Klein G,Ernberg I, Falk KI, 1999: Horizontal transfer of DNA bythe uptake of apoptotic bodies. Blood 93, .Hui L, 1989: Why does my newborn daughter resemble myformer husband? Family, 47.Invernizzi P, Biondi ML, Battezzati PM, Perego F, Selmi C,Cecchini F, Podda M, Simoni G, 2002: Presence of fetalDNA in maternal plasma decades after pregnancy. HumGenet 110, 587–591.Kohlbrugge JHF, 1910: Der Einfluss der Spermatozoiden aufden Uterus. Ein Beitrag zur Telegonie. Z Morphol Anthropol12, 359–368.Kohlbrugge JHF, 1913: Die Verbreitung der Spermatozodenim weiblichen Korper und m befruchteten Ei. Arch EntwicklungsmechOrg 35, 165–188.Lau LCT, 1975: Production of lobules in mouse L cellspenetrated with hamter sperms. Science 190, 684–686.Lau LCT, 1979: Sperm-cell multinucleate in Chinese ovarycells penetrated with rat spermatozoa. Cell Mol Biol 24,135–142.Ledoux L, Charles P, 1972: Fate of exogenous DNA inmammals. In: Ledoux L (ed.), Uptake of InformativeMolecules by Living Cells. North-Holland PublishingCompany Ltd, London, pp. 397–413.Lingard A, 1884: Hereditary transmission of hypospadias andits transmission by indirect atavism. Lancet 123, 703.Lissauer D, Piper K, Moss P, Kilby M, 2007: Persistence offetal cells in the mother: friend or foe? BJOG 114, 1321–1325.Liu Y-S, 2005: Reversion: going back to Darwin’s works.Trends Plant Sci 10, 459–460.Liu Y-S, 2008: A new perspective on Darwin’s Pangenesis. BiolRev 83, 141–149.Lo YM, Corbetta N, Chamberlain PF, Rai V, Sargent IL,Redman CW, Wainscoat JS, 1997: Presence of fetal DNA inmaternal plasma and serum. Lancet 350, 485–487.Lo YM, Tein MS, Lau TK, Haines CJ, Leung TN, Poon PM,
Wainscoat JS, Johnson PJ, Chang AM, Hjelm NM, 1998:Quantitative analysis of fetal DNA in maternal plasma andserum: implications for noninvasive prenatal diagnosis. AmJ Hum Genet 62, 768–775.Mei D, 2000: The son who resembles his mother’s formerhusband. Healthy Life 11, 37.Miller D, 2007: Spermatozoa RNA as reservoir, marker andcarrier of epigenetic information: implications for cloning.Reprod Domest anim 42(Suppl), 2–9.Mole, 2006: How we know I: strange dreams. J Cell Sci 119, 1–2.Morton L, 1821: A communication of a singular fact in naturalhistory. Philos Transact R Soc 111, 20–22.Nowacki M, Vijayan V, Zhou Y, Schotanus K, Doak TG,Landweber LF, 2008: RNA-mediated epigenetic programmingof a genome-rearrangement pathway. Nature 451,153–159.Ostermeier GC, Miller D, Huntriss JD, Diamond MP,Krawetz SA, 2004: Delivering spermatozoan RNA to theoocyte. Nature 429, 154.Parer I, Sobey WR, Conolly D, Morton R, 1995: Siretransmission of acquired resistance to myxomatosis. AustJ Zool 43, 459–465.Rabaud E, 1914: Telegony. J Hered 5, 389–399.Rassoulzadegan M, Grandjean V, Gounon P, Vincent S,Gillot I, Cuzin F, 2006: RNA-mediated non-Mendelianinheritance of an epigenetic change in the mouse. Nature441, 469–474.Rasweiler JJ, 1987: Prolonged receptivity to the male and thefate of spermatozoa in the female black mastiff bat. J reprodFertil 79, 643–654.Redfield CL, 1903: The Control of Heredity. Monarch BookCo, Chicago and Philadephia.Reid BL, Blackwell PM, 1967: Evidence for the possibility ofnuclear uptake of polymerized deoxyribonucleic acid ofsperm phagocytosed by macrophages. Aust J Exp Biol MedSci 45, 323–326.Rijsselaere T, Soom A, Cruchten SV, Coryn M, Gortz K,Maes D, de Kruif A, 2004: Sperm distribution in the genitaltract of the birth following artificial insemination inrelation to the time of ovulation. Reproduction 128, 801–811.Romanes GJ, 1893: An Examination of Weismannism. Green& Co, London, Longmans, pp. 191–209.Sedgwick W, 1896: Notes on the influence of heredity indisease. Br Med J 1, 458–462.Sievers-Altermann R, Engelbrecht DZ, 1990: Entry of spermatozoainto the cervical mucosa and transmission of theAIDS virus. S Afr Med J 77, 319.Sobey WR, Conolly D, 1986: Myxomatosis: non-geneticaspects of resistance to myxomatosis in rabbits, Oryctolaguscuniculus. Aust Wildl Res 13, 177–187.Spadafora C, 2007: Sperm-mediated gene transfer: mechanismsand implications. Spermatology 65, 459–467.
Spadafora C, 2008: Sperm-mediated ‘reverse’ gene transfer:a role of reverse transcriptase in the generation of newgenetic information. Hum Reprod 23, 735–740.Spencer H, 1893: Professor Weismann’s theories. ContempRev 63, 743–760.Steele EJ, 1979: Somatic Selection and Adaptive Evolution: Onthe Inheritance of Acquired Characters. Williams-Wallace,Toronto.Steele EJ, Lindley RA, Blanden RV, 1998: Lamarck’s Signature:How Retrogenes are Changing Darwin’s NaturalSelection Paradigm. Perseus Books, Massachusetts.Stein-Werblowsky R, 1973: Penetration of spermatozoa intothe uterine mucosa. Int J Fertil 18, 74–80.Storici F, Bebenek K, Kunkel TA, Gordenin DA, ResnickMA, 2007: RNA-templated DNA repair. Nature 447, 338–341.Stroun M, Lyautey J, Lederrey C, Olson-Sand A, Anker P,2001: About the possible origin and mechanisms of circulatingDNA: Apoptosis and active DNA release. Clin ChimActa 313, 139–142.Thomson JA, 1908: Heredity. John Murray, London, pp. 143–163Uchida TA, Mori T, Oh YK, 1984: Sperm invasion of theoviducal mucosa, fibroblastic phagocytosis and endometrialsloughing in the Japanese greater horseshoe bat Rhinolophusferrumequinum Nippon. Cell Tissue Res 236, 327–331.Watson JG, Carroll J, Chaykin S, 1983: Reproduction in mice:the fate of spermatozoa not involved in fertilization. GameteRes 7, 75–84.Weismann A, 1912: The Germ-Plasm – A Theory of Heredity.The Walter Scott Publishing Co., LTD, New York, pp. 383–386.Williams CK, Moore RJ, 1991: Inheritance of acquiredimmunity to myxomatosis. Aust J Zool 39, 307–311.Wolff JA, Malone RW, Williams P, Chong W, Acsadi G, JaniA, Felgner PL, 1990: Direct gene transfer into mouse musclein vivo. Science 247, .Zhelnin VA, 1964: The phenomenon of telegony in rabbits.Krolikovodstvo Zvehovodstvo 7, 20–21.Submitted: 14 Apr 2010; Accepted: 2 June 2010Author’s address (for correspondence): YS Liu, Department ofBiochemistry, University of Alberta, Edmonton, Alberta T6G 2H7,Canada. E-mail:
如何破？！
【作者】Liu YS； 　　【题名】Telegony, the Sire Effect and non-Mendelian Inheritance Mediated by Spermatozoa: A Historical Overview and Modern Mechanistic Speculations. 　　【中文题名】先父遗传，父辈的影响和非孟德尔遗传通过精子介导：一个历史回顾与现代机理的思考。 注意：机器翻译内容可能有误，仅供参考！ 　　【出处】Reprod Domest Anim .2010VN: 　　【相关链接】 SCI期刊查收 Google 引文 Pubmed相关文献 　　【通道揭示】 馆际互借通道 PUBMED 电子资源通道揭示 国内馆藏资源通道揭示
SCI在哪？。。。
第一篇： EI检索 Accession number: 96 Effects of presintering temperature and heating rate on the physical and mechanical properties of 引用
的话：SCI在哪？。。。
搜索了这个 作者 刘用生
刘用生，副教授，回国留学人员，现任河南科技学院园艺研究所所长应该是此人
植物学博士生
LZ右上角搜下…讨论过的…搬运工表示找不到了
的话：LZ右上角搜下…讨论过的…搬运工表示找不到了回复21楼 是这个吗？好短...
植物学博士生
的话：回复21楼 是这个吗？好短...不是这个…再找找……
的话：不是这个…再找找……实在找不到....
留学加拿大的访问学者刘用生副教授在二号合五教室为我校师生做了题为“从钱学森的嫁接改造学到达尔文的泛生论”的学术报告。会议由园林学院园艺系主任周俊国博士主持，教师学生代表200余人听取了报告。
此次报告的内容为刘用生老师在留学期间的研究成果。在加拿大期间，他刻苦钻研，通过查阅大量文献资料和严密的分析判断，为达尔文的泛生论提供了新的证据。此外，他在嫁接杂交与获得性遗传方面也取得了新的突破，对其机理提出了新的见解。相关研究发表在Biological Reviews（IF 8.833）、EMBO（IF 7.0）、Trends in plant Science（IF 8.0）等刊物上。其研究受到了许多国内外著名学者的高度评价。原英国皇家学会副会长、剑桥大学著名遗传与发育学家Anne Mclaren认为，刘用生的“嫁接杂交”研究具有“里程碑”的意义。
刘用生老师是园林学院副教授，于2002年2月作为访问学者赴加拿大阿尔伯特大学留学至今。他先后在国内《遗传》、《园艺学报》、《生物学通报》等刊物上发表学术论文50余篇，其中在SCI刊物上共发表16篇论文（个人独著12篇），累计被引用500多次刘用生博客地址：
植物学博士生
从中段看起…本来不是讨论这篇纱布文章的……应该还有哪个地方也讨论过…找不到了PS：你可以读读这篇文章查查他里面的“证据”有多不靠谱就知道了……PPS：这大叔归国后好像走向一条…莫名其妙的路线了
植物分子生物学博士
SCI IF低的期刊很多比国内期刊还不靠谱。
智能科学专业
楼主没必要复制全文的。。。。留个标题就行了。。。猪的签名：——微笑的猪头——帅气非凡！——
的话：SCI IF低的期刊很多比国内期刊还不靠谱。进了刘用生博客，看到刚才他还在线索性直接给他留了言，来回复此贴，估计没这个面子吧..刘用生的的对口专业好像是植物遗传和嫁接
植物分子生物学博士
的话：进了刘用生博客，看到刚才他还在线索性直接给他留了言，来回复此贴，估计没这个面子吧..刘用生的的对口专业好像是植物遗传和嫁接 我会告诉你他还发过“利用磁场能定向突变作物”的文章么？
这参考文献里居然参考个《家庭》杂志，无语……Hui L, 1989: Why does my newborn daughter resemble myformer husband? Family, 47.Mei D, 2000: The son who resembles his mother’s formerhusband. Healthy Life 11, 37.
还有尿道下裂的那个案例，本来也不一定是遗传病。与后父生的孩子有这个病不能诱来证实先父遗传。
人家作者自己都说“no good experimental evidence”啦，就不用纠结那几个19世纪的案例了。
的话：我会告诉你他还发过“利用磁场能定向突变作物”的文章么？虽然是刘写的 ，本文中我看过他举得案例有些是比较老的，而且不少都看到过Brodsky SV, Ivanov I, 2009: Spermatozoa-somatic cell fusion– A mechanism for micro-chimerism formation. J TheorBiol 259, 190–192.这个文献目测是他文中最新最奇葩的布罗德斯基和伊万诺夫（）Spermatozoa-somatic cell fusion-A mechanism for microchimerism formation（ 精子的体细胞融合，微嵌合体的形成机制）一文提出：游动精子可以穿透体细胞在体内，形成可行的嵌合体细胞，这可能会在体内长期存活时间...(这个论文万方医学网好像也有，但是需要职称认证很复杂 看来只有去谷歌一下了).这个比怀孕产生的微嵌合体更夸张啊，精子都能直接进入体细胞产生嵌合体了
的话：从中段看起…本来不是讨论这篇纱布文章的……应该还有哪个地方也讨论过…找不到了PS：你可以读读这篇文章查查他里面的“证据”有多不靠谱就知道了……PPS：这大叔归国后好像走向一条…莫名其妙的路线了找到了这个《Spermatozoa-somatic cell fusion-A mechanism for microchimerism formation》这个文摘The recent advantages in molecular biology and genetics revealed the presence of cells with XY-genotype in women, called microchimerism. Currently microchimerism is intensively studied as a possible mediator in autoimmune diseases. We propose that spermatozoids may interact with somatic cells in vivo, forming viable cells containing male chromosomes and surviving in the body for a long time. Chimeric cells may be more susceptible for malignant transformations and give rise to different tumors. ......游动精子在体内，形成含有男性染色体和可行的细胞在体内存活很长一段时间另一个文摘 还是来自《Spermatozoa-somatic cell fusion-A mechanism for microchimerism formation》一文Spermatozoa can enter the separated blastomeres of 8- and 16-cell stage embryos, the cells of blastulae and even somatic cells of the oesophagus wall of an adult sea urchin, under certain conditions. In the presence of egg jelly solution, the rate of entrance of spermatozoa is remarkably increased. In the case of the blastomere of 8-cell stage embryos, characteristic cytoplasmic protrusions are formed at the sites of sperm entry, in succession to the formation of the cytoplasmic bulge. These protrusions elongate until 4 min after insemination, and then they retract gradually. The nucleus of penetrated sperm swells and decondenses to form a pronucleus. In most cases, the pronucleus seems to fuse with the preexisting diploid nucleus of the blastomere. When the dissociated oesophagus cells were inseminated, a certain type of the cells was found to fuse with spermatozoa, although the percentage of fused cells was very low.在大多数情况下，原核似乎与已经存在的二倍体核的卵裂球融合。游离食管细胞进行人工授精时，发现某些类型的细胞与精子融合艹 这还真能进去 Sperm 岂不是毒品
既然刘老师都回复了，那我就发一下吧 引用
的话：我会告诉你他还发过“利用磁场能定向突变作物”的文章么？
既然刘老师都回复了，那我就发一下吧 我怎么看怎么觉得“那么多的报道不可能全都是伪造的”这句话有什么地方不对。看过谣言粉碎机的人都知道谣言有多么厉害吧。不过还好他说了“再婚夫妇不用担心”，冲着这句话，就没啥理由“非处不娶”了。
先父遗传都成日经了。
35楼的这个伊万诺夫和布罗德斯基所写论文 花了好多办法 搞出来了，而且这个论文很神秘 还不随便给人看也不允许复制，所以我花了好久时间用爪把他再完成 ，但绝对是原文，国内公布版首发....相关的其他论文还有一个，但是没写作者，按后一篇文中Experimental theory，貌视GAY都能中标
35楼的这个伊万诺夫和布罗德斯基所写论文 花了好多办法 搞出来了，而且这个论文很神秘 还不随便给人看也不允许复制，所以我花了好久时间用爪把他再完成 ，但绝对是原文，国内公布版首发....相关的其他论文还有一个，但是没写作者，按后一篇文中Experimental theory，貌视GAY都能中标辛苦了
这是一篇综述。我查看了这个杂志的当年当期的目录。发现这篇文章是被归类到综述的类别而非“论文”。请注意，综述与论文的差别。具体差异请自行百度。因为这是综合表述这一领域的现有的、情报性的东西。所以这里面都是别人的观点。
35楼的这个伊万诺夫和布罗德斯基所写论文 花了好多办法 搞出来了，而且这个论文很神秘 还不随便给人看也不允许复制，所以我花了好久时间用爪把他再完成 ，但绝对是原文，国内公布版首发....相关的其他论文还有一个，但是没写作者，按后一篇文中Experimental theory，貌视GAY都能中标辛苦了，还没时间看完全文，太长了。不过有一个疑问，我记得生物学里有提到只有生殖细胞能进行生殖遗传，精子能融合入体细胞不等于能完成精子遗传物质的遗传，被融入的体细胞除非能变成生殖细胞，否则不具备遗传作用。
的话：这是一篇综述。我查看了这个杂志的当年当期的目录。发现这篇文章是被归类到综述的类别而非“论文”。请注意，综述与论文的差别。具体差异请自行百度。因为这是综合表述这一领域的现有的、情报性的东西。所以这里面都是别人的观点。 此说法+1。这只是一篇Review Article而已，被网上发表到一本期刊上不代表它的可靠性。况且再看作者的reference，这只说明了很糟糕的peer review。看文章最重要还是要保持冷静头脑和独立思考能力。没人能保证将来“先父遗传”会被学术性质地承认，但可以肯定的一点，需要依赖的是实验数据，而不是Review。p.s.我至今不相信“先父遗传”，但我期待有文献改变我这个想法时刻的到来，但肯定不是现在这一篇
的话：此说法+1。这只是一篇Review Article而已，被网上发表到一本期刊上不代表它的可靠性。况且再看作者的reference，这只说明了很糟糕的peer review。看文章最重要还是要保持冷静头脑和独立思考能力。没人能保证将来“先父遗传”会被学术性质地承认，但可以肯定的一点，需要依赖的是实验数据，而不是Review。p.s.我至今不相信“先父遗传”，但我期待有文献改变我这个想法时刻的到来，但肯定不是现在这一篇总算识货之人出现了。
此说法+1。这只是一篇Review Article而已，被网上发表到一本期刊上不代表它的可靠性。况且再看作者的reference，这只说明了很糟糕的peer review。看文章最重要还是要保持冷静头脑和独立思考能力。没人能保证将来“先父遗传”会被学术性质地承认，但可以肯定的一点，需要依赖的是实验数据，而不是Review。p.s.我至今不相信“先父遗传”，但我期待有文献改变我这个想法时刻的到来，但肯定不是现在这一篇1.的确他用的是别人的文献来做指引构思，单他的文中，最难反驳的就是那个 尿道口开裂的遗传病案例，指的是某女嫁给患有尿道口开裂遗传病的人后生下几个孩子都有该遗传病，此后该女再嫁正常男生出的子代还是这样。2.还有的就是《Spermatozoa-somatic cell fusion-A mechanism for microchimerism formation》（ 精子的体细胞融合，微嵌合体的形成机制）这个文章我已经放在3.刘用生提出的这个理念他是把他定义为在雌性的首交之上，这个问题我也反问过他就是看了他的那些文献，即使精子和体细胞能融合，这和首交有什么关联？！他也没给出合理的解释...这个词的定义在早期西方指的是母性动物的前任或多任交配对象，谷歌搜索维基百科和其他链接大部分是这样的解释，单也有解释中说道是指第一次而产生，比如这个词的名词解释中就有写道，生物学上的定义指的首次交配影响到该母性动物与以后其他公性交配时子代所产生的遗传特征像首次公性叫做先父遗传...关键这个定义是从何而来，虽然这个话题有关生物学家支持和反对，但是辩论出发点不同，有些提到的是前任或多任 有些提到的则是首次.....生物学上有这样的首次定义吗？！这样cn都每天躲着精子走了，而且新鲜的精斑都不行。特异性的初次免疫应答，能把抗原体转化成自身抗原时只发生在胚胎期或者胎儿期 b细胞未成熟时，即使说道细胞学也符合不上啊。所以我觉得刘用生和其他部分生物学家 的首交理论和夸浮，直接跳跃了很多东西。这个理论如果成立那不光和遗传学大冲突，还大影响到了免疫 细胞 转基因学术理论颠覆。4.刘用生的东西中案例胜于雄辩的，包括所有的生物现象，重复案例和多出现案例，但目前观察到的许多案例，发现一个现象不少出现在孕后母体，如果一定要理论假设成立 那把他拆分开三部分来构思---孕后母体（微嵌合体“长子”细胞进入次子生殖细胞 ）----精子融合体细胞（即使进入 能否影响到生殖性细胞 而且理论也是很颠覆的）-----初次进入子宫的精子（是否会产生基因整合并保存 这个最颠覆）5.以上的理论都是很不完善的，前提条件要推翻多少原生物学原基础才能得到此荒谬理论，也许生物计算机的出现和更新才能解释其中的原委。
对所谓“先父遗传”无爱......
最具讨论的一个话题《Spermatozoa-somatic cell fusion-A mechanism for microchimerism formation》中提出的 ，嵌合体理论，活动的精子能够融合体细胞形成含有男性Y染色体的细胞，可能长时间存活于体内，同时作者伊万诺夫构成了以下4个环节的理论-----1.怀孕后母体内含有子代细胞（这个已经被证实）-----2.曾经提出的一个构思，有兄长（哥）的女性体内含有兄长的Y基因染色体抗体，这个论据被今年五月荷兰莱顿大学医学中心的Miranda Dierselhuis 在12个新生儿上所证明-----3.微嵌合体机制只在上述两种情况下发生的理论变的不完全可靠，在没有怀过孕的部分妇女（同时也没有兄长
因此不存在胎儿母体细胞转移的可能）也查到了y染色体细胞----4.其他相关精子融合体细胞的相关文献报道
感谢您的邀请由于英文水平有限不能读懂这篇论文尿道口开裂遗传病有可能是遗传，也有可能是受病毒感染生殖细胞先父遗传的只是病毒，而非基因首交可能是借用了某些人一生只会患一次的病影响，只有第一次有影响但
的话：感谢您的邀请由于英文水平有限不能读懂这篇论文尿道口开裂遗传病有可能是遗传，也有可能是受病毒感染生殖细胞先父遗传的只是病毒，而非基因首交可能是借用了某些人一生只会患一次的病影响，只有第一次有影响但这个用先父遗传是病毒来比喻的话，就难以说通了首先您说的首交理论构思成患病是自己的观点，有些病生过一次后不再生是因为体内有了这个免疫抗体。 而ml则不一样 不管是女性不管对任何男人都会产生抗精子抗体，哪怕里面只有一点点摩擦，都会造成理论上的抗精子抗体（理论上的那种是无法检测出来的），但是抗精子抗体在体内不接触同抗原的情况下，3-4个月就会消失，他不是长生抗体（毕竟这是要拿来怀孕的），国外有两种理论一种是前任遗传一种是第一任遗传，后者的说法来自法国人le Dentec1899年写的新达尔文理论，当时并没有科学家认同他的意见，这个理论被西方抛弃，但是在俄罗斯被敷衍下来，因为俄罗斯的斯拉夫雅利安人文化上追求这些东西他们追求的是处女的纯洁和灵魂（还像后期这些东西都被改写进了俄罗斯的教堂书籍），而在西方的一些文章中之处Dentec说的一些列子和自己开始的观点指的的第一次受精的影响，但他后期和美国人flint又做了另一些观点，就慢慢发展成了现在的说法，但是首交理论再西方不管是支持者还是反驳者都是百家争鸣，因为现实中毕竟也有案例是和该理论是矛盾的。在欧洲提到先父遗传都会提到Dentec和flint，尤尔特和魏斯曼 他们去查生物学上这个说法的来源而这里基本没有。 动物的毛色遗传的确很复杂，但是也有一些案例在欧洲变矛盾了，先父遗传是返祖现象的体现说这个说法不正确比如什么爱沙尼亚的无角羊和有角羊的杂交现象，后面无角母羊和同类公羊交配 的子代竟然还带着先父的羊角，上面说的尿道口开裂案例就是其中一个，俄罗斯有一些实验 得出的这个结论是精子融合的过程发生在 生发 上皮
能够进入未成熟的卵细胞（未成熟的卵细胞表层细胞质也还没成熟容易进入）我觉得最关键的问题在畜牧业，这个行业是最支持这个理论的，畜牧业的一些人士将这个理论运用到了动物的繁殖，比较常年在畜牧业的专家 亲生经验比理论更切实际让我感到最奇怪的是有些生物学家一直无法重复出这些东西，但是有些人却视这个现象视为频繁见贯不怪还能得出自己的看法和思路和述说自己观察到的许多案例来举例，就好像先父时刻在发生。
我无法证明先父遗传是否患病。但如果只是像或者相同的第一任或者前任部分特征遗传给下一代，那他的遗传基因会藏在哪里，是受着患病并遗传只是我的一种猜测。并非直接将基因遗传而是男方的影响，造成本身的一些隐性基因得到支持变位显性基因遗传。而并非男方的基因直接造成。在畜牧业更难说清，因为很多原因造成。因为动物的怀孕期通常比较短，并且怀孕后是否有再次交配而产生影响。而无角羊本身是否纯种，是否含有角的隐性基因。现在很多用于做实验的动物父辈或者祖父辈都可能是杂交而产生造成很多现象频繁出现，但却很难人为复制。我只是非专业人士理解
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