Journal articles: 'Replicating'

1

Coffman, Lucas C., Muriel Niederle, and Alistair J. Wilson. "A Proposal to Organize and Promote Replications." American Economic Review 107, no. 5 (May 1, 2017): 41–45. http://dx.doi.org/10.1257/aer.p20171122.

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We make a two-pronged proposal to (i) strengthen the incentives for replication work and (ii) better organize and draw attention to the replications that are conducted. First we propose that top journals publish short “replication reports.” These reports could summarize novel work replicating an existing high-impact paper, or they could highlight a replication result embedded in a wider-scope published paper. Second, we suggest incentivizing replications with the currency of our profession: citations. Enforcing a norm of citing replication work alongside the original would provide incentives for replications to both authors and journals.

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Robinson, D. R., and K. Gull. "The configuration of DNA replication sites within the Trypanosoma brucei kinetoplast." Journal of Cell Biology 126, no. 3 (August 1, 1994): 641–48. http://dx.doi.org/10.1083/jcb.126.3.641.

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The kinetoplast is a concatenated network of circular DNA molecules found in the mitochondrion of many trypanosomes. This mass of DNA is replicated in a discrete "S" phase in the cell cycle. We have tracked the incorporation of the thymidine analogue 5-bromodeoxyuridine into newly replicated DNA by immunofluorescence and novel immunogold labeling procedures. This has allowed the detection of particular sites of replicated DNA in the replicating and segregating kinetoplast. These studies provide a new method for observing kinetoplast DNA (kDNA) replication patterns at high resolution. The techniques reveal that initially the pattern of replicated DNA is antipodal and can be detected both on isolated complexes and in replicating kDNA in vivo. In Trypanosoma brucei the opposing edges of replicating kDNA never extend around the complete circumference of the network, as seen in other kinetoplastids. Furthermore, crescent-shaped labeling patterns are formed which give way to labeling of most of the replicating kDNA except the characteristic midzone. The configuration of these sites of replicated DNA molecules is different to previous studies on organisms such as Crithidia fasciculata, suggesting differences in the timing of replication of mini and maxicircles and/or organization of the replicative apparatus in the kinetoplast of the African trypanosome.

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Kelly, Clint D. "Rate and success of study replication in ecology and evolution." PeerJ 7 (September 10, 2019): e7654. http://dx.doi.org/10.7717/peerj.7654.

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The recent replication crisis has caused several scientific disciplines to self-reflect on the frequency with which they replicate previously published studies and to assess their success in such endeavours. The rate of replication, however, has yet to be assessed for ecology and evolution. Here, I survey the open-access ecology and evolution literature to determine how often ecologists and evolutionary biologists replicate, or at least claim to replicate, previously published studies. I found that approximately 0.023% of ecology and evolution studies are described by their authors as replications. Two of the 11 original-replication study pairs provided sufficient statistical detail for three effects so as to permit a formal analysis of replication success. Replicating authors correctly concluded that they replicated an original effect in two cases; in the third case, my analysis suggests that the finding by the replicating authors was consistent with the original finding, contrary the conclusion of “replication failure” by the authors.

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van ’t Wout, Angélique B., Hetty Blaak, Leonie J. Ran, Margreet Brouwer, Carla Kuiken, and Hanneke Schuitemaker. "Evolution of Syncytium-Inducing and Non-Syncytium-Inducing Biological Virus Clones in Relation to Replication Kinetics during the Course of Human Immunodeficiency Virus Type 1 Infection." Journal of Virology 72, no. 6 (June 1, 1998): 5099–107. http://dx.doi.org/10.1128/jvi.72.6.5099-5107.1998.

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ABSTRACT To investigate the temporal relationship between human immunodeficiency virus type 1 (HIV-1) replicative capacity and syncytium-inducing (SI) phenotype, biological and genetic characteristics of longitudinally obtained virus clones from two HIV-1-infected individuals who developed SI variants were studied. In one individual, the emergence of rapidly replicating SI and non-syncytium-inducing (NSI) variants was accompanied by a loss of the slowly replicating NSI variants. In the other subject, NSI variants were always slowly replicating, while the coexisting SI variants showed an increase in the rate of replication. Irrespective their replicative capacity, the NSI variants remained present throughout the infection in both individuals. Phylogenetic analysis of the V3 region showed early branching of the SI variants from the NSI tree. Successful SI conversion seemed a unique event since no SI variants were found among later-stage NSI variants. This was also confirmed by the increasing evolutionary distance between the two subpopulations. At any time point during the course of the infection, the variation within the coexisting SI and NSI populations did not exceed 2%, indicating continuous competition within each viral subpopulation.

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Quintini, G., K. Treuner, C. Gruss, and R. Knippers. "Role of amino-terminal histone domains in chromatin replication." Molecular and Cellular Biology 16, no. 6 (June 1996): 2888–97. http://dx.doi.org/10.1128/mcb.16.6.2888.

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Simian virus 40 minichromosomes were treated with trypsin to specifically remove the amino-terminal histone domains (tails). Trypsin treatment does not affect the spacing and the number of nucleosomes on minichromosomes but indices a more extended conformation, as shown by the reduced sedimentation coefficient of trypsinized minichromosomes compared with the untreated controls. Trypsinized minichromosomes replicate more efficiently than control minichromosomes in in vitro replication assays. The increased template efficiency appears to be due to higher rates of replicative fork movement. In vitro replication in the presence of protein-free competitor DNA shows that replicating trypsinized minichromosomes do not lose nucleosomes and replicating competitor DNA does not gain nucleosomes. This finding suggests that tailless nucleosomes are transferred from the unreplicated prefork stem to replicated DNA branches and excludes a participation of the basic histone domains in nucleosome transfer.

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Walker, Richard M., Gene A. Brewer, M. Jin Lee, Nicolai Petrovsky, and Arjen van Witteloostuijn. "Best Practice Recommendations for Replicating Experiments in Public Administration." Journal of Public Administration Research and Theory 29, no. 4 (August 14, 2018): 609–26. http://dx.doi.org/10.1093/jopart/muy047.

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Abstract Replication is an important mechanism through which broad lessons for theory and practice can be drawn in the applied interdisciplinary social science field of public administration. We suggest a common replication framework for public administration that is illustrated by experimental work in the field. Drawing on knowledge from other disciplines, together with our experience in replicating several experiments on topics such as decision making, organizational rules, and government–citizen relationships, we provide an overview of the replication process. We then distill this knowledge into seven decision points that offer a clear set of best practices on how to design and implement replications in public administration. We conclude by arguing that replication should be part of the normal scientific process in public administration to help to build valid middle-range theories and provide valuable lessons to practice.

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Hasse, Steven B., and Michele P. Calos. "Replication control of autonomously replicating human sequence." Nucleic Acids Research 19, no. 18 (1991): 5053–58. http://dx.doi.org/10.1093/nar/19.18.5053.

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8

Reggia, James A., Jason D. Lohn, and Hui-Hsien Chou. "Self-Replicating Structures: Evolution, Emergence, and Computation." Artificial Life 4, no. 3 (July 1998): 283–302. http://dx.doi.org/10.1162/106454698568594.

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Since von Neumann's seminal work around 1950, computer scientists and others have studied the algorithms needed to support self-replicating systems. Much of this work has focused on abstract logical machines (automata) embedded in two-dimensional cellular spaces. This research was motivated by the desire to understand the basic information-processing principles underlying self-replication, the potential long-term applications of programmable self-replicating machines, and the possibility of gaining insight into biological replication and the origins of life. We view past research as taking three main directions: early complex universal computer-constructors modeled after Turing machines, qualitatively simpler self-replicating loops, and efforts to view self-replication as an emergent phenomenon. We discuss our recent studies in the latter category showing that self-replicating structures can emerge from nonreplicating components, and that genetic algorithms can be applied to program automatically simple but arbitrary structures to replicate. We also describe recent work in which self-replicating structures are successfully programmed to do useful problem solving as they replicate. We conclude by identifying some implications and important research directions for the future.

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9

Avemann, K., R. Knippers, T. Koller, and J. M. Sogo. "Camptothecin, a specific inhibitor of type I DNA topoisomerase, induces DNA breakage at replication forks." Molecular and Cellular Biology 8, no. 8 (August 1988): 3026–34. http://dx.doi.org/10.1128/mcb.8.8.3026.

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The structure of replicating simian virus 40 minichromosomes, extracted from camptothecin-treated infected cells, was investigated by biochemical and electron microscopic methods. We found that camptothecin frequently induced breaks at replication forks close to the replicative growth points. Replication branches were disrupted at about equal frequencies at the leading and the lagging strand sides of the fork. Since camptothecin is known to be a specific inhibitor of type I DNA topoisomerase, we suggest that this enzyme is acting very near the replication forks. This conclusion was supported by experiments with aphidicolin, a drug that blocks replicative fork movement, but did not prevent the camptothecin-induced breakage of replication forks. The drug teniposide, an inhibitor of type II DNA topoisomerase, had only minor effects on the structure of these replicative intermediates.

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Avemann, K., R. Knippers, T. Koller, and J. M. Sogo. "Camptothecin, a specific inhibitor of type I DNA topoisomerase, induces DNA breakage at replication forks." Molecular and Cellular Biology 8, no. 8 (August 1988): 3026–34. http://dx.doi.org/10.1128/mcb.8.8.3026-3034.1988.

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The structure of replicating simian virus 40 minichromosomes, extracted from camptothecin-treated infected cells, was investigated by biochemical and electron microscopic methods. We found that camptothecin frequently induced breaks at replication forks close to the replicative growth points. Replication branches were disrupted at about equal frequencies at the leading and the lagging strand sides of the fork. Since camptothecin is known to be a specific inhibitor of type I DNA topoisomerase, we suggest that this enzyme is acting very near the replication forks. This conclusion was supported by experiments with aphidicolin, a drug that blocks replicative fork movement, but did not prevent the camptothecin-induced breakage of replication forks. The drug teniposide, an inhibitor of type II DNA topoisomerase, had only minor effects on the structure of these replicative intermediates.

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11

Jazwinski, S. M. "Participation of ATP in the binding of a yeast replicative complex to DNA." Biochemical Journal 246, no. 1 (August 15, 1987): 213–19. http://dx.doi.org/10.1042/bj2460213.

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The activity that replicates yeast DNA in vitro can be isolated from cells of the budding yeast Saccharomyces in a high-Mr (approximately 2 × 10(6] form. Several lines of evidence indicate that this fraction contains a multiprotein replicative complex. A functional assay has been developed for the analysis of the interaction of the replicating activity with DNA. Binding of the activity required Mg2+, but did not require the addition of ATP or the other ribo- or deoxynucleoside triphosphates. However, the ATP analogues adenosine 5′-[gamma-thio]triphosphate and adenosine 5′-[beta gamma-imido]triphosphate blocked the binding, suggesting that ATP participates in the interaction at some stage. The binding was template (origin)-specific in either the presence or the absence of ATP and the other nucleoside triphosphates; however, ATP stabilized the replicating activity. The preferential inhibition of binding that was observed in the presence of the DNA topoisomerase II inhibitor coumermycin suggests that the requirement for ATP may be at least partially accounted for by the involvement of this enzyme in the initial interaction of the replicating activity with DNA. Finally, the binding was rapid. In contrast, DNA synthesis displayed a lag when assayed directly without first allowing a period for the replicating activity to bind to the DNA. In addition, binding was ‘tight’, as judged by the resistance of the protein–DNA complexes to salt in comparison with the relative sensitivity of binding. The replicating activity was not readily displaced from the complexes by exogenous DNAs, either possessing or lacking yeast origins of replication. The results suggest that the interaction of the replicating activity with the DNA occurs in more than one stage.

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12

Hoggard, Timothy, Carolin A. Müller, Conrad A. Nieduszynski, Michael Weinreich, and Catherine A. Fox. "Sir2 mitigates an intrinsic imbalance in origin licensing efficiency between early- and late-replicating euchromatin." Proceedings of the National Academy of Sciences 117, no. 25 (June 8, 2020): 14314–21. http://dx.doi.org/10.1073/pnas.2004664117.

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A eukaryotic chromosome relies on the function of multiple spatially distributed DNA replication origins for its stable inheritance. The spatial location of an origin is determined by the chromosomal position of an MCM complex, the inactive form of the DNA replicative helicase that is assembled onto DNA in G1-phase (also known as origin licensing). While the biochemistry of origin licensing is understood, the mechanisms that promote an adequate spatial distribution of MCM complexes across chromosomes are not. We have elucidated a role for the Sir2 histone deacetylase in establishing the normal distribution of MCM complexes acrossSaccharomyces cerevisiaechromosomes. In the absence of Sir2, MCM complexes accumulated within both early-replicating euchromatin and telomeric heterochromatin, and replication activity within these regions was enhanced. Concomitantly, the duplication of several regions of late-replicating euchromatin were delayed. Thus, Sir2-mediated attenuation of origin licensing within both euchromatin and telomeric heterochromatin established the normal spatial distribution of origins across yeast chromosomes important for normal genome duplication.

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13

Iwasaki, Hiromichi, Peng Huang, Michael J. Keating, and William Plunkett. "Differential Incorporation of Ara-C, Gemcitabine, and Fludarabine Into Replicating and Repairing DNA in Proliferating Human Leukemia Cells." Blood 90, no. 1 (July 1, 1997): 270–78. http://dx.doi.org/10.1182/blood.v90.1.270.

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Abstract The major actions of nucleoside analogs such as arabinosylcytosine (ara-C) and fludarabine occurs after their incorporation into DNA, during either replication or repair synthesis. The metabolic salvage and DNA incorporation of the normal nucleoside, deoxycytidine, is functionally compartmentalized toward repair synthesis in a process regulated by ribonucleotide reductase. The aim of this study was to investigate the metabolic pathways by which nucleoside analogs that do (fludarabine, gemcitabine) or do not (ara-C) affect ribonucleotide reductase are incorporated into DNA in proliferating human leukemia cells. Using alkaline density-gradient centrifugation to separate repaired DNA from replicating DNA and unreplicated parental DNA strands, approximately 60% of ara-C nucleotide in DNA was incorporated by repair synthesis in CCRF-CEM cells; the remainder was incorporated by replication. In contrast, fludarabine and gemcitabine, nucleosides that inhibit ribonucleotide reductase and decreased deoxynucleotide pools, were incorporated mainly within replicating DNA. Hydroxyurea also depleted deoxynucleotide pools and increased the incorporation of ara-C into DNA by replicative synthesis. Stimulation of DNA repair activity by UV irradiation selectively enhanced the incorporation of all nucleosides tested through repair synthesis. These findings suggest that the pathways by which therapeutically useful nucleoside analogs are incorporated into DNA are affected by cellular dNTP pools from de novo synthesis and by the relative activities of DNA repair and replication. The antitumor activity of these drugs may be enhanced by combination with either ribonucleotide reductase inhibitors to increase their incorporation into replicating DNA or with agents that induce DNA damage and evoke the DNA repair process.

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Iwasaki, Hiromichi, Peng Huang, Michael J. Keating, and William Plunkett. "Differential Incorporation of Ara-C, Gemcitabine, and Fludarabine Into Replicating and Repairing DNA in Proliferating Human Leukemia Cells." Blood 90, no. 1 (July 1, 1997): 270–78. http://dx.doi.org/10.1182/blood.v90.1.270.270_270_278.

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The major actions of nucleoside analogs such as arabinosylcytosine (ara-C) and fludarabine occurs after their incorporation into DNA, during either replication or repair synthesis. The metabolic salvage and DNA incorporation of the normal nucleoside, deoxycytidine, is functionally compartmentalized toward repair synthesis in a process regulated by ribonucleotide reductase. The aim of this study was to investigate the metabolic pathways by which nucleoside analogs that do (fludarabine, gemcitabine) or do not (ara-C) affect ribonucleotide reductase are incorporated into DNA in proliferating human leukemia cells. Using alkaline density-gradient centrifugation to separate repaired DNA from replicating DNA and unreplicated parental DNA strands, approximately 60% of ara-C nucleotide in DNA was incorporated by repair synthesis in CCRF-CEM cells; the remainder was incorporated by replication. In contrast, fludarabine and gemcitabine, nucleosides that inhibit ribonucleotide reductase and decreased deoxynucleotide pools, were incorporated mainly within replicating DNA. Hydroxyurea also depleted deoxynucleotide pools and increased the incorporation of ara-C into DNA by replicative synthesis. Stimulation of DNA repair activity by UV irradiation selectively enhanced the incorporation of all nucleosides tested through repair synthesis. These findings suggest that the pathways by which therapeutically useful nucleoside analogs are incorporated into DNA are affected by cellular dNTP pools from de novo synthesis and by the relative activities of DNA repair and replication. The antitumor activity of these drugs may be enhanced by combination with either ribonucleotide reductase inhibitors to increase their incorporation into replicating DNA or with agents that induce DNA damage and evoke the DNA repair process.

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Pierron, Gérard, Dominick Pallotta, and Marianne Bénard. "The One-Kilobase DNA Fragment Upstream of theardC Actin Gene of Physarum polycephalum Is Both a Replicator and a Promoter." Molecular and Cellular Biology 19, no. 5 (May 1, 1999): 3506–14. http://dx.doi.org/10.1128/mcb.19.5.3506.

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ABSTRACT The 1-kb DNA fragment upstream of the ardC actin gene of Physarum polycephalum promotes the transcription of a reporter gene either in a transient-plasmid assay or as an integrated copy in an ectopic position, defining this region as the transcriptional promoter of the ardC gene (PardC). Since we mapped an origin of replication activated at the onset of S phase within this same fragment, we examined the pattern of replication of a cassette containing the PardCpromoter and the hygromycin phosphotransferase gene, hph, integrated into two different chromosomal sites. In both cases, we show by two-dimensional agarose gel electrophoresis that an efficient, early activated origin coincides with the ectopic PardC fragment. One of the integration sites was a normally late-replicating region. The presence of the ectopic origin converted this late-replicating domain into an early-replicating domain in which replication forks propagate with kinetics indistinguishable from those of the nativePardC replicon. This is the first demonstration that initiation sites for DNA replication in Physarum correspond to cis-acting replicator sequences. This work also confirms the close proximity of a replication origin and a promoter, with both functions being located within the 1-kb proximal region of theardC actin gene. A more precise location of the replication origin with respect to the transcriptional promoter must await the development of a functional autonomously replicating sequence assay inPhysarum.

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Suzuki, Keisuke, and Takashi Ikegami. "Spatial-Pattern-Induced Evolution of a Self-Replicating Loop Network." Artificial Life 12, no. 4 (October 2006): 461–85. http://dx.doi.org/10.1162/artl.2006.12.4.461.

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We study a system of self-replicating loops in which interaction rules between individuals allow competition that leads to the formation of a hypercycle-like network. The main feature of the model is the multiple layers of interaction between loops, which lead to both global spatial patterns and local replication. The network of loops manifests itself as a spiral structure from which new kinds of self-replicating loops emerge at the boundaries between different species. In these regions, larger and more complex self-replicating loops live for longer periods of time, managing to self-replicate in spite of their slower replication. Of particular interest is how micro-scale interactions between replicators lead to macro-scale spatial pattern formation, and how these macro-scale patterns in turn perturb the micro-scale replication dynamics.

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17

Makel, Matthew C., Jonathan A. Plucker, and Boyd Hegarty. "Replications in Psychology Research." Perspectives on Psychological Science 7, no. 6 (November 2012): 537–42. http://dx.doi.org/10.1177/1745691612460688.

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Recent controversies in psychology have spurred conversations about the nature and quality of psychological research. One topic receiving substantial attention is the role of replication in psychological science. Using the complete publication history of the 100 psychology journals with the highest 5-year impact factors, the current article provides an overview of replications in psychological research since 1900. This investigation revealed that roughly 1.6% of all psychology publications used the term replication in text. A more thorough analysis of 500 randomly selected articles revealed that only 68% of articles using the term replication were actual replications, resulting in an overall replication rate of 1.07%. Contrary to previous findings in other fields, this study found that the majority of replications in psychology journals reported similar findings to their original studies (i.e., they were successful replications). However, replications were significantly less likely to be successful when there was no overlap in authorship between the original and replicating articles. Moreover, despite numerous systemic biases, the rate at which replications are being published has increased in recent decades.

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Aguilar, Rhiannon R., and Jessica K. Tyler. "Thinking Outside the Cell: Replicating Replication In Vitro." Molecular Cell 65, no. 1 (January 2017): 5–7. http://dx.doi.org/10.1016/j.molcel.2016.12.019.

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19

Beare, Brendan K. "Distributional Replication." Entropy 23, no. 8 (August 17, 2021): 1063. http://dx.doi.org/10.3390/e23081063.

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A function which transforms a continuous random variable such that it has a specified distribution is called a replicating function. We suppose that functions may be assigned a price, and study an optimization problem in which the cheapest approximation to a replicating function is sought. Under suitable regularity conditions, including a bound on the entropy of the set of candidate approximations, we show that the optimal approximation comes close to achieving distributional replication, and close to achieving the minimum cost among replicating functions. We discuss the relevance of our results to the financial literature on hedge fund replication; in this case, the optimal approximation corresponds to the cheapest portfolio of market index options which delivers the hedge fund return distribution.

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Stauffer, André, and Moshe Sipper. "An Interactive Self-Replicator Implemented in Hardware." Artificial Life 8, no. 2 (April 2002): 175–83. http://dx.doi.org/10.1162/106454602320184239.

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Self-replicating loops presented to date are essentially worlds unto themselves, inaccessible to the observer once the replication process is launched. In this article we present the design of an interactive self-replicating loop of arbitrary size, wherein the user can physically control the loop's replication and induce its destruction. After introducing the BioWall, a reconfigurable electronic wall for bio-inspired applications, we describe the design of our novel loop and delineate its hardware implementation in the wall.

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Silverman, W. A. "Replicating Measurements." PEDIATRICS 112, no. 2 (August 1, 2003): 415–16. http://dx.doi.org/10.1542/peds.112.2.415.

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McCarthy, Nicola. "Replicating recurrence." Nature Reviews Cancer 9, no. 9 (August 13, 2009): 613. http://dx.doi.org/10.1038/nrc2722.

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Wärneryd, Karl. "Replicating contests." Economics Letters 71, no. 3 (June 2001): 323–27. http://dx.doi.org/10.1016/s0165-1765(01)00393-7.

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Burk, N. M. "Replicating Earth." IEEE Potentials 14, no. 2 (1995): 32–33. http://dx.doi.org/10.1109/45.376644.

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Wells, William A. "Replicating dominos." Journal of Cell Biology 160, no. 3 (January 27, 2003): 287. http://dx.doi.org/10.1083/jcb1603rr3.

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Ramachandran, Srinivas, and Steven Henikoff. "Replicating nucleosomes." Science Advances 1, no. 7 (August 2015): e1500587. http://dx.doi.org/10.1126/sciadv.1500587.

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Eukaryotic replication disrupts each nucleosome as the fork passes, followed by reassembly of disrupted nucleosomes and incorporation of newly synthesized histones into nucleosomes in the daughter genomes. In this review, we examine this process of replication-coupled nucleosome assembly to understand how characteristic steady-state nucleosome landscapes are attained. Recent studies have begun to elucidate mechanisms involved in histone transfer during replication and maturation of the nucleosome landscape after disruption by replication. A fuller understanding of replication-coupled nucleosome assembly will be needed to explain how epigenetic information is replicated at every cell division.

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L'Herault, Ron. "Replicating Surfaces." Microscopy Today 10, no. 5 (September 2002): 37. http://dx.doi.org/10.1017/s1551929500058375.

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Malcolm, Katy, Matt Bourne, and Ronnie Wilson. "Replicating Workschemes." A Life in the Day 3, no. 3 (August 1999): 4–6. http://dx.doi.org/10.1108/13666282199900022.

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Potter, Roberto Hugh, Timothy A. Akers, and Daniel Richard Bowman. "Replicating MISTERS." Journal of Correctional Health Care 19, no. 1 (January 1, 2013): 4–14. http://dx.doi.org/10.1177/1078345812458085.

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Moore, Pete. "Replicating success." Nature 435, no. 7039 (May 2005): 235. http://dx.doi.org/10.1038/435235a.

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Hou, Kewei, Chen Xue, and Lu Zhang. "Replicating Anomalies." Review of Financial Studies 33, no. 5 (December 10, 2018): 2019–133. http://dx.doi.org/10.1093/rfs/hhy131.

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Abstract Most anomalies fail to hold up to currently acceptable standards for empirical finance. With microcaps mitigated via NYSE breakpoints and value-weighted returns, 65% of the 452 anomalies in our extensive data library, including 96% of the trading frictions category, cannot clear the single test hurdle of the absolute $t$-value of 1.96. Imposing the higher multiple test hurdle of 2.78 at the 5% significance level raises the failure rate to 82%. Even for replicated anomalies, their economic magnitudes are much smaller than originally reported. In all, capital markets are more efficient than previously recognized. Received June 12, 2017; editorial decision October 29, 2018 by Editor Stijn Van Nieuwerburgh. Authors have furnished an Internet Appendix, which is available on the Oxford University Press Web site next to the link to the final published paper online.

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Kidder, David W., and Edward E. Gotts. "Replicating Research." Psychiatric Services 37, no. 8 (August 1986): 844. http://dx.doi.org/10.1176/ps.37.8.844.

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Vince, Andrew. "Replicating Tessellations." SIAM Journal on Discrete Mathematics 6, no. 3 (August 1993): 501–21. http://dx.doi.org/10.1137/0406040.

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Robinson, ES, PB Samollow, JL VandeBerg, and PG Johnston. "X-chromosome replication patterns in adult, newborn and prenatal opossums." Reproduction, Fertility and Development 6, no. 4 (1994): 533. http://dx.doi.org/10.1071/rd9940533.

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Somatic cells from the opossums Monodelphis domestica and Didelphis virginiana were labelled with 5-bromodeoxyuridine (BrdU), treated with colchicine, stained with acridine orange and examined using fluorescence microscopy. BrdU-incorporated metaphase spreads from females of M. domestica at developmental stages from late bilaminar blastocysts to adults showed replication asynchrony of the two (acrocentric) X chromosomes. The long arm of one X chromosome was the latest replicating region in the entire chromosome complement and is presumed to represent transcriptional inactivation and X dosage compensation. The minute short arm of the same X, which contains a nucleolar organizer region, was earlier replicating and synchronous with the short arm of its homologue and is thus assumed to escape inactivation. BrdU-incorporated spreads from cells of fetuses, neonates and adults of D. virginiana also showed a late replicating (submetacentric) X chromosome. The pattern was different from that of M. domestica because of the different morphology and the presence of large blocks of constitutive heterochromatin in both homologues. The timing and pattern of replication of the single X in males of both species resembled the earlier replicating X in females. The array of molecular techniques now available offers the best means for investigating X-chromosome replication and activity states of X-linked genes in the earliest stages of marsupial embryogenesis.

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Kim, Yusik, Rhonda Righter, and Ronald Wolff. "Job replication on multiserver systems." Advances in Applied Probability 41, no. 02 (June 2009): 546–75. http://dx.doi.org/10.1017/s0001867800003414.

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Parallel processing is a way to use resources efficiently by processing several jobs simultaneously on different servers. In a well-controlled environment where the status of the servers and the jobs are well known, everything is nearly deterministic and replicating jobs on different servers is obviously a waste of resources. However, in a poorly controlled environment where the servers are unreliable and/or their capacity is highly variable, it is desirable to design a system that is robust in the sense that it is not affected by the poorly performing servers. By replicating jobs and assigning them to several different servers simultaneously, we not only achieve robustness but we can also make the system more efficient under certain conditions so that the jobs are processed at a faster rate overall. In this paper we consider the option of replicating jobs and study how the performance of different ‘degrees’ of replication, ranging from no replication to full replication, affects the performance of a system of parallel servers.

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Kim, Yusik, Rhonda Righter, and Ronald Wolff. "Job replication on multiserver systems." Advances in Applied Probability 41, no. 2 (June 2009): 546–75. http://dx.doi.org/10.1239/aap/1246886623.

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Parallel processing is a way to use resources efficiently by processing several jobs simultaneously on different servers. In a well-controlled environment where the status of the servers and the jobs are well known, everything is nearly deterministic and replicating jobs on different servers is obviously a waste of resources. However, in a poorly controlled environment where the servers are unreliable and/or their capacity is highly variable, it is desirable to design a system that is robust in the sense that it is not affected by the poorly performing servers. By replicating jobs and assigning them to several different servers simultaneously, we not only achieve robustness but we can also make the system more efficient under certain conditions so that the jobs are processed at a faster rate overall. In this paper we consider the option of replicating jobs and study how the performance of different ‘degrees’ of replication, ranging from no replication to full replication, affects the performance of a system of parallel servers.

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Babudri, Nora, Alessandro Achilli, Chiara Martinelli, Elizabeth Moore, Hovirag Lancioni, and Yuri I. Pavlov. "The role of DNA polymerase alpha in the control of mutagenesis in Saccharomyces cerevisiae cells starved for nutrients." Ecological genetics 9, no. 1 (March 15, 2011): 53–61. http://dx.doi.org/10.17816/ecogen9153-61.

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In nature, microorganisms experience numerous environmental stresses and generally grow poorly most of the time. In the last two decades it has become evident that mutations arise not only in actively dividing cells but also in nonreplicating or slowly replicating cells starved for nutrients. In yeast, precise base selection and proofreading by replicative DNA polymerases δ and ε keep starvation-associated mutagenesis (SAM) at basal levels. Less is known about the role of replicative DNA polymerase α (Pol α). Here we provide evidence that Pol α is involved in the control of SAM in yeast cells starved for adenine by participation in sporadic replication and/or DNA repair under these conditions.

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Tunin, Karen, and Priscila Guimarães Otto. "Late-replicating X-chromosome: replication patterns in mammalian females." Genetics and Molecular Biology 25, no. 3 (2002): 305–8. http://dx.doi.org/10.1590/s1415-47572002000300009.

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Miller, D. G., M. A. Adam, and A. D. Miller. "Gene transfer by retrovirus vectors occurs only in cells that are actively replicating at the time of infection." Molecular and Cellular Biology 10, no. 8 (August 1990): 4239–42. http://dx.doi.org/10.1128/mcb.10.8.4239.

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Previous reports have shown that retrovirus infection is inhibited in nonreplicating (stationary-phase [hereafter called stationary]) cells. Infection of stationary cells was shown to occur when the cells were allowed to replicate at times up to a week after infection, suggesting that an unintegrated retrovirus could persist in a form that was competent to integrate after release of the block to replication. However, those studies were complicated by the use of replication-competent virus, which can spread in the infected cells. We have used a replication-defective retrovirus vector to compare the efficiency of gene transfer in stationary and replicating rat embryo fibroblasts. In agreement with previous results, gene transfer was inhibited 100-fold in stationary versus replicating cells. In contrast to previously reported results, the block to infection could not be relieved by stimulating stationary cells to divide at times from 6 h to 10 days after infection. Thus, for successful retroviral infection, the infected cells must be replicating at the time of infection. These results have important implications for the use of retroviral vectors for gene transfer.

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Miller, D. G., M. A. Adam, and A. D. Miller. "Gene transfer by retrovirus vectors occurs only in cells that are actively replicating at the time of infection." Molecular and Cellular Biology 10, no. 8 (August 1990): 4239–42. http://dx.doi.org/10.1128/mcb.10.8.4239-4242.1990.

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Previous reports have shown that retrovirus infection is inhibited in nonreplicating (stationary-phase [hereafter called stationary]) cells. Infection of stationary cells was shown to occur when the cells were allowed to replicate at times up to a week after infection, suggesting that an unintegrated retrovirus could persist in a form that was competent to integrate after release of the block to replication. However, those studies were complicated by the use of replication-competent virus, which can spread in the infected cells. We have used a replication-defective retrovirus vector to compare the efficiency of gene transfer in stationary and replicating rat embryo fibroblasts. In agreement with previous results, gene transfer was inhibited 100-fold in stationary versus replicating cells. In contrast to previously reported results, the block to infection could not be relieved by stimulating stationary cells to divide at times from 6 h to 10 days after infection. Thus, for successful retroviral infection, the infected cells must be replicating at the time of infection. These results have important implications for the use of retroviral vectors for gene transfer.

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Enver, T., A. C. Brewer, and R. K. Patient. "Role for DNA replication in beta-globin gene activation." Molecular and Cellular Biology 8, no. 3 (March 1988): 1301–8. http://dx.doi.org/10.1128/mcb.8.3.1301.

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Transcriptional activation of the Xenopus laevis beta-globin gene requires the synergistic action of the simian virus 40 enhancer and DNA replication in DEAE-dextran-mediated HeLa cell transfections. Replication does not act through covalent modification of the template, since its requirement was not obviated by the prior replication of the transfected DNA in eucaryotic cells. Transfection of DNA over a 100-fold range demonstrates that replication does not contribute to gene activation simply increasing template copy number. Furthermore, in cotransfections of replicating and nonreplicating constructs, only replicating templates were transcribed. Replication is not simply a requirement of chromatin assembly, since even unreplicated templates generated nucleosomal ladders. Stimulation of beta-globin transcription by DNA replication, though less marked, was also observed in calcium phosphate transfections. We interpret these results as revealing a dynamic role for replication in gene activation.

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Enver, T., A. C. Brewer, and R. K. Patient. "Role for DNA replication in beta-globin gene activation." Molecular and Cellular Biology 8, no. 3 (March 1988): 1301–8. http://dx.doi.org/10.1128/mcb.8.3.1301-1308.1988.

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Transcriptional activation of the Xenopus laevis beta-globin gene requires the synergistic action of the simian virus 40 enhancer and DNA replication in DEAE-dextran-mediated HeLa cell transfections. Replication does not act through covalent modification of the template, since its requirement was not obviated by the prior replication of the transfected DNA in eucaryotic cells. Transfection of DNA over a 100-fold range demonstrates that replication does not contribute to gene activation simply increasing template copy number. Furthermore, in cotransfections of replicating and nonreplicating constructs, only replicating templates were transcribed. Replication is not simply a requirement of chromatin assembly, since even unreplicated templates generated nucleosomal ladders. Stimulation of beta-globin transcription by DNA replication, though less marked, was also observed in calcium phosphate transfections. We interpret these results as revealing a dynamic role for replication in gene activation.

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Sobeck, Alexandra, Stacie Stone, Bendert deGraaf, Vincenzo Costanzo, Johan deWinter, Weidong Wang, Hans Joenje, Jean Gautier, and Maureen E. Hoatlin. "Coordinated Chromatin-Association of Fanconi Anemia Network Proteins Requires Replication-Coupled DNA Damage Recognition." Blood 104, no. 11 (November 16, 2004): 723. http://dx.doi.org/10.1182/blood.v104.11.723.723.

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Abstract Fanconi anemia (FA) is a genetic disorder characterized by hypersensitivity to DNA crosslinking agents and diverse clinical symptoms, including developmental anomalies, progressive bone marrow failure, and predisposition to leukemias and other cancers. FA is genetically heterogeneous, resulting from mutations in any of at least eleven different genes. The FA proteins function together in a pathway composed of a mulitprotein core complex that is required to trigger the DNA-damage dependent activation of the downstream FA protein, FANCD2. This activation is thought to be the key step in a DNA damage response that functionally links FA proteins to major breast cancer susceptibility proteins BRCA1 and BRCA2 (BRCA2 is FA gene FANCD1). The essential function of the FA proteins is unknown, but current models suggest that FA proteins function at the interface between cell cycle checkpoints, DNA repair and DNA replication, and are likely to play roles in the DNA damage response during S phase. To provide a platform for dissecting the key functional events during S-phase, we developed cell-free assays for FA proteins based on replicating extracts from Xenopus eggs. We identified the Xenopus homologs of human FANCD2 (xFANCD2) and several of the FA core complex proteins (xCCPs), and biochemically characterized these proteins in replicating cell-free extracts. We found that xCCPs and a modified isoform of xFANCD2 become associated with chromatin during normal and disrupted DNA replication. Blocking initiation of replication with geminin demonstrated that association of xCCPs and xFANCD2 with chromatin occurs in a strictly replication-dependent manner that is enhanced following DNA damage by crosslinking agents or by addition of aphidicolin, an inhibitor of replicative DNA polymerases. In addition, chromatin binding of xFANCD2, but not xBRCA2, is abrogated when xFANCA is quantitatively depleted from replicating extracts suggesting that xFANCA promotes the loading of xFANCD2 on chromatin. The chromatin-association of xFANCD2 and xCCPs is diminished in the presence of caffeine, an inhibitor of checkpoint kinases. Taken together, our data suggest a model in which the ordered loading of FA proteins on chromatin is required for processing a subset of DNA replication-blocking lesions that are resolved during late stages of replication.

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Mardiah, Rika, Hanita Hanita, and Farny Sutriany Jafar. "MENINGKATKAN KEMAMPUAN MENIRU BENTUK MELALUI STRATEGI PEMBELAJARAN GRADASI DENGAN MEDIA PLASTISIN PADA KELOMPOK B DI TK TUNAS BANGSA KERTA BUANA TENGGARONG SEBERANG TAHUN AJARAN 2016/2017." Jurnal Warna : Pendidikan dan Pembelajaran Anak Usia Dini 1, no. 2 (January 18, 2018): 32–44. http://dx.doi.org/10.24903/jw.v1i2.181.

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The researcher observed that students in Group B at TK Tunas Bangsa Kerta Buana Tenggarong Seberang had problems in replicating shapes. Therefore, to solve the problem, the researcher conducted a classroom action research, with purpose, to find out whether the implementation of gradation learning strategy by utilizing plasticine as the media of learning is able to enhance students’ ability in making shape replication. Moreover, the researcher involved 12 students; 7 males and 5 females, as the research subjects. To collect the data, the researcher employed observation and documentation technique during two cycles. It is important to note that each cycle consists of planning, implementation, observation and reflection. Meanwhile, for data analysis, the researcher applied percentages. Students’ ability in replicating shapes is measured based on five aspects; 1) ability in replicating the determined shape, 2) tidiness, 3) speed, 4) creation, and 5) accomplishing task without teacher’s help. At the first cycle, 27.77% were able to replicate the determined pattern. In the same way, 34.72% students were able to perform the task tidily. Regarding to speed aspect, 27.77% managed to finish the task fast. 38.88% students showed creativity in replicating various shapes, and 29.16% managed to accomplish the task independently. In brief, the percentage of success at Cycle 1 reached 63,31%, which means, the students were developed as expected. Furthermore, at Cycle 2, students experienced progress in each aspect. 44.44% students were able to reproduce shape which had been determined. 43% students managed to show the aspect of tidiness in replication. 37.49% managed to do the task fast. 37.49% students affirmed creativity in creating various shapes, and 37.49% were able to replicate the shapes without help from the teacher. Concisely, in Cycle 2, students’ ability in replicating shapes increased and reached 81%. It can be said that the students were developed very well in terms of replicating shapes.In conclusion, gradation learning strategy is effective for improving students’ ability in replicating shapes. Therefore, it is suggested for teachers to use this strategy later on.

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Robert-Guroff, Marjorie. "Replicating and non-replicating viral vectors for vaccine development." Current Opinion in Biotechnology 18, no. 6 (December 2007): 546–56. http://dx.doi.org/10.1016/j.copbio.2007.10.010.

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Gosert, Rainer, Denise Egger, Volker Lohmann, Ralf Bartenschlager, Hubert E. Blum, Kurt Bienz, and Darius Moradpour. "Identification of the Hepatitis C Virus RNA Replication Complex in Huh-7 Cells Harboring Subgenomic Replicons." Journal of Virology 77, no. 9 (May 1, 2003): 5487–92. http://dx.doi.org/10.1128/jvi.77.9.5487-5492.2003.

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ABSTRACT Formation of a membrane-associated replication complex, composed of viral proteins, replicating RNA, and altered cellular membranes, is a characteristic feature of plus-strand RNA viruses. Here, we demonstrate the presence of a specific membrane alteration, designated the membranous web, that contains hepatitis C virus (HCV) nonstructural proteins, as well as viral plus-strand RNA, in Huh-7 cells harboring autonomously replicating subgenomic HCV RNAs. Metabolic labeling with 5-bromouridine 5′-triphosphate in the presence of actinomycin D revealed that the membranous web is the site of viral RNA synthesis and therefore represents the replication complex of HCV.

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Lee-Chen, G. J., and M. Woodworth-Gutai. "Evolutionarily selected replication origins: functional aspects and structural organization." Molecular and Cellular Biology 6, no. 9 (September 1986): 3077–85. http://dx.doi.org/10.1128/mcb.6.9.3077.

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A selective replicative pressure occurs during the evolution of simian virus 40 variants. When the replication origin is duplicated as an inverted repeat, there is a dramatic enhancement of replication. Having regulatory sequences located between the inverted repeat of ori magnifies their enhancing effect on replication. A passage 20 variant and a passage 45 variant containing three pairs of an inverted repeat of ori replicated more efficiently than a passage 13 variant containing nine copies of ori arranged in tandem. A 69-base-pair cellular sequence inserted between inverted repeats of ori of both passage 40 and 45 variants enhanced simian virus 40 DNA replication. Differences in replication efficiencies became greater as the total number of replicating species was increased in the transfection mixture, under conditions where T antigen is limiting. In a competitive environment, sequences flanking the replication origin may be inhibitory to replication.

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48

Lee-Chen, G. J., and M. Woodworth-Gutai. "Evolutionarily selected replication origins: functional aspects and structural organization." Molecular and Cellular Biology 6, no. 9 (September 1986): 3077–85. http://dx.doi.org/10.1128/mcb.6.9.3077-3085.1986.

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A selective replicative pressure occurs during the evolution of simian virus 40 variants. When the replication origin is duplicated as an inverted repeat, there is a dramatic enhancement of replication. Having regulatory sequences located between the inverted repeat of ori magnifies their enhancing effect on replication. A passage 20 variant and a passage 45 variant containing three pairs of an inverted repeat of ori replicated more efficiently than a passage 13 variant containing nine copies of ori arranged in tandem. A 69-base-pair cellular sequence inserted between inverted repeats of ori of both passage 40 and 45 variants enhanced simian virus 40 DNA replication. Differences in replication efficiencies became greater as the total number of replicating species was increased in the transfection mixture, under conditions where T antigen is limiting. In a competitive environment, sequences flanking the replication origin may be inhibitory to replication.

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Taguchi, Naoko, and Shuai Li. "Replication research in contextual and individual influences in pragmatic competence: Taguchi, Xiao & Li (2016) and Bardovi-Harlig & Bastos (2011)." Language Teaching 52, no. 1 (September 5, 2017): 128–40. http://dx.doi.org/10.1017/s0261444817000222.

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Recent development in L2 pragmatics research in a study abroad context has witnessed an emerging line of studies investigating the joint influences of contextual and individual learner factors on second language (L2) pragmatic development. This paper argues for the replication of two representative quantitative studies in this new research direction. Situated within the field's increasing emphasis on explaining the development of L2 pragmatic competence, the first part of this paper makes a case for the necessity of replicating quantitative studies investigating the study abroad context, highlighting why and how the field can benefit from replication research. The second part of this paper presents detailed accounts of the two focus studies and suggests several options for approximate and conceptual replications.

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Pan, Zhijian, and James A. Reggia. "Computational Discovery of Instructionless Self-Replicating Structures in Cellular Automata." Artificial Life 16, no. 1 (January 2010): 39–63. http://dx.doi.org/10.1162/artl.2009.16.1.16104.

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Cellular automata models have historically been a major approach to studying the information-processing properties of self-replication. Here we explore the feasibility of adopting genetic programming so that, when it is given a fairly arbitrary initial cellular automata configuration, it will automatically generate a set of rules that make the given configuration replicate. We found that this approach works surprisingly effectively for structures as large as 50 components or more. The replication mechanisms discovered by genetic programming work quite differently than those of many past manually designed replicators: There is no identifiable instruction sequence or construction arm, the replicating structures generally translate and rotate as they reproduce, and they divide via a fissionlike process that involves highly parallel operations. This makes replication very fast, and one cannot identify which descendant is the parent and which is the child. The ability to automatically generate self-replicating structures in this fashion allowed us to examine the resulting replicators as their properties were systematically varied. Further, it proved possible to produce replicators that simultaneously deposited secondary structures while replicating, as in some past manually designed models. We conclude that genetic programming is a powerful tool for studying self-replication that might also be profitably used in contexts other than cellular spaces.

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Journal articles on the topic 'Replicating'

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