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    <title>Nature Precedings - Tag feed for regulation</title>
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    <description>Recently posted documents tagged with 'regulation'</description>
    <dc:publisher>Nature Publishing Group</dc:publisher>
    <dc:language>en</dc:language>
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      <title>Regulating Nanomedicine: A European perspective</title>
      <link>http://precedings.nature.com/documents/2388/version/1</link>
      <description>The potential impact of nanomedicine is foreseen to radically change health care; however it also challenges existing perceptions, dynamics and standards relating to ethics, safety and governance. This commentary briefly highlights aspects and approaches pertaining to nanomedical regulation in the European Union.</description>
      <guid>http://precedings.nature.com/documents/2388/version/1</guid>
      <pubDate>Tue, 14 Oct 2008 21:17:08 UTC</pubDate>
      <dc:title>Regulating Nanomedicine: A European perspective</dc:title>
      <dc:identifier>hdl:10101/npre.2008.2388.1</dc:identifier>
      <dc:date>2008-10-14</dc:date>
      <dc:creator>Joel D'Silva</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2008-10-14T21:17:08Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Biotechnology</prism:section>
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      <title>Just-in-time assembly of cell-cycle protein complexes</title>
      <link>http://dx.doi.org/10.1038/npre.2008.2273.1</link>
      <description>Our comparative analysis of eukaryotic cell-cycle complexes reveals that the identity of the periodically expressed subunits differs significantly between organisms and is often mirrored by changes in cell-cycle-dependent phosphorylation of the protein products. This indicates that many different solutions have evolved for just-in-time assembly of the same molecular machines.</description>
      <guid>http://dx.doi.org/10.1038/npre.2008.2273.1</guid>
      <pubDate>Tue, 09 Sep 2008 11:49:12 UTC</pubDate>
      <dc:title>Just-in-time assembly of cell-cycle protein complexes</dc:title>
      <dc:identifier>doi:10.1038/npre.2008.2273.1</dc:identifier>
      <dc:date>2008-09-09</dc:date>
      <dc:creator>Lars J. Jensen</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2008-09-09T11:49:12Z</prism:publicationDate>
      <prism:category>Poster</prism:category>
      <prism:section>Molecular Cell Biology</prism:section>
      <prism:section>Bioinformatics</prism:section>
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      <title>Invariant mRNA content and mitotic protein breakdown as a solution to the Russian Doll problem of the mammalian cell cycle</title>
      <link>http://precedings.nature.com/documents/1218/version/1</link>
      <description>It is widely accepted that numerous genes are expressed in a cell-cycle dependent manner, with cycle-specific variations in mRNA content or peaks of protein content during the cell cycle. These proposed variations raise the problem of how varying cell cycle gene expression is regulated. This is the &amp;#8220;infinite regression&amp;#8221; problem or Russian Doll problem where postulating a cell-cycle specific control element merely pushes the explanation of cell-cycle variation back one step to the problem of how that control element itself appears and disappears at particular times during the cell cycle. We present evidence that cyclin mRNA content is invariant during the cell cycle and calculations reveal that mRNA variation does not account for observed protein variations during the cell cycle. The experimental evidence for protein breakdown only at the end of the cell cycle leads to a general model for cell-cycle control that avoids the Russian Doll problem.</description>
      <guid>http://precedings.nature.com/documents/1218/version/1</guid>
      <pubDate>Thu, 11 Oct 2007 14:39:21 UTC</pubDate>
      <dc:title>Invariant mRNA content and mitotic protein breakdown as a solution to the Russian Doll problem of the mammalian cell cycle</dc:title>
      <dc:identifier>hdl:10101/npre.2007.1218.1</dc:identifier>
      <dc:date>2007-10-11</dc:date>
      <dc:creator>Stephen Cooper</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2007-10-11T14:39:21Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Molecular Cell Biology</prism:section>
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      <title>Evolution of malaria virulence in cross-generation transmission through selective immune pressure</title>
      <link>http://precedings.nature.com/documents/203/version/1</link>
      <description>Theoretical arguments and some mathematical models of host-parasite coevolution (e.g. [1- 6]) suggest host immunity as the driving source for the evolution of parasite virulence. Imperfect vaccines in particular, can play the role and recent work [7] sets to test these ideas experimentally, using the mouse malaria model, Plasmodium chabaudi. To this end the authors evolve parasite lines in immunized and nonimmunized (&#8220;na&#239;ve&#8221;) mice using serial passage of infected blood samples. They find parasite lines evolved in immunized mice become more virulent than those evolved in naive mice. Furthermore, this feature persisted even when the evolved strains were transmitted through mosquitoes. Here we develop a mathematical model of parasite dynamics that qualitatively reproduces the experimental results of [7]. Our model accounts for the basic in-host processes: (i) production and depletion of red blood cells (RBC); (ii) immune-modulated parasite growth/ replication, (iii) immune stimulation and clearing of parasite. Besides we introduce multiple parasite strains with variable levels of virulence, and allow random mutations during replication process. The virulence is represented by a single parameter &#8211; immune stimulation threshold. So more virulent strains have higher &#8220;tolerance levels&#8221;, hence increased RBC depletion (anemia). Numeric simulations with our model exhibit, as in [7] the overall evolution of virulence in serial passage of parasite strains, and its enhancement through partial (imperfect) immunization.</description>
      <guid>http://precedings.nature.com/documents/203/version/1</guid>
      <pubDate>Mon, 25 Jun 2007 05:21:52 UTC</pubDate>
      <dc:title>Evolution of malaria virulence in cross-generation transmission through selective immune pressure</dc:title>
      <dc:identifier>hdl:10101/npre.2007.203.1</dc:identifier>
      <dc:date>2009-03-04</dc:date>
      <dc:creator>David E. Gurarie</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2007-06-25T05:21:52Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Immunology</prism:section>
      <prism:section>Bioinformatics</prism:section>
      <prism:section>Evolutionary Biology</prism:section>
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