Catálogo de publicaciones - revistas

<jats:title>Bipolar Signature</jats:title> <jats:p> Atmospheric methane has increased approximately 2.5-fold since the start of the industrial revolution, a consequence of human activity. However, a smaller and more gradual rise began around 6000 years ago, near the time when human agriculture began to develop and expand. <jats:bold> Mitchell <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6161" page="964" related-article-type="in-this-issue" vol="342" xlink:href="10.1126/science.1238920">964</jats:related-article> ) present two, high-resolution ice core methane records of the past 2500 years, one from each pole. Methane emissions were primarily from the tropics, with secondary contributions from the higher latitudes where most humans lived. Thus, both natural and human sources are needed to explain the late-Holocene atmospheric methane record. </jats:p>

<jats:title>The Microbiota Makes for Good Therapy</jats:title> <jats:p> The gut microbiota has been implicated in the development of some cancers, such as colorectal cancer, but—given the important role our intestinal habitants play in metabolism—they may also modulate the efficacy of certain cancer therapeutics. <jats:bold> Iida <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6161" page="967" related-article-type="in-this-issue" vol="342" xlink:href="10.1126/science.1240527">967</jats:related-article> ) evaluated the impact of the microbiota on the efficacy of an immunotherapy [CpG (the cytosine, guanosine, phosphodiester link) oligonucleotides] and oxaliplatin, a platinum compound used as a chemotherapeutic. Both therapies were reduced in efficacy in tumor-bearing mice that lacked microbiota, with the microbiota important for activating the innate immune response against the tumors. <jats:bold> Viaud <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6161" page="971" related-article-type="in-this-issue" vol="342" xlink:href="10.1126/science.1240537">971</jats:related-article> ) found a similar effect of the microbiota on tumor-bearing mice treated with cyclophosphamide, but in this case it appeared that the microbiota promoted an adaptive immune response against the tumors. </jats:p>

<jats:title>The Microbiota Makes for Good Therapy</jats:title> <jats:p> The gut microbiota has been implicated in the development of some cancers, such as colorectal cancer, but—given the important role our intestinal habitants play in metabolism—they may also modulate the efficacy of certain cancer therapeutics. <jats:bold> Iida <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6161" page="967" related-article-type="in-this-issue" vol="342" xlink:href="10.1126/science.1240527">967</jats:related-article> ) evaluated the impact of the microbiota on the efficacy of an immunotherapy [CpG (the cytosine, guanosine, phosphodiester link) oligonucleotides] and oxaliplatin, a platinum compound used as a chemotherapeutic. Both therapies were reduced in efficacy in tumor-bearing mice that lacked microbiota, with the microbiota important for activating the innate immune response against the tumors. <jats:bold> Viaud <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6161" page="971" related-article-type="in-this-issue" vol="342" xlink:href="10.1126/science.1240537">971</jats:related-article> ) found a similar effect of the microbiota on tumor-bearing mice treated with cyclophosphamide, but in this case it appeared that the microbiota promoted an adaptive immune response against the tumors. </jats:p>

<jats:title>Flu Drift Limited</jats:title> <jats:p> Five antigenic sites in the virus surface hemagglutinin protein, which together comprise 131 amino acid positions, are thought to determine the full scope of antigenic drift of influenza A virus. <jats:bold> Koel <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6161" page="976" related-article-type="in-this-issue" vol="342" xlink:href="10.1126/science.1244730">976</jats:related-article> ) show that major antigenic change can be caused by single amino acid substitutions. These single substitutions substantially skew the way the immune system “sees” the virus. All substitutions of importance are located next to the receptor-binding site in the hemagglutinin. Because there are few positions of importance for antigenic drift, there are strict biophysical limitations to the substitutions at these positions, which restricts the number of new antigenic drift variants at any point in time. Thus, the evolution of influenza virus may be more predictable than previously thought. </jats:p>

<jats:title>From Yeast to Therapeutic?</jats:title> <jats:p> Yeast has shown some promise as a model system to generate lead compounds that could have therapeutic potential for the cellular problems associated with neurodegenerative diseases. Along these lines, <jats:bold> Tardiff <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6161" page="979" related-article-type="in-this-issue" vol="342" xlink:href="10.1126/science.1245321">979</jats:related-article> , published online 24 October) and <jats:bold> Chung <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6161" page="983" related-article-type="in-this-issue" vol="342" xlink:href="10.1126/science.1245296">983</jats:related-article> , published online 24 October) describe the results of multiple screens in yeast that lead to the identification of a potential therapeutic compound to combat the cytotoxic affect of α-synuclein accumulation. The compound was able to reverse the pathological hallmarks of Parkinson's disease in cultured neurons derived from patients with α-synuclein–induced Parkinson's disease dementia. </jats:p>

<jats:title>From Yeast to Therapeutic?</jats:title> <jats:p> Yeast has shown some promise as a model system to generate lead compounds that could have therapeutic potential for the cellular problems associated with neurodegenerative diseases. Along these lines, <jats:bold> Tardiff <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6161" page="979" related-article-type="in-this-issue" vol="342" xlink:href="10.1126/science.1245321">979</jats:related-article> , published online 24 October) and <jats:bold> Chung <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6161" page="983" related-article-type="in-this-issue" vol="342" xlink:href="10.1126/science.1245296">983</jats:related-article> , published online 24 October) describe the results of multiple screens in yeast that lead to the identification of a potential therapeutic compound to combat the cytotoxic affect of α-synuclein accumulation. The compound was able to reverse the pathological hallmarks of Parkinson's disease in cultured neurons derived from patients with α-synuclein–induced Parkinson's disease dementia. </jats:p>

<jats:title>Building Vocalization</jats:title> <jats:p> The transcription factor FoxP2 (forkhead box P2) affects language acquisition in humans and regulates the protein SRPX2 (sushi repeat-containing protein X-linked 2), which itself also affects language. <jats:bold> Sia <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6161" page="987" related-article-type="in-this-issue" vol="342" xlink:href="10.1126/science.1245079">987</jats:related-article> , published online 31 October; see the Perspective by <jats:bold> <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6161" page="944" related-article-type="in-this-issue" vol="342" xlink:href="10.1126/science.1247515">Lieberman</jats:related-article> </jats:bold> ) found that in the mouse brain, the FoxP2 transcription factor binds to the <jats:italic>SRPX2</jats:italic> gene. In tissue culture experiments, FoxP2, but not SRPX2, affected dendritic morphology, while both FoxP2 and SRPX2 affected the formation of excitatory synapses. Overexpression of SRPX2 in the mouse brain equivalent of the human brain's language area affected synapse density and disrupted the ultrasonic vocalizations emitted by mouse pups in search of their mothers. </jats:p>

<jats:title>Just Add Peroxide</jats:title> <jats:p> The HppE enzyme uses iron to catalyze oxidation of an alcohol to an epoxide ring in the biosynthesis of the antibiotic fosfomycin. Because this process is a two-electron oxidation, it has been unclear how the enzyme reduces its presumed oxidative partner O <jats:sub>2</jats:sub> all the way to water. Where do the two extra electrons come from? <jats:bold> Wang <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6161" page="991" related-article-type="in-this-issue" vol="342" xlink:href="10.1126/science.1240373">991</jats:related-article> , published 10 October; see the Perspective by <jats:bold> <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6161" page="943" related-article-type="in-this-issue" vol="342" xlink:href="10.1126/science.1247233">Raushel</jats:related-article> </jats:bold> ) now show that HppE is actually a peroxidase, and thus reduces H <jats:sub>2</jats:sub> O <jats:sub>2</jats:sub> , for which just two electrons are sufficient. The result expands the structural scope of iron-bearing peroxidase enzymes beyond heme motifs. </jats:p>

<jats:title>Limiting Tumor Initiation</jats:title> <jats:p> What is the competitive advantage of cells with frequently occurring mutations during tumor development? <jats:bold> Vermeulen <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6161" page="995" related-article-type="in-this-issue" vol="342" xlink:href="10.1126/science.1243148">995</jats:related-article> ; see the Perspective by <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6161" page="938" related-article-type="in-this-issue" vol="342" xlink:href="10.1126/science.1247887"> <jats:bold>Bozic and Nowak</jats:bold> </jats:related-article> ) quantified the advantages of <jats:italic>Apc</jats:italic> -loss, <jats:italic>Kras</jats:italic> activation, and <jats:italic>P53</jats:italic> mutation during tumor initiation in the mouse intestine. The mutations conferred only a limited clonal advantage. Indeed, many mutated stem cells were stochastically replaced by wild-type stem cells, helping to limit tumor initiation. </jats:p>

<jats:p>A weekly roundup of information on newly offered instrumentation, apparatus, and laboratory materials of potential interest to researchers.</jats:p>