Catálogo de publicaciones - revistas

<jats:title>Creating semiconductor nanocages</jats:title> <jats:p> The surface area of nanomaterials can be increased by creating open cage structures. Now it seems that the shape of nanocrystals can be used as a tool to manipulate crystal structure in nanocrystals. Wu <jats:italic>et al.</jats:italic> show how single nanocrystals of copper oxide are converted through anion exchange reactions to multiply twinned open cages of a copper sulfide in a process that changes the crystal lattice symmetries. These structures were then converted into cadmium sulfide nanocages through cation exchange. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6279" page="1306" related-article-type="in-this-issue" vol="351" xlink:href="10.1126/science.aad5520">1306</jats:related-article> </jats:p>

<jats:title>Gear-like rotation by a wobbly water duo</jats:title> <jats:p> The molecules in liquid water move about constantly, but on average they cling to each other through hydrogen bonds, like dancers who keep switching partners. Richardson <jats:italic>et al.</jats:italic> uncovered a fresh twist in this molecular dance (see the Perspective by Clary). Studying clusters of six molecules each—essentially the smallest three-dimensional water droplets—they observed coupled motion of two different molecules in the cluster. The process breaks two different hydrogen bonds concurrently in a pattern akin to rotating gears. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6279" page="1310" related-article-type="in-this-issue" vol="351" xlink:href="10.1126/science.aae0012">1310</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6279" page="1267" related-article-type="in-this-issue" vol="351" xlink:href="10.1126/science.aaf3061">1267</jats:related-article> </jats:p>

<jats:title>Transporting the hydrogen anion</jats:title> <jats:p> Hydrogen cation (H <jats:sup>+</jats:sup> ) transport is common in both biological systems and engineered ones such as fuel cells. In contrast, the transport of hydrogen anions (H <jats:sup>−</jats:sup> ) is far less common and is usually coupled with or compromised by the parallel transport of electrons. Kobayashi <jats:italic>et al.</jats:italic> examined the transport of H <jats:sup>−</jats:sup> in a series of rare-earth lithium oxyhydrides (see the Perspective by Yamaguchi). They prevented electronic conduction by using Li <jats:sup>+</jats:sup> as a countercation. In an electrochemical cell, the oxyhydride material acted as a solid-state electrolyte for H <jats:sup>−</jats:sup> , which suggests an alternative avenue for developing energy storage devices. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6279" page="1314" related-article-type="in-this-issue" vol="351" xlink:href="10.1126/science.aac9185">1314</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6279" page="1262" related-article-type="in-this-issue" vol="351" xlink:href="10.1126/science.aaf3361">1262</jats:related-article> </jats:p>

<jats:title>The magnitude of a major methane leak</jats:title> <jats:p> The Aliso Canyon underground gas storage facility outside Los Angeles, CA, houses enormous natural gas reserves. One well at the site experienced a blowout in late October 2015 and began leaking gas until it was sealed in February 2016. Over the course of 13 flights in the region, Conley <jats:italic>et al.</jats:italic> sampled the air column and determined daily release rates of methane (a powerful greenhouse gas) and ethane throughout the leak. The methane release rates were nearly double that of the entire Los Angeles region combined. Thus, single vulnerabilities can have major implications for state and federal climate policy. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6279" page="1317" related-article-type="in-this-issue" vol="351" xlink:href="10.1126/science.aaf2348">1317</jats:related-article> </jats:p>

<jats:title>A radical carboxyl migration</jats:title> <jats:p> The antibiotic nosiheptide, produced by <jats:italic>Streptomyces actuosus</jats:italic> , has high activity against multidrug-resistant pathogens. The enzymes involved in its biosynthesis include NosL, which cannibalizes tryptophan and forms a methylindolic acid precursor. Although NosL is included in a growing family of remarkable radical SAM enzymes, the mechanism by which it functions has been dif cult to identify. Using spectroscopic and theoretical approaches, Sicoli <jats:italic>et al.</jats:italic> show that an unexpected radical intermediate forms during the course of the reaction (see the Perspective by Bridwell-Rabb and Drennan). Unlike similar known enzymes, NosL cleaves a Cα-C bond, which results in the migration of tryptophan's carboxyl group to its side-chain indole. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6279" page="1320" related-article-type="in-this-issue" vol="351" xlink:href="10.1126/science.aad8995">1320</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6279" page="1266" related-article-type="in-this-issue" vol="351" xlink:href="10.1126/science.aaf4942">1266</jats:related-article> </jats:p>

<jats:title>Linking neurodegeneration and immune cells</jats:title> <jats:p> The expansion of a repetitive DNA sequence in the C9orf72 gene is the major genetic cause of amyotrophic lateral sclerosis and frontotemporal dementia. Although the expansion decreases C9orf72 expression, most research has focused on the toxic RNA and protein products it creates in neurons. O'Rourke <jats:italic>et al.</jats:italic> found that C9orf72 unexpectedly plays a key role in innate immune cells. Loss of C9orf72 in mice led to macrophage and microglial dysfunction and age-related neuroinflammation. This raises the possibility of a “dual-effect” disease mechanism, in which toxic byproducts in neurons are combined with microglial dysfunction from decreased C9orf72 expression, together promoting neurodegeneration. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6279" page="1324" related-article-type="in-this-issue" vol="351" xlink:href="10.1126/science.aaf1064">1324</jats:related-article> </jats:p>

<jats:title>Tuft cells help contain parasites</jats:title> <jats:p> Trillions of microbes inhabit our guts, including worms and other parasites. Epithelial cells that line the gut orchestrate parasite-targeted immune responses. Howitt <jats:italic>et al.</jats:italic> now identify a key cellular player in immunity to parasites: tuft cells (see the Perspective by Harris). Tuft cells make up a small fraction of gut epithelial cells but expand when parasites colonize or infect the gut. Parasites cause tuft cells to secrete large amounts of interleukin-25, a key cytokine for parasite clearance that also indirectly feeds back on tuft cells to expand their numbers. Tuft cells express chemosensory signaling machinery: disrupting this blocked parasite-triggered tuft cell expansion and weakened the ability of mice to control a parasitic infection. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6279" page="1329" related-article-type="in-this-issue" vol="351" xlink:href="10.1126/science.aaf1648">1329</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6279" page="1264" related-article-type="in-this-issue" vol="351" xlink:href="10.1126/science.aaf5215">1264</jats:related-article> </jats:p>

<jats:title>A prostaglandin barrier to inflammation</jats:title> <jats:p> Blood-borne bacterial infections and severe trauma can send the immune system into overdrive, causing it to pump out inflammatory mediators, sometimes at lethal doses. Duffin <jats:italic>et al.</jats:italic> now report on a role for prostaglandins in keeping systemic inflammation in check. Systemic inflammation correlates with decreased production of the prostaglandin E2 (PGE2). Blocking PGE2 signaling in mice led to severe inflammation associated with the translocation of gut bacteria. PGE2 acts on innate lymphoid cells, which produce interleukin-22, a secreted protein that helps promote intestinal integrity. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6279" page="1333" related-article-type="in-this-issue" vol="351" xlink:href="10.1126/science.aad9903">1333</jats:related-article> </jats:p>

<jats:title>Antibodies block Ebola virus entry</jats:title> <jats:p> The recent Ebola virus outbreak in West Africa illustrates the need for both an effective vaccine and therapies to treat infected individuals. Corti <jats:italic>et al.</jats:italic> isolated two monoclonal antibodies from a survivor of the 1995 Kikwit outbreak and demonstrated their therapeutic efficacy in Ebola virus–infected macaques. In fact, one antibody protected macaques when it was given up to 5 days after infection. Misasi <jats:italic>et al.</jats:italic> solved the crystal structures of fragments of the two antibodies bound to the Ebola virus glycoprotein (GP), which mediates viral cell entry. The two antibodies targeted different regions of GP, but in both cases blocked steps required for viral entry. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue pp. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6279" page="1339" related-article-type="in-this-issue" vol="351" xlink:href="10.1126/science.aad5224">1339</jats:related-article> &amp; <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6279" page="1343" related-article-type="in-this-issue" vol="351" xlink:href="10.1126/science.aad6117">1343</jats:related-article> </jats:p>

<jats:title>Antibodies block Ebola virus entry</jats:title> <jats:p> The recent Ebola virus outbreak in West Africa illustrates the need for both an effective vaccine and therapies to treat infected individuals. Corti <jats:italic>et al.</jats:italic> isolated two monoclonal antibodies from a survivor of the 1995 Kikwit outbreak and demonstrated their therapeutic efficacy in Ebola virus–infected macaques. In fact, one antibody protected macaques when it was given up to 5 days after infection. Misasi <jats:italic>et al.</jats:italic> solved the crystal structures of fragments of the two antibodies bound to the Ebola virus glycoprotein (GP), which mediates viral cell entry. The two antibodies targeted different regions of GP, but in both cases blocked steps required for viral entry. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue pp. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6279" page="1339" related-article-type="in-this-issue" vol="351" xlink:href="10.1126/science.aad5224">1339</jats:related-article> &amp; <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6279" page="1343" related-article-type="in-this-issue" vol="351" xlink:href="10.1126/science.aad6117">1343</jats:related-article> </jats:p>