Catálogo de publicaciones - revistas

<jats:title>Nanoparticle superalloy</jats:title> <jats:p> Improving the strength of a metal alloy is hard to do without sacrificing the ductility. Yang <jats:italic>et al.</jats:italic> designed an iron-nickel-cobalt (Fe-Ni-Co) alloy laced with aluminum-titanium (Al-Ti) nanoparticles with both high strength and ductility. The key was getting the composition tuned correctly, because the Fe-Ni-Co matrix reacts with the Al-Ti nanoparticles. This was vital for avoiding environmental embrittlement, enhancing work hardening, and improving ductility. </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="6417" page="933" related-article-type="in-this-issue" vol="362" xlink:href="10.1126/science.aas8815">933</jats:related-article> </jats:p>

<jats:title>Megaherbivore extinctions in Africa</jats:title> <jats:p> Human ancestors have been proposed as drivers of extinctions of Africa's diverse large mammal communities. Faith <jats:italic>et al.</jats:italic> challenge this view with an analysis of eastern African herbivore communities spanning the past ∼7 million years (see the Perspective by Bobe and Carvalho). Megaherbivores (for example, elephants, rhinos, and hippos) began to decline about 4.6 million years ago, preceding evidence for hominin consumption of animal tissues by more than 1 million years. Instead, megaherbivore decline may have been triggered by declining atmospheric carbon dioxide and expansion of grasslands. </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="6417" page="938" related-article-type="in-this-issue" vol="362" xlink:href="10.1126/science.aau2728">938</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6417" page="892" related-article-type="in-this-issue" vol="362" xlink:href="10.1126/science.aav6883">892</jats:related-article> </jats:p>

<jats:title>Protecting the colony</jats:title> <jats:p> When we get a cold and then stay home from work, we are not only taking care of ourselves but also protecting others. Such changes in behavior after infection are predicted in social animals but are difficult to quantify. Stroeymeyt <jats:italic>et al.</jats:italic> looked for such changes in the black garden ant and found that infected workers did alter their behavior—and healthy workers altered their behavior toward the sick. The changed behavior was especially valuable for protecting the most important and vulnerable members of the colony. </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="6417" page="941" related-article-type="in-this-issue" vol="362" xlink:href="10.1126/science.aat4793">941</jats:related-article> </jats:p>

<jats:title>Egocentric representation of objects</jats:title> <jats:p> The lateral entorhinal cortex (LEC) and medial entorhinal cortex (MEC) are the two major cortical projections to the hippocampus. The discovery of a variety of functional cell types in MEC has greatly advanced our understanding of the functional anatomy of entorhinal-hippocampal circuits. However, the function of LEC and the behavioral correlates of LEC cells are still not fully understood. Wang <jats:italic>et al.</jats:italic> analyzed the firing properties of LEC and MEC neurons. They found that LEC and MEC used different reference frames, with LEC encoding objects egocentrically. </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="6417" page="945" related-article-type="in-this-issue" vol="362" xlink:href="10.1126/science.aau4940">945</jats:related-article> </jats:p>

<jats:title>A single myosin sets chirality at all scales</jats:title> <jats:p> When viewed externally, most organisms appear symmetric between the left and right sides. However, many organs are left-right asymmetric. Whether macroscopic asymmetries are directly related to molecular-level chirality remains an open question. Working in <jats:italic>Drosophila</jats:italic> , Lebreton <jats:italic>et al.</jats:italic> found that the conserved molecular motor myosin 1D induced stereotyped chirality at all biological scales—from F-actin turning in vitro to the organ level and even organismal behavior. Thus, a single conserved myosin can generate de novo nano-to-macroscopic changes in form and direction through chiral interaction with the actin cytoskeleton. </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="6417" page="949" related-article-type="in-this-issue" vol="362" xlink:href="10.1126/science.aat8642">949</jats:related-article> </jats:p>

<jats:title>Visualizing TGF-β1 regulation by GARP</jats:title> <jats:p> Regulatory T cells (T <jats:sub>regs</jats:sub> ) can suppress immune responses through a variety of mechanisms. One such mechanism involves the activation of a surface-bound latent form of the cytokine transforming growth factor–β1 (TGF-β1). Within the cell, newly synthesized pro-TGF-β1 homodimers form disulfide bonds with the transmembrane protein GARP, which acts to chaperone and orient the cytokine for activation at the cell surface. Liénart <jats:italic>et al.</jats:italic> reveal how GARP interacts with TGF-β1, using a crystal structure in which the complex was stabilized using a Fab fragment from a monoclonal antibody (MHG-8) that binds to the complex. In so doing, they also demonstrate how MHG-8 prevents membrane-associated TGF-β1 release. These structural and mechanistic insights may inform treatments of diseases with altered TGF-β1 functionality and dysfunctional T <jats:sub>reg</jats:sub> activity, including cancer immunotherapy. </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="6417" page="952" related-article-type="in-this-issue" vol="362" xlink:href="10.1126/science.aau2909">952</jats:related-article> </jats:p>

<jats:title>Fine-tuning pyroptosis with ESCRT-III</jats:title> <jats:p> Pyroptosis is an inflammatory form of cell death induced by select caspases downstream of inflammasome complexes. These caspases cleave gasdermin D (GSDMD), whose N-terminal fragments quickly form large permeability pores that induce cell death. However, a large percentage of cells with active inflammasomes are resistant to pyroptosis. Rühl <jats:italic>et al.</jats:italic> found that the membrane-remodeling ESCRT-III machinery was recruited to the plasma membrane upon GSDMD activation. ESCRT-III–dependent membrane repair limited proinflammatory cytokine secretion and pyroptosis after activation of inflammasomes. </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="6417" page="956" related-article-type="in-this-issue" vol="362" xlink:href="10.1126/science.aar7607">956</jats:related-article> </jats:p>

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