Catálogo de publicaciones - revistas

<jats:title>ACHOO!-trophils?</jats:title> <jats:p> Why some individuals come down with a cold in any given year, whereas others are spared, is poorly understood. Habibi <jats:italic>et al.</jats:italic> exposed volunteers to respiratory syncytial virus (RSV), one of the pathogens responsible for the common cold, and then followed them over the ensuing 2 weeks (see the Perspective by Mirchandani and Walmsley). The main factor distinguishing the infected from the noninfected was that the former showed signs of airway neutrophil activation before exposure to RSV. Conversely, protected individuals showed enhanced interleukin-17 signaling soon after virus inoculation. Similarly, mice pretreated with a neutrophil chemoattractant were more susceptible to RSV infection and CD8 <jats:sup>+</jats:sup> T cell–driven disease. Neutrophil proteases, which can modulate cytokine activity, may explain the disparity and could provide therapeutic targets for RSV and other respiratory infections. </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" related-article-type="in-this-issue" xlink:href="10.1126/science.aba9301">eaba9301</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6513" page="166" related-article-type="in-this-issue" vol="370" xlink:href="10.1126/science.abe3685">166</jats:related-article> </jats:p>

<jats:title>Disentangling fatigue</jats:title> <jats:p> Metal fatigues when repeatedly loaded, ultimately failing when cracks form and propagate through the material. Lavenstein <jats:italic>et al.</jats:italic> studied the origins of this process in nickel. Using high-resolution observations, they tracked how dislocations evolved into microstructural features called persistent slip bands that preceded crack formation. The evolution of tangles of dislocations to a more regularly spaced pattern form the basis for the persistent slip bands and provide a road map for understanding fatigue cracking in metals. </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" related-article-type="in-this-issue" xlink:href="10.1126/science.abb2690">eabb2690</jats:related-article> </jats:p>

<jats:title>A moving target</jats:title> <jats:p> Abl kinase is an important signaling protein that is dysregulated in leukemia and other cancers and is the target of inhibitors such as imatinib. Like other kinases, Abl kinase is dynamic, and regulating conformational dynamics is key to regulating activity. Xie <jats:italic>et al.</jats:italic> used nuclear magnetic resonance to show that the Abl kinase domain interconverts between one active and two inactive states. Imatinib stabilizes an inactive conformation, and several resistance mutations act by destabilizing this conformation. In a construct that includes the regulatory domain, depending on the relative arrangement of the kinase and regulatory domains, the kinase domain is stabilized in either the active state or one of the inhibited states. Understanding the conformational dynamics of kinases can be leveraged to design selective drugs. </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" related-article-type="in-this-issue" xlink:href="10.1126/science.abc2754">eabc2754</jats:related-article> </jats:p>

<jats:title>Interface targeting skirts excitotoxicity</jats:title> <jats:p> Nearly all attempts to use traditional <jats:italic>N</jats:italic> -methyl- <jats:sc>d</jats:sc> -aspartate receptor (NMDAR) antagonists to treat neurodegenerative diseases have failed. This is because NMDARs are not only promoters of neuronal death but also have essential physiological roles in synaptic plasticity and cognitive functions such as learning and memory. Yan <jats:italic>et al.</jats:italic> explored the structural basis of NMDAR coupling to neuronal cell death (see the Perspective by Jones). The death-promoting activity, but not the essential physiological function, was mediated by the physical interaction of NMDARs with TRPM4, a calcium-impermeable ion channel activated by intracellular calcium, depolarization, and temperature. A subsequent structure-based computational drug screen led to the discovery of neuroprotective small molecules that block the NMDAR-TRPM4 interaction interface but spare the critical healthy NMDAR function. </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" related-article-type="in-this-issue" xlink:href="10.1126/science.aay3302">eaay3302</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6513" page="168" related-article-type="in-this-issue" vol="370" xlink:href="10.1126/science.abe2791">168</jats:related-article> </jats:p>

<jats:title>HIV-1 replication and integration in vitro</jats:title> <jats:p> To infect a host cell, HIV-1 must reverse transcribe its single-stranded RNA genome into a double-stranded DNA copy and integrate that copy into a host chromosome. Reverse transcription and integration have been characterized separately but have not been reconstituted together outside of the cell. Christensen <jats:italic>et al.</jats:italic> now report that viral core particles can complete full reverse transcription and integration in a cell-free system. The external capsid shell of the core is required for efficient reverse transcription, and the replicating DNA can loop out of capsid openings. Integration requires cell extract, and this cell-free system should be useful for analyzing how host factors contribute to the first half of the HIV life cycle. </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" related-article-type="in-this-issue" xlink:href="10.1126/science.abc8420">eabc8420</jats:related-article> </jats:p>

<jats:title>Electrolysis feels the heat</jats:title> <jats:p> Electricity infrastructure powered by sunlight and wind requires flexible storage capacity to compensate for the intermittency of these sources. In this context, Hauch <jats:italic>et al.</jats:italic> review progress in solid oxide electrolyzer technology to split water and/or carbon dioxide into chemical fuels. These devices, which rely on oxide conduction between cathode and anode, use nonprecious metals as catalysts and operate above 600°C, thereby benefiting from thermodynamic and kinetic efficiencies. The authors highlight recent optimizations of cell components as well as systems-level architecture. </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" related-article-type="in-this-issue" xlink:href="10.1126/science.aba6118">eaba6118</jats:related-article> </jats:p>

<jats:p>We are destroying the life-support systems of Earth rapidly, making our future uncertain. Ecosystems—the complex sets of organisms that form the globe's living landscape—regulate the atmosphere, water, and soils. They supply humanity its food, most medicines, and many other essential products, and they fill our lives with beauty. But they are falling apart as, one by one, their constituent species are lost. To save what we can and provide our children and grandchildren with a sustainable future, studies must be conducted not only in nature but also, to an increasing extent, on the billions of specimens preserved in the world's natural history collections. For many species barely hanging on in their endangered habitats, these samples will one day be all that we have.</jats:p>

<jats:p>A roundup of weekly science policy and related news.</jats:p>

<jats:p>Big carbon footprints and rising vulnerabilities push astronomers to take action.</jats:p>

<jats:p>Proposed comparison study could clarify safety and which vaccines work best.</jats:p>