Catálogo de publicaciones - revistas

<jats:title>Slower-motion bubble collapse</jats:title> <jats:p> The collapse of viscous bubbles is of practical interest to geophysics, glass manufacturing, and food processing. Previous studies have suggested that gravity or small punctures may play a role in the wrinkling and collapse of viscous bubbles. By studying bubbles with a range of viscosity and by tilting them both sideways and upside down, Oratis <jats:italic>et al.</jats:italic> conclude that gravity is not a factor. Instead, surface tension and dynamic stress of the compressed liquid seem to be the main driving mechanisms for the behavior of the bubbles and the wrinkling instability. </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="6504" page="685" related-article-type="in-this-issue" vol="369" xlink:href="10.1126/science.aba0593">685</jats:related-article> </jats:p>

<jats:title>A hair-splitting way to get dull</jats:title> <jats:p> Razors eventually become dull after shaving even though the blade is about 50 times harder than the hair. Whereas edge rounding and brittle cracking of a blade's hard coating were thought to be responsible, a detailed microstructural investigation by Roscioli <jats:italic>et al.</jats:italic> shows a different mechanism. A combination of out-of-plane bending, microstructural heterogeneity, and asperities—microscopic chips along the smooth edge—sometimes caused fracture to occur if the conditions lined up. This fracture originated at the hair-edge asperity interface and created chipping that dulled a blade faster than other processes. </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="6504" page="689" related-article-type="in-this-issue" vol="369" xlink:href="10.1126/science.aba9490">689</jats:related-article> </jats:p>

<jats:title>The magnetic field in the Sun's corona</jats:title> <jats:p> The solar corona is the outermost layer of the Sun's atmosphere, consisting of hot, diffuse, and highly ionized plasma. The magnetic field in this region is expected to drive many of its physical properties but has been difficult to measure with observations. Yang <jats:italic>et al.</jats:italic> used near-infrared imaging spectroscopy to determine the electron density and magnetohydrodynamic wave speed in the corona. By combining these measurements, they derived maps of the magnetic field throughout the entire observable corona. The method could potentially be used to produce routine magnetic field maps for the corona that are similar to those already available for the Sun's surface. </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="6504" page="694" related-article-type="in-this-issue" vol="369" xlink:href="10.1126/science.abb4462">694</jats:related-article> </jats:p>

<jats:title>Grafting success by cell wall remodeling</jats:title> <jats:p> Plants that produce great fruit may not always have great roots. Grafting of a productive scion onto a resilient rootstock has provided agriculturalists with solutions to this and other challenges. Notaguchi <jats:italic>et al.</jats:italic> have now studied why some plant grafts work better than others (see the Perspective by McCann). The tobacco relative <jats:italic>Nicotiana benthamiana</jats:italic> ( <jats:italic>Nb</jats:italic> ) turns out to be the superhero of grafting, able to form grafts with plants from a wide range of evolutionary families. A bit of <jats:italic>Nb</jats:italic> , set as a middleman between a tomato scion and an <jats:italic>Arabidopsis</jats:italic> rootstock, negotiated a successful junction between these two otherwise nonconversant plant species. The expression of β-1,4-glucanases secreted into the extracellular region turns out to be key in facilitating cell wall reconstruction. </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="6504" page="698" related-article-type="in-this-issue" vol="369" xlink:href="10.1126/science.abc3710">698</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6504" page="618" related-article-type="in-this-issue" vol="369" xlink:href="10.1126/science.abd1641">618</jats:related-article> </jats:p>

<jats:title>Air pollution epidemic</jats:title> <jats:p> The lockdown enforced in most cities in China in response to the outbreak of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) resulted in the virtual absence of motor vehicle traffic and sharply reduced manufacturing activity for several weeks. Le <jats:italic>et al.</jats:italic> report some of the anticipated and unanticipated effects that this had on air pollution there, including unexpectedly high levels of particulate matter abundances and severe haze formation in some areas. This natural experiment will help in the assessment of air pollution mitigation strategies. </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="6504" page="702" related-article-type="in-this-issue" vol="369" xlink:href="10.1126/science.abb7431">702</jats:related-article> </jats:p>

<jats:title>Interferons interfere with lung repair</jats:title> <jats:p> Interferons (IFNs) are central to antiviral immunity. Viral recognition elicits IFN production, which in turn triggers the transcription of IFN-stimulated genes (ISGs), which engage in various antiviral functions. Type I IFNs (IFN-α and IFN-β) are widely expressed and can result in immunopathology during viral infections. By contrast, type III IFN (IFN-λ) responses are primarily restricted to mucosal surfaces and are thought to confer antiviral protection without driving damaging proinflammatory responses. Accordingly, IFN-λ has been proposed as a therapeutic in coronavirus disease 2019 (COVID-19) and other such viral respiratory diseases (see the Perspective by Grajales-Reyes and Colonna). Broggi <jats:italic>et al.</jats:italic> report that COVID-19 patient morbidity correlates with the high expression of type I and III IFNs in the lung. Furthermore, IFN-λ secreted by dendritic cells in the lungs of mice exposed to synthetic viral RNA causes damage to the lung epithelium, which increases susceptibility to lethal bacterial superinfections. Similarly, using a mouse model of influenza infection, Major <jats:italic>et al.</jats:italic> found that IFN signaling (especially IFN-λ) hampers lung repair by inducing p53 and inhibiting epithelial proliferation and differentiation. Complicating this picture, Hadjadj <jats:italic>et al.</jats:italic> observed that peripheral blood immune cells from severe and critical COVID-19 patients have diminished type I IFN and enhanced proinflammatory interleukin-6– and tumor necrosis factor-α–fueled responses. This suggests that in contrast to local production, systemic production of IFNs may be beneficial. The results of this trio of studies suggest that the location, timing, and duration of IFN exposure are critical parameters underlying the success or failure of therapeutics for viral 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" issue="6504" page="706" related-article-type="in-this-issue" vol="369" xlink:href="10.1126/science.abc3545">706</jats:related-article> , p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6504" page="712" related-article-type="in-this-issue" vol="369" xlink:href="10.1126/science.abc2061">712</jats:related-article> , p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6504" page="718" related-article-type="in-this-issue" vol="369" xlink:href="10.1126/science.abc6027">718</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6504" page="626" related-article-type="in-this-issue" vol="369" xlink:href="10.1126/science.abd2208">626</jats:related-article> </jats:p>

<jats:title>Interferons interfere with lung repair</jats:title> <jats:p> Interferons (IFNs) are central to antiviral immunity. Viral recognition elicits IFN production, which in turn triggers the transcription of IFN-stimulated genes (ISGs), which engage in various antiviral functions. Type I IFNs (IFN-α and IFN-β) are widely expressed and can result in immunopathology during viral infections. By contrast, type III IFN (IFN-λ) responses are primarily restricted to mucosal surfaces and are thought to confer antiviral protection without driving damaging proinflammatory responses. Accordingly, IFN-λ has been proposed as a therapeutic in coronavirus disease 2019 (COVID-19) and other such viral respiratory diseases (see the Perspective by Grajales-Reyes and Colonna). Broggi <jats:italic>et al.</jats:italic> report that COVID-19 patient morbidity correlates with the high expression of type I and III IFNs in the lung. Furthermore, IFN-λ secreted by dendritic cells in the lungs of mice exposed to synthetic viral RNA causes damage to the lung epithelium, which increases susceptibility to lethal bacterial superinfections. Similarly, using a mouse model of influenza infection, Major <jats:italic>et al.</jats:italic> found that IFN signaling (especially IFN-λ) hampers lung repair by inducing p53 and inhibiting epithelial proliferation and differentiation. Complicating this picture, Hadjadj <jats:italic>et al.</jats:italic> observed that peripheral blood immune cells from severe and critical COVID-19 patients have diminished type I IFN and enhanced proinflammatory interleukin-6– and tumor necrosis factor-α–fueled responses. This suggests that in contrast to local production, systemic production of IFNs may be beneficial. The results of this trio of studies suggest that the location, timing, and duration of IFN exposure are critical parameters underlying the success or failure of therapeutics for viral 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" issue="6504" page="706" related-article-type="in-this-issue" vol="369" xlink:href="10.1126/science.abc3545">706</jats:related-article> , p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6504" page="712" related-article-type="in-this-issue" vol="369" xlink:href="10.1126/science.abc2061">712</jats:related-article> , p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6504" page="718" related-article-type="in-this-issue" vol="369" xlink:href="10.1126/science.abc6027">718</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6504" page="626" related-article-type="in-this-issue" vol="369" xlink:href="10.1126/science.abd2208">626</jats:related-article> </jats:p>

<jats:title>Interferons interfere with lung repair</jats:title> <jats:p> Interferons (IFNs) are central to antiviral immunity. Viral recognition elicits IFN production, which in turn triggers the transcription of IFN-stimulated genes (ISGs), which engage in various antiviral functions. Type I IFNs (IFN-α and IFN-β) are widely expressed and can result in immunopathology during viral infections. By contrast, type III IFN (IFN-λ) responses are primarily restricted to mucosal surfaces and are thought to confer antiviral protection without driving damaging proinflammatory responses. Accordingly, IFN-λ has been proposed as a therapeutic in coronavirus disease 2019 (COVID-19) and other such viral respiratory diseases (see the Perspective by Grajales-Reyes and Colonna). Broggi <jats:italic>et al.</jats:italic> report that COVID-19 patient morbidity correlates with the high expression of type I and III IFNs in the lung. Furthermore, IFN-λ secreted by dendritic cells in the lungs of mice exposed to synthetic viral RNA causes damage to the lung epithelium, which increases susceptibility to lethal bacterial superinfections. Similarly, using a mouse model of influenza infection, Major <jats:italic>et al.</jats:italic> found that IFN signaling (especially IFN-λ) hampers lung repair by inducing p53 and inhibiting epithelial proliferation and differentiation. Complicating this picture, Hadjadj <jats:italic>et al.</jats:italic> observed that peripheral blood immune cells from severe and critical COVID-19 patients have diminished type I IFN and enhanced proinflammatory interleukin-6– and tumor necrosis factor-α–fueled responses. This suggests that in contrast to local production, systemic production of IFNs may be beneficial. The results of this trio of studies suggest that the location, timing, and duration of IFN exposure are critical parameters underlying the success or failure of therapeutics for viral 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" issue="6504" page="706" related-article-type="in-this-issue" vol="369" xlink:href="10.1126/science.abc3545">706</jats:related-article> , p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6504" page="712" related-article-type="in-this-issue" vol="369" xlink:href="10.1126/science.abc2061">712</jats:related-article> , p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6504" page="718" related-article-type="in-this-issue" vol="369" xlink:href="10.1126/science.abc6027">718</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6504" page="626" related-article-type="in-this-issue" vol="369" xlink:href="10.1126/science.abd2208">626</jats:related-article> </jats:p>

<jats:title>Short path to a complex ring</jats:title> <jats:p> Nucleotide analogs are valuable tools and therapeutics because of their ability to interfere with processes such as DNA synthesis, which are vital to rapidly dividing cells and replicating viruses. These molecules are challenging to synthesize chemically. Meanwell <jats:italic>et al.</jats:italic> developed a “ribose last” synthetic strategy in which a fluorinated acyclic nucleic acid is formed by an <jats:sc>l</jats:sc> - or <jats:sc>d</jats:sc> -proline–catalyzed aldol reaction (see the Perspective by Miller). This intermediate can then be cyclized to yield the nucleic acid analog in one pot with control of anomeric conformation based on cyclization conditions. Nucleotide analogs accessible by this strategy include those with modifications at C2′ and C4′, purines and pyrimidines, and locked and protected products. </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="6504" page="725" related-article-type="in-this-issue" vol="369" xlink:href="10.1126/science.abb3231">725</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6504" page="623" related-article-type="in-this-issue" vol="369" xlink:href="10.1126/science.abd1283">623</jats:related-article> </jats:p>

<jats:title>Seeking broad protection</jats:title> <jats:p> As scientists develop therapeutic antibodies and vaccines against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the risk of emergent coronaviruses makes it important to also identify broadly protective antibodies. Wec <jats:italic>et al.</jats:italic> isolated and characterized hundreds of antibodies against the viral spike protein of SARS-CoV-2 from the memory B cells of a survivor of the 2003 outbreak caused by the related coronavirus, SARS-CoV. In both of these viruses, the spike protein facilitated viral entry by binding to the angiotensin-converting enzyme 2 (ACE2) receptor on human cells. The antibodies targeted multiple sites on the spike protein, but of nine antibodies that showed strong cross-neutralization, eight targeted the domain that binds to ACE2. These eight antibodies also neutralized a bat SARS-related virus. Illuminating the epitopes on the viral spike protein that bind cross-neutralizing antibodies could guide the design of broadly protective vaccines. </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="6504" page="731" related-article-type="in-this-issue" vol="369" xlink:href="10.1126/science.abc7424">731</jats:related-article> </jats:p>