Catálogo de publicaciones - revistas

<jats:title>Small-molecule defense</jats:title> <jats:p> Small-peptide defense molecules are produced by most organisms to fend off invasion by bacteria. The antimicrobial peptides that we know about so far show substantial diversity, synergism, and alternative functions. Lazzaro <jats:italic>et al.</jats:italic> review our knowledge of the evolution and diversity of antimicrobial peptides, the rapid pharmacodynamics of which make them promising candidates for translational applications to complement efforts to overcome antibiotic resistance. </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.aau5480">eaau5480</jats:related-article> </jats:p>

<jats:title>IL-13 hits the gym</jats:title> <jats:p> Interleukin-13 (IL-13) is a cytokine secreted by T cells, innate lymphoid cells (ILC2s), and granulocytes. It acts as a central mediator in allergy and antihelminth defense with various effects. Knudsen <jats:italic>et al.</jats:italic> report a distinct role for IL-13 in exercise and metabolism (see the Perspective by Correia and Ruas). Mice subjected to endurance training showed increases in circulating IL-13, which correlated with ILC2 expansion in the muscles. By contrast, exercise-induced increases in muscle fatty acid utilization and mitochondrial biogenesis were erased when mice lacked IL-13. Activation of signaling pathways downstream of the muscle IL-13 receptor was key to this effect. Intramuscular injection of adenoviral IL-13 could recapitulate exercise-induced metabolic reprogramming. This signaling pathway may have evolved to combat the metabolic stresses of parasite 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" related-article-type="in-this-issue" xlink:href="10.1126/science.aat3987">eaat3987</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6490" page="470" related-article-type="in-this-issue" vol="368" xlink:href="10.1126/science.abb4116">470</jats:related-article> </jats:p>

<jats:p>In April, the Democratic Republic of the Congo (DRC) was on the verge of good news—announcing an end to its tenth (and the world's second largest) Ebola outbreak. Unfortunately, since 10 April, new Ebola cases have been reported in Beni, the epicenter of the Ebola outbreak. Although the DRC has long struggled with political unrest, armed conflict, poverty, and infectious diseases, it must remain committed to ending the Ebola crisis while also applying the lessons learned in tackling this old viral enemy to combat a new one—severe acute respiratory syndrome–coronavirus 2 (SARS-CoV-2), the cause of coronavirus disease 2019 (COVID-19).</jats:p>

<jats:p>In response to the coronavirus disease 2019 (COVID-19) pandemic, countries are launching economic recovery programs to mitigate unemployment and stabilize core industries. Although it is understandably difficult to contemplate other hazards in the midst of this outbreak, it is important to remember that we face another major crisis that threatens human prosperity—climate change. Leveraging COVID-19 recovery programs to simultaneously advance the climate agenda presents a strategic opportunity to transition toward a more sustainable post–COVID-19 world.</jats:p>

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

<jats:p>Doctors debate how to treat patients with low blood oxygen but without trouble breathing.</jats:p>