Catálogo de publicaciones - revistas

<jats:title>Observing more massive stars</jats:title> <jats:p> The number of stars that form at each mass is known as the initial mass function (IMF). For most masses, the IMF follows a power-law distribution, first determined by Edwin Salpeter in 1955. Schneider <jats:italic>et al.</jats:italic> used observations of the nearby star-forming region 30 Doradus (also known as the Tarantula Nebula) and combined these with stellar modeling to determine its IMF. They found more stars above 30 solar masses than predicted by the Salpeter distribution. Because the most massive stars also have the biggest influence on their surroundings—for instance, through ultraviolet radiation, stellar winds, supernova explosions, and production of heavy elements—this excess will have wide-ranging implications. </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="6371" page="69" related-article-type="in-this-issue" vol="359" xlink:href="10.1126/science.aan0106">69</jats:related-article> </jats:p>

<jats:title>A healing squeeze</jats:title> <jats:p> The very long molecules found in synthetic polymers, and their tendency to entangle and partially crystallize, impart many of the polymers' useful properties. However, these same characteristics also mean that chain dynamics are slow, which impedes potential self-healing. Yanagisawa <jats:italic>et al.</jats:italic> developed a family of ether-thiourea linear polymers that form hydrogen-bonded networks and still manage to stay amorphous. The polymers are stiff, showing the strength of the hydrogen bonding; however, because these bonds can easily reform, the polymer is also able to self-heal when compressed. </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="6371" page="72" related-article-type="in-this-issue" vol="359" xlink:href="10.1126/science.aam7588">72</jats:related-article> </jats:p>

<jats:title>Heating up the quantum spin Hall effect</jats:title> <jats:p> Taking practical advantage of the topologically protected conducting edge states of topological insulators (TIs) has proven difficult. Semiconductor systems that have been identified as two-dimensional TIs must be cooled down to near liquid helium temperatures to bring out their topological character. Wu <jats:italic>et al.</jats:italic> fabricated a heterostructure consisting of a monolayer of WTe <jats:sub>2</jats:sub> placed between two layers of hexagonal boron nitride and found that its topological properties persisted up to a relatively high temperature of 100 K. Engineering this so-called quantum spin Hall effect in a van der Waals heterostructure makes it possible to apply many established experimental tools and functionalities. </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="6371" page="76" related-article-type="in-this-issue" vol="359" xlink:href="10.1126/science.aan6003">76</jats:related-article> </jats:p>

<jats:title>Not enough time for recovery</jats:title> <jats:p> Coral bleaching occurs when stressful conditions result in the expulsion of the algal partner from the coral. Before anthropogenic climate warming, such events were relatively rare, allowing for recovery of the reef between events. Hughes <jats:italic>et al.</jats:italic> looked at 100 reefs globally and found that the average interval between bleaching events is now less than half what it was before. Such narrow recovery windows do not allow for full recovery. Furthermore, warming events such as El Niño are warmer than previously, as are general ocean conditions. Such changes are likely to make it more and more difficult for reefs to recover between stressful events. </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="6371" page="80" related-article-type="in-this-issue" vol="359" xlink:href="10.1126/science.aan8048">80</jats:related-article> </jats:p>

<jats:title>Yellow warblers already in decline</jats:title> <jats:p> As the climate changes, species' ability to adapt to changing conditions may relate directly to their future persistence. Determining whether and when this will happen is challenging, however, because it is difficult to tease apart the causes of decline or maintenance. Bay <jats:italic>et al.</jats:italic> looked at the relationship between genomic variation and the environment in North American populations of the yellow warbler (see the Perspective by Fitzpatrick and Edelsparre). Genes linked to exploratory and migratory behavior were important for successful climate adaptation. Furthermore, populations identified as “genetically vulnerable” because of limited climate-associated genomic variation were already declining. </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="6371" page="83" related-article-type="in-this-issue" vol="359" xlink:href="10.1126/science.aan4380">83</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6371" page="29" related-article-type="in-this-issue" vol="359" xlink:href="10.1126/science.aar3920">29</jats:related-article> </jats:p>

<jats:title>Inhibiting natural killer cells in AIDS</jats:title><jats:p>The human leukocyte antigen (HLA) gene complex varies enormously among individuals and helps explain individual variation in immunity to infectious diseases. Ramsuran<jats:italic>et al.</jats:italic>examined data from almost 10,000 HIV infections. Expression of the<jats:italic>HLA-A</jats:italic>and -<jats:italic>B</jats:italic>alleles was associated with higher viral load, reduced CD4<jats:sup>+</jats:sup>T cell counts, and accelerated progression to AIDS. Higher levels of<jats:italic>HLA-A</jats:italic>expression increased expression of<jats:italic>HLA-E</jats:italic>, which blocks a specific receptor (NKG2A) on the immune cells that normally eliminate virus-infected cells. Thus, targeting NKG2A might provide a therapeutic avenue for HIV treatment.</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="6371" page="86" related-article-type="in-this-issue" vol="359" xlink:href="10.1126/science.aam8825">86</jats:related-article></jats:p>

<jats:title>Good bacteria help fight cancer</jats:title> <jats:p> Resident gut bacteria can affect patient responses to cancer immunotherapy (see the Perspective by Jobin). Routy <jats:italic>et al.</jats:italic> show that antibiotic consumption is associated with poor response to immunotherapeutic PD-1 blockade. They profiled samples from patients with lung and kidney cancers and found that nonresponding patients had low levels of the bacterium <jats:italic>Akkermansia muciniphila</jats:italic> . Oral supplementation of the bacteria to antibiotic-treated mice restored the response to immunotherapy. Matson <jats:italic>et al.</jats:italic> and Gopalakrishnan <jats:italic>et al.</jats:italic> studied melanoma patients receiving PD-1 blockade and found a greater abundance of “good” bacteria in the guts of responding patients. Nonresponders had an imbalance in gut flora composition, which correlated with impaired immune cell activity. Thus, maintaining healthy gut flora could help patients combat cancer. </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="6371" page="91" related-article-type="in-this-issue" vol="359" xlink:href="10.1126/science.aan3706">91</jats:related-article> , p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6371" page="104" related-article-type="in-this-issue" vol="359" xlink:href="10.1126/science.aao3290">104</jats:related-article> , p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6371" page="97" related-article-type="in-this-issue" vol="359" xlink:href="10.1126/science.aan4236">97</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6371" page="32" related-article-type="in-this-issue" vol="359" xlink:href="10.1126/science.aar2946">32</jats:related-article> </jats:p>

<jats:title>Good bacteria help fight cancer</jats:title> <jats:p> Resident gut bacteria can affect patient responses to cancer immunotherapy (see the Perspective by Jobin). Routy <jats:italic>et al.</jats:italic> show that antibiotic consumption is associated with poor response to immunotherapeutic PD-1 blockade. They profiled samples from patients with lung and kidney cancers and found that nonresponding patients had low levels of the bacterium <jats:italic>Akkermansia muciniphila</jats:italic> . Oral supplementation of the bacteria to antibiotic-treated mice restored the response to immunotherapy. Matson <jats:italic>et al.</jats:italic> and Gopalakrishnan <jats:italic>et al.</jats:italic> studied melanoma patients receiving PD-1 blockade and found a greater abundance of “good” bacteria in the guts of responding patients. Nonresponders had an imbalance in gut flora composition, which correlated with impaired immune cell activity. Thus, maintaining healthy gut flora could help patients combat cancer. </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="6371" page="91" related-article-type="in-this-issue" vol="359" xlink:href="10.1126/science.aan3706">91</jats:related-article> , p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6371" page="104" related-article-type="in-this-issue" vol="359" xlink:href="10.1126/science.aao3290">104</jats:related-article> , p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6371" page="97" related-article-type="in-this-issue" vol="359" xlink:href="10.1126/science.aan4236">97</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6371" page="32" related-article-type="in-this-issue" vol="359" xlink:href="10.1126/science.aar2946">32</jats:related-article> </jats:p>

<jats:title>Good bacteria help fight cancer</jats:title> <jats:p> Resident gut bacteria can affect patient responses to cancer immunotherapy (see the Perspective by Jobin). Routy <jats:italic>et al.</jats:italic> show that antibiotic consumption is associated with poor response to immunotherapeutic PD-1 blockade. They profiled samples from patients with lung and kidney cancers and found that nonresponding patients had low levels of the bacterium <jats:italic>Akkermansia muciniphila</jats:italic> . Oral supplementation of the bacteria to antibiotic-treated mice restored the response to immunotherapy. Matson <jats:italic>et al.</jats:italic> and Gopalakrishnan <jats:italic>et al.</jats:italic> studied melanoma patients receiving PD-1 blockade and found a greater abundance of “good” bacteria in the guts of responding patients. Nonresponders had an imbalance in gut flora composition, which correlated with impaired immune cell activity. Thus, maintaining healthy gut flora could help patients combat cancer. </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="6371" page="91" related-article-type="in-this-issue" vol="359" xlink:href="10.1126/science.aan3706">91</jats:related-article> , p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6371" page="104" related-article-type="in-this-issue" vol="359" xlink:href="10.1126/science.aao3290">104</jats:related-article> , p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6371" page="97" related-article-type="in-this-issue" vol="359" xlink:href="10.1126/science.aan4236">97</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6371" page="32" related-article-type="in-this-issue" vol="359" xlink:href="10.1126/science.aar2946">32</jats:related-article> </jats:p>

<jats:title>Mitosis-specific role of ATR</jats:title> <jats:p> The ATR (ataxia telangiectasia mutated and Rad3-related) kinase plays important roles in the S phase and during the DNA damage response to safeguard genome integrity. Kabeche <jats:italic>et al.</jats:italic> identified a distinct ATR activation pathway in mitosis that is also critical for suppressing genome instability (see the Perspective by Saldivar and Cimprich). ATR is recruited by Aurora A and activated by R loops at centromeres of mitotic chromosomes; this leads to Aurora B activation, which is necessary for accurate chromosome segregation. This mitotic, R loop–driven ATR signaling pathway could potentially be exploited in the search for cancer therapeutics. </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="6371" page="108" related-article-type="in-this-issue" vol="359" xlink:href="10.1126/science.aan6490">108</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6371" page="30" related-article-type="in-this-issue" vol="359" xlink:href="10.1126/science.aar4799">30</jats:related-article> </jats:p>