Catálogo de publicaciones - revistas

<jats:p>The widespread use of thermoelectric technology is constrained by a relatively low conversion efficiency of the bulk alloys, which is evaluated in terms of a dimensionless figure of merit (<jats:italic>zT</jats:italic>). The<jats:italic>zT</jats:italic>of bulk alloys can be improved by reducing lattice thermal conductivity through grain boundary and point-defect scattering, which target low- and high-frequency phonons. Dense dislocation arrays formed at low-energy grain boundaries by liquid-phase compaction in Bi<jats:sub>0.5</jats:sub>Sb<jats:sub>1.5</jats:sub>Te<jats:sub>3</jats:sub>(bismuth antimony telluride) effectively scatter midfrequency phonons, leading to a substantially lower lattice thermal conductivity. Full-spectrum phonon scattering with minimal charge-carrier scattering dramatically improved the<jats:italic>zT</jats:italic>to 1.86 ± 0.15 at 320 kelvin (K). Further, a thermoelectric cooler confirmed the performance with a maximum temperature difference of 81 K, which is much higher than current commercial Peltier cooling devices.</jats:p>

<jats:title>Young stars grow up and narrow their focus</jats:title> <jats:p> Stars are thought to grow by gathering spirals of material from a disk. If this is the case, to balance angular momentum, gas should flow out rapidly along the disk's rotation axis. Carrasco-Gonzalez <jats:italic>et al.</jats:italic> now seem to have glimpsed the “before” and “after” stages of the onset of such an outflow, over the course of just 18 years (see the Perspective by Hoare). Radio monitoring of the massive protostar W75N(B)-VLA2 reveals a transition from a spherical wind to a collimated one, giving critical insight into what happens as a massive star forms. </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="6230" page="114" related-article-type="in-this-issue" vol="348" xlink:href="10.1126/science.aaa7216">114</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6230" page="44" related-article-type="in-this-issue" vol="348" xlink:href="10.1126/science.aaa8915">44</jats:related-article> </jats:p>

<jats:title>Evolution in the Ebola virus outbreak</jats:title> <jats:p> Has rapid mutation produced alarming new virus characteristics in the 2013–2015 Ebola virus outbreak in West Africa? Hoenen <jats:italic>et al.</jats:italic> sequenced isolates obtained 9 months into the epidemic from cases in Mali. The nucleotide substitution rate was consistent with rates estimated from past Central African outbreaks. In contrast, analysis of sequence data from early in the outbreak indicated rapid mutation. This more recent finding offers confidence that diagnostic methods, vaccines, and other treatment interventions will remain effective. Nevertheless, vigilance must be maintained: A few mutations can radically change the biological properties of other RNA viruses. </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="6230" page="117" related-article-type="in-this-issue" vol="348" xlink:href="10.1126/science.aaa5646">117</jats:related-article> </jats:p>

<jats:title>Protecting against runaway defense systems</jats:title> <jats:p> RNA interference defends cells against invading genetic elements, such as viruses or transgenes. But while the invasive RNAs are under attack, what protects the normal endogenous RNAs? Zhang <jats:italic>et al.</jats:italic> identified, in the small plant <jats:italic>Arabidopsis</jats:italic> , a surveillance system to do just that: Preserve the normal transcriptome and keep the attack focused on invasive transcripts. </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="6230" page="120" related-article-type="in-this-issue" vol="348" xlink:href="10.1126/science.aaa2618">120</jats:related-article> </jats:p>

<jats:p>Immune checkpoint inhibitors, which unleash a patient’s own T cells to kill tumors, are revolutionizing cancer treatment. To unravel the genomic determinants of response to this therapy, we used whole-exome sequencing of non–small cell lung cancers treated with pembrolizumab, an antibody targeting programmed cell death-1 (PD-1). In two independent cohorts, higher nonsynonymous mutation burden in tumors was associated with improved objective response, durable clinical benefit, and progression-free survival. Efficacy also correlated with the molecular smoking signature, higher neoantigen burden, and DNA repair pathway mutations; each factor was also associated with mutation burden. In one responder, neoantigen-specific CD8+ T cell responses paralleled tumor regression, suggesting that anti–PD-1 therapy enhances neoantigen-specific T cell reactivity. Our results suggest that the genomic landscape of lung cancers shapes response to anti–PD-1 therapy.</jats:p>

<jats:title>Expressing variability under miRNA control</jats:title> <jats:p> MicroRNAs (miRNAs) repress gene expression by inhibiting translation and increasing mRNA degradation. Schmiedel <jats:italic>et al.</jats:italic> used single-cell reporter experiments and mathematical modeling to show that miRNAs can reduce not just expression but the expression variability of target genes (see the Perspective by Hoffman and Pilpel). Combinatorial targeting principles ensured reduced variability for most miRNA gene targets. Thus, miRNAs may provide safeguards for the precision of gene expression during development or cellular homeostasis. </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="6230" page="128" related-article-type="in-this-issue" vol="348" xlink:href="10.1126/science.aaa1738">128</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6230" page="41" related-article-type="in-this-issue" vol="348" xlink:href="10.1126/science.aaa9841">41</jats:related-article> </jats:p>

<jats:title>Inheritance of a covalent histone modification</jats:title> <jats:p> Genomic DNA is the repository of all genetic information and is packaged into chromatin. Chromatin is also a repository of regulatory information in the form of covalent marks added to the histones that package the DNA. These marks can determine tissue- and organ-specific gene expression patterns, which must be transmitted to daughter cells to maintain their identity. Ragunathan <jats:italic>et al.</jats:italic> and Audergon <jats:italic>et al.</jats:italic> show that in fission yeast, a chromatin mark, like genetic information, can be inherited across many cell generations. The mark can be inherited independently of DNA sequence, DNA methylation, or RNA interference. Thus, histone marks constitute true epigenetic information. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue <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.1258699">10.1126/science.1258699</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6230" page="132" related-article-type="in-this-issue" vol="348" xlink:href="10.1126/science.1260638">132</jats:related-article> </jats:p>

<jats:p>Immune cells, including natural killer (NK) cells, recognize transformed cells and eliminate them in a process termed immunosurveillance. It is thought that tumor cells evade immunosurveillance by shedding membrane ligands that bind to the NKG2D-activating receptor on NK cells and/or T cells, and desensitize these cells. In contrast, we show that in mice, a shed form of MULT1, a high-affinity NKG2D ligand, causes NK cell activation and tumor rejection. Recombinant soluble MULT1 stimulated tumor rejection in mice. Soluble MULT1 functions, at least in part, by competitively reversing a global desensitization of NK cells imposed by engagement of membrane NKG2D ligands on tumor-associated cells, such as myeloid cells. The results overturn conventional wisdom that soluble ligands are always inhibitory and suggest a new approach for cancer immunotherapy.</jats:p>

<jats:p>On this week's show: Five years of science following the Deepwater Horizon oil spill disaster in the Gulf of Mexico.</jats:p>

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