Catálogo de publicaciones - revistas

<jats:title>Friction in Microscopic Motor</jats:title> <jats:p> Friction arises because adhesive bonds between two bodies must be broken in order for them to move relative to each other. Now <jats:bold> Bormuth <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" page="870" related-article-type="in-this-issue" vol="325" xlink:href="10.1126/science.1174923">870</jats:related-article> ; see the Perspective by <jats:bold> <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="5942" page="826" related-article-type="in-this-issue" vol="325" xlink:href="10.1126/science.1178017">Veigel and Schmidt</jats:related-article> </jats:bold> ) have used single molecule measurements to characterize the frictional drag force of kinesin-8 motor proteins interacting with their microtubule track. Friction, arising from rupture of bonds with the track, constrains the speed and efficiency of the motor protein. </jats:p>

<jats:title>Dynamin-Related Proteins' Little Helper</jats:title> <jats:p> Dynamin-related proteins (DRPs) comprise a family of large guanosine triphosphatases that self-assemble to form different nucleotide-dependent structures that associate with and change the behavior of intracellular membranes. Many studies have focused on how dynamins function by themselves as machines. In cells, however, DRPs cannot function alone and require additional, associated proteins (DAPs) to perform their functions. The exact mechanistic roles that DAPs play are not known. <jats:bold> Lackner <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" page="874" related-article-type="in-this-issue" vol="325" xlink:href="10.1126/science.1176921">874</jats:related-article> ) address this question using the mitochondrial division machine that requires the DRP, Dnm1. The Dnm1-associated protein, Mdv1, functions as a conformational and structural nucleator for Dnm1 self-assembly. </jats:p>

<jats:title>Ironing Out Stress</jats:title> <jats:p> The peptide hormone, hepcidin, is secreted from the liver in response to extracellular factors, including inflammation, and regulates iron homeostasis by controlling transmembrane iron transport. <jats:bold> Vecchi <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" page="877" related-article-type="in-this-issue" vol="325" xlink:href="10.1126/science.1176639">877</jats:related-article> ) showed that intracellular stress signals in the endoplasmic reticulum also control hepcidin expression and can thus modulate local or systemic iron traffic. This mechanism occurs through the transcription factor CREBH, which is a known mediator of the inflammatory response. Collectively, the results suggest a direct link between the intracellular stress response, innate immunity, and iron metabolism. </jats:p>

<jats:title>Monkey See Human Do</jats:title> <jats:p> Imitation has been put forth as one mechanism through which cultural learning occurs. <jats:bold> Paukner <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" page="880" related-article-type="in-this-issue" vol="325" xlink:href="10.1126/science.1176269">880</jats:related-article> ; see the Perspective by <jats:bold> <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="5942" page="824" related-article-type="in-this-issue" vol="325" xlink:href="10.1126/science.1178714">Call and Carpenter</jats:related-article> </jats:bold> ) now demonstrate that imitation may also contribute to prosocial behaviors. Capuchin monkeys behaved in a more affiliative manner—as assessed by direction of gaze, physical proximity, and token exchange—toward humans who imitated them as compared to humans who performed the same movements, but did not do so simultaneously. </jats:p>

<jats:title>Diverting Asperger Deficit</jats:title> <jats:p> Placement of Asperger syndrome within the family of autism spectrum disorders (ASD) has always been a bit uneasy; although people with Asperger syndrome do exhibit the core impairments in social interaction and communication that are characteristic of ASD, they nevertheless perform well on tests that are thought to assess the ability to mentalize or to possess Theory of Mind skills. One of the classic tests of mentalizing ability is the false-belief task, in which subjects must be able to represent their own beliefs (true) and another's beliefs, which are false because they have not been given complete information, such as not having seen the transfer of a piece of candy from one drawer to another. People with Asperger syndrome succeed at the verbal form of the false-belief task, yet <jats:bold> Senju <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" page="883" related-article-type="in-this-issue" vol="325" xlink:href="10.1126/science.1176170">883</jats:related-article> , published online 16 July) show that this is owing entirely to their having learned how to cope with an existing and still demonstrable deficit in an implicit version of the false-belief task. That is, the core impairment is present, but conscious and explicit learning allows them to compensate. </jats:p>

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

<jats:p>The show includes how imitation affects affiliation, early humans' use of fire as an engineering tool, improving energy efficiency, and more.</jats:p>