Catálogo de publicaciones - revistas

<jats:title>Writing to Close Gaps</jats:title> <jats:p> Some have questioned whether findings in the laboratory obtained under controlled conditions and limited contexts bear any relevance to behavior in real-world environments in which ordinary people cope with real-life challenges. Recent studies have shown a replicable and long-term effect of a brief writing exercise on the academic performance of African-American seventh graders in an inner-city public school. <jats:bold> Miyake <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="1234" related-article-type="in-this-issue" vol="330" xlink:href="10.1126/science.1195996">1234</jats:related-article> ) extended this approach to show that a similar kind of writing exercise can help to reduce the gender gap observed in the performance of female students in an undergraduate physics class, where performance is measured not only via course grades and exam scores, but also on a standardized test. </jats:p>

<jats:title>Lynx Vision</jats:title> <jats:p> Early in development, correct visual experiences during the so-called “critical period” build the foundations for visual function in adulthood. Hence, when one eye is not working together with the other, an adult may be left with imperfect vision. The plasticity characteristic of the critical period does not persist into adulthood, and later readjustments to visual function may not be fully successful. <jats:bold> Morishita <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="1238" related-article-type="in-this-issue" vol="330" xlink:href="10.1126/science.1195320">1238</jats:related-article> , published online 11 November; see the Perspective by <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6008" page="1189" related-article-type="in-this-issue" vol="330" xlink:href="10.1126/science.1198983"> <jats:bold>Higley and Strittmatter</jats:bold> </jats:related-article> ) have identified a gene in mice called <jats:italic>Lynx1</jats:italic> , which shows increased expression after the critical period. The Lynx1 protein binds to and reduces the sensitivity of acetylcholine receptors, but if mice were treated to enhanced cholinergic signaling, their adult visual plasticity was improved and if mice lacked the <jats:italic>Lynx1</jats:italic> gene altogether, they were able to recover visual function even in adulthood. </jats:p>

<jats:title>By a Whisker</jats:title> <jats:p> Every student learns that the sensory cortex is used for processing sensation and the motor cortex is used for perceiving movement. However, in the real world, this may not always be so neatly arranged. <jats:bold> Matyas <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="1240" related-article-type="in-this-issue" vol="330" xlink:href="10.1126/science.1195797">1240</jats:related-article> ) have found that sensory and motor fields are specialized for different types of movement, such that in mice the motor cortex controlled the forward movement (protraction) of their whiskers and the sensory cortex controlled backwards movements (retraction) of whiskers. So if a whisker hits an object, then a reasonable first reaction might be a motor command for retraction. Similarly, the motor cortex stimulates protraction for more active exploration. Hence, the sensory cortex is also motor and the motor cortex is also sensory. In an ecological context, these combined reactions offer a repertoire useful for a mouse seeking food and shelter in a complex environment. </jats:p>

<jats:title>Self-Protection Mechanism</jats:title> <jats:p> Kaposi's sarcoma–associated herpesvirus (KSHV) causes an AIDS-associated cancer. During its lytic phase, the virus produces a noncoding polyadenylated nuclear RNA that accumulates to high levels in infected cells. This occurs because a helix-loop-helix element, called ENE within the RNA, that contains a uridine-rich internal loop, sequesters the poly(A) tail, preventing the initiation of RNA decay. <jats:bold> Mitton-Fry <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="1244" related-article-type="in-this-issue" vol="330" xlink:href="10.1126/science.1195858">1244</jats:related-article> ) have determined the 2.5 angstrom structure of the ENE core bound to the RNA. Instead of just binding to the uridine-rich loop, as was expected, the poly(A) tail interacts with the loop and lower stem to form a triple helix to prevent decay. Similar mechanisms may protect other noncoding RNAs from rapid turnover. </jats:p>

<jats:title>Promoting Apoptosis</jats:title> <jats:p> During acute disease, the promyelocytic leukemia (PML) protein becomes fused to another protein as a result of a chromosomal translocation. This protein appears to have multiple and varied functions, including the ability to form distinctive complexes in the nucleus that suppress tumorigenesis and promote apoptotic cell death. <jats:bold> Giorgi <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="1247" related-article-type="in-this-issue" vol="330" xlink:href="10.1126/science.1189157">1247</jats:related-article> , published online 28 October; see the Perspective by <jats:bold> <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6008" page="1183" related-article-type="in-this-issue" vol="330" xlink:href="10.1126/science.1199405">Culjkovic-Kraljacic and Borden</jats:related-article> </jats:bold> ) have proposed a mechanism by which PML influences the cellular signals that promote apoptosis. The protein was localized at sites of contact between the endoplasmic reticulum and mitochondria, where it associated with a calcium channel, a protein kinase, and a protein phosphatase, to regulate calcium mobilization into the mitochondrion, which then triggers the cell death program. </jats:p>

<jats:title>Cellular Devices</jats:title> <jats:p> Cellular control mechanisms might offer opportunities to build genetic devices capable of sensing aberrant cells and activate a regulatory signal that directs the cell to alter its biological state. <jats:bold> Culler <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="1251" related-article-type="in-this-issue" vol="330" xlink:href="10.1126/science.1192128">1251</jats:related-article> ; see the Perspective by <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6008" page="1185" related-article-type="in-this-issue" vol="330" xlink:href="10.1126/science.1199495"> <jats:bold>Liu and Arkin</jats:bold> </jats:related-article> ) present a proof of principle for a synthetic gene network in which cells were engineered to make an RNA-based device that detected molecules associated with disease states such as inflammation and cancer. Detection then triggered expression of a gene that made the cells more sensitive to a drug causing cell death. </jats:p>

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