Catálogo de publicaciones - revistas

<jats:title>A circuit controlling mechanical itch</jats:title> <jats:p> Considerable progress has been made in understanding and treating chemically induced itch. However, little is known about the mechanisms underlying mechanically evoked itch. Bourane <jats:italic>et al.</jats:italic> produced a model of mechanical itch by reducing the number of neuropeptide Y–expressing inhibitory spinal interneurons. This led to a selective increase in mechanically evoked itch-like behavior in mice. In contrast, chemically evoked itch or pain behavior remained unaffected. </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="6260" page="550" related-article-type="in-this-issue" vol="350" xlink:href="10.1126/science.aac8653">550</jats:related-article> </jats:p>

<jats:title>Circuits for brain building</jats:title> <jats:p>The brain is made up of circuits. Chen and Kriegstein analyzed how one particular circuit functions differently in developing and mature mouse brains (see the Perspective by Spitzer). This circuit connects the brain's diencephalon to the cortex. Early in development, the circuit is excitatory and affects how the cortical neurons it touches build their dendrites and synapses. Later on, after the fundamentals of brain construction are in place, the circuit switches to inhibitory functions, helping the brain resist epileptiform activity.</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="6260" page="554" related-article-type="in-this-issue" vol="350" xlink:href="10.1126/science.aac6472">554</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6260" page="510" related-article-type="in-this-issue" vol="350" xlink:href="10.1126/science.aad4876">510</jats:related-article> </jats:p>

<jats:title> The benefits of <jats:italic>Escherichia coli</jats:italic> </jats:title> <jats:p> Infection and intestinal damage can trigger severe muscle wasting and loss of fat in mice. How this happens is poorly understood. Palaferri Schieber <jats:italic>et al.</jats:italic> discovered a protective <jats:italic>Escherichia coli</jats:italic> strain in their mouse colony. Mice intestinally colonized with the <jats:italic>E. coli</jats:italic> and infected with the food-poisoning bug <jats:italic>Salmonella</jats:italic> or with the lung pathogen <jats:italic>Burkholderia</jats:italic> did not waste away. Without the <jats:italic>E. coli</jats:italic> , similarly infected mice became fatally ill. The protective <jats:italic>E. coli</jats:italic> stimulated an innate immune mechanism that ensured that muscle-signaling pathways were not damaged by infection. Thus, the friendly <jats:italic>E. coli</jats:italic> allowed its host to tolerate and survive the pathogens. </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="6260" page="558" related-article-type="in-this-issue" vol="350" xlink:href="10.1126/science.aac6468">558</jats:related-article> </jats:p>

<jats:title>A close up view of retrovirus spreading</jats:title> <jats:p> Viral infections typically begin with a small number of viral particles gaining access to the host at a specific tissue site. But how do viruses that cause systemic infections, such as HIV, spread more widely? Sewald <jats:italic>et al.</jats:italic> visualized how the retroviruses murine leukemia virus (MLV) and HIV spread within lymph nodes in mice (see the Perspective by Hope). Specific macrophages that line the lymph-draining sinuses in lymph nodes first captured the virus using the carbohydrate-binding protein CD169. These macrophages subsequently transferred virus to the B1 subclass of B lymphocytes, which migrated further into the lymph node, disseminating the virus more widely. </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="6260" page="563" related-article-type="in-this-issue" vol="350" xlink:href="10.1126/science.aab2749">563</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6260" page="511" related-article-type="in-this-issue" vol="350" xlink:href="10.1126/science.aad5409">511</jats:related-article> </jats:p>

<jats:title>Viral oncogenes remove the host's STING</jats:title> <jats:p> Cancer-causing viruses, such as the human papilloma virus (HPV) that causes cervical cancer, account for 12% of human cancers. One way they can cause cancer is by targeting tumor suppressor proteins in the host. Now Lau <jats:italic>et al.</jats:italic> report that DNA tumor viruses can also thwart the host's immune system. Oncogenes from HPV and human adenovirus bound to the protein STING, a key component of the cGAS-STING pathway that senses and defends against intracellular DNA. In this way, the viruses subvert the host's antiviral immunity and set up shop, which, for an unlucky few, eventually causes 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="6260" page="568" related-article-type="in-this-issue" vol="350" xlink:href="10.1126/science.aab3291">568</jats:related-article> </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>On this week's show: Where the Amazon Bason's stunning biodoversity comes from and a roundup of daily news stories.</jats:p>