Catálogo de publicaciones - revistas

<jats:p>The prospect of controlling the electronic properties of materials via the vacuum fields of cavity electromagnetic resonators is emerging as one of the frontiers of condensed matter physics. We found that the enhancement of vacuum field fluctuations in subwavelength split-ring resonators strongly affects one of the most paradigmatic quantum protectorates, the quantum Hall electron transport in high-mobility two-dimensional electron gases. The observed breakdown of the topological protection of the integer quantum Hall effect is interpreted in terms of a long-range cavity-mediated electron hopping where the anti-resonant terms of the light-matter coupling Hamiltonian develop into a finite resistivity induced by the vacuum fluctuations. Our experimental platform can be used for any two-dimensional material and provides a route to manipulate electron phases in matter by means of vacuum-field engineering.</jats:p>

<jats:p> Molecular knots are often prepared using metal helicates to cross the strands. We found that coordinatively mismatching oligodentate ligands and metal ions provides a more effective way to synthesize larger knots using Vernier templating. Strands composed of different numbers of tridentate 2,6-pyridinedicarboxamide groups fold around nine-coordinate lanthanide (III) ions to generate strand-entangled complexes with the lowest common multiple of coordination sites for the ligand strands and metal ions. Ring-closing olefin metathesis then completes the knots. A 3:2 (ditopic strand:metal) Vernier assembly produces +3 <jats:sub>1</jats:sub> #+3 <jats:sub>1</jats:sub> and −3 <jats:sub>1</jats:sub> #−3 <jats:sub>1</jats:sub> granny knots. Vernier complexes of 3:4 (tetratopic strand:metal) stoichiometry selectively form a 378-atom-long trefoil-of-trefoils triskelion knot with 12 alternating strand crossings or, by using opposing stereochemistry at the terminus of the strand, an inverted-core triskelion knot with six alternating and six nonalternating strand crossings. </jats:p>

<jats:p>Heterologous prime-boost immunization strategies have the potential to augment COVID-19 vaccine efficacy. We longitudinally profiled severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike (S)–specific serological and memory B cell (MBC) responses in individuals who received either homologous (ChAdOx1:ChAdOx1) or heterologous (ChAdOx1:mRNA-1273) prime-boost vaccination. Heterologous messenger RNA (mRNA) booster immunization induced higher serum neutralizing antibody and MBC responses against SARS-CoV-2 variants of concern (VOCs) compared with that of homologous ChAdOx1 boosting. Specificity mapping of circulating B cells revealed that mRNA-1273 boost immunofocused ChAdOx1-primed responses onto epitopes expressed on prefusion-stabilized S. Monoclonal antibodies isolated from mRNA-1273–boosted participants displayed overall higher binding affinities and increased breadth of reactivity against VOCs relative to those isolated from ChAdOx1-boosted individuals. Overall, the results provide molecular insight into the enhanced quality of the B cell response induced after heterologous mRNA booster vaccination.</jats:p>

<jats:p>The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) Omicron variant has become the dominant infective strain. We report the structures of the Omicron spike trimer on its own and in complex with angiotensin-converting enzyme 2 (ACE2) or an anti-Omicron antibody. Most Omicron mutations are located on the surface of the spike protein and change binding epitopes to many current antibodies. In the ACE2-binding site, compensating mutations strengthen receptor binding domain (RBD) binding to ACE2. Both the RBD and the apo form of the Omicron spike trimer are thermodynamically unstable. An unusual RBD-RBD interaction in the ACE2-spike complex supports the open conformation and further reinforces ACE2 binding to the spike trimer. A broad-spectrum therapeutic antibody, JMB2002, which has completed a phase 1 clinical trial, maintains neutralizing activity against Omicron. JMB2002 binds to RBD differently from other characterized antibodies and inhibits ACE2 binding.</jats:p>

<jats:p> Bivalent genes are ready for activation upon the arrival of developmental cues. Here, we report that BEND3 is a CpG island (CGI)–binding protein that is enriched at regulatory elements. The cocrystal structure of BEND3 in complex with its target DNA reveals the structural basis for its DNA methylation–sensitive binding property. Mouse embryos ablated of <jats:italic>Bend3</jats:italic> died at the pregastrulation stage. <jats:italic>Bend3</jats:italic> null embryonic stem cells (ESCs) exhibited severe defects in differentiation, during which hundreds of CGI-containing bivalent genes were prematurely activated. BEND3 is required for the stable association of polycomb repressive complex 2 (PRC2) at bivalent genes that are highly occupied by BEND3, which suggests a reining function of BEND3 in maintaining high levels of H3K27me3 at these bivalent genes in ESCs to prevent their premature activation in the forthcoming developmental stage. </jats:p>

<jats:p>We present a unique, extensive, and open synaptic physiology analysis platform and dataset. Through its application, we reveal principles that relate cell type to synaptic properties and intralaminar circuit organization in the mouse and human cortex. The dynamics of excitatory synapses align with the postsynaptic cell subclass, whereas inhibitory synapse dynamics partly align with presynaptic cell subclass but with considerable overlap. Synaptic properties are heterogeneous in most subclass-to-subclass connections. The two main axes of heterogeneity are strength and variability. Cell subclasses divide along the variability axis, whereas the strength axis accounts for substantial heterogeneity within the subclass. In the human cortex, excitatory-to-excitatory synaptic dynamics are distinct from those in the mouse cortex and vary with depth across layers 2 and 3.</jats:p>

<jats:p>Elucidating the wiring diagram of the human cell is a central goal of the postgenomic era. We combined genome engineering, confocal live-cell imaging, mass spectrometry, and data science to systematically map the localization and interactions of human proteins. Our approach provides a data-driven description of the molecular and spatial networks that organize the proteome. Unsupervised clustering of these networks delineates functional communities that facilitate biological discovery. We found that remarkably precise functional information can be derived from protein localization patterns, which often contain enough information to identify molecular interactions, and that RNA binding proteins form a specific subgroup defined by unique interaction and localization properties. Paired with a fully interactive website (opencell.czbiohub.org), our work constitutes a resource for the quantitative cartography of human cellular organization.</jats:p>

<jats:p>As the world reflects on 2 years of the COVID-19 pandemic, we need to change how to tackle the enormous challenges of the future. The good news is that the past 2 years of the COVID-19 pandemic have shown that change is possible.</jats:p>

<jats:p>The devastation and despair gripping Ukraine following the unprovoked invasion by neighboring Russia is heartbreaking and unthinkable. Such a loss of life and homeland has stirred wide concern around the world. This war sets back progress to establish a peaceful and sustainable world and to address important problems faced by all humanity, including climate change, environmental degradation, public health, and inequality. The international community of scientists cooperates extensively to address the challenges of our time, and a war that is destroying a stable and healthy nation and provoking a refugee crisis is no exception. What can the scientific community do most immediately to provide support and aid to its Ukrainian colleagues in their time of need? The community should focus on strengthening regional partnerships in Eastern Europe, networking to find refugees safe havens, speaking out forcefully against this invasion, and preparing to help rebuild Ukrainian science when the time is right.</jats:p>