Catálogo de publicaciones - revistas
Nature
Resumen/Descripción – provisto por la editorial en inglés
Nature is a weekly international journal publishing the finest peer-reviewed research in all fields of science and technology on the basis of its originality, importance, interdisciplinary interest, timeliness, accessibility, elegance and surprising conclusions. Nature also provides rapid, authoritative, insightful and arresting news and interpretation of topical and coming trends affecting science, scientists and the wider public.Palabras clave – provistas por la editorial
No disponibles.
Disponibilidad
| Institución detectada | Período | Navegá | Descargá | Solicitá |
|---|---|---|---|---|
| No detectada | desde jul. 2012 / hasta dic. 2023 | Nature.com | ||
| No detectada | desde jul. 2006 / hasta ago. 2012 | Ovid |
Información
Tipo de recurso:
revistas
ISSN impreso
0028-0836
ISSN electrónico
1476-4687
Editor responsable
Springer Nature
País de edición
Reino Unido
Fecha de publicación
1869-
Tabla de contenidos
Rational design of a new antibiotic class for drug-resistant infections
Thomas F. Durand-Reville; Alita A. Miller
; John P. O’Donnell; Xiaoyun Wu; Mark A. Sylvester; Satenig Guler; Ramkumar Iyer; Adam B. Shapiro; Nicole M. Carter; Camilo Velez-Vega; Samir H. Moussa; Sarah M. McLeod; April Chen; Angela M. Tanudra; Jing Zhang; Janelle Comita-Prevoir; Jan A. Romero; Hoan Huynh; Andrew D. Ferguson; Peter S. Horanyi; Stephen J. Mayclin; Henry S. Heine; George L. Drusano; Jason E. Cummings; Richard A. Slayden; Ruben A. Tommasi
Palabras clave: Multidisciplinary.
Pp. 698-702
Emergence and expansion of SARS-CoV-2 B.1.526 after identification in New York
Medini K. Annavajhala; Hiroshi Mohri; Pengfei Wang; Manoj Nair; Jason E. Zucker; Zizhang Sheng; Angela Gomez-Simmonds; Anne L. Kelley; Maya Tagliavia; Yaoxing Huang; Trevor Bedford; David D. Ho; Anne-Catrin Uhlemann
<jats:title>Abstract</jats:title><jats:p>SARS-CoV-2 infections have surged across the globe in recent months, concomitant with considerable viral evolution<jats:sup>1–3</jats:sup>. Extensive mutations in the spike protein may threaten the efficacy of vaccines and therapeutic monoclonal antibodies<jats:sup>4</jats:sup>. Two signature spike mutations of concern are E484K, which has a crucial role in the loss of neutralizing activity of antibodies, and N501Y, a driver of rapid worldwide transmission of the B.1.1.7 lineage. Here we report the emergence of the variant lineage B.1.526 (also known as the Iota variant<jats:sup>5</jats:sup>), which contains E484K, and its rise to dominance in New York City in early 2021. This variant is partially or completely resistant to two therapeutic monoclonal antibodies that are in clinical use and is less susceptible to neutralization by plasma from individuals who had recovered from SARS-CoV-2 infection or serum from vaccinated individuals, posing a modest antigenic challenge. The presence of the B.1.526 lineage has now been reported in all 50 states in the United States and in many other countries. B.1.526 rapidly replaced earlier lineages in New York, with an estimated transmission advantage of 35%. These transmission dynamics, together with the relative antibody resistance of its E484K sub-lineage, are likely to have contributed to the sharp rise and rapid spread of B.1.526. Although SARS-CoV-2 B.1.526 initially outpaced B.1.1.7 in the region, its growth subsequently slowed concurrently with the rise of B.1.1.7 and ensuing variants.</jats:p>
Palabras clave: Multidisciplinary.
Pp. 703-708
A lymphocyte–microglia–astrocyte axis in chronic active multiple sclerosis
Martina Absinta; Dragan Maric; Marjan Gharagozloo; Thomas Garton; Matthew D. Smith; Jing Jin; Kathryn C. Fitzgerald; Anya Song; Poching Liu; Jing-Ping Lin; Tianxia Wu; Kory R. Johnson; Dorian B. McGavern; Dorothy P. Schafer; Peter A. Calabresi; Daniel S. Reich
Palabras clave: Multidisciplinary.
Pp. 709-714
Acinar cell clonal expansion in pancreas homeostasis and carcinogenesis
Patrick Neuhöfer; Caitlin M. Roake; Stewart J. Kim; Ryan J. Lu; Robert B. West; Gregory W. Charville; Steven E. Artandi
Palabras clave: Multidisciplinary.
Pp. 715-719
Programmable RNA targeting with the single-protein CRISPR effector Cas7-11
Ahsen Özcan; Rohan Krajeski; Eleonora Ioannidi; Brennan Lee; Apolonia Gardner; Kira S. Makarova; Eugene V. Koonin; Omar O. Abudayyeh; Jonathan S. Gootenberg
Palabras clave: Multidisciplinary.
Pp. 720-725
UTX condensation underlies its tumour-suppressive activity
Bi Shi; Wei Li; Yansu Song; Zhenjia Wang; Rui Ju; Aleksandra Ulman; Jing Hu; Francesco Palomba; Yanfang Zhao; John Philip Le; William Jarrard; David Dimoff; Michelle A. Digman; Enrico Gratton; Chongzhi Zang; Hao Jiang
Palabras clave: Multidisciplinary.
Pp. 726-731
Structure-based classification predicts drug response in EGFR-mutant NSCLC
Jacqulyne P. Robichaux; Xiuning Le; R. S. K. Vijayan; J. Kevin Hicks; Simon Heeke; Yasir Y. Elamin; Heather Y. Lin; Hibiki Udagawa; Ferdinandos Skoulidis; Hai Tran; Susan Varghese; Junqin He; Fahao Zhang; Monique B. Nilsson; Lemei Hu; Alissa Poteete; Waree Rinsurongkawong; Xiaoshan Zhang; Chenghui Ren; Xiaoke Liu; Lingzhi Hong; Jianjun Zhang; Lixia Diao; Russell Madison; Alexa B. Schrock; Jennifer Saam; Victoria Raymond; Bingliang Fang; Jing Wang; Min Jin Ha; Jason B. Cross; Jhanelle E. Gray; John V. Heymach
<jats:title>Abstract</jats:title><jats:p>Epidermal growth factor receptor (<jats:italic>EGFR</jats:italic>) mutations typically occur in exons 18–21 and are established driver mutations in non-small cell lung cancer (NSCLC)<jats:sup>1–3</jats:sup>. Targeted therapies are approved for patients with ‘classical’ mutations and a small number of other mutations<jats:sup>4–6</jats:sup>. However, effective therapies have not been identified for additional <jats:italic>EGFR</jats:italic> mutations. Furthermore, the frequency and effects of atypical <jats:italic>EGFR</jats:italic> mutations on drug sensitivity are unknown<jats:sup>1,3,7–10</jats:sup>. Here we characterize the mutational landscape in 16,715 patients with <jats:italic>EGFR</jats:italic>-mutant NSCLC, and establish the structure–function relationship of <jats:italic>EGFR</jats:italic> mutations on drug sensitivity. We found that <jats:italic>EGFR</jats:italic> mutations can be separated into four distinct subgroups on the basis of sensitivity and structural changes that retrospectively predict patient outcomes following treatment with EGFR inhibitors better than traditional exon-based groups. Together, these data delineate a structure-based approach for defining functional groups of <jats:italic>EGFR</jats:italic> mutations that can effectively guide treatment and clinical trial choices for patients with <jats:italic>EGFR</jats:italic>-mutant NSCLC and suggest that a structure–function-based approach may improve the prediction of drug sensitivity to targeted therapies in oncogenes with diverse mutations.</jats:p>
Palabras clave: Multidisciplinary.
Pp. 732-737
How to shrink the gap that holds Black scientists back
Ingrid Torjesen
Palabras clave: Multidisciplinary.
Pp. 739-740
Stress testing avocados
Virginia Gewin
Palabras clave: Multidisciplinary.
Pp. 742-742
Sleeping flies and climate anxiety — the week in infographics
Palabras clave: Multidisciplinary.
Pp. No disponible