Catálogo de publicaciones - revistas
Science
Resumen/Descripción – provisto por la editorial
No disponible.
Palabras clave – provistas por la editorial
No disponibles.
Disponibilidad
Institución detectada | Período | Navegá | Descargá | Solicitá |
---|---|---|---|---|
No detectada | desde mar. 1997 / hasta dic. 2023 | Science Journals |
Información
Tipo de recurso:
revistas
ISSN impreso
0036-8075
ISSN electrónico
1095-9203
Editor responsable
American Association for the Advancement of Science (AAAS)
País de edición
Estados Unidos
Fecha de publicación
1880-
Cobertura temática
Tabla de contenidos
Aiming for fish-friendly hydropower plants
Ling Bai; Ling Zhou
Palabras clave: Multidisciplinary.
Pp. 1062-1063
Poland’s border wall threatens ancient forest
Bogdan Jaroszewicz; Katarzyna Nowak; Michał Żmihorski
Palabras clave: Multidisciplinary.
Pp. 1063-1063
Funders, diversify research grant awards
Sindy N. Escobar Alvarez; Wonder P. Drake; Lisa Evans; Elizabeth R. Myers
Palabras clave: Multidisciplinary.
Pp. 1063-1064
Green with phenology
Lin Meng
<jats:p>Warmer and brighter cities trick trees into thinking that spring arrives earlier</jats:p>
Palabras clave: Multidisciplinary.
Pp. 1065-1066
As cancer grows old
Adrian Baez-Ortega
<jats:p>Mutations trace the evolution of an ancient tumor lineage</jats:p>
Palabras clave: Multidisciplinary.
Pp. 1066-1066
Seeing fat inside the nucleus
Anete Romanauska
<jats:p>The inner nuclear membrane has an expanded role in lipid metabolism</jats:p>
Palabras clave: Multidisciplinary.
Pp. 1066-1066
Fat for heat
Wenfei Sun
<jats:p>The distinct properties of brown adipose tissue may be harnessed to mitigate obesity</jats:p>
Palabras clave: Multidisciplinary.
Pp. 1066-1066
Inflammation
Gemma Alderton; Seth Thomas Scanlon
Palabras clave: Multidisciplinary.
Pp. 1068-1069
The spectrum of inflammatory responses
Ruslan Medzhitov
Palabras clave: Multidisciplinary.
Pp. 1070-1075
Dying cells fan the flames of inflammation
Kim Newton; Vishva M. Dixit; Nobuhiko Kayagaki
<jats:p>Inflammatory processes that recruit leukocytes to injured or infected tissues are crucial for tissue repair and the elimination of pathogens. However, excessive or chronic inflammation promotes tissue damage and disease, as in arthritis, atherosclerosis, inflammatory bowel disease, and COVID-19. Intracellular constituents released from dying cells are among the stimuli that trigger proinflammatory gene expression programs in innate immune cells. We explore how programmed cell death mechanisms—apoptosis, necroptosis, and pyroptosis—may contribute to inflammatory disease. We discuss inhibition of cell death as a potential therapeutic strategy, focusing on the targets RIPK1 (receptor interacting serine/threonine kinase 1), NLRP3 (NLR family pyrin domain containing 3), and GSDMD (gasdermin D) as important mediators of lytic cell death. We also consider the potential benefits of limiting membrane rupture rather than cell death by targeting NINJ1.</jats:p>
Palabras clave: Multidisciplinary.
Pp. 1076-1080