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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

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 MedzhitovORCID

Palabras clave: Multidisciplinary.

Pp. 1070-1075

Dying cells fan the flames of inflammation

Kim NewtonORCID; Vishva M. DixitORCID; Nobuhiko KayagakiORCID

<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