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Wen Yang
Researcher at Beijing Institute of Technology
Publications - 599
Citations - 19015
Wen Yang is an academic researcher from Beijing Institute of Technology. The author has contributed to research in topics: Chemistry & Computer science. The author has an hindex of 64, co-authored 501 publications receiving 14385 citations. Previous affiliations of Wen Yang include University of Washington & Max Planck Society.
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Efficient metal-free oxygen reduction in alkaline medium on high-surface-area mesoporous nitrogen-doped carbons made from ionic liquids and nucleobases.
TL;DR: It is demonstrated that the resulting nitrogen-doped carbons show very high catalytic activity, even in the metal-free case in the oxygen reduction reaction (ORR) for fuel cells, and is regarded as a first step toward an all-sustainable fuel cell, avoiding noble metals.
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A Mitochondrial Superoxide Signal Triggers Increased Longevity in Caenorhabditis elegans
Wen Yang,Siegfried Hekimi +1 more
TL;DR: The study of long-lived C. elegans mutants suggests that mitochondrial oxidants can actually help reduce aging by acting as stress signals, rather than acting solely as toxic molecules.
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Keratin: Structure, mechanical properties, occurrence in biological organisms, and efforts at bioinspiration
TL;DR: Keratin can be classified as α- and β-types as discussed by the authors, and α-types have a characteristic filament-matrix structure: 7nm diameter intermediate filaments for α-keratin, and 3nm diameter filament for β-kkeratin.
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Natural Flexible Dermal Armor
Wen Yang,Irene H. Chen,Bernd Gludovatz,Elizabeth A. Zimmermann,Robert O. Ritchie,Robert O. Ritchie,Marc A. Meyers +6 more
TL;DR: Fish, reptiles, and mammals can possess flexible dermal armor for protection by examining the scales from several fish, and osteoderms from armadillos, alligators, and leatherback turtles, to find the means by which Nature derives its protection.
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The Intrinsic Apoptosis Pathway Mediates the Pro-Longevity Response to Mitochondrial ROS in C. elegans
TL;DR: It is shown that the mtROS signal is relayed by the conserved, mitochondria-associated, intrinsic apoptosis signaling pathway, triggered by CED-13, an alternative BH3-only protein, which results in extended longevity whenmtROS generation is inappropriately elevated.