Results 231 to 240 of about 119,871 (297)

Memristive Physical Reservoir Computing

open access: yesAdvanced Science, EarlyView.
Memristors’ nonlinear dynamics and input‐dependent memory effects make them ideal candidates for high‐performance physical reservoir computing (RC). Based on their conductance modulation, memristors can be classified as electronic or optoelectronic types.
Dian Jiao   +9 more
wiley   +1 more source

Traumatic injuries and outcomes during the Libyan Civil War: a systematic review. [PDF]

open access: yesBMJ Mil Health
Abdulshafea M   +3 more
europepmc   +1 more source

Drug‐Induced Cuproptosis Defines the Therapeutic Window of Celecoxib in Intervertebral Disc Degeneration via the HSP90‐RBX1 Axis

open access: yesAdvanced Science, EarlyView.
This study reveals the dual role of celecoxib in intervertebral disc degeneration. While low concentrations are protective, high concentrations induce toxicity by upregulating HSP90, which synergizes with USP15 to deubiquitinate and stabilize RBX1. This leads to degradation of COMMD1/ATP7B, copper dyshomeostasis, and ultimately, cuproptosis.
Youfeng Guo   +11 more
wiley   +1 more source

“Membrane‐Guided” Repair Strategy: Precision Delivery of GGT1 Degrader for Targeted Repair and Regeneration of Spinal Cord Neurons

open access: yesAdvanced Science, EarlyView.
This study confirms that GGT1 is a key driver of neuronal ferroptosis following spinal cord injury. We developed NSCm@EA, a biomimetic delivery system coated with neural stem cell membranes, for precise delivery of enocyanin to injured neurons. By combining targeted delivery with ubiquitination degradation mechanisms, this system promotes MGRN1 ...
Tao Yang   +14 more
wiley   +1 more source

CK2α Deficiency Drives Myocardial Fibrosis via Desmin‐Induced Mitochondrial Dysfunction

open access: yesAdvanced Science, EarlyView.
CK2α preserves mitochondrial homeostasis by phosphorylating Desmin to recruit Cryab, ensuring proper filament assembly. CK2α deficiency disrupts this interaction, causing mitochondrial dysfunction, metabolic shifts, bioenergetic failure, and oxidative stress—ultimately establishing a pro‐fibrotic environment that drives cardiac fibrosis.
Canjie Ma   +12 more
wiley   +1 more source

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