Results 221 to 230 of about 273,197 (337)
Bilirubin Targeting WNK1 to Alleviate NLRP3‐Mediated Neuroinflammation
At physiological concentrations, bilirubin binds to the kinase domain of WNK1, thereby augmenting its activity and facilitating the phosphorylation of downstream SPAK/OSR1. This phosphorylation inhibits KCC2 activity, leading to elevate intracellular chloride levels in neurons.
Linfei Mao+14 more
wiley +1 more source
The contribution of brain injury to the overall injury severity of brain-injured patients
Daniel Fife, Janine Jagger
openalex +1 more source
Tirilazad treatment does not decrease early brain injury after transient focal ischemia in cats. [PDF]
Reiko Takeshima+3 more
openalex +1 more source
Neurological manifestations of encephalitic alphaviruses, traumatic brain injuries, and organophosphorus nerve agent exposure. [PDF]
VanderGiessen M+6 more
europepmc +1 more source
Traditional Chinese Medicine (TCM), while holistic and historically esteemed, faces challenges in “miracle cures” due to slow onset, long cycles, and difficulty controlling quality. This study obtains the active ingredients, glabridin (GLA) and puerarin (PUE), from Ge‐Gen Decoction (GGD), developing a safe and effective drug delivery system, GLA‐PUE ...
Jianhong Qi+7 more
wiley +1 more source
Investigating the Impact of Turmeric on Neuroinflammation and Degenerative Changes in Repetitive Traumatic Brain Injuries: Insights from Murine Model. [PDF]
Siahaan AMP+6 more
europepmc +1 more source
D‐galactose (D‐gal) induced inner ear hair cell senescence by inhibiting TFEB transcription. RONIN/HCF1 promotes TFEB transcription to prevent cochlear HCs from D‐gal‐induced senescence through autophagy activation. Abstract Age‐related hearing loss is characterized by senescent inner ear hair cells (HCs) and reduced autophagy.
Yongjie Wei+18 more
wiley +1 more source
Editorial: Revisiting mouse models of traumatic brain injuries: a focus on intracellular mechanisms. [PDF]
Omais S, Kobeissy F, Zibara K, Shaito A.
europepmc +1 more source
USP42 is identified as a novel DUB of PPARγ in hepatocytes. USP42 mediated PPARγ deubiquitylation determines its transcriptional preference on proliferative and redox balance genes. USP42 knockdown exacerbates liver damage and delays regeneration. FGF2 is the upstream signal that initiates and activates the USP42‐PPARγ axis.
Nanfei Yang+16 more
wiley +1 more source