Results 141 to 150 of about 607,889 (300)
A comparative study of some convulsant substances as γ‐aminobutyric acid antagonists in the feline cerebral cortex [PDF]
R.G. Hill +2 more
openalex +1 more source
Cerebral Cortex Thickness in Patients with Temporal Lobe Epilepsy Using Magnetic Resonance Imaging [PDF]
Iman Sarbisheh +6 more
openalex +1 more source
Particulate matter ≤2.5 µm (PM2.5) elevates risks of neurological and chronic metabolic diseases, but the underlying mechanisms linking PM2.5‐induced central nervous system (CNS) injury to metabolic dysfunction remain unclear. Hypothalamic pro‐opiomelanocortin‐expressing (POMC+) neurons regulate systemic metabolic homeostasis, and tripartite motif ...
Chenxu Ge +21 more
wiley +1 more source
CYTOMETRIC PARAMETERS OF CEREBRAL CORTEX NEURONS IN COVID-19 [PDF]
T.I. Kuznetsova +4 more
openalex +1 more source
Nurr1 Orchestrates Claustrum Development and Functionality
Nurr1 (Nr4a2) is the master transcription factor to control claustrum morphogenesis and cell fate decision postmitotically by inhibiting intracellular G‐protein signaling. Nurr1 deficiency alters the transcriptomic profiles of subcortical claustral neurons into neocortical insular neurons, resulting in defected claustrum development, impaired axonal ...
Kuo Yan +12 more
wiley +1 more source
This study reveals that the E3 ubiquitin ligase TRIM56 exacerbates neuronal ferroptosis and brain damage by mediating K48‐linked ubiquitination and degradation of KLF4, leading to suppression of the xCT/GSH/GPX4 axis. Targeting TRIM56 alleviates cerebral ischemia‐reperfusion injury in vivo and in vitro, highlighting its therapeutic potential.
Qiangping Wang +15 more
wiley +1 more source
Whole transcriptome cerebral cortex gene analysis in Alzheimer’s diseases
Sharma Pooja +4 more
openalex +1 more source
Comprehensive analysis of circRNA expression profiles in rat cerebral cortex after moderate traumatic brain injury [PDF]
Gang Li +5 more
openalex +1 more source
NAD⁺ homeostasis maintains neuronal integrity through opposing actions of NMNAT2 and SARM1. Loss of NMNAT2 in glutamatergic neurons reprograms cortical metabolism from glucose to lipid catabolism, depletes lipid stores, and triggers inflammation and neurodegeneration.
Zhen‐Xian Niou +9 more
wiley +1 more source

