Results 231 to 240 of about 129,622 (343)

NEAT1 Promotes Epileptogenesis in Tuberous Sclerosis Complex

open access: yesAdvanced Science, EarlyView.
The primary neurological manifestations of tuberous sclerosis complex (TSC) are intractable epilepsy and intellectual disability. NEAT1 is differentially expressed in TSC‐related epilepsy and influences neuronal excitability by regulating the PI3K/AKT/mTOR signaling pathway.
Suhui Kuang   +8 more
wiley   +1 more source

Forelimb Motor Learning and Memory Consolidation Drives Distinct Oligodendrocyte Plasticity to Regulate Task‐related Neuronal Activity

open access: yesAdvanced Science, EarlyView.
Genetic and chemical tracking of oligodendrogenesis, combining fiber photometric neuronal activity recording, reveals that distinct oligodendrocyte plasticities are adopted during different phases of motor learning to fine‐tune task‐related neuronal activity, with a preferential involvement of oligodendrogenesis suppression and node lengthening (type 2
Shuming Wang   +10 more
wiley   +1 more source

Effectiveness of an AI-Assisted Digital Workflow for Complete-Arch Implant Impressions: An In Vitro Comparative Study. [PDF]

open access: yesDent J (Basel)
Tallarico M   +9 more
europepmc   +1 more source

Elevated Apolipoprotein E Expression in Hippocampal Microglia Drives Temporal Lobe Epilepsy Progression

open access: yesAdvanced Science, EarlyView.
In temporal lobe epilepsy, hippocampal APOE is markedly upregulated predominantly in microglia. APOE overexpression in microglia drives TLR4 and cGAS/STING‐dependent neuroinflammation, engages bidirectional crosstalk with neurons and astrocytes, increases neuronal excitability, and perturbs hippocampal lipid metabolism. These findings suggest that APOE‐
Jianwei Shi   +10 more
wiley   +1 more source

Onion‐Mitochondria Inhibit Lipopolysaccharide‐Induced Acute Lung Injury by Shaping Lung Macrophage Mitochondrial Function

open access: yesAdvanced Science, EarlyView.
Proposed model of orally administered onion mitochondria (O‐Mit) uptake by lung macrophages and fuse with macrophage mitochondria (M‐Mit). This fusion reprograms the metabolism of dysfunctional M‐Mit in lipopolysaccharide‐induced murine acute lung injury by modulating dynamin‐related protein 1 (DRP1) phosphorylation and cardiolipin peroxidation ...
Qingbo Xu   +13 more
wiley   +1 more source

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