Neuroscience
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Ferroptosis is an iron-dependent form of regulated cell death, which is driven by loss of activity of the lipid repair enzyme glutathione peroxidase 4 (GPX4) and subsequent accumulation of lipid peroxidation. Ferroptosis is implicated in various diseases involving neuronal injury. However, the role of ferroptosis in hypoxic-ischemic brain damage (HIBD) has not been elucidated. ⋯ These changes resulted in diminished cellular antioxidant capacity and mitochondrial damage, causing neuronal ferroptosis in the cerebral cortex. We conclude that ferroptosis plays a role in HIBD in neonatal rats. Ferroptosis-related mechanisms such as abnormalities in iron metabolism, amino acid metabolism, and lipid peroxidation regulation play important roles in HIBD.
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This study uses simple tasks to induce self-conscious emotions and event-related potentials to investigate the effects of pride, neutral, and shame emotions on cognitive flexibility. The behavior results revealed that the switching tasks had a longer reaction time and a lower accuracy rate than the repetitive tasks. Furthermore, the reaction time was longer, and the accuracy rate was lower for individuals in the shame and pride emotions group than the neutral group. ⋯ These findings imply that pride and shame may inhibit conversion ability and consistently affect cognitive flexibility. This consistency may be manifested in late decision-making tasks. Our finds provide a theoretical basis for management of students' pride and shame.
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Previous studies have reported altered neuroimaging features in right temporal lobe epilepsy (rTLE). However, the alterations in degree centrality (DC) as a diagnostic method for rTLE have not been reported. Therefore, we aimed to explore abnormalities in the DC of the rTLE and whether such alterations could be applied to the diagnosis of rTLE. ⋯ The highest diagnostic accuracy of 99.34% (150/151), based on SVM analysis, was demonstrated for the combination of abnormal DC in the right IPL and the left SFGdor, along with a sensitivity of 100% (82/82), and a specificity of 98.55% (68/69) for the differentiation of rTLE patients from healthy controls. The study demonstrated abnormal functional connectivity in rTLE patients. Thus, a distinctive DC pattern may serve as an imaging marker for the diagnosis of rTLE patients.
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G-protein coupled receptors (GPCRs) modulate brain function by signaling through heterotrimeric Gq/11, Gs, and Gi/o protein subtypes. Researchers frequently study neuromodulation via these GPCR-subtypes on a 'cell-by-cell' basis. Although useful to explore a small number of interactions among neuromodulatory systems under controlled settings, this approach fails to account for a global organization of GPCRs in the brain. ⋯ Correlation strength increased with age but dropped when randomly removing genes from their corresponding groups. These findings suggest that the expression patterns of GPCR subtypes and receptor families are intricately intertwined. Well-orchestrated interactions by neuromodulatory-GPCR ensembles could be crucial for the brain to function as a highly integrated complex system.
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The experimental investigations on the pathogenesis of remifentanil-induced hyperalgesia (RIH) have been primarily conducted, but the effective treatment of RIH remains unclear. Recent reports highlight the necessity of ionotropic glutamate receptors in oxidative damage in spinal nociceptive transduction. Artesunate, the 1st-line anti-malaria drug, has been identified to be valid in removing superoxide in several pathological conditions. ⋯ Moreover, hyperalgesia and peroxiredoxin-3 hyperacetylation were attenuated after the combination of artesunate (1 μg) and MPEP (1 nmol). Additionally, artesunate treatment reversed acute pain and peroxiredoxin-3 hyperacetylation following spinal exposure to DHPG. In conclusion, intrathecal injection of artesunate impairs RIH by down-regulating spinal mGluR5 expression and peroxiredoxin-3 hyperacetylation-mediated oxidative stress in rats.