Neuroscience
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Peripheral nerve injury (PNI) is a common clinical disease that causes the partial loss of segmental exercise and sensory and autonomic nervous function, placing a heavy burden on patients and their families. A previous study confirmed that exendin-4 can effectively improve nerve regeneration and functional recovery after PNI. However, the specific mechanisms by which exendin-4-mediates this repair have not been clarified. ⋯ In vitro, exendin-4 could significantly promote the proliferation and migration of SCs by activating the Jak-STAT pathway, which promoted peripheral nerve regeneration. Our results indicate that exendin-4 promotes SC proliferation, migration and nerve regeneration after PNI by activating the Jak-STAT pathway. Our findings provide a basis and direction for further elucidation of the mechanisms of exendin-4 in the repair of PNI and provide a new way to treat PNI.
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Long non-coding RNAs (lncRNAs) play critical roles in regulating the progression of cerebral ischemia. LncRNA H19 was significantly up-regulated under ischemia-reperfusion (I/R) damage and implicatedin I/R injury progression, but the mechanisms remain unclear. Mice were subjected to middle cerebral artery occlusion (MCAO)/R (1 h/24 h) to build an I/R injury model and the infarct volume and neurological deficit were assessed. ⋯ H19 knockdown and miR-19a-3p overexpression relieved I/R or OGD/R induced neuronal cell oxidative stress and apoptosis. H19/miR-19a-3p/PTEN axis could promote cerebral I/R injury via PI3K/AKT pathway. These demonstrated a mechanism how H19 participates in I/R injury, and provided us a potential target for I/R injury diagnosis and treatment.
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We tested several predictions of the theory of motor control with spatial referent coordinates related to effects of muscle coactivation on force production and perception. In particular, we predicted that subjects would produce unintentional force increase by finger flexors and be unaware of this force increase. Healthy subjects performed steady force production task in isometric conditions with visual feedback on the force level. ⋯ The results confirm the earlier hypothesis on the reciprocal command being hierarchically higher than the coactivation command. The observations suggest that verbal reports and force matching use different neural mechanisms of force perception; the former are dominated by sense of effort, which reflects primarily the magnitude of the reciprocal command. There were only minor differences between the dominant and non-dominant hands, likely reflecting the faster unintentional drifts of control variables in the dominant hand.
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The main neuropathological hallmarks of Parkinson's disease (PD) are loss of dopaminergic neurons in the substantia nigra and intraneuronal protein aggregates immunoreactive for α-synuclein phosphorylated at serine 129 (pS129). Most cases of PD are idiopathic; however, genetic mutations have been identified in several genes linked to familial PD. Mutations in the gene encoding α-synuclein are causally linked to dominantly inherited forms of PD and mutations in the PTEN-induced kinase-1 (PINK1) gene are linked to recessively inherited forms of PD. ⋯ Moreover, the synuclein extracted from the brains of PFF-injected PINK1 KO rats was more insoluble compared to PFF-injected WT littermates, suggesting greater progression of α-synuclein pathology in PINK1 KO rats. Four weeks post-injection, PFFs caused significant loss of dopaminergic neurons in the substantia nigra of PINK1 KO rats, but not WT controls. Together, our results indicate that PINK1 deficiency increases vulnerability to α-synuclein aggregation and dopaminergic neurodegeneration in vivo.
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Physical exercise practice has been increasingly recommended in the prevention and treatment of chronic diseases, causing a positive effect from body weight/fat loss to improved cognitive function. Maternal exercise seems to induce the same positive lifelong adaptations to the offspring. We hypothesized that maternal exercise can prevent redox imbalance in adult offspring's hippocampus exposed to a high-fat diet (HFD). ⋯ In the hippocampus, both maternal exercise intensities could increase antioxidant defense. Hippocampal redox homeostasis was impaired by HFD, causing increased superoxide levels, which was prevented by exercise without load, while overload caused only a reduction of the effect. In summary, the practice of swimming exercise without overload during pregnancy seems to be more beneficial when evaluated in animal model, preventing HFD induced redox imbalance and increasing antioxidant defense while overload swimming exercise during pregnancy demonstrated a negative effect on offspring submitted to HFD consumption.