Musical stimuli can induce a variety of emotions in individuals. We sought to determine whether different valenced music would induce EEG profile changes and self-reported emotional states in individuals following the viewing of a complex video with a concrete narrative and emotional ambivalence. We used a five-minute video titled "El Empleo", coupled with either joyful, fearful, or no music. EEG recordings were taken throughout the duration of the experiment and a self-reported questionnaire on emotional state was administered after viewing of the video. We found self-reported measures of happiness increased following viewing of the video paired with joyful music, while EEG data demonstrated that the following brain regions displayed significant changes in activity following both fearful and joyful music the right inferior parietal lobule, left uncus, and left insula. Additionally, we found that anxiety self-report scores correlated negatively with average gamma activity within the insula within each group. The convergence of self-reported data and quantitative EEG data was consistent across 27 participants. These data indicate that different valenced music can alter EEG activity in emotion specific regions, reflected in participants perceived emotional state.Growth arrest and DNA damage-inducible protein 34 (GADD34), one of the key effectors of negative feedback loops, is induced by stress and subsequently attempts to restore homeostasis. It plays a critical role in response to DNA damage and endoplasmic reticulum stress. GADD34 has opposing effects on different stimulus-induced cell apoptosis events in many nervous system diseases, but its role in ischemic stroke is unclear. In this study, we evaluated the role of GADD34 and its distribution in a rat cerebral ischemic model. The results showed that GADD34 was increased in the cortex and contributed to brain injury in ischemic rats. Furthermore, treatment with a GADD34 inhibitor reduced the infarct volume, improved functional outcomes, and inhibited neuronal apoptosis in the cortical penumbra after ischemia. The role of GADD34 in ischemic stroke was associated with the dephosphorylation of eukaryotic translation initiation factor 2α (eIF2α) and phosphorylation of p53. In addition, the GADD34 level was increased in plasma exosomes of cerebral ischemic rats. These findings indicate that GADD34 could be a potential therapeutic target and biomarker for ischemic stroke.Neuroinflammation is one of the main causes of Alzheimer's disease (AD). The presence of Lipopolysaccharide (LPS) in senile plaques (SP) of AD suggests that it plays a role in AD pathogenesis. ATP5A1 (F1F0-ATP synthase F1 α subunit) is abundant in SP. Further, the protein has recently been found to have an anti-infection role in zebrafish embryos. In the present study, we observed that LPS levels were higher in the brains of APP/PS1 mice than in control mice, and LPS co-localised with ATP5A1 in amyloid plaques. The interaction of recombinant ATP5A1(rATP5A1) and LPS was evidenced by cellular thermal shift assay and enzyme-linked immunosorbent assay-based binding assay in vitro.  https://www.selleckchem.com/products/c188-9.html  Neuroinflammation in the brain of a mouse model was induced by intracerebroventricular injection of LPS. The addition of rATP5A1 relieved LPS-induced reduction of spontaneous locomotor ability, depressive-like behaviour, and working memory impairment. Furthermore, rATP5A1 suppressed the activation of astrocytes and microglia, IL-1β accumulation, and tau phosphorylation induced by LPS. Taken together, findings suggest that ATP5A1 is involved in the regulation of LPS-mediated neuroinflammation in AD.The study of functional corticomuscular coupling can reflect the interaction between the cerebral cortex and muscle tissue, thereby helping to understand how the brain controls muscle tissue and the effect of muscle movement on brain function. This study proposes a detection model of the coupling strength between the cortex and muscles. The detection model uses an adaptive selector to choose the optimal long short-term memory network, uses this network to extract the features of electroencephalography and electromyography, and finally transforms time characteristics into the frequency domain. The transfer entropy is used to represent the interaction intensity of signals in different frequency bands. Using this model, we analyze the coupling relationship between the cortex and muscles in the three movements of wrist flexion, wrist extension, and clench fist, and compare the model with traditional wavelet coherence analysis and deep canonical correlation analysis. The experimental results show that our model can not only express the bidirectional coupling relationship between different frequency bands but also suppress the possible false coupling that traditional methods may detect. Our research shows that the proposed model has great potential in medical rehabilitation, movement decoding, and other fields.Phase-amplitude coupling (PAC) of local field potential (LFP) has been recognized as higher-order representation of brain states. Neuronal loss in the striatum leads to Parkinson's disease (PD) symptoms and modifies LFP oscillation. However, PAC in the striatum of PD mouse model induced by 6-hydroxydopamne (6-OHDA) remained to be investigated. Male Swiss albino ICR mice were implanted with intracranial electrode and injected with 6-OHDA to the left striatum. Levodopa (L-dopa) (10 mg/kg, oral) was used for treatment once a day from day 15-19. Locomotor activity and resting LFP signals were selectively analyzed on day 15 and 19. One-way ANOVA revealed significant decreases in travelled distance induced by 6-OHDA on both days (p ≤ 0.05). However, the decreased travelled distances were significantly reversed by L-dopa. On day 15, LFP powers of theta, alpha, beta and low gamma waves were significantly increased by 6-OHDA injection and the powers of beta and low gamma were significantly reversed to control level by treatment with L-dopa. On day 19, LFP powers of delta, theta, alpha, beta and low gamma waves were significantly increased by 6-OHDA injection and the powers of low gamma were significantly reversed to control level by treatment with L-dopa. Theta-gamma PAC analyses also confirmed significant increase in modulation index (MI) induced by 6-OHDA on day 19. However, L-dopa failed to significantly reverse the MI to control level. These findings indicated theta-gamma coupling in the striatum of PD mouse model. Taken together, change in striatal theta-gamma PAC might be one of biomarkers in addition to hypokinesia and increased LFP powers that reflect disrupted neural mechanisms in PD mouse model.