Neuroscience
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Allergic asthma is a common chronic inflammatory condition associated with psychiatric comorbidities. Notably depression, correlated with adverse outcomes in asthmatic patients. Peripheral inflammation's role in depression has been shown previously. ⋯ Moreover, mPFC and vHipp activity were altered in asthmatic animals. Allergen disrupted the strength and direction of functional connectivity in the mPFC-vHipp circuit so that, unlike normal conditions, mPFC causes and modulates vHipp activity. Our results provide new insight into the underlying mechanism of allergic inflammation-induced psychiatric disorders, aiming to develop new interventions and therapeutic approaches for improving asthma complications.
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Functional magnetic resonance imaging (fMRI) is a convolution of latent neural activity and the hemodynamic response function (HRF). According to prior studies, the neurodegenerative process in idiopathic Parkinson's Disease (PD) interacts significantly with neuromuscular abnormalities. Although these underlying neuromuscular changes might influence the temporal characteristics of HRF and fMRI signals, relatively few studies have explored this possibility. ⋯ The results suggested that neglecting HRF variability may cultivate false-positive and false-negative FC group differences. Furthermore, HRF was related to dopamine receptor type 2 (DRD2) gene expression (P < 0.001, t = -7.06, false discover rate-corrected). Taken together, these findings reveal HRF variation and its possible underlying molecular mechanism in PD, and suggest that deconvolution could reduce the impact of HRF variation on FC group differences.
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Numerous blood oxygenation level-dependent (BOLD) imaging studies have shown that generalized anxiety disorder (GAD) can lead to abnormal activation of specific brain regions in patients. However, these methods lack sufficient temporal resolution to explain the underlying brain dynamics of GAD. The electroencephalogram (EEG) microstate allows us to explore brain dynamics at the subsecond level. ⋯ The optimal configuration combined the spatial features of source-level data with microstate features and achieved the highest classification accuracy. Collectively, the statistical results indicated remarkable differences in dynamic brain parameters between the two groups, and patients with GAD may have abnormalities in their higher sensory cortex that affect the processing of anxiety signals. Furthermore, our proposed fusion framework provides a reliable method for GAD automatic detection.
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Deferoxamine (DFO) is a potent iron chelator for clinical treatment of various diseases. Recent studies have also shown its potential to promote vascular regeneration during peripheral nerve regeneration. However, the effect of DFO on the Schwann cell function and axon regeneration remains unclear. ⋯ Moreover, the appropriate concentration of DFO promotes axon regeneration in DRG. Our findings demonstrate that DFO, with suitable concentration and duration of action, can positively affect multiple stages of peripheral nerve regeneration, thereby improving the effectiveness of nerve injury repair. This study also enriches the theory of DFO promoting peripheral nerve regeneration and provides a basis for the design of sustained-release DFO nerve grafts.
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Understanding the role and mechanism of astrocytes in inflammation and oxidative response is crucial for developing therapeutic strategies to reduce inflammation and oxidative injury in cerebral ischemia-reperfusion injury (CIRI). In this study, we investigated the regulatory effects of phosphoglycerate kinase 1 (PGK1) on inflammation and oxidative response after CIRI in male adult Sprague-Dawley (SD) rats and using primary astrocytes obtained from neonatal SD rats, and explored its related mechanisms. We established a rat model of middle cerebral artery occlusion-reperfusion (MCAO/R) by suture occlusion, and an oxygen-glucose deprivation/reoxygenation model of astrocytes using oxygen-free, glucose-free, and serum-free cultures. ⋯ Further rescue experiments showed that Nrf2 knockdown eliminated the protective effect of CBR-470-1 (a PGK1 inhibitor) on CIRI. Lastly, we confirmed that PGK1 aggravates CIRI by inhibiting the Nrf2/ARE pathway. In conclusion, our findings suggest that inhibiting PGK1 attenuates CIRI by reducing the release of inflammatory and oxidative factors from astrocytes by activating the Nrf2/ARE signaling pathway.