Neuroscience
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A right-left dichotomy of olfactory processes has been recognized on several levels of the perception or processing of olfactory input. On a clinical level, the lateralization of components of human olfaction is contrasted by the predominantly birhinal olfactory testing. The present analyses aimed at investigation of the relation of such side-differences related with the subject's age, sex and with the cause or degree of olfactory loss. ⋯ The observation particularly owed to olfactory loss attributed to head trauma, which may hint at a different impact on the left or right hemisphere processing of olfactory input. Thus, between-nostrils agreement in odor identification is limited and the common unilateral olfactory testing probably misses important information. Lateral differences owe to age, sex, kind of odor and etiology of olfactory loss.
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The causal connections among small-scale regions based on resting-state fMRI data have been extensively studied and a lot of achievements have been demonstrated. However, the causal connection among large-scale regions was seldom discussed. In this paper, we applied global Granger causality analysis to construct the causal connections in the whole-brain network among 103 healthy subjects (33 M/66F, ages 20-23) based on a resting-state fMRI dataset. ⋯ There were 817 directed edges identified as significant among the 8010 possible causal connections; seven driving hubs and ten driven hubs were identified in the whole-brain network. In CEN, dorsolateral prefrontal cortex (DlPFC) and superior parietal cortex (SPC) were the driven and driving hubs, respectively; in DMN, they were posterior cingulate cortex (PCC) and medial prefrontal cortex (MPFC); in DAN, they were frontal eye fields (FEF) and intraparietal sulcus (IPS); and in SN, they were frontoinsular cortex (FIC) and medial frontal cortex (MFC). These findings may provide insights into our understanding of human brain function mechanisms and the diagnosis of brain diseases.
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Psychopath and neuropath often exhibit similar symptoms in clinical functional performances. However, few studies ever demonstrate the existence of overlapped brain functional mechanism between neurological and psychiatric disorders. ⋯ In these overlapped functions, we also find that the brain regions of neuropsychopathic disorders exhibit different cooperative patterns at different levels of brain activities. For example, strong-strong cooperative patterns were observed at high levels of brain activities in epilepsy, ADHD and schizophrenia.
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It has long been known that each neuron in both the central and peripheral nervous system has a large number of active zones. Nonetheless, how active zones are regulated to maintain a homeostatic release state and response to the constantly changing environment remains poorly understood. Due to its relatively simple structure and easy accessibility, the neuromuscular synapse (NM-synapse) continues to be used as a model synapse to examine the basic nature of synaptic neurotransmission. ⋯ Furthermore, evoked quantal release has been shown to be highly non-uniform between active zones along nerve terminal branches. How these large numbers of active zones along the same nerve terminal are functionally correlated remains unclear. This review starts with the basic features of quantal neurotransmitter release, then progresses to the current knowledge on how the active zones interact with each other along the same nerve terminal.
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After ischemic stroke, the degenerated myelin caused by ischemic injury cannot be rapidly cleared away by microglia and interferes with the recovery process. Complement receptor 3 (CR3, CD11b/CD18), belonging to β2 integrin family primarily expressed in phagocytes, is involved in the microglial phagocytosis of myelin debris. We previously found that pseudoginsenoside-F11 (PF11), an ocotillol-type saponin, exerts neuroprotective effects against ischemic stroke and neuroinflammation. ⋯ Meanwhile, PF11 strengthened the OGD-activated RhoA/ROCK signaling associated with the internalization during myelin debris phagocytosis through CR3. Consistently, the anti-CD11b mAb could markedly attenuated the nrueoprotective effects of PF11 (12 mg/kg, i.v.) on infarction and brain edema, neurological functions and loss of neurons of pMCAO rats. These findings suggest that PF11 accelerates the phagocytosis of myelin debris by microglia mainly through CR3, which may likely contribute to its neuroprotection against ischemic stroke.