Neuroscience
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Impaired balance may limit mobility and daily activities, and plays a key role in the elderly falling. Maintaining balance requires a concerted action of the sensory, nervous and motor systems, whereby cause and effect mutually affect each other within a closed loop. Aforementioned systems and their connecting pathways are prone to chronological age and disease-related deterioration. ⋯ This paper outlines the multiple deteriorations of the underlying systems that may be involved in standing balance, which have to be detected early to prevent impaired standing balance. An overview of clinically used balance tests shows that early detection of impaired standing balance and identification of causal mechanisms is difficult with current tests, thereby hindering the development of well-timed and target-oriented interventions as described next. Finally, a new approach to assess standing balance and to detect the underlying deteriorations is proposed.
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Although extensively investigated in socio-cognitive neuroscience, empathy is difficult to study. The first difficulty originates in its multifaceted nature. According to the multidimensional model, empathy combines emotional, automatic (simulation), cognitive (mentalizing) and regulatory (executive functions) processes. ⋯ However, at 333-424ms, empathy triggered greater co-activations in the right IFG and dorsolateral prefrontal cortex (dlPFC) (executive functions). Linking together our present and prior (Thirioux et al., 2010) findings from the same dataset, we suggest that this greater recruitment of the right dlPFC monitors the shift from egocentered and first-person-like mechanisms in the MNS to heterocentered and second-person-like mechanisms in the left temporo-parietal junction within the MENT, i.e., reflecting the onset of perspective-change processes in the neural time course of empathy. Contrasting with sympathy, this recruitment of the executive functions could modulate the output end of the mirroring processing in the premotor and sensorimotor cortices.
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Curculigoside A may be a powerful way of protecting the brain against a wide variety of injury. In the present study, we sought to elucidate whether Curculigoside A contributes to induce angiogenesis and its mechanisms. To this end, we examined the role of Curculigoside A on proliferation, invasion, and tube formation in the human brain microvascular endothelial cell line (HBMEC) in vitro. ⋯ VEGF expression was increased by Curculigoside A and counteracted by the soluble VEGF receptor 1 (sFlt-1, VEGF antagonist) and KG-501 in HMBEC. Tube formation was enhanced by Curculigoside A and counteracted by VEGF receptor blocker-SU1498, KG-501 and Egr-3 siRNA. It may be suggested that Curculigoside A induces angiogenesis in vitro via a programed VCAM-1/Egr-3/CREB/VEGF signaling axis.
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Opiate analgesia in the spinal cord is impaired during neuropathic pain. We hypothesized that this is caused by a decrease in μ-opioid receptor inhibition of neurotransmitter release from primary afferents. To investigate this possibility, we measured substance P release in the spinal dorsal horn as neurokinin 1 receptor (NK1R) internalization in rats with chronic constriction injury (CCI) of the sciatic nerve. ⋯ In contrast, DAMGO still inhibited substance P release after inflammation of the hind paw with complete Freund's adjuvant and in naïve rats. This loss of inhibition was not due to μ-opioid receptor downregulation in primary afferents, because their colocalization with substance P was unchanged, both in dorsal root ganglion neurons and primary afferent fibers in the dorsal horn. In conclusion, nerve injury eliminates the inhibition of substance P release by μ-opioid receptors, probably by hindering their signaling mechanisms.
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Neuropathologic processes such as cerebral ischemia can enhance neurogenesis. Angiopoietin-1 (Ang1) emerges as a critical regulator of physiological and pathological angiogenesis during embryonic and postnatal life. Although Ang1 could protect peripheral vasculature from vascular leakage following ischemic injury, the role of Ang1 in long-term neurological recovery after ischemic stroke remains elusive. ⋯ Our results demonstrated that lentivirus-mediated Ang1 gene transfer led to improved neurological behavior and reduced infarction volume, and protected against blood-brain barrier (BBB) leakage in the ischemic rats. In addition, we revealed that these effects of Ang1 are related to the ability of Ang1 to increase vascular density and accelerate endogenous neuronal differentiation. These findings suggest that Ang1 is a promising agent for the treatment of cerebral ischemia.