Neuroscience
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The cerebellum harbors a specialized area on the roof of the fourth ventricle that is composed of glial cells and neurons that interface with the cerebrospinal fluid. This region includes the so-called ventromedial cord (VMC), which is composed of cells that are glial fibrillary acidic protein (GFAP)-positive and nestin-positive and distributes along the midline in association with blood vessels. We hypothesized that these cells should compare to GFAP and nestin-positive cells that are known to exist in other areas of the brain, which undergo proliferation and differentiation under hypoxic conditions. ⋯ This EGFP loss was supported by western blot analysis, which also showed a loss in the astrocyte-markers GFAP and ALDH1L1. On the other hand, other cell-markers appeared to be upregulated in the blots (including nestin, NeuN, and Iba1). Finally, we found that HPC does not remarkably affect the incorporation of BrdU into cells on the cerebellum, but strongly augments BrdU incorporation into periventricular cells on the floor of the fourth ventricle over the adjacent medulla.
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Excessive expression of vascular endothelial growth factor (VEGF) is a common cause of blood-brain barrier (BBB) breakdown that triggers severe complications following traumatic brain injury (TBI). It has been shown that inhibition of VEGF activities may attenuate cerebral edema in pathological conditions. Vascular endothelial growth inhibitor (VEGI; also known as TNFSF15), a cytokine produced largely by vascular endothelial cells, is capable of downregulating VEGF expression and inhibiting VEGF receptor-2 (VEGFR2) activation. ⋯ VEGI treatment resulted in a marked decrease of BBB permeability and concomitant restoration of normal ratios of VEGF/VEGI and Angpt2/Angpt1. Consistently, alleviated edema, decreased neuron cell death, and improved neurological functions were observed when the experimental animals were treated with VEGI in the early phase of TBI. Our findings suggest that administration of VEGI recombinant protein at early phases of TBI is beneficial to stabilization of the disease conditions.
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Case Reports
Damage to the Intraparietal Sulcus Impairs Magnitude Representations of Results of Complex Arithmetic Problems.
Past research investigating the role of the intraparietal sulcus (IPS) in numerical processes focused mainly on quantity and numerical comparisons as well on single digit arithmetic. The present study investigates the involvement of the IPS in estimating the results of multi-digit multiplication problems. For this purpose, the performance a 24-year-old female (JD) with brain damage in the left IPS was compared to an age-matched control group in the computation estimation task. ⋯ Most control participants used both the approximated calculation strategy that involves rounding and calculation procedures and the sense of magnitude strategy that relies on an intuitive approximated magnitude representation of the results. In contrast, JD used only the former but not the latter strategy. Together, these findings suggest that the damage to the IPS impaired JD's representations of magnitude that play an important role in this computation estimation task.
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White matter lesions are common when global cerebral ischemia (GCI) occurs in the elderly, and cause damage to neurological and psychological functions. Remyelination often fails because of the limited recruitment of oligodendrocyte progenitor cells (OPCs) to the demyelinated site or the inefficient differentiation of OPCs to mature oligodendrocytes (OLs). The activation of microglia, the most important immune cells in the central nervous system, and subsequent inflammation have been implicated in myelination repair disorder. ⋯ No effect was found on myelin in the corpus callosum. Besides, hippocampal neurons were protected by anti-FKR treatment after GCI. Collectively, our data demonstrated that downregulating of the Fractalkine/CX3CR1 signaling pathway had an anti-depressant and cognition-improvement effect by inhibiting microglia activation, promoting OPCs maturation and remyelination.