Wittallison3189

Western blot analysis and immunohistochemistry results showed that Ndufv2, Maob and Gria3 expression and positive cell count in the dexamethasone-treated group were significantly greater than those in the model group. These findings suggest that dexamethasone may promote a compensatory increase in complex I subunits (Ndufs2 and Ndufv2), increase the expression of mitochondrial enzyme Maob, and upregulate synaptic-transmission-related protein Gria3. These changes may be caused by nerve injury after traumatic brain injury treatment by dexamethasone. The study was approved by Institutional Ethics Committee of Beijing Neurosurgical Institute (approval No. 201802001) on June 6, 2018.In recent years, mental practice (MP) using laterally inverted video of a subject's non-paralyzed upper limb to improve the vividness of presented motor imagery (MI) has been shown to be effective for improving the function of a paralyzed upper limb. However, no studies have yet assessed the activity of cortical regions engaged during MI task performance using inverse video presentations and neurophysiological indicators. This study sought to investigate changes in MI vividness and hemodynamic changes in the cerebral cortex during MI performance under the following three conditions in near-infrared spectroscopy MI-only without inverse video presentation (MI-only), MI with action observation (AO) of an inverse video presentation of another person's hand (AO + MI (other hand)), and MI with AO of an inverse video presentation of a participant's own hand (AO + MI (own hand)). Participants included 66 healthy right-handed adults (41 men and 25 women; mean age 26.3 ± 4.3 years). There were 23 patients in the MI-only group (mean age 26.4 ± 4.1 years), 20 in the AO + MI (other hand) group (mean age 25.9 ± 5.0 years), and 23 in the AO + MI (own hand) group (mean age 26.9 ± 4.1 years). The MI task involved transferring 1 cm × 1 cm blocks from one plate to another, once per second, using chopsticks held in the non-dominant hand. Based on a visual analog scale (VAS), MI vividness was significantly higher in the AO + MI (own hand) group than in the MI-only group and the AO + MI (other hand) group. A main effect of condition was revealed in terms of MI vividness, as well as regions of interest (ROIs) in certain brain areas associated with motor processing. The data suggest that inverse video presentation of a person's own hand enhances the MI vividness and increases the activity of motor-related cortical areas during MI. This study was approved by the Institutional Ethics Committee of Nagasaki University Graduate School of Biomedical and Health Sciences (approval No. 18121303) on January 18, 2019.Lithium has been used in the treatment of bipolar disorders for decades, but the exact mechanisms of action remain elusive to this day. Recent evidence suggests that lithium is critically involved in a variety of signaling pathways affecting apoptosis, inflammation, and neurogenesis, all of which contributing to the complex pathophysiology of various neurological diseases. As a matter of fact, preclinical work reports both acute and long-term neuroprotection in distinct neurological disease models such as Parkinson's disease, traumatic brain injury, Alzheimer's disease, and ischemic stroke. Lithium treatment reduces cell injury, decreases α synuclein aggregation and Tau protein phosphorylation, modulates inflammation and even stimulates neuroregeneration under experimental conditions of Parkinson's disease, traumatic brain injury, and Alzheimer's disease. The therapeutic impact of lithium under conditions of ischemic stroke was also studied in numerous preclinical in vitro and in vivo studies, giving rise to entioned neurological diseases. A detailed understanding of the lithium-induced mechanisms, however, is important for prospective clinical trials which may pave the way for a successful bench-to-bedside translation in the future. In this review, we will give an overview of lithium-induced neuroprotective mechanisms under various pathological conditions, with special emphasis on ischemic stroke.In the porcine model discussed in this review, the acute subdural hematoma was induced by subdural injection of autologous blood over the left parietal cortex, which led to a transient elevation of the intracerebral pressure, measured by bilateral neuromonitoring. The hematoma-induced brain injury was associated with albumin extravasation, oxidative stress, reactive astrogliosis and microglial activation in the ipsilateral hemisphere. Further proteins and injury markers were validated to be used for immunohistochemistry of porcine brain tissue. The cerebral expression patterns of oxytocin, oxytocin receptor, cystathionine-γ-lyase and cystathionine-β-synthase were particularly interesting these four proteins all co-localized at the base of the sulci, where pressure-induced brain injury elicits maximum stress. In this context, the pig is a very relevant translational model in contrast to the rodent brain. The structure of the porcine brain is very similar to the human the presence of gyri and sulci (gyrencephalic brain), white matter to grey matter proportion and tentorium cerebelli. Thus, pressure-induced injury in the porcine brain, unlike in the rodent brain, is reflective of the human pathophysiology.A long-standing goal of spinal cord injury research is to develop effective repair strategies, which can restore motor and sensory functions to near-normal levels. Recent advances in clinical management of spinal cord injury have significantly improved the prognosis, survival rate and quality of life in patients with spinal cord injury. In addition, a significant progress in basic science research has unraveled the underlying cellular and molecular events of spinal cord injury. Such efforts enabled the development of pharmacologic agents, biomaterials and stem-cell based therapy. L-α-Phosphatidylcholine datasheet Despite these efforts, there is still no standard care to regenerate axons or restore function of silent axons in the injured spinal cord. These challenges led to an increased focus on another therapeutic approach, namely neuromodulation. In multiple animal models of spinal cord injury, epidural electrical stimulation of the spinal cord has demonstrated a recovery of motor function. Emerging evidence regarding the efficacy of epidural electrical stimulation has further expanded the potential of epidural electrical stimulation for treating patients with spinal cord injury.