Modulations of visual and somatosensory perception by action

This thesis aimed to further investigate the effects of movements on modulations of visual and somatosensory perception. The first experiment (Chapter 2) investigated spatial mislocalisation of visual stimuli presented before saccade using a pointing paradigm and found that a predictive remapping of visual space occurred before saccade and the post-saccadic remapping employed spatially as well as temporally accurate memory of pre-saccadic visual stimuli. The second experiment (Chapter 3) examined relevance of saccadic chronostasis to remapping of visual space using a target displacement paradigm and found that it did not serve as a mechanism that fills in a perceptual gap during saccadic suppression. The third (Chapter 4) and fourth (Chapter 5) experiments adopted a target blanking paradigm and found that the pre-saccadic stimuli predictively remapped before saccade were anchored to the location of the pre-saccadic target remapped using a precise efference copy and neither saccade landing sites nor remembered locations of pre-saccadic targets were used in this process. Behavioural (Chapter 6) and fMRI (Chapter 7) studies were conducted to investigate modulations of tactile perception by manual movements and found that the tactile attention induced by the cued index finger facilitated processing of tactile stimuli presented to the responded hand. The somatosensory ROIs mainly showed a bias towards contralateral tactile stimulation in comparison with ipsilateral tactile stimulation. The right primary motor cortex (right M1), the left precuneus (left PreC) and the left middle frontal gyrus (left MFG) showed significant modulations of somatosensory processing by the Moving condition compared to the Non Moving condition. The final chapter included summaries and conclusions of each chapter and proposals for future investigations

Modulations of visual and somatosensory perception by action

This thesis aimed to further investigate the effects of movements on modulations of visual and somatosensory perception. The first experiment (Chapter 2) investigated spatial mislocalisation of visual stimuli presented before saccade using a pointing paradigm and found that a predictive remapping of visual space occurred before saccade and the post-saccadic remapping employed spatially as well as temporally accurate memory of pre-saccadic visual stimuli. The second experiment (Chapter 3) examined relevance of saccadic chronostasis to remapping of visual space using a target displacement paradigm and found that it did not serve as a mechanism that fills in a perceptual gap during saccadic suppression. The third (Chapter 4) and fourth (Chapter 5) experiments adopted a target blanking paradigm and found that the pre-saccadic stimuli predictively remapped before saccade were anchored to the location of the pre-saccadic target remapped using a precise efference copy and neither saccade landing sites nor remembered locations of pre-saccadic targets were used in this process. Behavioural (Chapter 6) and fMRI (Chapter 7) studies were conducted to investigate modulations of tactile perception by manual movements and found that the tactile attention induced by the cued index finger facilitated processing of tactile stimuli presented to the responded hand. The somatosensory ROIs mainly showed a bias towards contralateral tactile stimulation in comparison with ipsilateral tactile stimulation. The right primary motor cortex (right M1), the left precuneus (left PreC) and the left middle frontal gyrus (left MFG) showed significant modulations of somatosensory processing by the Moving condition compared to the Non Moving condition. The final chapter included summaries and conclusions of each chapter and proposals for future investigations

Initial Nutritional Status and Clinical Outcomes in Patients With Deep Neck Infection

Objectives The current study aims to determine the correlation between nutritional status upon presentation and disease severity, as well as treatment and survival outcomes. Methods Patients who were diagnosed with deep neck infection, underwent at least one surgical drainage/debridement, and had more than 1 week of hospitalization at a tertiary medical center from 2007 to 2015 were retrospectively included. Thereafter, initial serum albumin, C-reactive protein (CRP), and body mass index (BMI) were reviewed. Results A total of 135 patients were included in the final analysis. Accordingly, the proportion of patients with simultaneous mediastinitis (21.0%), necrotizing fasciitis (12.9%), disease extent >1 cervical level (72.6%), mean CRP (22.4 mg/dL), mean length of hospitalization (25.0 days), and mean 1-week follow-up CRP (7.2 mg/dL) was significantly higher in the hypoalbuminemia group (initial serum albumin 1 cervical level (2.12), initial serum CRP over 20 mg/dL (3.79), hospitalization of more than 14 days (4.10), 1-week follow-up CRP over 5 mg/dL (3.78), and increased duration for an over 50% decrease in initial CRP (2.70) (all P<0.05). Although intravascular albumin replenishment decreased the proportion of patients with hypoalbuminemia after 2 weeks (P<0.05), it did not significantly predict better treatment outcomes. Conclusion Among the markers reflecting an individual’s nutritional state, an initial serum albumin of less than 3.0 g/dL was an independent serologic marker predicting increased disease severity and complications in patients with deep neck infection

Trans-Differentiation of Neural Stem Cells: A Therapeutic Mechanism Against the Radiation Induced Brain Damage

Radiation therapy is an indispensable therapeutic modality for various brain diseases. Though endogenous neural stem cells (NSCs) would provide regenerative potential, many patients nevertheless suffer from radiation-induced brain damage. Accordingly, we tested beneficial effects of exogenous NSC supplementation using in vivo mouse models that received whole brain irradiation. Systemic supplementation of primarily cultured mouse fetal NSCs inhibited radiation-induced brain atrophy and thereby preserved brain functions such as short-term memory. Transplanted NSCs migrated to the irradiated brain and differentiated into neurons, astrocytes, or oligodendrocytes. In addition, neurotrophic factors such as NGF were significantly increased in the brain by NSCs, indicating that both paracrine and replacement effects could be the therapeutic mechanisms of NSCs. Interestingly, NSCs also differentiated into brain endothelial cells, which was accompanied by the restoration the cerebral blood flow that was reduced from the irradiation. Inhibition of the VEGF signaling reduced the migration and trans-differentiation of NSCs. Therefore, trans-differentiation of NSCs into brain endothelial cells by the VEGF signaling and the consequential restoration of the cerebral blood flow would also be one of the therapeutic mechanisms of NSCs. In summary, our data demonstrate that exogenous NSC supplementation could prevent radiation-induced functional loss of the brain. Therefore, successful combination of brain radiation therapy and NSC supplementation would provide a highly promising therapeutic option for patients with various brain diseases

Immunohistochemical identification and quantitative analysis of cytoplasmic Cu/Zn superoxide dismutase in mouse organogenesis

Cytoplasmic Cu/Zn superoxide dismutase (SOD1) is an antioxidant enzyme that converts superoxide to hydrogen peroxide in cells. Its spatial distribution matches that of superoxide production, allowing it to protect cells from oxidative stress. SOD1 deficiencies result in embryonic lethality and a wide range of pathologies in mice, but little is known about normal SOD1 protein expression in developing embryos. In this study, the expression pattern of SOD1 was investigated in post-implantation mouse embryos and extraembryonic tissues, including placenta, using Western blotting and immunohistochemical analyses. SOD1 was detected in embryos and extraembryonic tissues from embryonic day (ED) 8.5 to 18.5. The signal in embryos was observed at the lowest level on ED 9.5-11.5, and the highest level on ED 17.5-18.5, while levels remained constant in the surrounding extraembryonic tissues during all developmental stages examined. Immunohistochemical analysis of SOD1 expression on ED 13.5-18.5 revealed its ubiquitous distribution throughout developing organs. In particular, high levels of SOD1 expression were observed in the ependymal epithelium of the choroid plexus, ganglia, sensory cells of the olfactory and vestibulocochlear epithelia, blood cells and vessels, hepatocytes and hematopoietic cells of the liver, lymph nodes, osteogenic tissues, and skin. Thus, SOD1 is highly expressed at late stages of embryonic development in a cell- and tissue-specific manner, and can function as an important antioxidant enzyme during organogenesis in mouse embryos

SALM4 suppresses excitatory synapse development by cis-inhibiting trans-synaptic SALM3-LAR adhesion

Synaptic adhesion molecules regulate various aspects of synapse development, function and plasticity. These functions mainly involve trans-synaptic interactions and positive regulations, whereas cis-interactions and negative regulation are less understood. Here we report that SALM4, a member of the SALM/Lrfn family of synaptic adhesion molecules, suppresses excitatory synapse development through cis inhibition of SALM3, another SALM family protein with synaptogenic activity. Salm4-mutant (Salm4) mice show increased excitatory synapse numbers in the hippocampus. SALM4 cis-interacts with SALM3, inhibits trans-synaptic SALM3 interaction with presynaptic LAR family receptor tyrosine phosphatases and suppresses SALM3-dependent presynaptic differentiation. Importantly, deletion of Salm3 in Salm4 mice (Salm3, Salm4) normalizes the increased excitatory synapse number. These results suggest that SALM4 negatively regulates excitatory synapses via cis inhibition of the trans-synaptic SALM3-LAR adhesion. © The Author(s) 2016110101sciescopu