Geometric Visual Illusion Effects on Visual Perception and Visuomotor Control: Emphasis on the Vertical-Horizontal Illusion

The focus of this dissertation was to explore the effects of potential vertical-horizontal (V-H) illusory influences on perceptuomotor control. As part of this focus, we examined the potential use of separate cortical visual streams: the ventral visual stream for perception and the dorsal visual stream for action. Three studies were conducted to determine the effects of the V-H illusion influences on length estimations using upper limb point-to-point movements and lower limb stepping movements, involving various illusory configurations, movement directions, gaze directions. After a short introduction (Chapter 1) and a more detailed review of existing literature (Chapter 2), we present manuscripts on three studies. In the first study, we determined that manual length estimations of perpendicular segment lengths using curved point-to-point reaches corresponded to V-H illusory influences for movements, which began on the V-H illusion configurations rather than away from the illusion center. We concluded that encouraging gaze fixation on the center of the configuration likely contributed to the greater illusory influences over sensorimotor control. In the second study (Chapter 4), we directly assessed whether restricting gaze on the configuration or movement would alter V-H illusory influences on manual length estimations. Results revealed that restricting gaze on the configuration or movement space did alter general V-H illusory influences over sensorimotor control. We determine that the exploitation of V-H illusory cues can guide of upper limb movements given the specific gaze parameters. In Chapter 5 we assessed whether restricting gaze to the configuration or movement space also maintained V-H illusory effects on length estimations using stepping movements. Results demonstrated illusory influences, which did not exist for length estimations using movements of the lower limb with different gaze restrictions, did exist for movement planning and early movement execution. We concluded that the exploitation of vertically presented V-H illusory cues cannot guide the completion of lower limb horizontal plane movements, even given specific gaze parameters. Taken together, these data provide evidence to support that given the right circumstances exploitation of simple deceptive cues can influence relative aspects of perceptuomotor control; however, people can utilize the separate pathways involving visual control for perception and action to produce manual length estimations which differ from perception

Improve Food Safety of Chinese Restaurants in Kansas through Multicultural Intervening Measures

Chinese restaurants\u27 food safety problems have attracted the attention of food safety regulators. According to the many feedback of the state food safety inspectors, there are more problems in the operations of Chinese restaurants than in those others. The probability of repeating the same mistakes is also high in the review of the violation items in the inspection reports. Due to the number of violating behaviors in Chinese restaurants, food safety inspectors have to do many follow-up inspections, and this causes much waste of human resources. The purpose of this study was to enable Chinese restaurant practitioners to understand US health regulations, adjust and change their practices through multicultural interventions, improve behavior compliance and reduce the number of violations. The specific objectives of the study are: (1) To determine whether independent operated Chinese restaurants in Kansas truly have more food safety problems as described by the inspectors. (2) To develop practical multicultural intervening measures to help restaurant practitioners improve food safety knowledge, awareness, and acting ability. (3) The numbers of the restaurant violations after the multicultural intervening measures should be examined with the numbers of before interventions and non-intervening restaurants to analyze the effectiveness of the interventions; it also can be compared with other types of non-Chinese restaurants in Kansas to evaluate the actual effects of this study. The comparisons should also be made between those restaurants which implement different types and numbers of intervening measures to assess the pros and cons of the interventions and their cumulative effect

A SERIAL-PARALLEL HYBRID ROBOT FOR MACHINING OF COMPLEX SURFACES

Ph.DDOCTOR OF PHILOSOPH

NR2B-dependent cyclophilin D translocation suppresses the recovery of synaptic transmission after oxygen-glucose deprivation

N-methyl d-aspartate receptor (NMDA) subunit 2B (NR2B)-containing NMDA receptors and mitochondrial protein cyclophilin D (CypD) are well characterized in mediating neuronal death after ischemia, respectively. However, whether and how NR2B and CypD work together in mediating synaptic injury after ischemia remains elusive. Using an ex vivo ischemia model of oxygen–glucose deprivation (OGD) in hippocampal slices, we identified a NR2B-dependent mechanism for CypD translocation onto the mitochondrial inner membrane. CypD depletion (CypD null mice) prevented OGD-induced impairment in synaptic transmission recovery. Overexpression of neuronal CypD mice (CypD +) exacerbated OGD-induced loss of synaptic transmission. Inhibition of CypD-dependent mitochondrial permeability transition pore (mPTP) opening by cyclosporine A (CSA) attenuated ischemia-induced synaptic perturbation in CypD + and non-transgenic (non-Tg) mice. The treatment of antioxidant EUK134 to suppress mitochondrial oxidative stress rescued CypD-mediated synaptic dysfunction following OGD in CypD + slices. Furthermore, OGD provoked the interaction of CypD with P53, which was enhanced in slices overexpressing CypD but was diminished in CypD-null slices. Inhibition of p53 using a specific inhibitor of p53 (pifithrin-μ) attenuated the CypD/p53 interaction following OGD, along with a restored synaptic transmission in both non-Tg and CypD + hippocampal slices. Our results indicate that OGD-induced CypD translocation potentiates CypD/P53 interaction in a NR2B dependent manner, promoting oxidative stress and loss of synaptic transmission. We also evaluate a new ex vivo chronic OGD-induced ischemia model for studying the effect of oxidative stress on synaptic damage

NR2B-dependent cyclophilin D translocation suppresses the recovery of synaptic transmission after oxygen-glucose deprivation

N-methyl d-aspartate receptor (NMDA) subunit 2B (NR2B)-containing NMDA receptors and mitochondrial protein cyclophilin D (CypD) are well characterized in mediating neuronal death after ischemia, respectively. However, whether and how NR2B and CypD work together in mediating synaptic injury after ischemia remains elusive. Using an ex vivo ischemia model of oxygen–glucose deprivation (OGD) in hippocampal slices, we identified a NR2B-dependent mechanism for CypD translocation onto the mitochondrial inner membrane. CypD depletion (CypD null mice) prevented OGD-induced impairment in synaptic transmission recovery. Overexpression of neuronal CypD mice (CypD +) exacerbated OGD-induced loss of synaptic transmission. Inhibition of CypD-dependent mitochondrial permeability transition pore (mPTP) opening by cyclosporine A (CSA) attenuated ischemia-induced synaptic perturbation in CypD + and non-transgenic (non-Tg) mice. The treatment of antioxidant EUK134 to suppress mitochondrial oxidative stress rescued CypD-mediated synaptic dysfunction following OGD in CypD + slices. Furthermore, OGD provoked the interaction of CypD with P53, which was enhanced in slices overexpressing CypD but was diminished in CypD-null slices. Inhibition of p53 using a specific inhibitor of p53 (pifithrin-μ) attenuated the CypD/p53 interaction following OGD, along with a restored synaptic transmission in both non-Tg and CypD + hippocampal slices. Our results indicate that OGD-induced CypD translocation potentiates CypD/P53 interaction in a NR2B dependent manner, promoting oxidative stress and loss of synaptic transmission. We also evaluate a new ex vivo chronic OGD-induced ischemia model for studying the effect of oxidative stress on synaptic damage

Genetic deficiency of neuronal RAGE protects against AGE-induced synaptic injury

Synaptic dysfunction and degeneration is an early pathological feature of aging and age-related diseases, including Alzheimer's disease (AD). Aging is associated with increased generation and deposition of advanced glycation endproducts (AGEs), resulting from nonenzymatic glycation (or oxidation) proteins and lipids. AGE formation is accelerated in diabetes and AD-affected brain, contributing to cellular perturbation. The extent of AGEs' involvement, if at all, in alterations in synaptic structure and function is currently unknown. Here we analyze the contribution of neuronal receptor of AGEs (RAGE) signaling to AGE-mediated synaptic injury using novel transgenic neuronal RAGE knockout mice specifically targeted to the forebrain and transgenic mice expressing neuronal dominant-negative RAGE (DN-RAGE). Addition of AGEs to brain slices impaired hippocampal long-term potentiation (LTP). Similarly, treatment of hippocampal neurons with AGEs significantly decreases synaptic density. Such detrimental effects are largely reversed by genetic RAGE depletion. Notably, brain slices from mice with neuronal RAGE deficiency or DN-RAGE are resistant to AGE-induced LTP deficit. Further, RAGE deficiency or DN-RAGE blocks AGE-induced activation of p38 signaling. Taken together, these data show that neuronal RAGE functions as a signal transducer for AGE-induced synaptic dysfunction, thereby providing new insights into a mechanism by which the AGEs–RAGE-dependent signaling cascade contributes to synaptic injury via the p38 MAP kinase signal transduction pathway. Thus, RAGE blockade may be a target for development of interventions aimed at preventing the progression of cognitive decline in aging and age-related neurodegenerative diseases

Notoginsenoside R1 increases neuronal excitability and ameliorates synaptic and memory dysfunction following amyloid elevation

Neurodegeneration and synaptic dysfunction observed in Alzheimer's disease (AD) have been associated with progressive decrease in neuronal activity. Here, we investigated the effects of Notoginsenoside R1 (NTR1), a major saponin isolated from Panax notoginseng, on neuronal excitability and assessed the beneficial effects of NTR1 on synaptic and memory deficits under the Aβ-enriched conditions in vivo and in vitro. We assessed the effects of NTR1 on neuronal excitability, membrane ion channel activity, and synaptic plasticity in acute hippocampal slices by combining electrophysiological extracellular and intracellular recording techniques. We found that NTR1 increased the membrane excitability of CA1 pyramidal neurons in hippocampal slices by lowering the spike threshold possibly through a mechanism involving in the inhibition of voltage-gated K+ currents. In addition, NTR1 reversed Aβ1-42 oligomers-induced impairments in long term potentiation (LTP). Reducing spontaneous firing activity with 10 nM tetrodotoxin (TTX) abolished the protective effect of NTR1 against Aβ-induced LTP impairment. Finally, oral administration of NTR1 improved the learning performance of the APP/PS1 mouse model of AD. Our work reveals a novel mechanism involving in modulation of cell strength, which contributes to the protective effects of NTR1 against Aβ neurotoxicity

Alternating magnetic field-promoted nanoparticle mixing: the on-chip immunocapture of serum neuronal exosomes for Parkinson’s disease diagnostics

The analysis of cargo proteins in exosome subpopulations has considerable value in diagnostics but a translatable impact has been limited by lengthy or complex exosome extraction protocols. We describe herein a scalable, fast, and low-cost exosome extraction using an alternating (AC) magnetic field to support the dynamic mixing of antibody-coated magnetic beads (MBs) with serum samples within 3D-printed microfluidic chips. Zwitterionic polymer-coated MBs are, specifically, magnetically agitated and support ultraclean exosome capture efficiencies >70% from <50 μL of neat serum in 30 min. Applied herein to the immunocapture of neuronal exosomes using anti-L1CAM antibodies, prior to the array-based assaying of α-synuclein (α-syn) content by a standard duplex electrochemical sandwich ELISA, sub pg/mL detection was possible with an excellent coefficient of variation and a sample-to-answer time of ∼75 min. The high performance and semiautomation of this approach hold promise in underpinning low-cost Parkinson’s disease diagnostics and is of value in exosomal biomarker analyses more generally