The Effect of Interaction with Therapy Horses on University Students\u27 Perceived Stress Level

This research project investigates how university students are affected by interacting with therapy horses. Stress is the factor that will be evaluated in this particular study. The self-rated stress scores will be acquired from University of Arkansas students both before and after interacting with specially trained therapy horses during an Equine Assisted Activity and Therapy (EAAT) class offered at the University. Stress will be evaluated by students taking a survey inquiring about daily stressors including finances, school, work and relationships. The data collected will be compared by pre- and post- interactions with the horses. We expect that the pre- and post- survey results will indicate lower stress levels following interaction with the therapy horses. Therapy horses’ calming and therapeutic effect on humans could result in stress relieving benefits for the University of Arkansas students participating in this study. This study could support the utilization of therapy horses to decrease stress for college students. Overall there was no significant evidence supporting a decrease in students stress levels in this study. Future studies will require a larger sample size as well as a control group. The possibility of horse therapy use in the decrease of stress levels of university students is valuable and should be studied further

FGF-2 Induces Neuronal Death through Upregulation of System xc-

The cystine/glutamate antiporter (system xc-) transports cystine into cell in exchange for glutamate. Fibroblast growth factor-2 (FGF-2) upregulates system xc- selectively on astrocytes, which leads to increased cystine uptake, the substrate for glutathione production, and increased glutamate release. While increased intracellular glutathione can limit oxidative stress, the increased glutamate release can potentially lead to excitotoxicity to neurons. To test this hypothesis, mixed neuronal and glial cortical cultures were treated with FGF-2. Treatment with FGF-2 for 48 h caused a significant neuronal death in these cultures. Cell death was not observed in neuronal-enriched cultures, or astrocyte-enriched cultures, suggesting the toxicity was the result of neuron-glia interaction. Blocking system xc- eliminated the neuronal death as did the AMPA/kainate receptor antagonist 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo[f]quinoxaline-2,3-dione (NBQX), but not the NMDA receptor antagonist memantine. When cultures were exposed directly to glutamate, both NBQX and memantine blocked the neuronal toxicity. The mechanism of this altered profile of glutamate receptor mediated toxicity by FGF-2 is unclear. The selective calcium permeable AMPA receptor antagonist 1-naphthyl acetyl spermine (NASPM) failed to offer protection. The most likely explanation for the results is that 48 h FGF-2 treatment induces AMPA/kainate receptor toxicity through increased system xc- function resulting in increased release of glutamate. At the same time, FGF-2 alters the sensitivity of the neurons to glutamate toxicity in a manner that promotes selective AMPA/kainate receptor mediated toxicity

Initial state of the QGP from perturbative QCD + saturation

The production of the initial state of the QGP in very high-energy $AA$ collisions is discussed within the framework of perturbative QCD and saturation. The next-to-leading order computation of the transverse energy of minijets is reviewed. Saturation of parton production, conjectured to occur at a dynamically determinable perturbative scale, leads to estimates of the initial densities. The final state multiplicities are predicted by assuming an isentropic hydrodynamical further evolution. Comparison with RHIC data is shown.Comment: 10 pages, 8 figures. Invited talk at the International Conference on Statistical QCD, August 2001, Bielefel

A study to determine the factors which influence primiparas to accept or reject breast feeding

Thesis (M.S.)--Boston Universit

Phase Retrieval via Randomized Kaczmarz: Theoretical Guarantees

We consider the problem of phase retrieval, i.e. that of solving systems of quadratic equations. A simple variant of the randomized Kaczmarz method was recently proposed for phase retrieval, and it was shown numerically to have a computational edge over state-of-the-art Wirtinger flow methods. In this paper, we provide the first theoretical guarantee for the convergence of the randomized Kaczmarz method for phase retrieval. We show that it is sufficient to have as many Gaussian measurements as the dimension, up to a constant factor. Along the way, we introduce a sufficient condition on measurement sets for which the randomized Kaczmarz method is guaranteed to work. We show that Gaussian sampling vectors satisfy this property with high probability; this is proved using a chaining argument coupled with bounds on VC dimension and metric entropy.Comment: Revised after comments from referee

Outcomes in language and social skills as seen in children with autism and developmental disabilities participating in equine assisted activities

Individuals with developmental disabilities commonly present characteristics that include deficits in social and communicative abilities. A number of intervention strategies have been implemented, but none have proven to be most effective. A somewhat novel approach known as equine assisted activities and therapies (EAAT) involves the utilization of horses during intervention and has shown to be effective in areas concerning quality of life, social functioning, self-regulation, adaptive behaviors, motor control, and motivation. The purpose of the current study is to examine the effects of EAA on social skills and expressive language in 2-4 children diagnosed with developmental disability. Participants engaged in 6 weeks of EAA at Equestrian Bridges, a local not-for-profit organization. Sessions were one hour and occurred once a week. Prior to the first session, participants’ guardians completed the Social Skills Improvement System (SSIS) and the Behavior Rating Inventory of Executive Function (BRIEF) questionnaires. A conversational language sample was elicited from each of the participants. Each session consisted of time spent learning a new vocabulary word, greeting and brushing miniature horses, leading the horses while engaging in activities, and reviewing the vocabulary word of the day. The final 3 sessions also included horseback riding. Following the last session, participants’ guardians completed the SSIS and BRIEF questionnaires again, and a second conversational language sample was elicited. Results suggested EAA may contribute to increased social skills, fewer problem behaviors, and improved executive function. Gains in expressive language were also noted, such as increased length and ease of conversation

Transport of BMAA into Neurons and Astrocytes by System x\u3csub\u3ec\u3c/sub\u3e-

The study of the mechanism of β-N-methylamino-l-alanine (BMAA) neurotoxicity originally focused on its effects at the N-methyl-d-aspartate (NMDA) receptor. In recent years, it has become clear that its mechanism of action is more complicated. First, there are certain cell types, such as motor neurons and cholinergic neurons, where the dominate mechanism of toxicity is through action at AMPA receptors. Second, even in cortical neurons where the primary mechanism of toxicity appears to be activation of NMDA receptors, there are other mechanisms involved. We found that along with NMDA receptors, activation of mGLuR5 receptors and effects on the cystine/glutamate antiporter (system xc-) were involved in the toxicity. The effects on system xc- are of particular interest. System xc- mediates the transport of cystine into the cell in exchange for releasing glutamate into the extracellular fluid. By releasing glutamate, system xc- can potentially cause excitotoxicity. However, through providing cystine to the cell, it regulates the levels of cellular glutathione (GSH), the main endogenous intracellular antioxidant, and in this way may protect cells against oxidative stress. We have previously published that BMAA inhibits cystine uptake leading to GSH depletion and had indirect evidence that BMAA is transported into the cells by system xc-. We now present direct evidence that BMAA is transported into both astrocytes and neurons through system xc-. The fact that BMAA is transported by system xc- also provides a mechanism for BMAA to enter brain cells potentially leading to misincorporation into proteins and protein misfolding