Exploring the long-term training of sport-based youth development coaches serving with coach across America

Thesis (Ed.D.)--Boston UniversityThis study sought to examine the impact on coaches' experiences, and perceptions of coaching efficacy, of an ongoing coach training program designed to support a diverse sample of sport-based youth development coaches serving with Coach Across America (CAA). This multi-modal training program consisted of an intensive three-day training, highlighting holistic youth development, monthly webinars and formal mentoring/peer- leadership. Participants were recruited from two years (2011-2012 and 2012-2013) of the CAA program. In year one, 82 coaches (52.4% male, 47.6% female; 43.9% Caucasian, 22% Hispanic, 14.6% African American, 6.1% Asian American, 11% Other, 2.3% Unidentified) completed the quantitative measures, and five coaches participated in focus groups. In year two, 160 coaches (48.4% male, 50.6% female, 0.6% transgender; 38.8% Caucasian, 20.6% Hispanic, 20% African American, 2.5% Asian American, 1.9% Native North American Indian, 14.4% Unidentified) completed the quantitative measures, and seven coaches participated in focus groups. Quantitative analyses examining dimensions of coaching efficacy (CES-11 dimensions: motivation, technique, game strategy, character building and total coaching efficacy) (Feltz, Chase, Mortiz & Sullivan, 1999) revealed several significant findings, including: coaching satisfaction was the only predictive factor of CES-II scores; number of webinars viewed did not predict CES-II scores; character building efficacy scores increased following attendance at the three-day training; and CES-II scores increased for all but technique efficacy over the course of the year. Focus groups provided a more robust picture of coaches' perceptions and experiences. Analysis revealed five higher order themes: overall positive impact of the training program, experiences at host site, factors facilitating a mentoring relationship, factors hindering a mentoring relationship, and suggestions for future support. In particular, coaches highlighted the need for content focused on holistic youth development, connection between theory and practice, addressing contextual challenges of coaching in an underserved community, and relationships with knowledgeable, engaged and available mentors/peers. Results support the potential efficacy of long-term training for youth coaches in positively impacting coaches' experiences and perceptions of coaching efficacy, with a particular focus on encouraging youth development principles, building relationships and responding to current coach challenges. Based on the data, specific implications and directions for future research are discussed

Endocannabinoids-related compounds in gastrointestinal diseases

The endocannabinoid system (ECS) is an endogenous signalling pathway involved in the control of several gastrointestinal (GI) functions at both peripheral and central levels. In recent years, it has become apparent that the ECS is pivotal in the regulation of GI motility, secretion and sensitivity, but endocannabinoids (ECs) are also involved in the regulation of intestinal inflammation and mucosal barrier permeability, suggesting their role in the pathophysiology of both functional and organic GI disorders. Genetic studies in patients with irritable bowel syndrome (IBS) or inflammatory bowel disease have indeed shown significant associations with polymorphisms or mutation in genes encoding for cannabinoid receptor or enzyme responsible for their catabolism, respectively. Furthermore, ongoing clinical trials are testing EC agonists/antagonists in the achievement of symptomatic relief from a number of GI symptoms. Despite this evidence, there is a lack of supportive RCTs and relevant data in human beings, and hence, the possible therapeutic application of these compounds is raising ethical, political and economic concerns. More recently, the identification of several EC-like compounds able to modulate ECS function without the typical central side effects of cannabino-mimetics has paved the way for emerging peripherally acting drugs. This review summarizes the possible mechanisms linking the ECS to GI disorders and describes the most recent advances in the manipulation of the ECS in the treatment of GI diseases

Palmitoylethanolamide exerts neuroprotective effects in mixed neuroglial cultures and organotypic hippocampal slices via peroxisome proliferator-activated receptor-α

<p>Abstract</p> <p>Background</p> <p>In addition to cytotoxic mechanisms directly impacting neurons, β-amyloid (Aβ)-induced glial activation also promotes release of proinflammatory molecules that may self-perpetuate reactive gliosis and damage neighbouring neurons, thus amplifying neuropathological lesions occurring in Alzheimer's disease (AD). Palmitoylethanolamide (PEA) has been studied extensively for its anti-inflammatory, analgesic, antiepileptic and neuroprotective effects. PEA is a lipid messenger isolated from mammalian and vegetable tissues that mimics several endocannabinoid-driven actions, even though it does not bind to cannabinoid receptors. Some of its pharmacological properties are considered to be dependent on the expression of peroxisome proliferator-activated receptors-α (PPARα).</p> <p>Findings</p> <p>In the present study, we evaluated the effect of PEA on astrocyte activation and neuronal loss in models of Aβ neurotoxicity. To this purpose, primary rat mixed neuroglial co-cultures and organotypic hippocampal slices were challenged with Aβ_1-42and treated with PEA in the presence or absence of MK886 or GW9662, which are selective PPARα and PPARγ antagonists, respectively. The results indicate that PEA is able to blunt Aβ-induced astrocyte activation and, subsequently, to improve neuronal survival through selective PPARα activation. The data from organotypic cultures confirm that PEA anti-inflammatory properties implicate PPARα mediation and reveal that the reduction of reactive gliosis subsequently induces a marked rebound neuroprotective effect on neurons.</p> <p>Conclusions</p> <p>In line with our previous observations, the results of this study show that PEA treatment results in decreased numbers of infiltrating astrocytes during Aβ challenge, resulting in significant neuroprotection. PEA could thus represent a promising pharmacological tool because it is able to reduce Aβ-evoked neuroinflammation and attenuate its neurodegenerative consequences.</p

Synthesis, Structure-Activity, and Structure-Stability Relationships of 2-Substituted- N

N-Acylethanolamine acid amidase (NAAA) is a cysteine amidase that preferentially hydrolyzes saturated or monounsaturated fatty acid ethanolamides (FAEs), such as palmitoylethanolamide (PEA) and oleoylethanolamide (OEA), which are endogenous agonists of nuclear peroxisome proliferator-activated receptor-α (PPAR-α). Compounds that feature an α-amino-β-lactone ring have been identified as potent and selective NAAA inhibitors and have been shown to exert marked anti-inflammatory effects that are mediated through FAE-dependent activation of PPAR-α. We synthesized and tested a series of racemic, diastereomerically pure β-substituted α-amino-β-lactones, as either carbamate or amide derivatives, investigating the structure-activity and structure-stability relationships (SAR and SSR) following changes in β-substituent size, relative stereochemistry at the α- and β-positions, and α-amino functionality. Substituted carbamate derivatives emerged as more active and stable than amide analogues, with the cis configuration being generally preferred for stability. Increased steric bulk at the β-position negatively affected NAAA inhibitory potency, while improving both chemical and plasma stability

Tetracosahexaenoylethanolamide, a novel -acylethanolamide, is elevated in ischemia and increases neuronal output.

-acylethanolamines (NAEs) are endogenous lipid-signaling molecules derived from fatty acids that regulate numerous biological functions, including in the brain. Interestingly, NAEs are elevated in the absence of fatty acid amide hydrolase (FAAH) and following CO-induced ischemia/hypercapnia, suggesting a neuroprotective response. Tetracosahexaenoic acid (THA) is a product and precursor to DHA; however, the NAE product, tetracosahexaenoylethanolamide (THEA), has never been reported. Presently, THEA was chemically synthesized as an authentic standard to confirm THEA presence in biological tissues. Whole brains were collected and analyzed for unesterified THA, total THA, and THEA in wild-type and FAAH-KO mice that were euthanized by either head-focused microwave fixation, CO + microwave, or CO only. PPAR activity by transient transfection assay and ex vivo neuronal output in medium spiny neurons (MSNs) of the nucleus accumbens by patch clamp electrophysiology were determined following THEA exposure. THEA in the wild-type mice was nearly doubled ( 0.05) transcriptional activity of PPARs relative to control, but 100 nM of THEA increased ( < 0.001) neuronal output in MSNs of the nucleus accumbens. Here were identify a novel NAE, THEA, in the brain that is elevated upon ischemia/hypercapnia and by KO of the FAAH enzyme. While THEA did not activate PPAR, it augmented the excitability of MSNs in the nucleus accumbens. Overall, our results suggest that THEA is a novel NAE that is produced in the brain upon ischemia/hypercapnia and regulates neuronal excitation