Examining the Role of Life Skills in Mediating the Relationship between the Basic Psychological Needs and Subjective Well-Being of Taekwondo Student-Athletes.

Various theories in the field of positive youth development (PYD) through sport argue that student athletes' satisfaction with basic psychological needs, life skills development, and well-being are closely related to each other. This study identified the structural relationship among three basic psychological needs, life skills, and subjective well-being. Korean Taekwondo student athletes (N = 302, Mage = 17.67, range = 17-19) completed a survey evaluating basic psychological needs (autonomy, competence, and relatedness), life skills (teamwork, goal setting, social skills, time management, and leadership), and subjective well-being (life satisfaction, positive/negative affect). Data were analyzed by using descriptive statistics, correlation, and the Structural Equation Model (SEM). The model's goodness of fit was Ï°2/df = 2.78, TLI = 0.90, CFI = 0.90, RMSEA = 0.077 (95% CI = 0.70, 0.80), and SRMR = 0.085. The three basic psychological needs were positively related to life skills and subjective well-being. In addition, life skills had a mediation effect between the three basic psychological needs and subjective well-being. The interpretation of the results indicated that life skills development and well-being depend on basic psychological needs. Thus, coaches should encourage a PYD climate to satisfy their athletes' psychological needs.

Applications of psychological skills training for Paralympic table tennis athletes.

This study examined effects of psychological skills training (PST) for Korean national table tennis athletes with spinal cord injuries (SCI), who were training for the 2012 London Paralympics. Participants were three male table tennis players with level two SCI, and all participants attended a total of eight sessions of PST over a period of 3 months. The PST consisted of self-talk, imagery, cognitive reconstructing, and routine. To examine the effectiveness of mental coaching, the Test of Performance Strategies questionnaire was administered over three different periods of time: pre-PST, post-PST, and postcompetition. Pre- and posttest outcomes indicated that there were positive changes in self-talk, emotional control, and goal setting of athletes with SCI. With the exception of relaxation, Athlete 1 was able to maintain and use all of the improved mental skills in Paralympic competitions. However, although the mental skills of the athletes 2 and 3 generally improved, they were not able to take full advantage of these improvements in Paralympic competitions. PST can be developed and effectively utilized by athletes with SCI. Disability-specific issues should be considered to provide a better intervention program.

Oral administration of a small molecule targeted to block proNGF binding to p75 promotes myelin sparing and functional recovery after spinal cord injury.

The lack of effective therapies for spinal cord injury points to the need for identifying novel targets for therapeutic intervention. Here we report that a small molecule, LM11A-31, developed to block proNGF-p75 interaction and p75-mediated cell death crosses the blood-brain barrier efficiently when delivered orally. Administered starting 4 h postinjury, LM11A-31 promotes functional recovery without causing any toxicity or increased pain in a mouse model of spinal contusion injury. In both weight-bearing open-field tests and nonweight-bearing swim tests, LM11A-31 was effective in improving motor function and coordination. Such functional improvement correlated with a >50% increase in the number of surviving oligodendrocytes and myelinated axons. We also demonstrate that LM11A-31 indeed inhibits proNGF-p75 interaction in vivo, thereby curtailing the JNK3-mediated apoptotic cascade. These results thus highlight p75 as a novel therapeutic target for an orally delivered treatment for spinal cord injury.

JNK3 perpetuates metabolic stress induced by Aß peptides.

Although Aß peptides are causative agents in Alzheimer's disease (AD), the underlying mechanisms are still elusive. We report that Aß42 induces a translational block by activating AMPK, thereby inhibiting the mTOR pathway. This translational block leads to widespread ER stress, which activates JNK3. JNK3 in turn phosphorylates APP at T668, thereby facilitating its endocytosis and subsequent processing. In support, pharmacologically blocking translation results in a significant increase in Aß42 in a JNK3-dependent manner. Thus, JNK3 activation, which is increased in human AD cases and a familial AD (FAD) mouse model, is integral to perpetuating Aß42 production. Concomitantly, deletion of JNK3 from FAD mice results in a dramatic reduction in Aß42 levels and overall plaque loads and increased neuronal number and improved cognition. This reveals AD as a metabolic disease that is under tight control by JNK3.