Understanding Players' Sportspersonship Attitude, Expectancy-Related Beliefs, and Subjective Task Values in Field Hockey: An Integrated Approach.

(1) Background: The purpose of this study was to examine the relationship between expectancy-value components and attitudes toward sportspersonship among Malaysian adolescent field hockey players. This study also examined the effect of expectancy beliefs, task values, and sportspersonship attitude on the motivation of adolescent field hockey players by gender and age group. (2) Methods: The Malay versioned Expectancy Value Model Questionnaire and the Malay versioned Multidimensional Sportspersonship Orientations Scale were administered on 730 respondents (µ = 15.46 ± 1.83 years). (3) Results: The expectancy values and attainment value (r = 0.894), utility value and attainment value (r = 0.833) were highly correlated. There was no significant gender difference in expectancy, task values, and sportspersonship attitude dimensions. The main effect of age group was significant on task values: F (2724) = 4.19; p = 0.01. The difference was indicated between age groups of 15-16 years and 12-14 years (p = 0.02, d = 0.014) under task values variable. (4) Conclusions: There is no significant relationships between sportspersonship attitude (MSOS-M) and of expectancy beliefs and task values (EVMQ-M). To conclude, female and younger players demonstrate lower expectancy beliefs, task values, and sportspersonship attitudes than male and older field hockey players.

Sport Commitment among Malaysian Racquet Sports Athletes.

BACKGROUND: The Sport Commitment Model is widely used to understand the motivation and commitment of athletes to continue playing sports. However, the factors influencing athletes' commitment to racquet sports have not received much research attention, especially in Malaysia. PURPOSE: This study aims to use the Sport Commitment Questionnaire-2 (SCQ-2) to examine Malaysian athletes' commitment to racquet sports. METHODS: A total of 612 athletes (367 males/245 females, µ age= 30.32 ± 11.56) completed the SCQ-2, which measures seven factors and two dimensions of sport commitment. RESULTS: The results revealed that sport enjoyment was the main factor contributing to the athletes' commitment in all sports. Two-way ANOVA analyses showed significant differences in athletes' enthusiastic commitment [F(3,604) = 44.92, P = 0.00] and constrained commitment [F (3,604) = 15.32, P = 0.00] across four sports. There were also significant differences in both enthusiastic commitment [F(3,604) = 7.53, P = 0.00] and constraint commitment [F(3,604) = 18.82, P = 0.00] across age groups. CONCLUSION: Enjoyment is the main factor in sport commitment. Tennis athletes possess the highest level of enthusiastic commitment across all the racquet sports. Moreover, male athletes showed higher levels of enthusiastic commitment than female athletes.

Intracellular Bacterial Pathogens Trigger the Formation of U Small Nuclear RNA Bodies (U Bodies) through Metabolic Stress Induction.

Invasive bacterial pathogens induce an amino acid starvation (AAS) response in infected host cells that controls host defense in part by promoting autophagy. However, whether AAS has additional significant effects on the host response to intracellular bacteria remains poorly characterized. Here we showed that Shigella, Salmonella, and Listeria interfere with spliceosomal U snRNA maturation in the cytosol. Bacterial infection resulted in the rerouting of U snRNAs and their cytoplasmic escort, the survival motor neuron (SMN) complex, to processing bodies, thus forming U snRNA bodies (U bodies). This process likely contributes to the decline in the cytosolic levels of U snRNAs and of the SMN complex proteins SMN and DDX20 that we observed in infected cells. U body formation was triggered by membrane damage in infected cells and was associated with the induction of metabolic stresses, such as AAS or endoplasmic reticulum stress. Mechanistically, targeting of U snRNAs to U bodies was regulated by translation initiation inhibition and the ATF4/ATF3 pathway, and U bodies rapidly disappeared upon removal of the stress, suggesting that their accumulation represented an adaptive response to metabolic stress. Importantly, this process likely contributed to shape the host response to invasive bacteria because down-regulation of DDX20 expression using short hairpin RNA (shRNA) amplified ATF3- and NF-κB-dependent signaling. Together, these results identify a critical role for metabolic stress and invasive bacterial pathogens in U body formation and suggest that this process contributes to host defense.

Post-transcriptional inhibition of luciferase reporter assays by the Nod-like receptor proteins NLRX1 and NLRC3.

Luciferase reporter assays (LRAs) are widely used to assess the activity of specific signal transduction pathways. Although powerful, rapid and convenient, this technique can also generate artifactual results, as revealed for instance in the case of high throughput screens of inhibitory molecules. Here we demonstrate that the previously reported inhibitory effect of the Nod-like receptor (NLR) protein NLRX1 on NF-κB- and type I interferon-dependent pathways in LRAs was a nonspecific consequence of the overexpression of the NLRX1 leucine-rich repeat (LRR) domain. By comparing luciferase activity and luciferase gene expression using quantitative PCR from the same samples, we showed that NLRX1 inhibited LRAs in a post-transcriptional manner. In agreement, NLRX1 also repressed LRAs if luciferase was expressed under the control of a constitutive promoter, although the degree of inhibition by NLRX1 seemed to correlate with the dynamic inducibility of luciferase reporter constructs. Similarly, we observed that overexpression of another NLR protein, NLRC3, also resulted in artifactual inhibition of LRAs; thus suggesting that the capacity to inhibit LRAs at a post-transcriptional level is not unique to NLRX1. Finally, we demonstrate that host type I interferon response to Sendai virus infection was normal in NLRX1-silenced human HEK293T cells. Our results thus highlight the fact that LRAs are not a reliable technique to assess the inhibitory function of NLRs, and possibly other overexpressed proteins, on signal transduction pathways.

Amino acid starvation induced by invasive bacterial pathogens triggers an innate host defense program.

Autophagy, which targets cellular constituents for degradation, is normally inhibited in metabolically replete cells by the metabolic checkpoint kinase mTOR. Although autophagic degradation of invasive bacteria has emerged as a critical host defense mechanism, the signals that induce autophagy upon bacterial infection remain unclear. We find that infection of epithelial cells with Shigella and Salmonella triggers acute intracellular amino acid (AA) starvation due to host membrane damage. Pathogen-induced AA starvation caused downregulation of mTOR activity, resulting in the induction of autophagy. In Salmonella-infected cells, membrane integrity and cytosolic AA levels rapidly normalized, favoring mTOR reactivation at the surface of the Salmonella-containing vacuole and bacterial escape from autophagy. In addition, bacteria-induced AA starvation activated the GCN2 kinase, eukaryotic initiation factor 2α, and the transcription factor ATF3-dependent integrated stress response and transcriptional reprogramming. Thus, AA starvation induced by bacterial pathogens is sensed by the host to trigger protective innate immune and stress responses.

Nod-like receptors in intestinal homeostasis, inflammation, and cancer.

NLRs have been shown in a number of models to protect against microbial infection through their ability to participate in "pattern recognition" and their triggering of inflammatory pathways to control infection. Over the past few years, however, the role of NLRs, especially Nod1, Nod2, and NLRP3, in intestinal homeostasis has been highlighted. Indeed, these specific NLRs have been implicated in IBD, in particular, the association of Nod2 with CD, yet a clear understanding of how dysfunctional NLR activation leads to aberrant inflammation is still the focus of much investigation. In this review, we will examine how NLRs participate in the maintenance of gut homeostasis and how upset of this regulation can tip the balance toward chronic inflammation and intestinal cancer.