Children's Perception of Food Marketing Across Digital Media Platforms.

Introduction: Exposure to food marketing increases the risk of poor diet. Children's perception and interpretation of food marketing across digital media platforms is understudied. Children aged 9-11 years are uniquely susceptible to food marketing because children may watch content alone, and it is unclear whether embedded ads are decipherable by children (e.g., social media influencers) and if children are receptive to advertisements. Methods: The authors collected data from 21 child-parent dyads in 2022 to fill this gap. Children were interviewed about their food marketing exposure and media use and were asked to share their perspectives on food advertisements. Parents completed a survey for household digital devices, demographics, and perception of their child's food advertising knowledge. Results: This study found that all children generally recognized direct food advertisements, could describe them with varying levels of confidence, and shared examples. Despite self-identifying ads and understanding the intent of advertising, many children are still receptive to advertisements on the basis of engaging content (e.g., liking the ads as entertainment, watching ads even when given the chance to skip the ad) and the food items marketed (e.g., liking the taste of foods). Conclusions: These findings suggest that knowledge of advertisement exposure and intent of advertising are not sufficient to reduce receptiveness of unhealthy food ad exposure. Additional research on the potential impacts of embedded ads, such as through social media influencers, is needed to understand children's interaction with the current digital media landscape.

Top 10 Research Questions Related to Teaching Games for Understanding.

In this article, we elaborate on 10 current research questions related to the "teaching games for understanding" (TGfU) approach with the objective of both developing the model itself and fostering game understanding, tactical decision making, and game-playing ability in invasion and net/wall games: (1) How can existing scientific approaches from different disciplines be used to enhance game play for beginners and proficient players? (2) How can state-of-the-art technology be integrated to game-play evaluations of beginners and proficient players by employing corresponding assessments? (4) How can complexity thinking be utilized to shape day-to-day physical education (PE) and coaching practices? (5) How can game making/designing be helpfully utilized for emergent learning? (6) How could purposeful game design create constraints that enable tactical understanding and skill development through adaptive learning and distributed cognition? (7) How can teacher/coach development programs benefit from game-centered approaches? (8) How can TGfU-related approaches be implemented in teacher or coach education with the goal of facilitating preservice and in-service teachers/coaches' learning to teach and thereby foster their professional development from novices to experienced practitioners? (9) Can the TGfU approach be considered a helpful model across different cultures? (10) Can physical/psychomotor, cognitive, affective/social, and cultural development be fostered via TGfU approaches? The answers to these questions are critical not only for the advancement of teaching and coaching in PE and sport-based clubs, but also for an in-depth discussion on new scientific avenues and technological tools.

Impact of the functional status of saeRS on in vivo phenotypes of Staphylococcus aureus†sarA mutants.

We investigated the in vivo relevance of the impact of sarA and saeRS on protease production using derivatives of the USA300 strain LAC. The results confirmed that mutation of saeRS or sarA reduces virulence in a bacteremia model to a comparable degree. However, while eliminating protease production restored virulence in the sarA mutant, it had little impact in the saeRS mutant. Additionally, constitutive activation of saeRS (saeRS(C)) enhanced the virulence of LAC and largely restored virulence in the isogenic sarA mutant. Based on these results, together with our analysis of the representative virulence factors alpha toxin, protein A (Spa), and extracellular nucleases, we propose a model in which the attenuation of saeRS mutants is defined primarily by decreased production of such factors, while constitutive activation of saeRS increases virulence, and reverses the attenuation of sarA mutants, because it results in both increased production and decreased protease-mediated degradation of these same factors. This regulatory balance was also apparent in a murine model of catheter-associated infection, with the results suggesting that the impact of saeRS on nuclease production plays an important role during the early stages of these infections that is partially offset by increased protease production in sarA mutants.

saeRS and sarA act synergistically to repress protease production and promote biofilm formation in Staphylococcus aureus.

Mutation of the staphylococcal accessory regulator (sarA) limits biofilm formation in diverse strains of Staphylococcus aureus, but there are exceptions. One of these is the commonly studied strain Newman. This strain has two defects of potential relevance, the first being mutations that preclude anchoring of the fibronectin-binding proteins FnbA and FnbB to the cell wall, and the second being a point mutation in saeS that results in constitutive activation of the saePQRS regulatory system. We repaired these defects to determine whether either plays a role in biofilm formation and, if so, whether this could account for the reduced impact of sarA in Newman. Restoration of surface-anchored FnbA enhanced biofilm formation, but mutation of sarA in this fnbA-positive strain increased rather than decreased biofilm formation. Mutation of sarA in an saeS-repaired derivative of Newman (P18L) or a Newman saeRS mutant (ΔsaeRS) resulted in a biofilm-deficient phenotype like that observed in clinical isolates, even in the absence of surface-anchored FnbA. These phenotypes were correlated with increased production of extracellular proteases and decreased accumulation of FnbA and/or Spa in the P18L and ΔsaeRS sarA mutants by comparison to the Newman sarA mutant. The reduced accumulation of Spa was reversed by mutation of the gene encoding aureolysin, while the reduced accumulation of FnbA was reversed by mutation of the sspABC operon. These results demonstrate that saeRS and sarA act synergistically to repress the production of extracellular proteases that would otherwise limit accumulation of critical proteins that contribute to biofilm formation, with constitutive activation of saeRS limiting protease production, even in a sarA mutant, to a degree that can be correlated with increased enhanced capacity to form a biofilm. Although it remains unclear whether these effects are mediated directly or indirectly, studies done with an sspA::lux reporter suggest they are mediated at a transcriptional level.

Impact of extracellular nuclease production on the biofilm phenotype of Staphylococcus aureus under in vitro and in vivo conditions.

Recent studies suggest that extracellular DNA promotes biofilm formation in Staphylococcus aureus and, conversely, that extracellular nucleases limit the ability to form a biofilm. S. aureus produces at least two extracellular nucleases, and in the study described in this report, we examined the impact of each of these nucleases on biofilm formation under both in vitro and in vivo conditions. Our results demonstrate that both nucleases impact biofilm formation in the clinical isolate UAMS-1. Under certain in vitro conditions, this impact is negative, with mutation of either or both of the nuclease genes (nuc1 and nuc2) resulting in an enhanced capacity to form a biofilm. However, this effect was not apparent in vivo in a murine model of catheter-associated biofilm formation. Rather, mutation of either or both nuclease genes appeared to limit biofilm formation to a degree that could be correlated with increased susceptibility to daptomycin.

Defining the strain-dependent impact of the Staphylococcal accessory regulator (sarA) on the alpha-toxin phenotype of Staphylococcus aureus.

We demonstrate that mutation of the staphylococcal accessory regulator (sarA) limits the accumulation of alpha-toxin and phenol-soluble modulins (PSMs) in Staphylococcus aureus isolates of the USA300 clonal lineage. Degradation assays and experiments done with protease inhibitors suggested that this was due to the increased production of extracellular proteases rather than differences associated with the impact of sarA on transcription of the target gene (hla) or the accessory gene regulator (agr). This was confirmed by demonstrating that concomitant mutation of the gene encoding aureolysin (aur) reversed the alpha-toxin and PSM-deficient phenotypes of a USA300 sarA mutant. Mutation of sarA had little impact on the alpha-toxin or PSM phenotypes of the commonly studied strain Newman, which is known to have a mutation in saeS that results in constitutive activation of the saeRS regulatory system, and we also demonstrate that repair of this defect resulted in the increased production of extracellular proteases and reversed both the alpha-toxin and PSM-positive phenotypes of a Newman sarA mutant.

Epistatic relationships between sarA and agr in Staphylococcus aureus biofilm formation.

BACKGROUND: The accessory gene regulator (agr) and staphylococcal accessory regulator (sarA) play opposing roles in Staphylococcus aureus biofilm formation. There is mounting evidence to suggest that these opposing roles are therapeutically relevant in that mutation of agr results in increased biofilm formation and decreased antibiotic susceptibility while mutation of sarA has the opposite effect. To the extent that induction of agr or inhibition of sarA could potentially be used to limit biofilm formation, this makes it important to understand the epistatic relationships between these two loci. METHODOLOGY/PRINCIPAL FINDINGS: We generated isogenic sarA and agr mutants in clinical isolates of S. aureus and assessed the relative impact on biofilm formation. Mutation of agr resulted in an increased capacity to form a biofilm in the 8325-4 laboratory strain RN6390 but had little impact in clinical isolates S. aureus. In contrast, mutation of sarA resulted in a reduced capacity to form a biofilm in all clinical isolates irrespective of the functional status of agr. This suggests that the regulatory role of sarA in biofilm formation is independent of the interaction between sarA and agr and that sarA is epistatic to agr in this context. This was confirmed by demonstrating that restoration of sarA function restored the ability to form a biofilm even in the corresponding agr mutants. Mutation of sarA in clinical isolates also resulted in increased production of extracellular proteases and extracellular nucleases, both of which contributed to the biofilm-deficient phenotype of sarA mutants. However, studies comparing different strains with and without proteases inhibitors and/or mutation of the nuclease genes demonstrated that the agr-independent, sarA-mediated repression of extracellular proteases plays a primary role in this regard. CONCLUSIONS AND SIGNIFICANCE: The results we report suggest that inhibitors of sarA-mediated regulation could be used to limit biofilm formation in S. aureus and that the efficacy of such inhibitors would not be limited by spontaneous mutation of agr in the human host.

The causal pathway model and cerebral palsy.

This article reviews possible prenatal, perinatal, and postnatal causes of cerebral palsy. The interactive effects of various causes are evaluated. Groups of intervention strategies are then presented based on the causal pathway model.