2,415 research outputs found

    Exploring the Impact of Tourist Motivations on Thailand's Gastronomic Tourism: A Structural Equation Modeling Approach

    Get PDF
    This study investigates the impact of tourist motivations on Thailand's appeal as a gastronomic tourism destination, addressing a gap in the existing literature by examining the specific factors that attract tourists to the country's culinary offerings. The primary research objective is to identify and analyze the motivations driving tourists to choose Thailand as a gastronomic destination, while also assessing the implications of these motivations for tourism stakeholders. Data was collected from 163 valid participants who had experiences with Thailand's gastronomic tourism. Using a combination of exploratory and confirmatory factor analyses, this study identifies four distinct factors that contribute to tourism motivation in Thailand: social interaction with novelty, relaxation, regression, and escape from boredom. Structural equation modeling is then employed to analyze the relationships between these factors and Thailand's appeal as a gastronomic tourism destination. The results indicate that social interaction with novelty, regression, and escape from boredom have a significant positive effect on Thailand's gastronomic destination, while relaxation is found to have no significant impact. These findings challenge existing assumptions about the role of relaxation in tourists' destination choices and provide valuable insights for tourism stakeholders seeking to capitalize on the growing popularity of gastronomic tourism. This research contributes to the understanding of gastronomic tourism motivations in Thailand, offering valuable insights for tourism stakeholders and paving the way for further exploration and understanding of the factors driving tourists' destination choices in the context of gastronomic tourism

    Chromatin-binding protein PHF6 regulates activity-dependent transcriptional networks to promote hunger response

    Get PDF
    Understanding the mechanisms of activity-dependent gene transcription underlying adaptive behaviors is challenging at neuronal-subtype resolution. Using cell-type specific molecular analysis in agouti-related peptide (AgRP) neurons, we reveal that the profound hunger-induced transcriptional changes greatly depend on plant homeodomain finger protein 6 (PHF6), a transcriptional repressor enriched in AgRP neurons. Loss of PHF6 in the satiated mice results in a hunger-state-shifting transcriptional profile, while hunger fails to further induce a rapid and robust activity-dependent gene transcription in PHF6-deficient AgRP neurons. We reveal that PHF6 binds to the promoters of a subset of immediate-early genes (IEGs) and that this chromatin binding is dynamically regulated by hunger state. Depletion of PHF6 decreases hunger-driven feeding motivation and makes the mice resistant to body weight gain under repetitive fasting-refeeding conditions. Our work identifies a neuronal subtype-specific transcriptional repressor that modulates transcriptional profiles in different nutritional states and enables adaptive eating behavior

    Conference on Best Practices for Managing Daubert Questions

    Get PDF
    When we are talking about overstatement, is it so apparent that surely the jury could understand that? Or that on cross at trial, would the opposing counsel make that apparent so that the jury would deal with it on its own? Or is it overstatement, in ways that you normally see, in that it becomes opaque and therefore misleading to the jury and the jury would never be able to figure it out

    GEMC1 and MCIDAS interactions with SWI/SNF complexes regulate the multiciliated cell-specific transcriptional program

    Get PDF
    Multiciliated cells (MCCs) project dozens to hundreds of motile cilia from their apical surface to promote the movement of fluids or gametes in the mammalian brain, airway or reproductive organs. Differentiation of MCCs requires the sequential action of the Geminin family transcriptional activators, GEMC1 and MCIDAS, that both interact with E2F4/5-DP1. How these factors activate transcription and the extent to which they play redundant functions remains poorly understood. Here, we demonstrate that the transcriptional targets and proximal proteomes of GEMC1 and MCIDAS are highly similar. However, we identified distinct interactions with SWI/SNF subcomplexes; GEMC1 interacts primarily with the ARID1A containing BAF complex while MCIDAS interacts primarily with BRD9 containing ncBAF complexes. Treatment with a BRD9 inhibitor impaired MCIDAS-mediated activation of several target genes and compromised the MCC differentiation program in multiple cell based models. Our data suggest that the differential engagement of distinct SWI/SNF subcomplexes by GEMC1 and MCIDAS is required for MCC-specific transcriptional regulation and mediated by their distinct C-terminal domains

    Requirement for YAP1 signaling in myxoid liposarcoma

    Full text link
    Myxoid liposarcomas (MLS), malignant tumors of adipocyte origin, are driven by the FUS-DDIT3 fusion gene encoding an aberrant transcription factor. The mechanisms whereby FUS-DDIT3 mediates sarcomagenesis are incompletely understood, and strategies to selectively target MLS cells remain elusive. Here we show, using an unbiased functional genomic approach, that FUS-DDIT3-expressing mesenchymal stem cells and MLS cell lines are dependent on YAP1, a transcriptional co-activator and central effector of the Hippo pathway involved in tissue growth and tumorigenesis, and that increased YAP1 activity is a hallmark of human MLS Mechanistically, FUS-DDIT3 promotes YAP1 expression, nuclear localization, and transcriptional activity and physically associates with YAP1 in the nucleus of MLS cells. Pharmacologic inhibition of YAP1 activity impairs the growth of MLS cells in vitro and in vivo These findings identify overactive YAP1 signaling as unifying feature of MLS development that could represent a novel target for therapeutic intervention

    Effects of omega-3 polyunsaturated fatty acid supplementation on cognitive functioning in youth at ultra-high risk for psychosis: secondary analysis of the NEURAPRO randomised controlled trial

    Full text link
    BACKGROUND: Cognitive impairments are well-established features of psychotic disorders and are present when individuals are at ultra-high risk for psychosis. However, few interventions target cognitive functioning in this population. AIMS: To investigate whether omega-3 polyunsaturated fatty acid (n-3 PUFA) supplementation improves cognitive functioning among individuals at ultra-high risk for psychosis. METHOD: Data (N = 225) from an international, multi-site, randomised controlled trial (NEURAPRO) were analysed. Participants were given omega-3 supplementation (eicosapentaenoic acid and docosahexaenoic acid) or placebo over 6 months. Cognitive functioning was assessed with the Brief Assessment of Cognition in Schizophrenia (BACS). Mixed two-way analyses of variance were computed to compare the change in cognitive performance between omega-3 supplementation and placebo over 6 months. An additional biomarker analysis explored whether change in erythrocyte n-3 PUFA levels predicted change in cognitive performance. RESULTS: The placebo group showed a modest greater improvement over time than the omega-3 supplementation group for motor speed (ηp_{p}2^{2} = 0.09) and BACS composite score (ηp_{p}2^{2} = 0.21). After repeating the analyses without individuals who transitioned, motor speed was no longer significant (ηp_{p}2^{2} = 0.02), but the composite score remained significant (ηp_{p}2^{2} = 0.02). Change in erythrocyte n-3 PUFA levels did not predict change in cognitive performance over 6 months. CONCLUSIONS: We found no evidence to support the use of omega-3 supplementation to improve cognitive functioning in ultra-high risk individuals. The biomarker analysis suggests that this finding is unlikely to be attributed to poor adherence or consumption of non-trial n-3 PUFAs

    Neural network solution for suboptimal control of non-holonomic chained form system

    Get PDF
    In this paper, we develop fixed-final time nearly optimal control laws for a class of non-holonomic chained form systems by using neural networks to approximately solve a Hamilton-Jacobi-Bellman equation. A certain time-folding method is applied to recover uniform complete controllability for the chained form system. This method requires an innovative design of a certain dynamic control component. Using this time-folding method, the chained form system is mapped into a controllable linear system for which controllers can systematically be designed to ensure exponential or asymptotic stability as well as nearly optimal performance. The result is a neural network feedback controller that has time-varying coefficients found by a priori offline tuning. The results of this paper are demonstrated in an example

    Centrosome-dependent microtubule modifications set the conditions for axon formation

    Get PDF
    Microtubule (MT) modifications are critical during axon development, with stable MTs populating the axon. How these modifications are spatially coordinated is unclear. Here, via high-resolution microscopy, we show that early developing neurons have fewer somatic acetylated MTs restricted near the centrosome. At later stages, however, acetylated MTs spread out in soma and concentrate in growing axon. Live imaging in early plated neurons of the MT plus-end protein, EB3, show increased displacement and growth rate near the MTOC, suggesting local differences that might support axon selection. Moreover, F-actin disruption in early developing neurons, which show fewer somatic acetylated MTs, does not induce multiple axons, unlike later stages. Overexpression of centrosomal protein 120 (Cep120), which promotes MT acetylation/stabilization, induces multiple axons, while its knockdown downregulates proteins modulating MT dynamics and stability, hampering axon formation. Collectively, we show how centrosome-dependent MT modifications contribute to axon formation
    • …
    corecore