568 research outputs found
Altering HIF-1α through 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure affects coronary vessel development.
Differential tissue hypoxia drives normal cardiogenic events including coronary vessel development. This requirement renders cardiogenic processes potentially susceptible to teratogens that activate a transcriptional pathway that intersects with the hypoxia-inducible factor (HIF-1) pathway. The potent toxin 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is known to cause cardiovascular defects by way of reduced myocardial hypoxia, inhibition of angiogenic stimuli, and alterations in responsiveness of endothelial cells to those stimuli. Our working hypothesis is that HIF-1 levels and thus HIF-1 signaling in the developing myocardium will be reduced by TCDD treatment in vivo during a critical stage and in particularly sensitive sites during heart morphogenesis. This inadequate HIF-1 signaling will subsequently result in outflow tract (OFT) and coronary vasculature defects. Our current data using the chicken embryo model showed a marked decrease in the intensity of immunostaining for HIF-1α nuclear expression in the OFT myocardium of TCDD-treated embryos. This area at the base of the OFT is particularly hypoxic during normal development; where endothelial cells initially form a concentrated anastomosing network known as the peritruncal ring; and where the left and right coronary arteries eventually connect to the aortic lumen. Consistent with this finding, anomalies of the proximal coronaries were detected after TCDD treatment and HIF-1α protein levels decreased in a TCDD dose-dependent manner
Examination of the Robustness of the Resilience Scale Using Multigroup Analysis
This study aimed to investigate the factor invariance and robustness of a resilience scale using multigroup analysis to allow for a relative comparison of models. Participants were 2568 high school students (male: 1211, female: 1357) in Japan. They answered the questionnaire about their respective general attributes (gender, grade) and the resilience scale. The resilience scale included 9 items and 3 factors (building relationship, overcome power, and breakthrough strength). To investigate whether the resilience scale responds appropriately to the participants in this study, a separate confirmatory factor analysis was conducted for each gender. After examining the construct validity of the resilience scale, a multigroup analysis was conducted for groups by gender. The multigroup analysis confirmed configural invariance, measurement invariance, weak factorial invariance, and strong factorial invariance. The results of the confirmatory factor analysis for each gender was a good fit. Configural invariance was adopted for multigroup analysis. The validity of interpreting resilience in male and female participants using the same model was established in this study. We expect that the current findings will help interpret gender differences in resilience in the field of mental health
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Closer to critical resting-state neural dynamics in individuals with higher fluid intelligence
According to the critical brain hypothesis, the brain is considered to operate near criticality and realize efficient neural computations. Despite the prior theoretical and empirical evidence in favor of the hypothesis, no direct link has been provided
between human cognitive performance and the neural criticality. Here we provide such a key link by analyzing resting-state dynamics of functional magnetic resonance imaging (fMRI) networks at a whole-brain level. We develop a data-driven analysis method, inspired from statistical physics theory of spin systems, to map out the whole-brain neural dynamics onto a phase diagram. Using this tool, we show evidence that neural dynamics of human participants with higher fluid intelligence quotient scores are closer to a critical state, i.e., the boundary between the paramagnetic phase and the spin-glass (SG) phase. The present results are consistent with the notion of “edge-of-chaos” neural computation
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Cutaneous T-cell lymphoma developing during nivolumab treatment for metastatic melanoma
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