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Human risk behavior is the subject of growing research in the field of psychology as well as economics. One central topic is the influence of psychological variables on risk behavior. Studies contained in this work investigated the impact of arousal, framing and motivation on risk behavior.
Arousal can on the one hand be a temporarily stable trait and on the other hand a situation-dependent variable. We showed that low trait arousal, measured via resting heart rate, predicted risky behavior. After physical exercise, state arousal was heightened in the experiment. Participants tended to act less risky after physical exercise. Taken together, the results suggest an inverse relation of arousal and risk behavior. Most studies investigating risk behavior employ a payment method that we call pay-one method: although the gambles that are used consist of many trials, only one trial is paid out. We investigated the effect of the payment method on risk behavior by employing both the pay-one and a pay-all method, which pays out all trials, in a within-subjects design. We found that participants acted about 10% less risky in the pay-one condition compared to the pay-all condition. This result suggests that risk-aversion is over-estimated in common risk paradigms that use the pay-one method.
When we worked on a hard task before, we like to engage in a more likable task afterwards. That observation led to the general classification of tasks in want-to and have-to tasks. Our body system strives towards a balance between those two task types in the sense of a homeostasis. We assessed event-related potentials (ERPs) in a risk game that we treated as a want-to task. When participants worked on a difficult have-to task before, amplitudes of the ERP-components in the risk game were raised compared to a condition where participants worked on an easy task before. We conclude that the motivation shift towards a want-to task after a have-to task can be assessed via ERP amplitudes.
In conclusion, it was shown that arousal, framing and motivation are important psychological variables that influence risk behavior. The specific mechanisms of these influences have been investigated and discussed.
Background
Preterm birth, low birth weight, and infant catch-up growth seem associated with an increased risk of respiratory diseases in later life, but individual studies showed conflicting results.
Objectives
We performed an individual participant data meta-analysis for 147,252 children of 31 birth cohort studies to determine the associations of birth and infant growth characteristics with the risks of preschool wheezing (1-4 years) and school-age asthma (5-10 years).
Methods
First, we performed an adjusted 1-stage random-effect meta-analysis to assess the combined associations of gestational age, birth weight, and infant weight gain with childhood asthma. Second, we performed an adjusted 2-stage random-effect meta-analysis to assess the associations of preterm birth (gestational age <37 weeks) and low birth weight (<2500 g) with childhood asthma outcomes.
Results
Younger gestational age at birth and higher infant weight gain were independently associated with higher risks of preschool wheezing and school-age asthma (P < .05). The inverse associations of birth weight with childhood asthma were explained by gestational age at birth. Compared with term-born children with normal infant weight gain, we observed the highest risks of school-age asthma in children born preterm with high infant weight gain (odds ratio [OR], 4.47; 95% CI, 2.58-7.76). Preterm birth was positively associated with an increased risk of preschool wheezing (pooled odds ratio [pOR], 1.34; 95% CI, 1.25-1.43) and school-age asthma (pOR, 1.40; 95% CI, 1.18-1.67) independent of birth weight. Weaker effect estimates were observed for the associations of low birth weight adjusted for gestational age at birth with preschool wheezing (pOR, 1.10; 95% CI, 1.00-1.21) and school-age asthma (pOR, 1.13; 95% CI, 1.01-1.27).
Conclusion
Younger gestational age at birth and higher infant weight gain were associated with childhood asthma outcomes. The associations of lower birth weight with childhood asthma were largely explained by gestational age at birth."
Extraintestinal pathogenic and intestinal pathogenic (diarrheagenic) Escherichia coli differ phylogenetically and by virulence profiles. Classic theory teaches simple linear descent in this species, where non-pathogens acquire virulence traits and emerge as pathogens. However, diarrheagenic Shiga toxin-producing E.coli (STEC) O2:H6 not only possess and express virulence factors associated with diarrheagenic and uropathogenic E.coli but also cause diarrhea and urinary tract infections. These organisms are phylogenetically positioned between members of an intestinal pathogenic group (STEC) and extraintestinal pathogenic E.coli. STEC O2:H6 is, therefore, a 'heteropathogen,' and the first such hybrid virulent E.coli identified. The phylogeny of these E.coli and the repertoire of virulence traits they possess compel consideration of an alternate view of pathogen emergence, whereby one pathogroup of E.coli undergoes phased metamorphosis into another. By understanding the evolutionary mechanisms of bacterial pathogens, rational strategies for counteracting their detrimental effects on humans can be developed.