Personalidade e conflito : Uma aplicação do modelo da dupla mediação

Dissertação de Mestrado apresentada ao ISPA - Instituto UniversitárioEscolher entre duas opções gera conflito intrapessoal. O modelo da dupla mediação (Scholten & Sherman, 2006) defende que este conflito é gerado pela preocupação com os sacrifícios envolvidos na escolha de uma opção em detrimento de outra, e pela preocupação com os argumentos que podem ser construídos a favor de cada opção. Estas duas fontes de conflito originam uma relação entre tamanho de troca (entre os atributos das opções) e conflito em U-invertido. O presente estudo investiga se a personalidade, especificamente o modo de processamento de informação, tem impacto nesta relação, usando a perspectiva dualista da Cognitive-Experiential Self Theory (Epstein, 1973). Os resultados indicaram que pessoas com baixa racionalidade e experiencialidade apresentam o maior nível de conflito e que pessoas mais experienciais sentem um menor conflito que pessoas pouco experienciais. Este efeito é atenuado pelo nível de racionalidade e é mais forte em trocas pequenas do que em intermédias, e em trocas intermédias do que em grandes. No que respeita à relação entre tamanho de troca e conflito, verifica-se que, em pessoas mais racionais, uma menor experiencialidade origina uma relação menos positiva, e que em pessoas mais experienciais, uma menor racionalidade torna a relação também menos positiva. Parece que pessoas mais racionais contemplam as opções durante mais tempo, deixando-as mais alertas a possíveis sacrifícios, e que pessoas mais experienciais têm menos dificuldades em encontrar argumentos, gerando uma relação mais positiva.ABSTRACT: Choosing between options generates intrapersonal conflict. The double-meditation model (Scholten & Sherman, 2006) claims that both concern about the sacrifices involved in choosing one option instead of the other and concern about the possible arguments in favour of each option are sources of conflict, and that these lead to an inverse U-shaped relation between tradeoff size (between the attributes of the options) and conflict. This study investigates whether personality, more specifically the mode of information processing, has an impact on this relation, using the dual-process framework of the Cognitive-Experiential Self Theory (Epstein, 1973). Results showed that people that are less experiential and less rational experience a superior conflict than their more rational and/or more experiential counterparts. Moreover, more experiential subjects experienced less conflict than less experiential subjects. This relation is attenuated by their level of rationality and this effect applies more to small tradeoff sizes than to large ones, and to intermediate tradeoff sizes than to extreme ones. Moreover, the more rational experiential people are, and the more experiential rational people are, the less positive becomes the relation between tradeoff size and final conflict. Apparently more rational people contemplate more, leaving them more aware of possible sacrifices, and more experiential people experience less difficulties in finding an argument, leading both to a more positive relation

FM stars II: a Fourier view of pulsating binary stars - determining binary orbital parameters photometrically for highly eccentric cases

Continuous and precise space-based photometry has made it possible to measure the orbital frequency modulation of pulsating stars in binary systems with extremely high precision over long time spans. Frequency modulation caused by binary orbital motion manifests itself as a multiplet with equal spacing of the orbital frequency in the Fourier transform. The amplitudes and phases of the peaks in these multiplets reflect the orbital properties, hence the orbital parameters can be extracted by analysing such precise photometric data alone. We derive analytically the theoretical relations between the multiplet properties and the orbital parameters, and present a method for determining these parameters, including the eccentricity and the argument of periapsis, from a quintuplet or a higher order multiplet. This is achievable with the photometry alone, without spectroscopic radial velocity measurements. We apply this method to Kepler mission data of KIC 8264492, KIC 9651065, and KIC 10990452, each of which is shown to have an eccentricity exceeding 0.5. Radial velocity curves are also derived from the Kepler photometric data. We demonstrate that the results are in good agreement with those obtained by another technique based on the analysis of the pulsation phases

Lessons to be learned from periodontitis

Purpose of reviewThis article reviews the link between periodontitis and rheumatoid arthritis (RA) with regard to similarities in genetic risk factors and immunopathogenesis. Emphasis is paid to the potential role of the periodontal pathogen Porphyromonas gingivalis in the etiopathogenesis of both periodontitis and RA, in particular by post-translational modification of arginine into citrulline.Recent findingsP. gingivalis, a major periodontal pathogen, is presently known as the only bacterium in the oral flora which contains a peptidyl arginine deiminase enzyme (PAD). This enzyme is necessary for citrullination. As a result, citrullinated proteins and P. gingivalis PAD, PAD2 and PAD4 (expressed by infiltrating neutrophils) are found in periodontal tissues. Autoantibodies directed to citrullinated proteins, so-called anticitrullinated protein antibodies (ACPAs), are found to be present in gingival crevicular fluid originating from inflamed gingival tissue. Furthermore, treatment studies have revealed that nonsurgical periodontal treatment, that is removal of sub-gingival calculus and biofilm deposits, is accompanied by a reduction in the severity of RA.SummaryIn this study the similarities in immune response and tissue degradation between RA and periodontitis are reviewed. It is shown that the two diseases share the same environmental and genetic risk factors, apart from the fact that there is a link between both diseases via citrullination of proteins by human PAD and P. gingivalis PAD.</p

The role of fitness in the association between fatness and cardiometabolic risk from childhood to adolescence

Background Fatness and fitness both influence cardiometabolic risk. Objective The purpose of this study was to investigate whether childhood fatness and increasing fatness from childhood to adolescence are associated with cardiometabolic risk during adolescence and how fitness affects this association. Subjects and methods Of 565 adolescents (283 boys and 282 girls) from the TRacking Adolescents Individual Life Survey (TRAILS) data on anthropometric parameters (age 11 and 16), metabolic parameters, and fitness (age 16) were available. Body mass index and skinfolds were used as measures for fatness. Increasing fatness was calculated by subtracting Z-scores for fatness at age 11 from Z-score fatness at age 16. Cardiometabolic risk was calculated as the average of the standardized means of mean arterial pressure, fasting serum triglycerides, high-density lipoprotein-cholesterol, glucose, and waist circumference. Insulin resistance was calculated by homeostasis model assessment-insulin resistance (HOMA-IR). Fitness was estimated as maximal oxygen consumption (VO2max) during a shuttle run test. Results Boys showed a higher clustered cardiometabolic risk when compared to girls (p < 0.01). Childhood fatness (age 11) and increasing fatness were independently associated with cardiometabolic risk during adolescence. In boys, high fitness was related to a reduced effect of increasing fatness on clustered cardiometabolic risk. Childhood fatness, increasing fatness, and fitness were independently associated with HOMA-IR. Moreover, in boys this association was dependent of fatness. Conclusions Childhood fatness and increasing fatness are associated with increased cardiometabolic risk and HOMA-IR during adolescence, but a good fitness attenuates this association especially in fat boys

Understanding the combined effects of sleep deprivation and acute social stress on cognitive performance using a comprehensive approach

Background: Sleep deprivation (SD) and acute social stress are common, often unavoidable, and frequently co-occurring stressors in high-risk professions. Both stressors are known to acutely induce inflammatory responses and an increasing body of literature suggests this may lead to cognitive impairment. This study examined the combined effects of total SD and acute social stress on cognitive performance and took a comprehensive approach to explore their (shared) underlying mechanism leading to cognitive decline. Method: We recorded cognitive performance on a response inhibition task and a multitask and monitored a range of inflammatory, psychophysiological and self-reported markers in 101 participants, both before and after one night of either sleep (control group: N = 48) or SD (N = 53), and both before and after a social stressor (Trier Social Stress Test). Results: SD decreased cognitive performance. The social stress test also results in cognitive performance decline in the control group on the response inhibition task, but improved rather than decreased performance of sleep deprived participants on both tasks. The subjective ratings of mental effort also reflect this antagonistic interaction, indicating that the social stressor when sleep-deprived also reduced mental effort. In the inflammatory and physiological measures, this pattern was only reflected by IL-22 in blood. SD reduced blood IL-22 concentrations, and the social stress reduced IL-22 in the control group as well, but not in sleep-deprived participants. There were no interactive effects of SD and social stress on any other inflammatory or psychophysiological measures. The effects of the social stress test on autonomic measures and subjective results suggest that increased arousal may have benefited sleep-deprived participants’ cognitive performance. Discussion: SD generally decreased cognitive performance and increased required mental effort. By contrast, the isolated effects of a social stressor were not generic, showing a positive effect on cognitive performance when sleep deprived. Our study is the first that studied combined effects of sleep deprivation and acute social stress on cognitive performance and inflammatory markers. It provides a comprehensive overview of effects of these stressors on a range of variables. We did not show unequivocal evidence of an underlying physiological mechanism explaining changes in performance due to (the combination of) sleep deprivation and social stress, but consider IL-22 as a possible cytokine involved in this mechanism and certainly worth following up on in future research.</p

Understanding the effects of sleep deprivation and acute social stress on cognitive performance using a comprehensive approach

Different professionals (e.g. in the military) have to perform cognitive challenging tasks in multi-stressor environments. However, our understanding how combined stressors interact and affect cognitive performance is limited (Van Dongen &amp; Belenky, 2009). This study examined how sleep deprivation (SD) and acute social stress affect cognitive performance in isolation and in combination, and used a comprehensive approach to find evidence for a (shared) mechanism. Recent research suggests that SD leads to higher amounts of proinflammatory markers (i.e. cytokines) in the blood, which assumedly contribute to a decline in cognitive performance (Irwin, 2019; Shields et al., 2017). In addition, acute social stressors have also been shown to elicit an immune response, as reflected by circulating cytokines in blood (Marsland et al., 2017; Prather et al., 2014). These findings suggest that different stressors may affect cognitive performance through an effect on the immune system. We therefore hypothesize that individuals showing a high proinflammatory response to a combination of two stressors (SD and acute social stress) are more vulnerable to cognitive decline compared to individuals showing a lower proinflammatory response. To test this hypothesis, we measured not only cognitive performance, but also the physiological response and biochemical determinants of metabolism and inflammation at baseline and after SD, but also in response to an acute social stressor (Tkacheenko &amp; Dinges, 2018)

Levels of Anti-Citrullinated Protein Antibodies and Rheumatoid Factor, Including IgA Isotypes, and Articular Manifestations in Ulcerative Colitis and Crohn's Disease

Systemic presence of arthritis autoantibodies (AAb) is specific for rheumatoid arthritis (RA). AAb initiation might be triggered by chronic mucosal inflammation, such as in inflammatory bowel disease (IBD). We assessed the prevalence of anti-citrullinated protein antibodies (ACPA) and rheumatoid factor (RF) in ulcerative colitis (UC) and Crohn&rsquo;s disease (CD) patients, with regard to the prevalence of joint complaints in AAb+ versus AAb&minus; IBD patients. RA patients and healthy subjects (HC) served as controls. Serum was collected from 226 UC, 165 CD and 86 RA patients, and 36 HCs. One-hundred-and-ten UC (48.7%) and 76 CD (46.1%) patients were seropositive for at least one autoantibody, compared to 4 (13.9%) HCs and 81 (94.2%) RA patients. Eighty-three (37%) UC and 52 (32%) CD patients were seropositive for the anti-cyclic citrullinated protein antibody (anti-CCP2) of the immunoglobulin A type (IgA anti-CCP2), compared to 1 (2.8%) HC and 64 (74%) RA patients. RF of the immunoglobulin G type (IgG RF) and IgA RF seropositivity in UC and CD patients was comparable to HCs and low compared to RA patients. Arthralgia was reported by 34 (18.7%) UC and 50 (33.1%) CD patients, but presence of arthralgia was not increased in AAb+ patients. AAbs are frequently present in IBD patients, supporting the hypothesis that inflammation of intestinal mucosa induces low systemic levels of ACPA