Aversion and attraction to harmful plant secondary compounds jointly shape the foraging ecology of a specialist herbivore.

Most herbivorous insect species are restricted to a narrow taxonomic range of host plant species. Herbivore species that feed on mustard plants and their relatives in the Brassicales have evolved highly efficient detoxification mechanisms that actually prevent toxic mustard oils from forming in the bodies of the animals. However, these mechanisms likely were not present during the initial stages of specialization on mustard plants ~100 million years ago. The herbivorous fly Scaptomyza nigrita (Drosophilidae) is a specialist on a single mustard species, bittercress (Cardamine cordifolia; Brassicaceae) and is in a fly lineage that evolved to feed on mustards only in the past 10-20 million years. In contrast to many mustard specialists, S. nigrita does not prevent formation of toxic breakdown products (mustard oils) arising from glucosinolates (GLS), the primary defensive compounds in mustard plants. Therefore, it is an appealing model for dissecting the early stages of host specialization. Because mustard oils actually form in the bodies of S. nigrita, we hypothesized that in lieu of a specialized detoxification mechanism, S. nigrita may mitigate exposure to high GLS levels within plant tissues using behavioral avoidance. Here, we report that jasmonic acid (JA) treatment increased GLS biosynthesis in bittercress, repelled adult female flies, and reduced larval growth. S. nigrita larval damage also induced foliar GLS, especially in apical leaves, which correspondingly displayed the least S. nigrita damage in controlled feeding trials and field surveys. Paradoxically, flies preferred to feed and oviposit on GLS-producing Arabidopsis thaliana despite larvae performing worse in these plants versus non-GLS-producing mutants. GLS may be feeding cues for S. nigrita despite their deterrent and defensive properties, which underscores the diverse relationship a mustard specialist has with its host when lacking a specialized means of mustard oil detoxification

Neuroticism and polymorphisms in the serotonin transporter gene

Background. There is evidence for an association between two different polymorphisms of the human serotonin transporter gene (5-HTT) and the personality trait of neuroticism and affective disorder.Methods. We studied the association between neuroticism and polymorphisms in the 5HTT-linked promoter region and in a variable number tandem repeat region (VNTR) of the 5-HTT gene in 204 people aged over 60 derived from a random sample of men and women in the general population. Approximately half of the subjects were in the top 20% of neuroticism scorers and half in the bottom 20%.Results. There were no significant differences in allelic or genotypic frequencies between the high and low neuroticism scorers. There was highly significant linkage disequilibrium between the two 5-HTT gene polymorphisms, and haplotype analysis showed no association between neuroticism level and haplotype.Conclusions. Reports of an association between two 5-HTT gene polymorphisms and the personality trait of neuroticism are not supported by these results.</jats:p

Common non-synonymous SNPs associated with breast cancer susceptibility: findings from the Breast Cancer Association Consortium.

Candidate variant association studies have been largely unsuccessful in identifying common breast cancer susceptibility variants, although most studies have been underpowered to detect associations of a realistic magnitude. We assessed 41 common non-synonymous single-nucleotide polymorphisms (nsSNPs) for which evidence of association with breast cancer risk had been previously reported. Case-control data were combined from 38 studies of white European women (46 450 cases and 42 600 controls) and analyzed using unconditional logistic regression. Strong evidence of association was observed for three nsSNPs: ATXN7-K264R at 3p21 [rs1053338, per allele OR = 1.07, 95% confidence interval (CI) = 1.04-1.10, P = 2.9 × 10(-6)], AKAP9-M463I at 7q21 (rs6964587, OR = 1.05, 95% CI = 1.03-1.07, P = 1.7 × 10(-6)) and NEK10-L513S at 3p24 (rs10510592, OR = 1.10, 95% CI = 1.07-1.12, P = 5.1 × 10(-17)). The first two associations reached genome-wide statistical significance in a combined analysis of available data, including independent data from nine genome-wide association studies (GWASs): for ATXN7-K264R, OR = 1.07 (95% CI = 1.05-1.10, P = 1.0 × 10(-8)); for AKAP9-M463I, OR = 1.05 (95% CI = 1.04-1.07, P = 2.0 × 10(-10)). Further analysis of other common variants in these two regions suggested that intronic SNPs nearby are more strongly associated with disease risk. We have thus identified a novel susceptibility locus at 3p21, and confirmed previous suggestive evidence that rs6964587 at 7q21 is associated with risk. The third locus, rs10510592, is located in an established breast cancer susceptibility region; the association was substantially attenuated after adjustment for the known GWAS hit. Thus, each of the associated nsSNPs is likely to be a marker for another, non-coding, variant causally related to breast cancer risk. Further fine-mapping and functional studies are required to identify the underlying risk-modifying variants and the genes through which they act.BCAC is funded by Cancer Research UK (C1287/A10118, C1287/A12014) and by the European Community’s Seventh Framework Programme under grant agreement n8 223175 (HEALTH-F2–2009-223175) (COGS). Meetings of the BCAC have been funded by the European Union COST programme (BM0606). Genotyping of the iCOGS array was funded by the European Union (HEALTH-F2-2009-223175), Cancer Research UK (C1287/A10710), the Canadian Institutes of Health Research for the ‘CIHR Team in Familial Risks of Breast Cancer’ program and the Ministry of Economic Development, Innovation and Export Trade of Quebec (PSR-SIIRI-701). Additional support for the iCOGS infrastructure was provided by the National Institutes of Health (CA128978) and Post-Cancer GWAS initiative (1U19 CA148537, 1U19 CA148065 and 1U19 CA148112—the GAME-ON initiative), the Department of Defence (W81XWH-10-1-0341), Komen Foundation for the Cure, the Breast Cancer Research Foundation, and the Ovarian Cancer Research Fund. The ABCFS and OFBCR work was supported by grant UM1 CA164920 from the National Cancer Institute (USA). The content of this manuscript does not necessarily reflect the views or policies of the National Cancer Institute or any of the collaborating centers in the Breast Cancer Family Registry (BCFR), nor does mention of trade names, commercial products or organizations imply endorsement t by the US Government or the BCFR. The ABCFS was also supported by the National Health and Medical Research Council of Australia, the New South Wales Cancer Council, the Victorian Health Promotion Foundation (Australia) and the Victorian Breast Cancer Research Consortium. J.L.H. is a National Health and Medical Research Council (NHMRC) Senior Principal Research Fellow and M.C.S. is a NHMRC Senior Research Fellow. The OFBCR work was also supported by the Canadian Institutes of Health Research ‘CIHR Team in Familial Risks of Breast Cancer’ program. The ABCS was funded by the Dutch Cancer Society Grant no. NKI2007-3839 and NKI2009-4363. The ACP study is funded by the Breast Cancer Research Trust, UK. The work of the BBCC was partly funded by ELAN-Programme of the University Hospital of Erlangen. The BBCS is funded by Cancer Research UK and Breakthrough Breast Cancer and acknowledges NHS funding to the NIHR Biomedical Research Centre, and the National Cancer Research Network (NCRN). E.S. is supported by NIHR Comprehensive Biomedical Research Centre, Guy’s & St. Thomas’ NHS Foundation Trust in partnership with King’s College London, UK. Core funding to the Wellcome Trust Centre for Human Genetics was provided by the Wellcome Trust (090532/Z/09/Z). I.T. is supported by the Oxford Biomedical Research Centre. The BSUCH study was supported by the Dietmar-Hopp Foundation, the Helmholtz Society and the German Cancer Research Center (DKFZ). The CECILE study was funded by the Fondation de France, the French National Institute of Cancer (INCa), The National League against Cancer, the National Agency for Environmental l and Occupational Health and Food Safety (ANSES), the National Agency for Research (ANR), and the Association for Research against Cancer (ARC). The CGPS was supported by the Chief Physician Johan Boserup and Lise Boserup Fund, the Danish Medical Research Council and Herlev Hospital.The CNIO-BCS was supported by the Genome Spain Foundation the Red Temática de Investigación Cooperativa en Cáncer and grants from the Asociación Española Contra el Cáncer and the Fondo de Investigación Sanitario PI11/00923 and PI081120). The Human Genotyping-CEGEN Unit, CNIO is supported by the Instituto de Salud Carlos III. D.A. was supported by a Fellowship from the Michael Manzella Foundation (MMF) and was a participant in the CNIO Summer Training Program. The CTS was initially supported by the California Breast Cancer Act of 1993 and the California Breast Cancer Research Fund (contract 97-10500) and is currently funded through the National Institutes of Health (R01 CA77398). Collection of cancer incidence e data was supported by the California Department of Public Health as part of the statewide cancer reporting program mandated by California Health and Safety Code Section 103885. HAC receives support from the Lon V Smith Foundation (LVS39420). The ESTHER study was supported by a grant from the Baden Württemberg Ministry of Science, Research and Arts. Additional cases were recruited in the context of the VERDI study, which was supported by a grant from the German Cancer Aid (Deutsche Krebshilfe). The GENICA was funded by the Federal Ministry of Education and Research (BMBF) Germany grants 01KW9975/5, 01KW9976/8, 01KW9977/0 and 01KW0114, the Robert Bosch Foundation, Stuttgart, Deutsches Krebsforschungszentrum (DKFZ), Heidelberg Institute for Prevention and Occupational Medicine of the German Social Accident Insurance, Institute of the Ruhr University Bochum (IPA), as well as the Department of Internal Medicine , Evangelische Kliniken Bonn gGmbH, Johanniter Krankenhaus Bonn, Germany. The HEBCS was supported by the Helsinki University Central Hospital Research Fund, Academy of Finland (132473), the Finnish Cancer Society, The Nordic Cancer Union and the Sigrid Juselius Foundation. The HERPACC was supported by a Grant-in-Aid for Scientific Research on Priority Areas from the Ministry of Education, Science, Sports, Culture and Technology of Japan, by a Grant-in-Aid for the Third Term Comprehensive 10-Year strategy for Cancer Control from Ministry Health, Labour and Welfare of Japan, by a research grant from Takeda Science Foundation , by Health and Labour Sciences Research Grants for Research on Applying Health Technology from Ministry Health, Labour and Welfare of Japan and by National Cancer Center Research and Development Fund. The HMBCS was supported by short-term fellowships from the German Academic Exchange Program (to N.B), and the Friends of Hannover Medical School (to N.B.). Financial support for KARBAC was provided through the regional agreement on medical training and clinical research (ALF) between Stockholm County Council and Karolinska Institutet, the Stockholm Cancer Foundation and the Swedish Cancer Society. The KBCP was financially supported by the special Government Funding (EVO) of Kuopio University Hospital grants, Cancer Fund of North Savo, the Finnish Cancer Organizations, the Academy of Finland and by the strategic funding of the University of Eastern Finland. kConFab is supported by grants from the National Breast Cancer Foundation , the NHMRC, the Queensland Cancer Fund, the Cancer Councils of New South Wales, Victoria, Tasmania and South Australia and the Cancer Foundation of Western Australia. The kConFab Clinical Follow Up Study was funded by the NHMRC (145684, 288704, 454508). Financial support for the AOCS was provided by the United States Army Medical Research and Materiel Command (DAMD17-01-1-0729), the Cancer Council of Tasmania and Cancer Foundation of Western Australia and the NHMRC (199600). G.C.T. and P.W. are supported by the NHMRC. LAABC is supported by grants (1RB-0287, 3PB-0102, 5PB-0018 and 10PB-0098) from the California Breast Cancer Research Program. Incident breast cancer cases were collected by the USC Cancer Surveillance Program (CSP) which is supported under subcontract by the California Department of Health. The CSP is also part of the National Cancer Institute’s Division of Cancer Prevention and Control Surveillance, Epidemiology, and End Results Program, under contract number N01CN25403. LMBC is supported by the ‘Stichting tegen Kanker’ (232-2008 and 196-2010). The MARIE study was supported by the Deutsche Krebshilfe e.V. (70-2892-BR I), the Federal Ministry of Education Research (BMBF) Germany (01KH0402), the Hamburg Cancer Society and the German Cancer Research Center (DKFZ). MBCSG is supported by grants from the Italian Association ciation for Cancer Research (AIRC) and by funds from the Italian citizens who allocated a 5/1000 share of their tax payment in support of the Fondazione IRCCS Istituto Nazionale Tumori, according to Italian laws (INT-Institutional strategic projects ‘5 × 1000’). The MCBCS was supported by the NIH grants (CA122340, CA128978) and a Specialized Program of Research Excellence (SPORE) in Breast Cancer (CA116201), the Breast Cancer Research Foundation and a generous gift from the David F. and Margaret T. Grohne Family Foundation and the Ting Tsung and Wei Fong Chao Foundation. MCCS cohort recruitment was funded by VicHealth and Cancer Council Victoria. The MCCS was further supported by Australian NHMRC grants 209057, 251553 and 504711 and by infrastructure provided by Cancer Council Victoria. The MEC was supported by NIH grants CA63464, CA54281, CA098758 and CA132839. The work of MTLGEBCS was supported by the Quebec Breast Cancer Foundation, the Canadian Institutes of Health Research (grant CRN-87521) and the Ministry of Economic Development, Innovation and Export Trade (grant PSR-SIIRI-701). MYBRCA is funded by research grants from the Malaysian Ministry of Science, Technology and Innovation (MOSTI), Malaysian Ministry of Higher Education (UM.C/HlR/MOHE/06) and Cancer Research Initiatives Foundation (CARIF). Additional controls were recruited by the Singapore Eye Research Institute, which was supported by a grant from the Biomedical Research Council (BMRC08/1/35/19,tel:08/1/35/19./550), Singapore and the National medical Research Council, Singapore (NMRC/CG/SERI/2010). The NBCS was supported by grants from the Norwegian Research council (155218/V40, 175240/S10 to A.L.B.D., FUGE-NFR 181600/ V11 to V.N.K. and a Swizz Bridge Award to A.L.B.D.). The NBHS was supported by NIH grant R01CA100374. Biological sample preparation was conducted the Survey and Biospecimen Shared Resource, which is supported by P30 CA68485. The OBCS was supported by research grants from the Finnish Cancer Foundation, the Sigrid Juselius Foundation, the Academy of Finland, the University of Oulu, and the Oulu University Hospital. The ORIGO study was supported by the Dutch Cancer Society (RUL 1997-1505) and the Biobanking and Biomolecular Resources Research Infrastructure (BBMRI-NLCP16). The PBCS was funded by Intramural Research Funds of the National Cancer Institute, Department of Health and Human Services, USA. pKARMA is a combination of the KARMA and LIBRO-1 studies. KARMA was supported by Ma¨rit and Hans Rausings Initiative Against Breast Cancer. KARMA and LIBRO-1 were supported the Cancer Risk Prediction Center (CRisP; www.crispcenter.org), a Linnaeus Centre (Contract ID 70867902) financed by the Swedish Research Council. The RBCS was funded by the Dutch Cancer Society (DDHK 2004-3124, DDHK 2009-4318). SASBAC was supported by funding from the Agency for Science, Technology and Research of Singapore (A∗STAR), the US National Institute of Health (NIH) and the Susan G. Komen Breast Cancer Foundation KC was financed by the Swedish Cancer Society (5128-B07-01PAF). The SBCGS was supported primarily by NIH grants R01CA64277, R01CA148667, and R37CA70867. Biological sample preparation was conducted the Survey and Biospecimen Shared Resource, which is supported by P30 CA68485. The SBCS was supported by Yorkshire Cancer Research S305PA, S299 and S295. Funding for the SCCS was provided by NIH grant R01 CA092447. The Arkansas Central Cancer Registry is fully funded by a grant from National Program of Cancer Registries, Centers for Disease Control and Prevention (CDC). Data on SCCS cancer cases from Mississippi were collected by the Mississippi Cancer Registry which participates in the National Program of Cancer Registries (NPCR) of the Centers for Disease Control and Prevention (CDC). The contents of this publication are solely the responsibility of the authors and do not necessarily represent the official views of the CDC or the Mississippi Cancer Registry. SEARCH is funded by a programme grant from Cancer Research UK (C490/A10124) and supported by the UK National Institute for Health Research Biomedical Research Centre at the University of Cambridge. The SEBCS was supported by the BRL (Basic Research Laboratory) program through the National Research Foundation of Korea funded by the Ministry of Education, Science and Technology (2012-0000347). SGBCC is funded by the National Medical Research Council Start-up Grant and Centre Grant (NMRC/CG/NCIS /2010). The recruitment of controls by the Singapore Consortium of Cohort Studies-Multi-ethnic cohort (SCCS-MEC) was funded by the Biomedical Research Council (grant number: 05/1/21/19/425). SKKDKFZS is supported by the DKFZ. The SZBCS was supported by Grant PBZ_KBN_122/P05/2004. K. J. is a fellow of International PhD program, Postgraduate School of Molecular Medicine, Warsaw Medical University, supported by the Polish Foundation of Science. The TNBCC was supported by the NIH grant (CA128978), the Breast Cancer Research Foundation , Komen Foundation for the Cure, the Ohio State University Comprehensive Cancer Center, the Stefanie Spielman Fund for Breast Cancer Research and a generous gift from the David F. and Margaret T. Grohne Family Foundation and the Ting Tsung and Wei Fong Chao Foundation. Part of the TNBCC (DEMOKRITOS) has been co-financed by the European Union (European Social Fund – ESF) and Greek National Funds through the Operational Program ‘Education and Life-long Learning’ of the National Strategic Reference Framework (NSRF)—Research Funding Program of the General Secretariat for Research & Technology: ARISTEIA. The TWBCS is supported by the Institute of Biomedical Sciences, Academia Sinica and the National Science Council, Taiwan. The UKBGS is funded by Breakthrough Breast Cancer and the Institute of Cancer Research (ICR). ICR acknowledges NHS funding to the NIHR Biomedical Research Centre. Funding to pay the Open Access publication charges for this article was provided by the Wellcome Trust.This is the advanced access published version distributed under a Creative Commons Attribution License 2.0, which can also be viewed on the publisher's webstie at: http://hmg.oxfordjournals.org/content/early/2014/07/04/hmg.ddu311.full.pdf+htm

Fine-Scale Mapping of the 4q24 Locus Identifies Two Independent Loci Associated with Breast Cancer Risk

Background: A recent association study identified a common variant (rs9790517) at 4q24 to be associated with breast cancer risk. Independent association signals and potential functional variants in this locus have not been explored. Methods: We conducted a fine-mapping analysis in 55,540 breast cancer cases and 51,168 controls from the Breast Cancer Association Consortium. Results: Conditional analyses identified two independent association signals among women of European ancestry, represented by rs9790517 [conditional P = 2.51 × 10−4; OR, 1.04; 95% confidence interval (CI), 1.02–1.07] and rs77928427 (P = 1.86 × 10−4; OR, 1.04; 95% CI, 1.02–1.07). Functional annotation using data from the Encyclopedia of DNA Elements (ENCODE) project revealed two putative functional variants, rs62331150 and rs73838678 in linkage disequilibrium (LD) with rs9790517 (r2 ≥ 0.90) residing in the active promoter or enhancer, respectively, of the nearest gene, TET2. Both variants are located in DNase I hypersensitivity and transcription factor–binding sites. Using data from both The Cancer Genome Atlas (TCGA) and Molecular Taxonomy of Breast Cancer International Consortium (METABRIC), we showed that rs62331150 was associated with level of expression of TET2 in breast normal and tumor tissue. Conclusion: Our study identified two independent association signals at 4q24 in relation to breast cancer risk and suggested that observed association in this locus may be mediated through the regulation of TET2. Impact: Fine-mapping study with large sample size warranted for identification of independent loci for breast cancer risk

Subverting the Patriarchy: Artistic Manipulations of the Female Trope in Weimar Germany

Gendered social anxieties prevailed during the Weimar Republic as women gained the right to vote. With the rapid departure of men from Germany at the onset of World War I, women were thrust into the public sphere to fulfill necessary labor roles. This cross-over from the domestic to the public sphere incited anxiety in the male population, who felt a loss of control and dominance in an otherwise patriarchal society. In reaction to this fear, men began to both physically and societally exert their dominance over women through the science-based process of classification. By breaking the collective idea of women down into categories, men created a distinction between their idea of a woman and all those who deviated from it. The avant-garde male artists were especially influential in German society, as they visually depicted the gendered changes around them. By depicting women as subjects of these classifications, they effectively reinforced these classifications and created concrete tropes. The four main tropes that this research will address are the Neue Frau, the Garçonne, the Prostituierte, and the Mutter. In looking closely at these classifications, this research intends to reveal the flawed misconceptions of female autonomy and sexuality by visually comparing male and female artistic renderings of women in the Weimar Republic. Through more intimate and sympathetic renderings of female subjects, women artists utilized stereotypical female classifications as a way to subvert the male-created trope, painting a more complex and authentic picture of female sexuality and autonomy in the Weimar Republic

Creating a Cult: How the Canterbury Monks Capitalized on the Myth of Thomas Becket in Popular Culture, Visual and Textual Imagery, and Branding

The brutal murder of Archbishop Thomas Becket in his own cathedral sent tremors throughout medieval Europe, prompting a subsequent interest in Canterbury Cathedral. Immediately following Becket’s death, people began to proclaim miracles in his name. Thus, the cult of Becket originated. Over the next four centuries, Canterbury would be a primary pilgrimage site, drawing pious pilgrims and curious spectators alike. This rapid influx of pilgrims can be linked to both the myth of Thomas Becket in popular culture and the Canterbury monks’ superiority in cultivating a cult culture. This research addresses three key points. One is the importance of miracle accounts in creating a populist cult. Laypeople were the first to convey miraculous accounts. In this way, they appropriated the miracle experience and attached themselves to the cult of Becket. The second key point is the superior marketing techniques the monks at Canterbury employed in attracting the masses. This includes capitalizing on the pilgrimage experience, which can be seen in an array of souvenirs produced near Canterbury (e.g., pilgrimage badges). The third key point is creating a sensorial environment that must be experienced. By engaging the pilgrim’s senses at every station of the cathedral, the monks strategically heightened the feeling of awe one feels at experiencing something spectacular. Much of this sensorial environment is created through the cathedral’s visual culture. This essay will provide new readings of the use of visual and textual culture in the manipulation of the pilgrim’s experience – an issue relevant to both the medieval and modern pilgrimage experience

Effect of emotion on attentional processing

Previous research on the relationship between emotion and attention has focused primarily on attention to emotionally valenced stimuli; trait anxiety and attentional biases for threat; or the relationship between emotion and attention in clinical contexts. Few studies have investigated the effect of emotion on attentional processing irrespective of the valence of the stimuli that is being attended. However, such studies are important as they shed light on issues central to emotions theory such as whether the experience of discrete emotions is associated with distinct patterns of attentional processing. In this thesis six experiments and one correlational study are described. The experimental studies investigate whether the experience of discrete emotions - specifically amusement, happiness, sadness and fear - influence attentional processing in comparison to a neutral condition. Film clips, emotional images and music were used to elicit a target emotional state. A modified version of the Attention Network Test (ANT) was used to assess three forms of attention – phasic alerting, covert exogenous orienting and executive attention. The correlational study required participants to complete a set of emotion-related questionnaires including the Basic Emotion Scale (BES) and to perform the ANT. The results suggest that: i) fear reduces executive attention costs, ii) sadness reduces intrinsic alerting, but does not influence alerting, orienting or executive attention, iii) amusement and happiness do not differentially influence alerting, orienting or executive attention, iv) individual differences in the tendency to experience high arousal negative emotions are associated with phasic alerting, i.e. faster mobilisation of attentional resources in response to an impending stimulus and v) exogenous orienting of attention may be impervious to the influence of emotion, at least in context of neutrally valenced stimuli. Results relating to anxiety, emotion regulation and attention network performance are also discussed. Taken together these findings provide only limited support for the broaden-and-build theory (Fredrickson, 1998) of positive emotions. Amusement and happiness did not result in broadening (as assessed by executive attention costs) in the present studies. An attentional narrowing effect was found for fear but not for sadness. It is proposed that fear, but not sadness, facilitates inhibition and reduces executive attention costs, indicative of more focused attention. The results here also suggest a relationship between negative emotions characterised by high arousal and phasic alerting – an aspect of attention which has received little coverage in emotions research to date. Implications relating to the use of the ANT as a measure of attentional performance, and the challenges associated with manipulating emotion in a lab setting are discussed.EThOS - Electronic Theses Online ServiceGBUnited Kingdo

Latent variable modelling of personality-health associations : measures, models and extensions

Functional health status, morbidity and mortality are determined partly by health behaviours (World Health Organization, 2002), which have determinants of their own. Personality traits, such as Conscientiousness, have a strong association with health behaviours (Bogg & Roberts, 2004). There is a less consistent and generally weaker association between traits and health outcomes (e.g. Neuroticism and mortality). The central problem in this thesis is how to measure, model, maximize, and extend trait-health associations. Conceptual issues associated with modelling traits and health are discussed in chapter one. The next three chapters concern such measurement issues about: personality traits (chapter two), health behaviours (chapter three) and health outcomes, with particular reference to functional health status (chapter four). These chapters are followed by a move to modelling (chapter five), with particular reference to the generalized latent variable modelling (LVM) framework (Muth´en & Muth´en, 1998–2007). The HAPPLE study is introduced (chapter six) which is used to model associations between Conscientiousness and health criteria within the LVMframework (chapter seven). Moving beyond self-reported outcomes, which are a mono-method approach, the role of multiple health behaviours in predicting cardiovascular mortality is considered (chapter eight). In a third section, cortisol is introduced, which is a biomarker of stress reactivity. The diurnal profile of cortisol output is described (chapter nine). Latent growth curve modelling is used to illustrate its association with Neuroticism, in a sample of student volunteers (chapter 10). Taken together, the results highlight the need for a general framework of modelling techniques, in personality-health research. I conclude that biopsychosocial models with excellent explanatory power, which are still parsimonious, can be achieved with LVM and its extensions. However, trait researchers will need to state more clearly the intended destinations of their work in order to attract contributions from, and share knowledge with, other disciplines.EThOS - Electronic Theses Online ServiceGBUnited Kingdo

Emotional intelligence, personality, social networks, and social perception

Emotional Intelligence (EI) is a relatively new concept in the field of psychology, introduced by Salovey and Mayer in 1990. Research on EI has found associations among EI and social network size, health and well-being, and job performance.(Austin, Saklofske, & Egan, 2003; Brackett, Mayer, & Warner, 2003; Petrides & Furnham, 2003; Saklofske, Austin, & Minski, 2001). Two different types of EI, trait EI and ability EI, have been identified in the literature. Trait EI was identified by Petrides and Furnham, and is a non-cognitive ability which allows an individual to regulate his/her mood, recognize and make the most of emotions, and utilize social skills, and is measured by self report. Ability EI is the ability of an individual to understand, generate, and manage emotions. Ability EI is measured using a performance measure which assesses the capacity of an individual to perceive emotions in him/herself, others, and the environment. Emotional intelligence has been linked to aspects of well-being, such as social network quality. In order to examine how EI related to social networks, both trait and ability EI were measured along with the Big Five factors of personality and social network quality and size. A study of 268 participants investigated the relationships amongst trait EI, personality, and social network quality and size. The Big Five factors of personality were all significantly positively correlated with EI (p< .01), and were also significantly correlated with social network quality and size. EI was significantly related to social network quality and size. When controlling for personality, EI was no longer significantly correlated with any of the social network quality or size variables. A subset of participants (n=78) completed an ability measure of EI, the Mayer Salovey Caruso Emotional Intelligence Test (MSCEIT). There were no significant correlations between MSCEIT scores and any of the other variables. A follow-up study was then carried out looking at the relationship of the original study variables with ability EI (MSCEIT), life stress, measured using the Uplifts and Hassles scale, and depression, measured using the Beck Depression Inventory (BDI), in the original participants. The results from this study indicated that emotional stability was significantly correlated with the Uplifts portion of the life stress scale, but not with Hassles. Conscientiousness was significantly negatively correlated with both the Hassle subscale of life stress and the BDI score. Emotional stability was also significantly negatively correlated with the BDI score. The total ability EI score measured by the MSCEIT did not show significant relationships with any other variables. Given that EI has been linked to social network quality and size, and one of the facets of EI is the capacity of an individual to recognize emotions in others, it would seem that individuals who are high in EI should have larger and better quality social networks as they are theoretically able to recognize and appropriately respond to the emotions of others. In order to test this, a social perception inspection time task was carried out in which participants were required to identify if a face was happy, sad, or angry. The faces used were both Caucasian and Far-East Asian, the hypothesis being that a person high in EI would recognize the facially expressed emotions regardless of whether the face shown was of their own race or not. Results from this study indicated that EI was not related to correctly identifying facial expressions. The results of these studies are discussed along with suggestions for future research in this area.EThOS - Electronic Theses Online ServiceGBUnited Kingdo