The genetic basis of human height : the role of estrogen

Height is a complex physical trait that displays strong heritability. Adult height is related to length of the long bones, which is determined by growth at the epiphyseal growth plate. Longitudinal bone growth occurs via the process of endochondral ossification, where bone forms over the differentiating cartilage template at the growth plate. Estrogen plays a major role in regulating longitudinal bone growth and is responsible for inducing the pubertal growth spurt and fusion of the epiphyseal growth plate. However, the mechanism by which estrogen promotes epiphyseal fusion is poorly understood. It has been hypothesised that estrogen functions to regulate growth plate fusion by stimulating chondrocyte apoptosis, angiogenesis and bone cell invasion in the growth plate. Another theory has suggested that estrogen exposure exhausts the proliferative capacity of growth plate chondrocytes, which accelerates the process of chondrocyte senescence, leading to growth plate fusion. The overall objective of this study was to gain a greater understanding of the molecular mechanisms behind estrogen-mediated growth and height attainment by examining gene regulation in chondrocytes and the role of some of these genes in normal height inheritance. With the heritability of height so well established, the initial hypothesis was that genetic variation in candidate genes associated with longitudinal bone growth would be involved in normal adult height variation. The height-related genes FGFR3, CBFA1, ER and CBFA1 were screened for novel polymorphisms using denaturing HPLC and RFLP analysis. In total, 24 polymorphisms were identified. Two SNPs in ER (rs3757323 C>T and rs1801132 G>C) were strongly associated with adult male height and displayed an 8 cm and 9 cm height difference between homozygous genotypes, respectively. The TC haplotype of these SNPs was associated with a 6 cm decrease in height and remarkably, no homozygous carriers of the TC haplotype were identified in tall subjects. No significant associations with height were found for polymorphisms in the FGFR3, CBFA1 or VDR genes. In the epiphyseal growth plate, chondrocyte proliferation, matrix synthesis and chondrocyte hypertrophy are all major contributors to long bone growth. As estrogen plays such a significant role in both growth and final height attainment, another hypothesis of this study was that estrogen exerted its effects in the growth plate by influencing chondrocyte proliferation and mediating the expression of chondrocyte marker genes. The examination of genes regulated by estrogen in chondrocyte-like cells aimed to identify potential regulators of growth plate fusion, which may further elucidate mechanisms involved in the cessation of linear growth. While estrogen did not dramatically alter the proliferation of the SW1353 cell line, gene expression experiments identified several estrogen regulated genes. Sixteen chondrocyte marker genes were examined in response to estrogen concentrations ranging from 10-12 M to 10-8 M over varying time points. Of the genes analysed, IHH, FGFR3, collagen II and collagen X were not readily detectable and PTHrP, GHR, ER, BMP6, SOX9 and TGF1 mRNAs showed no significant response to estrogen treatments. However, the expression of MMP13, CBFA1, BCL-2 and BAX genes were significantly decreased. Interestingly, the majority of estrogen regulated genes in SW1353 cells are expressed in the hypertrophic zone of the growth plate. Estrogen is also known to regulate systemic GH secretion and local GH action. At the molecular level, estrogen functions to inhibit GH action by negatively regulating GH signalling. GH treated SW1353 cells displayed increases in MMP9 mRNA expression (4.4-fold) and MMP13 mRNA expression (64-fold) in SW1353 cells. Increases were also detected in their respective proteins. Treatment with AG490, an established JAK2 inhibitor, blocked the GH mediated stimulation of both MMP9 and MMP13 mRNA expression. The application of estrogen and GH to SW1353 cells attenuated GH-stimulated MMP13 levels, but did not affect MMP9 levels. Investigation of GH signalling revealed that SW1353 cells have high levels of activated JAK2 and exposure to GH, estrogen, AG490 and other signalling inhibitors did not affect JAK2 phosphorylation. Interestingly, AG490 treatment dramatically decreased ERK2 signalling, although GH did stimulate ERK2 phosphorylation above control levels. AG490 also decreased CBFA1 expression, a transcription factor known to activate MMP9 and MMP13. Finally, GH and estrogen treatment increased expression of SOCS3 mRNA, suggesting that SOCS3 may regulate JAK/STAT signalling in SW1353 cells. The modulation of GH-mediated MMP expression by estrogen in SW1353 cells represents a potentially novel mechanism by which estrogen may regulate longitudinal bone growth. However, further investigation is required in order to elucidate the precise mechanisms behind estrogen and GH regulation of MMP13 expression in SW1353 cells. This study has provided additional evidence that estrogen and the ER gene are major factors in the regulation of growth and the determination of adult height. Newly identified polymorphisms in the ER gene not only contribute to our understanding of the genetic basis of human height, but may also be useful in association studies examining other complex traits. This study also identified several estrogen regulated genes and indicated that estrogen modifies the expression of genes which are primarily expressed in the hypertrophic region of the epiphyseal growth plate. Furthermore, synergistic studies incorporating GH and estrogen have revealed the ability of estrogen to attenuate the effects of GH on MMP13 expression, revealing potential pathways by which estrogen may modulate growth plate fusion, longitudinal bone growth and even arthritis.

Mutation frequency of non-ESBL phenotype SENTRY (Asia-Pacific) isolates of Klebsiella pneumoniae conversion to an ESBL positive phenotype

Extended spectrum β-lactamases or ESBLs, which are derived from non-ESBL precursors by point mutation of β-lactamase genes (bla), are spreading rapidly all over the world and have caused considerable problems in the treatment of infections caused by bacteria which harbour them. The mechanism of this resistance is not fully understood and a better understanding of these mechanisms might significantly impact on choosing proper diagnostic and treatment strategies. Previous work on SHV β-lactamase gene, blaSHV, has shown that only Klebsiella pneumoniae strains which contain plasmid-borne blaSHV are able to mutate to phenotypically ESBL-positive strains and there was also evidence of an increase in blaSHV copy number. Therefore, it was hypothesised that although specific point mutation is essential for acquisition of ESBL activity, it is not yet enough, and blaSHV copy number amplification is also essential for an ESBL-positive phenotype, with homologous recombination being the likely mechanism of blaSHV copy number expansion. In this study, we investigated the mutation rate of non-ESBL expressing K. pneumoniae isolates to an ESBL-positive status by using the MSS-maximum likelihood method. Our data showed that blaSHV mutation rate of a non-ESBL expressing isolate is lower than the mutation rate of the other single base changes on the chromosome, even with a plasmid-borne blaSHV gene. On the other hand, mutation rate from a low MIC ESBL-positive (≤ 8 µg/mL for cefotaxime) to high MIC ESBL-positive (≥16 µg/mL for cefotaxime) is very high. This is because only gene copy number increase is needed which is probably mediated by homologous recombination that typically takes place at a much higher frequencies than point mutations. Using a subinhibitory concentration of novobiocin, as a homologous recombination inhibitor, revealed that this is the case.

Listening, sharing understanding and facilitating consumer, family and community empowerment through a priority driven partnership in Far North Queensland

Objectives: This paper provides an example of a mental health research partnership underpinned by empowerment principles that seeks to foster strength among community organizations to support better outcomes for consumers, families and communities. It aims to raise awareness among researchers and service providers that empowerment approaches to assist communities to address mental health problems are not too difficult to be practical but require long-term commitment and appropriate support. Methods: A collaborative research strategy that has become known as the Priority Driven Research (PDR) Partnership emerged through literature review,consultations, Family Wellbeing Program delivery with community groups and activities in two discrete Indigenous communities. Progress to date on three of the four components of the strategy is described. Results: The following key needs were identified in a pilot study and are now being addressed in a research-based implementation phase: (i) gaining two-way understanding of perspectives on mental health and promoting universal awareness; (ii) supporting the empowerment of carers, families, consumers and at-risk groups through existing community organizations to gain greater understanding and control of their situation; (iii) developing pathways of care at the primary health centre level to enable support of social and emotional wellbeing as well as more integrated mental health care; (iv) accessing data to enable an ongoing process of analysis/sharing/planning and monitoring to inform future activity. Conclusion: One of the key learnings to emerge in this project so far is that empowerment through partnership becomes possible when there is a concerted effort to strengthen grassroots community organizations. These include social health teams and men’s and women’s groups that can engage local people in an action orientation. Key words: Aboriginal, empowerment, Indigenous, mental health.

The Queensland study of melanoma : Environmental and genetic associations (Q-MEGA); Study design, baseline characteristics, and repeatability of phenotype and sun exposure measures

Cutaneous malignant melanoma (CMM) is a major health issue in Queensland, Australia, which has the world’s highest incidence. Recent molecular and epidemiologic studies suggest that CMM arises through multiple etiological pathways involving gene-environment interactions. Understanding the potential mechanisms leading to CMM requires larger studies than those previously conducted. This article describes the design and baseline characteristics of Q-MEGA, the Queensland Study of Melanoma: Environmental and Genetic Associations, which followed up 4 population-based samples of CMM patients in Queensland, including children, adolescents, men aged over 50, and a large sample of adult cases and their families, including twins. Q-MEGA aims to investigate the roles of genetic and environmental factors, and their interaction, in the etiology of melanoma. Three thousand, four hundred and seventy-one participants took part in the follow-up study and were administered a computer-assisted telephone interview in 2002-2005. Updated data on environmental and phenotypic risk factors, and 2777 blood samples were collected from interviewed participants as well as a subset of relatives. This study provides a large and well-described population-based sample of CMM cases with follow-up data. Characteristics of the cases and repeatability of sun exposure and phenotype measures between the baseline and the follow-up surveys, from 6 to 17 years later, are also described.

Seeing is understanding : the effect of visualisation in understanding programming concepts

How and why visualisations support learning was the subject of this qualitative instrumental collective case study. Five computer programming languages (PHP, Visual Basic, Alice, GameMaker, and RoboLab) supporting differing degrees of visualisation were used as cases to explore the effectiveness of software visualisation to develop fundamental computer programming concepts (sequence, iteration, selection, and modularity). Cognitive theories of visual and auditory processing, cognitive load, and mental models provided a framework in which student cognitive development was tracked and measured by thirty-one 15-17 year old students drawn from a Queensland metropolitan secondary private girls’ school, as active participants in the research. Seventeen findings in three sections increase our understanding of the effects of visualisation on the learning process. The study extended the use of mental model theory to track the learning process, and demonstrated application of student research based metacognitive analysis on individual and peer cognitive development as a means to support research and as an approach to teaching. The findings also forward an explanation for failures in previous software visualisation studies, in particular the study has demonstrated that for the cases examined, where complex concepts are being developed, the mixing of auditory (or text) and visual elements can result in excessive cognitive load and impede learning. This finding provides a framework for selecting the most appropriate instructional programming language based on the cognitive complexity of the concepts under study.

Spaces of care in the third sector : Understanding the effects of professionalization

Increasingly the health and welfare needs of individuals and communities are being met by third sector, or not-for-profit, organizations. Since the 1980s third sector organizations have been subject to significant, sector-wide changes, such as the development of contractual funding and an increasing need to collaborate with governments and other sectors. In particular, the processes of ‘professionalization’ and ‘bureaucratization’ have received significant attention and are now well documented in third sector literature. These processes are often understood to create barriers between organizations and their community groups and neutralize alternative forms of service provision. In this article we provide a case study of an Australian third sector organization undergoing professionalization. The case study draws on ethnographic and qualitative interviews with staff and volunteers at a health-based third sector organization involved in service provision to marginalized community groups. We examine how professionalization alters organizational spaces and dynamics and conclude that professionalized third sector spaces may still be ‘community’ spaces where individuals may give and receive care and services. Moreover, we suggest that these community spaces hold potential for resisting the neutralizing effects of contracting.

Nonlinear pedagogy : implications for teaching games for understanding (TGfU)

Nonlinear Dynamics, provides a framework for understanding how teaching and learning processes function in Teaching Games for Understanding (TGfU). In Nonlinear Pedagogy, emergent movement behaviors in learners arise as a consequence of intrinsic self-adjusted processes shaped by interacting constraints in the learning environment. In a TGfU setting, representative, conditioned games provide ideal opportunities for pedagogists to manipulate key constraints so that self-adjusted processes by players lead to emergent behaviors as they explore functional movement solutions. The implication is that, during skill learning, functional movement variability is necessary as players explore different motor patterns for effective skill execution in the context of the game. Learning progressions in TGfU take into account learners’ development through learning stages and have important implications for organisation of practices, instructions and feedback. A practical application of Nonlinear Pedagogy in a national sports institute is shared to exemplify its relevance for TGfU practitioners.

Biochemical characterization of Aprataxin, the protein deficient in Ataxia with Oculomotor Apraxia type 1

Neurodegenerative disorders are heterogenous in nature and include a range of ataxias with oculomotor apraxia, which are characterised by a wide variety of neurological and ophthalmological features. This family includes recessive and dominant disorders. A subfamily of autosomal recessive cerebellar ataxias are characterised by defects in the cellular response to DNA damage. These include the well characterised disorders Ataxia-Telangiectasia (A-T) and Ataxia-Telangiectasia Like Disorder (A-TLD) as well as the recently identified diseases Spinocerebellar ataxia with axonal neuropathy Type 1 (SCAN1), Ataxia with Oculomotor Apraxia Type 2 (AOA2), as well as the subject of this thesis, Ataxia with Oculomotor Apraxia Type 1 (AOA1). AOA1 is caused by mutations in the APTX gene, which is located at chromosomal locus 9p13. This gene codes for the 342 amino acid protein Aprataxin. Mutations in APTX cause destabilization of Aprataxin, thus AOA1 is a result of Aprataxin deficiency. Aprataxin has three functional domains, an N-terminal Forkhead Associated (FHA) phosphoprotein interaction domain, a central Histidine Triad (HIT) nucleotide hydrolase domain and a C-terminal C2H2 zinc finger. Aprataxins FHA domain has homology to FHA domain of the DNA repair protein 5’ polynucleotide kinase 3’ phosphatase (PNKP). PNKP interacts with a range of DNA repair proteins via its FHA domain and plays a critical role in processing damaged DNA termini. The presence of this domain with a nucleotide hydrolase domain and a DNA binding motif implicated that Aprataxin may be involved in DNA repair and that AOA1 may be caused by a DNA repair deficit. This was substantiated by the interaction of Aprataxin with proteins involved in the repair of both single and double strand DNA breaks (XRay Cross-Complementing 1, XRCC4 and Poly-ADP Ribose Polymerase-1) and the hypersensitivity of AOA1 patient cell lines to single and double strand break inducing agents. At the commencement of this study little was known about the in vitro and in vivo properties of Aprataxin. Initially this study focused on generation of recombinant Aprataxin proteins to facilitate examination of the in vitro properties of Aprataxin. Using recombinant Aprataxin proteins I found that Aprataxin binds to double stranded DNA. Consistent with a role for Aprataxin as a DNA repair enzyme, this binding is not sequence specific. I also report that the HIT domain of Aprataxin hydrolyses adenosine derivatives and interestingly found that this activity is competitively inhibited by DNA. This provided initial evidence that DNA binds to the HIT domain of Aprataxin. The interaction of DNA with the nucleotide hydrolase domain of Aprataxin provided initial evidence that Aprataxin may be a DNA-processing factor. Following these studies, Aprataxin was found to hydrolyse 5’adenylated DNA, which can be generated by unscheduled ligation at DNA breaks with non-standard termini. I found that cell extracts from AOA1 patients do not have DNA-adenylate hydrolase activity indicating that Aprataxin is the only DNA-adenylate hydrolase in mammalian cells. I further characterised this activity by examining the contribution of the zinc finger and FHA domains to DNA-adenylate hydrolysis by the HIT domain. I found that deletion of the zinc finger ablated the activity of the HIT domain against adenylated DNA, indicating that the zinc finger may be required for the formation of a stable enzyme-substrate complex. Deletion of the FHA domain stimulated DNA-adenylate hydrolysis, which indicated that the activity of the HIT domain may be regulated by the FHA domain. Given that the FHA domain is involved in protein-protein interactions I propose that the activity of Aprataxins HIT domain may be regulated by proteins which interact with its FHA domain. We examined this possibility by measuring the DNA-adenylate hydrolase activity of extracts from cells deficient for the Aprataxin-interacting DNA repair proteins XRCC1 and PARP-1. XRCC1 deficiency did not affect Aprataxin activity but I found that Aprataxin is destabilized in the absence of PARP-1, resulting in a deficiency of DNA-adenylate hydrolase activity in PARP-1 knockout cells. This implies a critical role for PARP-1 in the stabilization of Aprataxin. Conversely I found that PARP-1 is destabilized in the absence of Aprataxin. PARP-1 is a central player in a number of DNA repair mechanisms and this implies that not only do AOA1 cells lack Aprataxin, they may also have defects in PARP-1 dependant cellular functions. Based on this I identified a defect in a PARP-1 dependant DNA repair mechanism in AOA1 cells. Additionally, I identified elevated levels of oxidized DNA in AOA1 cells, which is indicative of a defect in Base Excision Repair (BER). I attribute this to the reduced level of the BER protein Apurinic Endonuclease 1 (APE1) I identified in Aprataxin deficient cells. This study has identified and characterised multiple DNA repair defects in AOA1 cells, indicating that Aprataxin deficiency has far-reaching cellular consequences. Consistent with the literature, I show that Aprataxin is a nuclear protein with nucleoplasmic and nucleolar distribution. Previous studies have shown that Aprataxin interacts with the nucleolar rRNA processing factor nucleolin and that AOA1 cells appear to have a mild defect in rRNA synthesis. Given the nucleolar localization of Aprataxin I examined the protein-protein interactions of Aprataxin and found that Aprataxin interacts with a number of rRNA transcription and processing factors. Based on this and the nucleolar localization of Aprataxin I proposed that Aprataxin may have an alternative role in the nucleolus. I therefore examined the transcriptional activity of Aprataxin deficient cells using nucleotide analogue incorporation. I found that AOA1 cells do not display a defect in basal levels of RNA synthesis, however they display defective transcriptional responses to DNA damage. In summary, this thesis demonstrates that Aprataxin is a DNA repair enzyme responsible for the repair of adenylated DNA termini and that it is required for stabilization of at least two other DNA repair proteins. Thus not only do AOA1 cells have no Aprataxin protein or activity, they have additional deficiencies in PolyADP Ribose Polymerase-1 and Apurinic Endonuclease 1 dependant DNA repair mechanisms. I additionally demonstrate DNA-damage inducible transcriptional defects in AOA1 cells, indicating that Aprataxin deficiency confers a broad range of cellular defects and highlighting the complexity of the cellular response to DNA damage and the multiple defects which result from Aprataxin deficiency. My detailed characterization of the cellular consequences of Aprataxin deficiency provides an important contribution to our understanding of interlinking DNA repair processes.

Postpartum fatigue and driving : relating experiences, thoughts and opinions 12 weeks post-birth

Fatigue in the postnatal period is such a common experience for most mothers that the term ‘postpartum fatigue’ (PPF) has been coined to describe it. When new mothers experience extreme fatigue, it follows that their physical health, mental health, and social-wellbeing is negatively affected. It is interesting to note that there is a distinct lack of empirical investigations focusing on the link between PPF and increased risk of injury; particularly when the links between fatigue and increased risk of road crashes are well documented. The purpose of this investigation was to undertake pilot research to develop an understanding of the duration of PPF and the performance impairments experienced by new mothers when involved in safety-sensitive activities, such as driving a motor vehicle. Semi-structured interviews were undertaken with women (N = 24) at 12 weeks postpartum living in South-east Queensland, Australia. Key themes were identified; with a particular emphasis towards understanding the link between the participant’s experience of postpartum fatigue and the impact this has on their overall cognitive and physiological functioning, as well as their experience of the driving task. Further, sleep/wake data was collected and using the Karolinska Sleepiness Scale (KSS) the potential crash risk for this group of mothers is discussed. It is proposed that the findings of this investigation could be used to improve current knowledge among new mothers and practitioners regarding the mechanisms and consequences of fatigue and to inform interventions that lead to a decreased risk of injury associated with postpartum fatigue.

Deepening our understanding about school leadership : learning from educators and non-educators

Increasingly, leadership is argued as a way forward to improve performance and practice in a variety of contexts. School leadership is no different. There is little doubt that in the current globalised world characterized by change and complexity, effective school leadership is a key requirement. The contribution of this chapter is framed around a synthesis of current research, writing and theoretical insights regarding leadership. It draws upon three bodies of writing, Firstly, it begins by distilling several key themes and trends regarding educational leadership from the current research and writing. Secondly, it reports on the findings of a current research project carried out by the authors that explored the leadership stories of ten outstanding leaders from non-educational settings in Australia. Finally, it concludes by referring to some of the paradoxes and tensions inherent in the work of school leaders. It is argued that understanding and endeavouring to reconcile these dilemmas is a pre-requisite for school leaders as they continue to operate in an environment fraught with change and complexity.

Understanding the psychosocial factors influencing the risky behaviour of young drivers

Young people aged 17–24 years are at high risk of being killed in road crashes around the world. Road safety interventions consider some influences upon young driver behaviour; for example, imposing passenger restrictions on young novice drivers indirectly minimises the potential negative social influences of peers as passengers. To change young driver risky behaviour, the multitude of psychosocial influences upon its initiation and maintenance must be identified. A study questionnaire was developed to investigate the relationships between risky driving and Akers’ social learning theory, social identity theory, and thrill seeking variables. The questionnaire was completed by 165 participants (105 women,60 men) residing in south-east Queensland, Australia. The sociodemographic variables of age, gender, and exposure explained 19% of the variance in self-reported risky driving behaviour, whilst Akers’ social learning variables explained an additional 42%. Thrill seeking and social identity variables did not explain any significant additional variance. Significant predictors of risky driving included imitation of the driving behaviours of, and anticipated rewards and punishments administered by, parents and peers. Road safety policy that directly considers and incorporates these factors in their design, implementation, and enforcement of young driver road safety interventions should prove more efficacious than current approaches.

Mechanisms of improvement in treatment for depression : test of a self-efficacy and performance model

Tested D. J. Kavanagh's (1983) depression model's explanation of response to cognitive-behavioral treatment among 19 20–60 yr old Ss who received treatment and 24 age-matched Ss who were assigned to a waiting list. Measures included the Beck Depression Inventory and self-efficacy (SE) and self-monitoring scales. Rises in SE and self-monitored performance of targeted skills were closely associated with the improved depression scores of treated Ss. Improvements in the depression of waiting list Ss occurred through random, uncontrolled events rather than via a systematic increase in specific skills targeted in treatment. SE regarding assertion also predicted depression scores over a 12-wk follow-up.

A Proposed Framework for Understanding Information Security Culture and Practices in the Saudi Context

An examination of Information Security (IS) and Information Security Management (ISM) research in Saudi Arabia has shown the need for more rigorous studies focusing on the implementation and adoption processes involved with IS culture and practices. Overall, there is a lack of academic and professional literature about ISM and more specifically IS culture in Saudi Arabia. Therefore, the overall aim of this paper is to identify issues and factors that assist the implementation and the adoption of IS culture and practices within the Saudi environment. The goal of this paper is to identify the important conditions for creating an information security culture in Saudi Arabian organizations. We plan to use this framework to investigate whether security culture has emerged into practices in Saudi Arabian organizations.

Understanding how to enhance business creativity

This PhD study examines some of what happens in an individual’s mind regarding creativity during problem solving within an organisational context. It presents innovations related to creative motivation, cognitive style and framing effects that can be applied by managers to enhance individual employee creativity within the organisation and thereby assist organisations to become more innovative. The project delivers an understanding of how to leverage natural changes in creative motivation levels during problem solving. This pattern of response is called Creative Resolve Response (CRR). The project also presents evidence of how framing effects can be used to influence decisions involving creative options in order to enhance the potential for managers get employees to select creative options more often for implementation. The study’s objectives are to understand: • How creative motivation changes during problem solving • How cognitive style moderates these creative motivation changes • How framing effects apply to decisions involving creative options to solve problems • How cognitive style moderate these framing effects The thesis presents the findings from three controlled experiments based around self reports during contrived problem solving and decision making situations. The first experiment suggests that creative motivation varies in a predictable and systematic way during problem solving as a function of the problem solver’s perception of progress. The second experiment suggests that there are specific framing effects related to decisions involving creativity. It seems that simply describing an alternative as innovative may activate perceptual biases that overcome risk based framing effects. The third experiment suggests that cognitive style moderates decisions involving creativity in complex ways. It seems that in some contexts, decision makers will prefer a creative option, regardless of their cognitive style, if this option is both outside the bounds of what is officially allowed and yet ultimately safe. The thesis delivers innovation on three levels: theoretical, methodological and empirical. The highlights of these findings are outlined below: 1. Theoretical innovation with the conceptualisation of Creative Resolve Response based on an extension of Amabile’s research regarding creative motivation. 2. Theoretical innovation linking creative motivation and Kirton’s research on cognitive style. 3. Theoretical innovation linking both risk based and attribute framing effects to cognitive style. 4. Methodological innovation for defining and testing preferences for creative solution implementation in the form of operationalised creativity decision alternatives. 5. Methodological innovation to identify extreme decision options by applying Shafir’s findings regarding attribute framing effects in reverse to create a test. 6. Empirical innovation with statistically significant research findings which indicate creative motivation varies in a systematic way. 7. Empirical innovation with statistically significant research findings which identify innovation descriptor framing effects 8. Empirical innovation with statistically significant research findings which expand understanding of Kirton’s cognitive style descriptors including the importance of safe rule breaking. 9. Empirical innovation with statistically significant research findings which validate how framing effects do apply to decisions involving operationalised creativity. Drawing on previous research related to creative motivation, cognitive style, framing effects and supervisor interactions with employees, this study delivers insights which can assist managers to increase the production and implementation of creativity in organisations. Hopefully this will result in organisations which are more innovative. Such organisations have the potential to provide ongoing economic and social benefits.

Negotiating selves: exploring cultures of disclosure

If identity is a construct—and, more critically, a construct defined and developed through relationships with others in public and private spheres—then an understanding of the processes, mechanisms and platforms by which individuals disclose information about themselves is crucial in understanding the way identity, community and culture function, and the way individuals can intervene in the functioning of culture.