940 resultados para Ptolemaios son of Chairemon (see also O.Mich. I, 650)
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Raman spectroscopy has been used to study a selection of vivianites from different origins. A band is identified at around 3480 cm-1 whose intensity is sample dependent. The band is attributed to the stretching vibration of Fe3+ OH units which are formed through the autooxidation of the vivianite minerals either by self-oxidation or by photocatalytic oxidation according to the reaction: (Fe2+)3(PO4)2·8H2O + 1/2O2 (Fe2+)3– x(Fe3+)x(PO4)2(OH)x·(8–x)H2O in which some of the water of crystallization is converted to hydroxyl anions. Complexity of the OH stretching region through the overlap of broad bands is reflected in the water HOH deformation modes at 1660 cm–1. Using the infrared bands at 3281, 3105 and 3025 cm–1, hydrogen bond distances of 2.734(5), 2.675(2) and 2.655(2) Å are calculated. Vivianites are characterised by an intense band at 950 cm–1 assigned to the PO4 symmetric stretching vibration. Low Raman intensity bands are observed at ~1077, ~1050, 1015 and ~ 985 cm–1 assigned to the phosphate PO4 antisymmetric stretching vibrations. Multiple antisymmetric stretching vibrations are due to the reduced tetrahedral symmetry. This loss of degeneracy is also reflected in the bending modes. Two bands are observed at ~ 423 and ~ 456 cm–1 assigned to the2bending modes. For the vivianites four bands are observed at ~ 584, ~ 571, ~ 545 and ~ 525 cm–1 assigned to the 4modes of vivianite.
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The release of ultrafine particles (UFP) from laser printers and office equipment was analyzed using a particle counter (FMPS; Fast Mobility Particle Sizer) with a high time resolution, as well as the appropriate mathematical models. Measurements were carried out in a 1 m³ chamber, a 24 m³ chamber and an office. The time-dependent emission rates were calculated for these environments using a deconvolution model, after which the total amount of emitted particles was calculated. The total amounts of released particles were found to be independent of the environmental parameters and therefore, in principle, they were appropriate for the comparison of different printers. On the basis of the time-dependent emission rates, “initial burst” emitters and constant emitters could also be distinguished. In the case of an “initial burst” emitter, the comparison to other devices is generally affected by strong variations between individual measurements. When conducting exposure assessments for UFP in an office, the spatial distribution of the particles also had to be considered. In this work, the spatial distribution was predicted on a case by case basis, using CFD simulation.
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This work is concerned with the genetic basis of normal human pigmentation variation. Specifically, the role of polymorphisms within the solute carrier family 45 member 2 (SLC45A2 or membrane associated transporter protein; MATP) gene were investigated with respect to variation in hair, skin and eye colour ― both between and within populations. SLC45A2 is an important regulator of melanin production and mutations in the gene underly the most recently identified form of oculocutaneous albinism. There is evidence to suggest that non-synonymous polymorphisms in SLC45A2 are associated with normal pigmentation variation between populations. Therefore, the underlying hypothesis of this thesis is that polymorphisms in SLC45A2 will alter the function or regulation of the protein, thereby altering the important role it plays in melanogenesis and providing a mechanism for normal pigmentation variation. In order to investigate the role that SLC45A2 polymorphisms play in human pigmentation variation, a DNA database was established which collected pigmentation phenotypic information and blood samples of more than 700 individuals. This database was used as the foundation for two association studies outlined in this thesis, the first of which involved genotyping two previously-described non-synonymous polymorphisms, p.Glu272Lys and p.Phe374Leu, in four different population groups. For both polymorphisms, allele frequencies were significantly different between population groups and the 272Lys and 374Leu alleles were strongly associated with black hair, brown eyes and olive skin colour in Caucasians. This was the first report to show that SLC45A2 polymorphisms were associated with normal human intra-population pigmentation variation. The second association study involved genotyping several SLC45A2 promoter polymorphisms to determine if they also played a role in pigmentation variation. Firstly, the transcription start site (TSS), and hence putative proximal promoter region, was identified using 5' RNA ligase mediated rapid amplification of cDNA ends (RLM-RACE). Two alternate TSSs were identified and the putative promoter region was screened for novel polymorphisms using denaturing high performance liquid chromatography (dHPLC). A novel duplication (c.–1176_–1174dupAAT) was identified along with other previously described single nucleotide polymorphisms (c.–1721C>G and c.–1169G>A). Strong linkage disequilibrium ensured that all three polymorphisms were associated with skin colour such that the –1721G, +dup and –1169A alleles were associated with olive skin in Caucasians. No linkage disequilibrium was observed between the promoter and coding region polymorphisms, suggesting independent effects. The association analyses were complemented with functional data, showing that the –1721G, +dup and –1169A alleles significantly decreased SLC45A2 transcriptional activity. Based on in silico bioinformatic analysis that showed these alleles remove a microphthalmia-associated transcription factor (MITF) binding site, and that MITF is a known regulator of SLC45A2 (Baxter and Pavan, 2002; Du and Fisher, 2002), it was postulated that SLC45A2 promoter polymorphisms could contribute to the regulation of pigmentation by altering MITF binding affinity. Further characterisation of the SLC45A2 promoter was carried out using luciferase reporter assays to determine the transcriptional activity of different regions of the promoter. Five constructs were designed of increasing length and their promoter activity evaluated. Constitutive promoter activity was observed within the first ~200 bp and promoter activity increased as the construct size increased. The functional impact of the –1721G, +dup and –1169A alleles, which removed a MITF consensus binding site, were assessed using electrophoretic mobility shift assays (EMSA) and expression analysis of genotyped melanoblast and melanocyte cell lines. EMSA results confirmed that the promoter polymorphisms affected DNA-protein binding. Interestingly, however, the protein/s involved were not MITF, or at least MITF was not the protein directly binding to the DNA. In an effort to more thoroughly characterise the functional consequences of SLC45A2 promoter polymorphisms, the mRNA expression levels of SLC45A2 and MITF were determined in melanocyte/melanoblast cell lines. Based on SLC45A2’s role in processing and trafficking TYRP1 from the trans-Golgi network to stage 2 melanosmes, the mRNA expression of TYRP1 was also investigated. Expression results suggested a coordinated expression of pigmentation genes. This thesis has substantially contributed to the field of pigmentation by showing that SLC45A2 polymorphisms not only show allele frequency differences between population groups, but also contribute to normal pigmentation variation within a Caucasian population. In addition, promoter polymorphisms have been shown to have functional consequences for SLC45A2 transcription and the expression of other pigmentation genes. Combined, the data presented in this work supports the notion that SLC45A2 is an important contributor to normal pigmentation variation and should be the target of further research to elucidate its role in determining pigmentation phenotypes. Understanding SLC45A2’s function may lead to the development of therapeutic interventions for oculocutaneous albinism and other disorders of pigmentation. It may also help in our understanding of skin cancer susceptibility and evolutionary adaptation to different UV environments, and contribute to the forensic application of pigmentation phenotype prediction.
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In this article, we take a close look at the literacy demands of one task from the ‘Marvellous Micro-organisms Stage 3 Life and Living’ Primary Connections unit (Australian Academy of Science, 2005). One lesson from the unit, ‘Exploring Bread’, (pp 4-8) asks students to ‘use bread labels to locate ingredient information and synthesise understanding of bread ingredients’. We draw upon a framework offered by the New London Group (2000), that of linguistic, visual and spatial design, to consider in more detail three bread wrappers and from there the complex literacies that students need to interrelate to undertake the required task. Our findings are that although bread wrappers are an example of an everyday science text, their linguistic, visual and spatial designs and their interrelationship are not trivial. We conclude by reinforcing the need for teachers of science to also consider how the complex design elements of everyday science texts and their interrelated literacies are made visible through instructional practice.
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I argue that a divergence between popular culture as “object” and “subject” of journalism emerged during the nineteenth century in Britain. It accounts not only for different practices of journalism, but also for differences in the study of journalism, as manifested in journalism studies and cultural studies respectively. The chapter offers an historical account to show that popular culture was the source of the first mass circulation journalism, via the pauper press, but that it was later incorporated into the mechanisms of modern government for a very different purpose, the theorist of which was Walter Bagehot. Journalism’s polarity was reversed – it turned from “subjective” to “objective.” The paper concludes with a discussion of YouTube and the resurgence of self-made representation, using the resources of popular culture, in current election campaigns. Are we witnessing a further reversal of polarity, where popular culture and self-representation once again becomes the “subject” of journalism?
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It has previously been found that complexes comprised of vitronectin and growth factors (VN:GF) enhance keratinocyte protein synthesis and migration. More specifically, these complexes have been shown to significantly enhance the migration of dermal keratinocytes derived from human skin. In view of this, it was thought that these complexes may hold potential as a novel therapy for healing chronic wounds. However, there was no evidence indicating that the VN:GF complexes would retain their effect on keratinocytes in the presence of chronic wound fluid. The studies in this thesis demonstrate for the first time that the VN:GF complexes not only stimulate proliferation and migration of keratinocytes, but also these effects are maintained in the presence of chronic wound fluid in a 2-dimensional (2-D) cell culture model. Whilst the 2-D culture system provided insights into how the cells might respond to the VN:GF complexes, this investigative approach is not ideal as skin is a 3-dimensional (3-D) tissue. In view of this, a 3-D human skin equivalent (HSE) model, which reflects more closely the in vivo environment, was used to test the VN:GF complexes on epidermopoiesis. These studies revealed that the VN:GF complexes enable keratinocytes to migrate, proliferate and differentiate on a de-epidermalised dermis (DED), ultimately forming a fully stratified epidermis. In addition, fibroblasts were seeded on DED and shown to migrate into the DED in the presence of the VN:GF complexes and hyaluronic acid, another important biological factor in the wound healing cascade. This HSE model was then further developed to enable studies examining the potential of the VN:GF complexes in epidermal wound healing. Specifically, a reproducible partial-thickness HSE wound model was created in fully-defined media and monitored as it healed. In this situation, the VN:GF complexes were shown to significantly enhance keratinocyte migration and proliferation, as well as differentiation. This model was also subsequently utilized to assess the wound healing potential of a synthetic fibrin-like gel that had previously been demonstrated to bind growth factors. Of note, keratinocyte re-epitheliasation was shown to be markedly improved in the presence of this 3-D matrix, highlighting its future potential for use as a delivery vehicle for the VN:GF complexes. Furthermore, this synthetic fibrin-like gel was injected into a 4 mm diameter full-thickness wound created in the HSE, both keratinocytes and fibroblasts were shown to migrate into this gel, as revealed by immunofluorescence. Interestingly, keratinocyte migration into this matrix was found to be dependent upon the presence of the fibroblasts. Taken together, these data indicate that reproducible wounds, as created in the HSEs, provide a relevant ex vivo tool to assess potential wound healing therapies. Moreover, the models will decrease our reliance on animals for scientific experimentation. Additionally, it is clear that these models will significantly assist in the development of novel treatments, such as the VN:GF complexes and the synthetic fibrin-like gel described herein, ultimately facilitating their clinical trial in the treatment of chronic wounds.
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The end of the Korean War in 1953 marked the beginning of Seoul’s transformation from the shattered capital city of South Korea to one of the most connected, populous, and fast-changing hubs of global economy. Seoul’s technosocial development has been celebrated nationally and internationally. To the outside, young Koreans’ swift and extensive adoption and adaptation to digital technologies has been a subject of exotification; to adults in Korea, it has been a subject of criticism (see Yoon in this volume). With the understanding that ‘the city is connections,’ it is crucial to study not only the macro-level design of the city as a network (through policy, for example), but also its micro-level construction at the intersection of people, place, and technology. Accordingly, this chapter explores this exact intersection to comprehensively portray the constant renewal of the city as imagined and experienced by young Koreans. The chapter is based on fieldwork conducted in Seoul, South Korea, from 2007 to 2008 as part of a research project on the mobile play culture of Seoul transyouth, the transitional demographic situated between youth and adulthood, and the pioneers of the Korean ‘broadband miracle’ (Hazlett, 2004). The study draws upon transdisciplinary research data including interviews, questionnaires, diaries, and Shared Visual Ethnography (SVE) to render the everyday urban social networking of young Seoulites with and through which they interact to constantly (re)create the city and the self.
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Think back to your teaching experiences over the past four years. Were there a number of children or adolescents in your classes who seemed to have learning difficulties? What area of their learning seemed to be of greatest concern for these students? Did most of these struggling learners have difficulty with reading? Was expressing their thoughts in writing also a challenge? Did some of these students also have difficulty in listening to and following directions? And did some of these students seem hesitant when asked to speak to the class?
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This paper describes an approach to introducing fraction concepts using generic software tools such as Microsoft Office's PowerPoint to create "virtual" materials for mathematics teaching and learning. This approach replicates existing concrete materials and integrates virtual materials with current non-computer methods of teaching primary students about fractions. The paper reports a case study of a 12-year-old student, Frank, who had an extremely limited understanding of fractions. Frank also lacked motivation for learning mathematics in general and interacted with his peers in a negative way during mathematics lessons. In just one classroom session involving the seamless integration of off-computer and on-computer activities, Frank acquired a basic understanding of simple common equivalent fractions. Further, he was observed as the session progressed to be an enthusiastic learner who offered to share his learning with his peers. The study's "virtual replication" approach for fractions involves the manipulation of concrete materials (folding paper regions) alongside the manipulation of their virtual equivalent (shading screen regions). As researchers have pointed out, the emergence of new technologies does not mean old technologies become redundant. Learning technologies have not replaced print and oral language or basic mathematical understanding. Instead, they are modifying, reshaping, and blending the ways in which humankind speaks, reads, writes, and works mathematically. Constructivist theories of learning and teaching argue that mathematics understanding is developed from concrete to pictorial to abstract and that, ultimately, mathematics learning and teaching is about refinement and expression of ideas and concepts. Therefore, by seamlessly integrating the use of concrete materials and virtual materials generated by computer software applications, an opportunity arises to enhance the teaching and learning value of both materials.
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It's hard to be dispassionate about Reyner Banham. For me, and for the plethora of other people with strong opinions about Banham, his writing is compelling, and one’s connection to him as a figure quite personal. For me, frankly, he rocks. As a landscape architect, I gleaned most of my knowledge about Modern architecture from Banham. His Theory and Design in the First Machine Age, along with Rowe and Koetter’s Collage City and Venturi’s Complexity and Contradiction in Architecture were the most influential books in my library, by far. Later, as a budding “real scholar”, I was disappointed to find that, while these authors had serious credibility, the writings themselves were regarded as “polemical” – when in fact what I admired about them most was their ability and willingness to make rough groupings and gross generalizations, and to offer fickle opinions. It spoke to me of a real personal engagement and an active, participatory reading of the architectural culture they discussed. They were at their best in their witty, cutting, but generally pithy, creative prose, such as in Rowe’s extrapolation of the modern citizen as the latest “noble savage”, or Banham railing against conservative social advocates and their response to high density housing: “those who had just re-discovered ‘community’ in the slums would fear megastructure as much as any other kind of large-scale renewal program, and would see to it that the people were never ready.” Any reader of Banham will be able to find a gem that will relate, somehow, personally, to what they are doing right now. For Banham, it was all personal, and the gaps in his scholarship, rather, were the dispassionate places: “Such bias is essential – an unbiased historian is a pointless historian – because history is an essentially critical activity, a constant re-scrutiny and rearrangement of the profession.” Reyner Banham: Historian of the Immediate Future, Nigel Whiteley’s recent “intellectual biography” (the MIT Press, 2002), allowed me to revisit Banham’s passionate mode of criticism and to consider what his legacy might be. The book examines Banham’s body of work, grouped according to his various primary fascinations, as well as his relationship to contemporaneous theoretical movements, such as postmodernism. His mode of practice, as a kind of creative critic, is also considered in some depth. While there are points where the book delves into Banham’s personal life, on the whole Whiteley is very rigorous in considering and theorizing the work itself: more than 750 articles and twelve books. In academic terms, this is good practice. However, considering the entirely personal nature of Banham’s writing itself, this separation seems artificial. Banham, as he himself noted, “didn’t mind a gossip”, and often when reading the book I was curious about what was happening to him at the time. Banham’s was an amazing type of intellectual practice, and one that academics (a term he hated) could do well to learn from. While Whiteley spends a lot of time arguing for his practice to be regarded as such, and makes strong points about both the role of the critic, and the importance of journalism, rather than scholarly publishing, I found myself wondering what his study looked like. What books he had in his library. Did he smoke when he wrote? What sort of teaching load did he have? He is an inspiration to design writers and thinkers, and I, personally, wanted to know how he did it.
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The recent Supreme Court decision of Queensland v B [2008] 2 Qd R 562 has significant implications for the law that governs consent and abortions. The judgment purports to extend the ratio of Secretary, Department of Health and Community Services (NT) v JWB and SMB (1991) 175 CLR 218 (Marion’s Case) and impose a requirement of court approval for terminations of pregnancy for minors who are not Gillick-competent. This article argues against the imposition of this requirement on the ground that such an approach is an unjustifiable extension of the reasoning in Marion’s Case. The decision, which is the first judicial consideration in Queensland of the position of medical terminations, also reveals systemic problems with the criminal law in that State. In concluding that the traditional legal excuse for abortions will not apply to those which are performed medically, Queensland v B provides further support for calls to reform this area of law.
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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.
Resumo:
This paper presents the author characteristics of papers published in The Australian Sociological Association (TASA) journal, the Journal of Sociology (formerly the Australian and New Zealand Journal of Sociology) between 1965 and 2008. The aim of the paper is empirically to identify trends in authorship. The review examines all articles published in the period (excluding book reviews). The rationale of the study is to reveal trends in who publishes in the journal in terms of authors’ academic rank, gender, institution, and country. A table of those who have published the greatest number of papers is also presented. Findings show that over time the gap between the proportion of males and females publishing has closed; more PhD students and research fellows are publishing in the journal in recent decades; the highest proportion of authors consistently come from the Australian National University and The University of Queensland; and most authors are located in Australia. Information such as this can inform editorial practices and serve to inform the membership and readership on the nature of the journal.
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A subset of novice drivers exhibit executive function impairments which may adversely impact on the learn-to-drive period and subsequent driving experience, potentially explaining their overrepresentation in traffic offences and crashes. This paper presents the results of a qualitative analysis of a small series of in-depth semi-structured interviews undertaken individually with affected young drivers (n = 7) and each of their parent supervisors (n = 6). Young drivers were selected on the basis of their ADHD diagnosis, as a sample particularly affected by executive function impairments. Standardised rating scale measures confirmed the currency of the young drivers’ ADHD symptoms and executive function impairment. Results are discussed in terms of common experiences of the young affected drivers and those of their parents as supervising drivers of the learn-to-drive process and subsequent driving behaviour. Key themes included difficulties that were related to core executive function impairments symptomatic of ADHD. Themes also included common emotions that the young drivers associated with driving, with particular types of impact on their driving behaviour. Common strategies that were used by both the young driver and their parent during this learning process and their perceived effectiveness are also discussed. Those that were perceived to be most effective tended to focus on reducing the cognitive load for the young driver when introducing new information and skills.
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Rather than understanding the recurrent failure of various attempts at crime control as unfortunate and undesirable aberrations, all too familiar glitches an otherwise uninterrupted teleological march to a better society, such failures are instead positioned as part of the fabric of late modernity itself. That is, society changes not according to a predetermined logic along neatly defined and clearly reasoned tracks, rather it hurtles from crisis to crisis, from failure to failure, and it is the regulation of that failure which produces new initiatives and new forms of governance. Utilising the example of the modern prison, this chapter contends that too great an emphasis upon this institution’s ‘failure’ results not only in a neglect of the many other functions that it serves in the regulation of difference, but also, and more generally, it results in an underestimation of the importance of failure in providing new impetus for social transformation.