title: The Modern Dragon: Contemporary Representations from Tolkein to Present

authors: Sheridan, Brendan Daniel

subjects: Dragon

abstract: ‘Every century has its dragons.’  I intend to examine depiction of dragons from 1937  onwards to try to determine how we perceive the dragon in the modern world. To this end I will examine dragons in a variety of contemporary media, from film and television, as well as literature. They will include, but not be limited to: Game of Thrones , Eragon , The Hobbit , Dragonflight , Guards! Guards! , and How to Train Your Dragon.

Framed by adaptation studies, this thesis analyses the way in which contemporary texts re-interpret and re-imagine the dragon. In so doing, it draws on related theories, in particular human-animal studies, the uncanny, the other, and gender studies, in order to understand the enduring fascination with this mythical creature and the way in which modern authors and directors draw on and depart from both Eastern and Western mythological tradition and folklore.

The first section examines the shape of the dragon and how they are depicted, not only in literary text, but also in television, film, and art work. This involves identifying the literary and mythological forebears of these current depictions, as well as what the presentation reveals about contemporary culture. Having identified recent adaptations of the dragon’s physical form, I move to a discussion of the nature of the dragon, in particular its intelligence and morality. Throughout this section, I draw on human-animal studies to analyse the dragon’s familiarity and otherness.  

Turning to the interrelation between dragons and magic, I look at how dragons are presented as magical beings who at times exhibit magical abilities and at times are themselves the source of magic. As in my discussion of the dragon’s nature, it is the strangeness of the dragon which is apparent here: it is a creature of fantasy, beyond the realm of the rational, belonging to what J.R.R. Tolkein refers to as ‘Of Faërie’.  In the fourth chapter, the focus on dragon-slayers and dragon-riders highlights the human impulse to tame and control or destroy this mystical creature. At the same time, I reveal the human belief in their capacity to domesticate the dragon’s essential wildness to be delusive. I conclude with an analysis of the gender ambiguity of the dragon and its particular association with women, foregrounding their mutual marginalisation by society.

text: The Modern Dragon: Contemporary Representations from Tolkein to Present ‘Every century has its dragons.’  I intend to examine depiction of dragons from 1937  onwards to try to determine how we perceive the dragon in the modern world. To this end I will examine dragons in a variety of contemporary media, from film and television, as well as literature. They will include, but not be limited to: Game of Thrones , Eragon , The Hobbit , Dragonflight , Guards! Guards! , and How to Train Your Dragon.

Framed by adaptation studies, this thesis analyses the way in which contemporary texts re-interpret and re-imagine the dragon. In so doing, it draws on related theories, in particular human-animal studies, the uncanny, the other, and gender studies, in order to understand the enduring fascination with this mythical creature and the way in which modern authors and directors draw on and depart from both Eastern and Western mythological tradition and folklore.

The first section examines the shape of the dragon and how they are depicted, not only in literary text, but also in television, film, and art work. This involves identifying the literary and mythological forebears of these current depictions, as well as what the presentation reveals about contemporary culture. Having identified recent adaptations of the dragon’s physical form, I move to a discussion of the nature of the dragon, in particular its intelligence and morality. Throughout this section, I draw on human-animal studies to analyse the dragon’s familiarity and otherness.  

Turning to the interrelation between dragons and magic, I look at how dragons are presented as magical beings who at times exhibit magical abilities and at times are themselves the source of magic. As in my discussion of the dragon’s nature, it is the strangeness of the dragon which is apparent here: it is a creature of fantasy, beyond the realm of the rational, belonging to what J.R.R. Tolkein refers to as ‘Of Faërie’.  In the fourth chapter, the focus on dragon-slayers and dragon-riders highlights the human impulse to tame and control or destroy this mystical creature. At the same time, I reveal the human belief in their capacity to domesticate the dragon’s essential wildness to be delusive. I conclude with an analysis of the gender ambiguity of the dragon and its particular association with women, foregrounding their mutual marginalisation by society.

year: 2015

title: A neural and behavioural investigation of aberrant feeding in animal models of autism spectrum disorder

authors: Harvey, Savannah

abstract: Autism spectrum disorder (ASD), a  neurodevelopmental disorder  affecting approximately 1.85% of the population, is underpinned by complex interplay between genetics and environment. Thus far, ASD research has focused predominantly on abnormal social communication, anxiety, and cognitive impairments. It omits, however, dysregulated food intake, which is the symptom present in over 60% of ASD individuals. Data suggest that feeding abnormalities include heightened food selectivity, neophobia and food refusal, as well as pica (consumption of non-food items). The current knowledge of the scope and magnitude of abnormal appetite in ASD as well as neuropathology underlying this phenomenon is extremely limited. Thus, the overarching goal of this thesis was to provide systematic evidence pertaining to aberrant food intake in ASD and identify the relevant mechanisms, by utilizing two key animal models of this disorder (one in which ASD stems from a genetic mutation, and the other, in which ASD is induced pharmacologically).
In Specific Aim 1 of this thesis, I investigated the hypothesis that ASD mutant male mice overconsume palatable foods beyond the level observed in neurotypical controls. In this animal model, ASD stems from the deletion of the contactin-associated protein like 2 (CNTNAP2) gene encoding a transmembrane neuronal protein which clusters K+ channels in the nodes of Ranvier. My studies show for the first time that Cntnap2-/- males drink more of sucrose, saccharin and intralipid solutions compared to wild-type (WT) controls. A c-Fos immunoreactivity analysis revealed that at the end of a sucrose solution meal, Cntnap2-/- mice have blunted activation in key regions associated with satiety and reward. Specifically in the central amygdala (CEA), dorsomedial hypothalamus (DMH), ventromedial hypothalamus (VMH) and the nucleus accumbens (Acb). Excessive consumption palatable sucrose  sucrose was  was ameliorated  in mutants  by intraperitoneal administration of oxytocin (OT), a satiety promoting neuropeptide whose dysregulated release is also associated with the broad symptomology of ASD, from anxiety to sociality impairments. In line with the injection experiment, the double staining for c-Fos and OT showed blunted OT neuronal activation in the hypothalamus of the mutants after a meal of sucrose. Overall, the data indicate that ASD Cntnap2-/-male mice show excessive intake of palatable foods, and it is associated with atypical neural activation (including the OT system) in response to a palatable meal. 
In Specific Aim 2, I examined whether the overconsumption of sucrose observed in male Cntnap2-/- mice also occurs in females. Research on ASD animal models often focuses on males due to concerns about oestrus driven behavioural variability and the subtler presentation of ASD-related behaviours in females. However, feeding issues in ASD affect both sexes. To address this, I evaluated sucrose intake in female Cntnap2-/- mice and compared their consummatory behaviour across different stages of the oestrous cycle. Female Cntnap2-/- mice exhibited overconsumption of sucrose, which remained consistent across all oestrous phases. This study suggests that palatability-driven overconsumption of sugar occurs in female Cntnap2-/- mice and does not appear to be influenced by oestrus phase.
In Specific Aim 3, I investigated the hypothesis that Cntnap2-/- mice exhibit heightened hyponeophagia, a common feeding issue associated with ASD. I assessed hyponeophagia in Cntnap2-/- mice both in a novel environment and in their home cage. In both contexts, Cntnap2-/- mice displayed a significantly greater latency to approach novel food compared to WTs. Notably, in the home cage more instances of presentation of that food were required for the latency in Cntnap2-/- mice to decrease to match that of WTs. The analysis of c-Fos immunoreactivity revealed different densities of activation in key brain regions associated with reward, feeding, and fear processing between Cntnap2-/- and WT mice in response to novel food presentation. These regions included the ventral tegmental area (VTA), CEA, and arcuate nucleus (ARC). These findings suggest potential impairments in neural processing of food-related novelty cues, which may contribute to the exaggerated neophobic behaviours observed.
Valproate (VPA), an anti-epileptic drug and known teratogen, induces an ASD phenotype in offspring when administered during the period of neural tube closure. Specific Aim 4 tested whether rats prenatally exposed to VPA exhibit impaired acquisition of the conditioned taste aversion (CTA), a protective learning mechanism against ingestion of foods inducing nausea/malaise. Feeding issues in ASD, such as pica, may reflect disruptions in aversion-based learning. Additionally, OT has been implicated in CTA acquisition, and VPA rats exhibit OT signaling abnormalities. Using a standard CTA paradigm with lithium chloride (LiCl) as a nausea-inducing agent, I found that VPA rats failed to acquire a CTA response. Gene expression analysis via qPCR revealed altered expression of catecholamine metabolism-, reward-, aversion-, and satiety-related genes in the CEA in LiCl-treated VPA rats compared to controls. These findings suggest that prenatal VPA exposure disrupts neural mechanisms critical for aversion-based learning, with the CEA playing a key role.
In summary, this thesis provides novel insights into the neuromolecular mechanisms underlying feeding behaviours in ASD, highlighting distinct anomalies in palatable food intake, food neophobia, and aversive learning. Using Cntnap2-/- mice and VPA-exposed rats, the studies demonstrate significant overconsumption of palatable foods in both sexes, prolonged neophobic responses, and disrupted conditioned taste aversion acquisition, all underpinned by aberrant brain activation and gene expression.

text: A neural and behavioural investigation of aberrant feeding in animal models of autism spectrum disorder Autism spectrum disorder (ASD), a  neurodevelopmental disorder  affecting approximately 1.85% of the population, is underpinned by complex interplay between genetics and environment. Thus far, ASD research has focused predominantly on abnormal social communication, anxiety, and cognitive impairments. It omits, however, dysregulated food intake, which is the symptom present in over 60% of ASD individuals. Data suggest that feeding abnormalities include heightened food selectivity, neophobia and food refusal, as well as pica (consumption of non-food items). The current knowledge of the scope and magnitude of abnormal appetite in ASD as well as neuropathology underlying this phenomenon is extremely limited. Thus, the overarching goal of this thesis was to provide systematic evidence pertaining to aberrant food intake in ASD and identify the relevant mechanisms, by utilizing two key animal models of this disorder (one in which ASD stems from a genetic mutation, and the other, in which ASD is induced pharmacologically).
In Specific Aim 1 of this thesis, I investigated the hypothesis that ASD mutant male mice overconsume palatable foods beyond the level observed in neurotypical controls. In this animal model, ASD stems from the deletion of the contactin-associated protein like 2 (CNTNAP2) gene encoding a transmembrane neuronal protein which clusters K+ channels in the nodes of Ranvier. My studies show for the first time that Cntnap2-/- males drink more of sucrose, saccharin and intralipid solutions compared to wild-type (WT) controls. A c-Fos immunoreactivity analysis revealed that at the end of a sucrose solution meal, Cntnap2-/- mice have blunted activation in key regions associated with satiety and reward. Specifically in the central amygdala (CEA), dorsomedial hypothalamus (DMH), ventromedial hypothalamus (VMH) and the nucleus accumbens (Acb). Excessive consumption palatable sucrose  sucrose was  was ameliorated  in mutants  by intraperitoneal administration of oxytocin (OT), a satiety promoting neuropeptide whose dysregulated release is also associated with the broad symptomology of ASD, from anxiety to sociality impairments. In line with the injection experiment, the double staining for c-Fos and OT showed blunted OT neuronal activation in the hypothalamus of the mutants after a meal of sucrose. Overall, the data indicate that ASD Cntnap2-/-male mice show excessive intake of palatable foods, and it is associated with atypical neural activation (including the OT system) in response to a palatable meal. 
In Specific Aim 2, I examined whether the overconsumption of sucrose observed in male Cntnap2-/- mice also occurs in females. Research on ASD animal models often focuses on males due to concerns about oestrus driven behavioural variability and the subtler presentation of ASD-related behaviours in females. However, feeding issues in ASD affect both sexes. To address this, I evaluated sucrose intake in female Cntnap2-/- mice and compared their consummatory behaviour across different stages of the oestrous cycle. Female Cntnap2-/- mice exhibited overconsumption of sucrose, which remained consistent across all oestrous phases. This study suggests that palatability-driven overconsumption of sugar occurs in female Cntnap2-/- mice and does not appear to be influenced by oestrus phase.
In Specific Aim 3, I investigated the hypothesis that Cntnap2-/- mice exhibit heightened hyponeophagia, a common feeding issue associated with ASD. I assessed hyponeophagia in Cntnap2-/- mice both in a novel environment and in their home cage. In both contexts, Cntnap2-/- mice displayed a significantly greater latency to approach novel food compared to WTs. Notably, in the home cage more instances of presentation of that food were required for the latency in Cntnap2-/- mice to decrease to match that of WTs. The analysis of c-Fos immunoreactivity revealed different densities of activation in key brain regions associated with reward, feeding, and fear processing between Cntnap2-/- and WT mice in response to novel food presentation. These regions included the ventral tegmental area (VTA), CEA, and arcuate nucleus (ARC). These findings suggest potential impairments in neural processing of food-related novelty cues, which may contribute to the exaggerated neophobic behaviours observed.
Valproate (VPA), an anti-epileptic drug and known teratogen, induces an ASD phenotype in offspring when administered during the period of neural tube closure. Specific Aim 4 tested whether rats prenatally exposed to VPA exhibit impaired acquisition of the conditioned taste aversion (CTA), a protective learning mechanism against ingestion of foods inducing nausea/malaise. Feeding issues in ASD, such as pica, may reflect disruptions in aversion-based learning. Additionally, OT has been implicated in CTA acquisition, and VPA rats exhibit OT signaling abnormalities. Using a standard CTA paradigm with lithium chloride (LiCl) as a nausea-inducing agent, I found that VPA rats failed to acquire a CTA response. Gene expression analysis via qPCR revealed altered expression of catecholamine metabolism-, reward-, aversion-, and satiety-related genes in the CEA in LiCl-treated VPA rats compared to controls. These findings suggest that prenatal VPA exposure disrupts neural mechanisms critical for aversion-based learning, with the CEA playing a key role.
In summary, this thesis provides novel insights into the neuromolecular mechanisms underlying feeding behaviours in ASD, highlighting distinct anomalies in palatable food intake, food neophobia, and aversive learning. Using Cntnap2-/- mice and VPA-exposed rats, the studies demonstrate significant overconsumption of palatable foods in both sexes, prolonged neophobic responses, and disrupted conditioned taste aversion acquisition, all underpinned by aberrant brain activation and gene expression.

year: 2025

title: Using the curriculum guidelines for the teaching and learning of te reo Māori in Years 1 - 13 of New Zealand schools to create lessons for young learners

authors: Diane, Johnson

subjects: New Zealand

abstract: In 2009, The New Zealand Ministry of Education published curriculum guidelines for te reo Māori in Years 1 - 13 of English-medium New Zealand schools, that is, from age 5 upwards. These guidelines recommend a communicative approach to the teaching and learning of te reo Māori. In this article, we discuss communicative approaches and provide examples of ways in which teachers can design communicative language lessons that are appropriate for very young learners, lessons that are not only fun but also effective in developing genuine communicative competence in te reo Māori.

text: Using the curriculum guidelines for the teaching and learning of te reo Māori in Years 1 - 13 of New Zealand schools to create lessons for young learners In 2009, The New Zealand Ministry of Education published curriculum guidelines for te reo Māori in Years 1 - 13 of English-medium New Zealand schools, that is, from age 5 upwards. These guidelines recommend a communicative approach to the teaching and learning of te reo Māori. In this article, we discuss communicative approaches and provide examples of ways in which teachers can design communicative language lessons that are appropriate for very young learners, lessons that are not only fun but also effective in developing genuine communicative competence in te reo Māori.

year: 2009-09