title: Youth, action sports and political agency in the Middle East: Lessons from a grassroots parkour group in Gaza

authors: Thorpe, Holly Aysha

subjects: youth

abstract: In this paper we build upon recent scholarship on the globalization of youth culture and sport to examine the growing popularity of action sports in the Middle East. We focus on the development of the urban physical practice of parkour (also known as free running)—the act of running, jumping, leaping through an urban environment as fluidly, efficiently and creatively as possible—among Middle Eastern youth. Drawing upon interviews and media analysis of various print, digital and social media, we reveal how youth (particularly young men) in Gaza developed their own unique parkour group, despite various social, cultural, economic, physical and psychological obstacles. We explain the proactive approaches adopted by these young men to find appropriate training spaces, to develop the skills of local children and youth, and to support their peer groups. In particular, we describe how these young men are creatively engaging social media (e.g., YouTube, Facebook, Twitter) to gain inspiration from the transnational parkour community, and also for opening new dialogue and establishing informal cultural exchanges with parkour enthusiasts around the world. We conclude by offering some broader comments for the Sport for Development and Peace Building (SDP) movement, encouraging youth-focused SDP initiatives to move beyond the ‘deficit model’ and toward more collaborative projects that provide space for local voices and acknowledge youth agency.

text: Youth, action sports and political agency in the Middle East: Lessons from a grassroots parkour group in Gaza In this paper we build upon recent scholarship on the globalization of youth culture and sport to examine the growing popularity of action sports in the Middle East. We focus on the development of the urban physical practice of parkour (also known as free running)—the act of running, jumping, leaping through an urban environment as fluidly, efficiently and creatively as possible—among Middle Eastern youth. Drawing upon interviews and media analysis of various print, digital and social media, we reveal how youth (particularly young men) in Gaza developed their own unique parkour group, despite various social, cultural, economic, physical and psychological obstacles. We explain the proactive approaches adopted by these young men to find appropriate training spaces, to develop the skills of local children and youth, and to support their peer groups. In particular, we describe how these young men are creatively engaging social media (e.g., YouTube, Facebook, Twitter) to gain inspiration from the transnational parkour community, and also for opening new dialogue and establishing informal cultural exchanges with parkour enthusiasts around the world. We conclude by offering some broader comments for the Sport for Development and Peace Building (SDP) movement, encouraging youth-focused SDP initiatives to move beyond the ‘deficit model’ and toward more collaborative projects that provide space for local voices and acknowledge youth agency.

year: 2013

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: Te Tarata

authors: Maxwell, Te Kahautu

subjects: Haka

abstract: He whakamārama mō te haka 
Ko tēnei haka he whakamauharatanga ki te riri whenua i waenganui i Te Whakatōhea me te Karauna i te 23 o Poutūterangi 1865. Ko te ingoa o te pakanga nei ko Te Tarata. Hai tēnei marama kua eke ki te kotahi rau e rima tekau tau mai i tēnei pakanga. Ka kōrerotia te patunga i te mihinare a Te Wākana i te 2 o Poutūterangi i te tau kotahi mano e waru rau e ono tekau mā rima (1865). Nā Kereopa o Ngāti Rangiwewehi i patu a Te Wākana. I haramai a Te Kereopa i raro i te Paimārire (Hauhau) ki Ōpōtiki. Ko tā Te Paimārire kaupapa i tae atu ai ko te kauhau i te whakapono hou a Te Ua Haumēne o Taranaki. Ko ngā āpōtoro i tukuna atu e Te Ua Haumēne ko Pātara Rakataura me Te Kereopa, hoi anō ko te kauhau i te rongopai tā Te Ua Haumēne i whakahau ai. Hoi anō he take tā Te Kereopa, tā te mea i kōhurutia tana wahine me āna tamāhine tokorua ki te whare karakia i Rangiaowhia ki roto o Tainui. Nara i pau a Ngāti Apakura ki te mate ki roto i te ahi, i tahuna te whare karakia e ngā hoia me te iwi o Ngāti Apakura ki roto. Ā i patua anō tana tamāhine hoki ki te pakanga i Hairini. Koiarā tā Kereopa he rānaki i te mate o tana whānau i pau i te ahi nukarau a te Karauna. Nā tēnei patunga i a Te Wākana i riro ai te 250,000 eka o Te Whakatōhea. I tēnei rā tonu o Te Matatini i tēnei tau 2015 kua eke ki te kotahi rau e rima tekau (150) tau o te parekuranui o Te Whakatōhea mō te patunga i te tangata kotahi nā tētahi atu ko Te Kereopa o Ngāti Rangiwewehi. Ko te kōhuru i a Te Whakatōhea me āna tamariki, āna mokopuna, ko te tāwharona i ngā tāne, i ngā wāhine, ko te ekeeke kino te rarahu i ngā wāhine me ngā tamariki kōtiro, tāne hoki. Mutu ana te rarahu ko te kōhuru i a rātou ki te pū, ki te mata o te pēneti ko te tahu rānei. Ko te urupatu anō tērā ko te tahu i ngā pā, i ngā whare tīpuna, i ngā māra, i ngā mira mahi paura, i ngā kaipuke tauhokohoko ki Tāmaki, ki Poihākena, ki Ingarangi. Ko te parekura nui tēnei o Te Whakatōhea, ko te kōhuru i tō mātou katoa, tō mātou ao, tō mātou wairua, tō mātou hinengaro, tō mātou tinana o Te Whakatōhea mō te mate kotahi a te tangata kotahi. Ahakoa he mihingare, he pūrahorua hoki he kawe o kōrero nōna ki a Kāwana Kerei mō ngā nekeneke a Te Whakatōhea ki te tautoko i a Kīngi Tāwhiao me ngā pakanga whenua i Rangiriri, i Ōrakau i te tau kotahi mano e waru rau e ono tekau mā whā (1864). Ki te pakanga o Te Tarata, 14 ngā Māori i mate i tēnei pakanga me ngā hoia pākeha, ngā maemanerau 26. E 500 ngā manemanerau i roto i te ope taua a Kuini Wikitōria. I tēnei pakanga nā Hira Te Popo te rangatira o Ngāti Ira, hapū o Te Whakatōhea i herehangaia ngā tīkouka me ōna rau ki ngā pou o te tūwatawata. Nara i pupuhi ngā pūrepō ngā ki te pā o Te Tarata i hinga ngā tūwatawata me te tū anō. Koirā te mahi a te tīkouka he rākau māmā kāore i whati pēnei i te mānuka me ngā rākau mārō ehara ko tāna he tiaki i te tūwatawata ka tūohu ka tū anō me te maka anō i ngā kariri o te pūrepō ki ngā hōia a te Karauna. Ana nā te tīkouka i āhei a Te Whakatōhea me ōna haumi te rere whakauta ki te tuawhenua. I huihui rātou ki tētahi pā anō ki Kohipawa kīhai i tareka e te Karauna.

text: Te Tarata He whakamārama mō te haka 
Ko tēnei haka he whakamauharatanga ki te riri whenua i waenganui i Te Whakatōhea me te Karauna i te 23 o Poutūterangi 1865. Ko te ingoa o te pakanga nei ko Te Tarata. Hai tēnei marama kua eke ki te kotahi rau e rima tekau tau mai i tēnei pakanga. Ka kōrerotia te patunga i te mihinare a Te Wākana i te 2 o Poutūterangi i te tau kotahi mano e waru rau e ono tekau mā rima (1865). Nā Kereopa o Ngāti Rangiwewehi i patu a Te Wākana. I haramai a Te Kereopa i raro i te Paimārire (Hauhau) ki Ōpōtiki. Ko tā Te Paimārire kaupapa i tae atu ai ko te kauhau i te whakapono hou a Te Ua Haumēne o Taranaki. Ko ngā āpōtoro i tukuna atu e Te Ua Haumēne ko Pātara Rakataura me Te Kereopa, hoi anō ko te kauhau i te rongopai tā Te Ua Haumēne i whakahau ai. Hoi anō he take tā Te Kereopa, tā te mea i kōhurutia tana wahine me āna tamāhine tokorua ki te whare karakia i Rangiaowhia ki roto o Tainui. Nara i pau a Ngāti Apakura ki te mate ki roto i te ahi, i tahuna te whare karakia e ngā hoia me te iwi o Ngāti Apakura ki roto. Ā i patua anō tana tamāhine hoki ki te pakanga i Hairini. Koiarā tā Kereopa he rānaki i te mate o tana whānau i pau i te ahi nukarau a te Karauna. Nā tēnei patunga i a Te Wākana i riro ai te 250,000 eka o Te Whakatōhea. I tēnei rā tonu o Te Matatini i tēnei tau 2015 kua eke ki te kotahi rau e rima tekau (150) tau o te parekuranui o Te Whakatōhea mō te patunga i te tangata kotahi nā tētahi atu ko Te Kereopa o Ngāti Rangiwewehi. Ko te kōhuru i a Te Whakatōhea me āna tamariki, āna mokopuna, ko te tāwharona i ngā tāne, i ngā wāhine, ko te ekeeke kino te rarahu i ngā wāhine me ngā tamariki kōtiro, tāne hoki. Mutu ana te rarahu ko te kōhuru i a rātou ki te pū, ki te mata o te pēneti ko te tahu rānei. Ko te urupatu anō tērā ko te tahu i ngā pā, i ngā whare tīpuna, i ngā māra, i ngā mira mahi paura, i ngā kaipuke tauhokohoko ki Tāmaki, ki Poihākena, ki Ingarangi. Ko te parekura nui tēnei o Te Whakatōhea, ko te kōhuru i tō mātou katoa, tō mātou ao, tō mātou wairua, tō mātou hinengaro, tō mātou tinana o Te Whakatōhea mō te mate kotahi a te tangata kotahi. Ahakoa he mihingare, he pūrahorua hoki he kawe o kōrero nōna ki a Kāwana Kerei mō ngā nekeneke a Te Whakatōhea ki te tautoko i a Kīngi Tāwhiao me ngā pakanga whenua i Rangiriri, i Ōrakau i te tau kotahi mano e waru rau e ono tekau mā whā (1864). Ki te pakanga o Te Tarata, 14 ngā Māori i mate i tēnei pakanga me ngā hoia pākeha, ngā maemanerau 26. E 500 ngā manemanerau i roto i te ope taua a Kuini Wikitōria. I tēnei pakanga nā Hira Te Popo te rangatira o Ngāti Ira, hapū o Te Whakatōhea i herehangaia ngā tīkouka me ōna rau ki ngā pou o te tūwatawata. Nara i pupuhi ngā pūrepō ngā ki te pā o Te Tarata i hinga ngā tūwatawata me te tū anō. Koirā te mahi a te tīkouka he rākau māmā kāore i whati pēnei i te mānuka me ngā rākau mārō ehara ko tāna he tiaki i te tūwatawata ka tūohu ka tū anō me te maka anō i ngā kariri o te pūrepō ki ngā hōia a te Karauna. Ana nā te tīkouka i āhei a Te Whakatōhea me ōna haumi te rere whakauta ki te tuawhenua. I huihui rātou ki tētahi pā anō ki Kohipawa kīhai i tareka e te Karauna.

year: 2017