title: An autopoietic approach to custody and contact decisions and the welfare and best interests of the child

authors: Schrenk, Amelda

abstract: All over the common law world complaints are heard about the manner in which the courts decide the living arrangements for children when their parents separate. A large body of contributions from scholars and commentators from various disciplines exist, and are still being contributed, that highlights problems, critique outcomes, and make recommendations relating to these types of legal decisions. Will their work make a difference to legal outcomes and, if so, why? 
This thesis uses the socio-legal theory of Niklas Luhmann to show that it is because of how the legal system operates that the expectations of parents, scholars and interest groups, will invariably be disappointment and that ultimately what is required for these types of decisions, cannot be achieved by the legal system. Luhmann argued that the legal system operates in a closed, self-referential manner to produce its own messages as regards the values of legal and illegal. This manner of functioning is called autopoiesis. By its operations the system self-selects and simplifies information generated outside of the system in a manner that will stabilise normative expectations, which is all that the law does. Normative expectations are created with society in mind and not individuals. This challenges the individualistic approach that is required in custody and contact decisions after parental separation. The research starts at the historical point when the common law legal system gained jurisdiction over children. The research follows the development of the ‘welfare principle’ upon which custody decisions are based and illustrates the relevance and application of Luhmann’s theory. This study investigates the limitations of the legal system to make decisions about children’s welfare and best interests in the context of custody and contact decisions.

text: An autopoietic approach to custody and contact decisions and the welfare and best interests of the child All over the common law world complaints are heard about the manner in which the courts decide the living arrangements for children when their parents separate. A large body of contributions from scholars and commentators from various disciplines exist, and are still being contributed, that highlights problems, critique outcomes, and make recommendations relating to these types of legal decisions. Will their work make a difference to legal outcomes and, if so, why? 
This thesis uses the socio-legal theory of Niklas Luhmann to show that it is because of how the legal system operates that the expectations of parents, scholars and interest groups, will invariably be disappointment and that ultimately what is required for these types of decisions, cannot be achieved by the legal system. Luhmann argued that the legal system operates in a closed, self-referential manner to produce its own messages as regards the values of legal and illegal. This manner of functioning is called autopoiesis. By its operations the system self-selects and simplifies information generated outside of the system in a manner that will stabilise normative expectations, which is all that the law does. Normative expectations are created with society in mind and not individuals. This challenges the individualistic approach that is required in custody and contact decisions after parental separation. The research starts at the historical point when the common law legal system gained jurisdiction over children. The research follows the development of the ‘welfare principle’ upon which custody decisions are based and illustrates the relevance and application of Luhmann’s theory. This study investigates the limitations of the legal system to make decisions about children’s welfare and best interests in the context of custody and contact decisions.

year: 2012

title: Characterisation of an acute anorexigenic action of l-tryptophan: a link with neural mechanisms regulating appetite

authors: Gartner, Sarah Nicole

subjects: Tryptophan

abstract: Recent evidence suggests that individual amino acids may promote hypophagia, however, our understanding of processes underlying their anorexigenic action is extremely limited. The few human and laboratory animal studies performed to date suggest that a free essential amino acid, l-tryptophan (TRP) reduces food intake. It is unclear, however, whether TRP acutely affects consumption driven by energy needs or by palatability, and whether central mechanisms underlie TRP-induced hypophagia. This thesis provides a detailed characterisation of ingestive behavioural effects induced by TRP administered intragastrically or (in order to bypass the gut) via an intraperitoneal (IP) injection in laboratory rodents prior to a meal as well as relevant neural processes triggered by TRP.
The first set of experiments explored whether an intragastric preload of TRP affects energy- and palatability-induced feeding in mice. A conditioned taste aversion (CTA) test was used to assess whether hypophagia is unrelated to sickness. Finally, c-Fos immunohistochemistry was employed to detect changes in activation of feeding-related brain sites induced by an anorexigenic dose of intragastric TRP. TRP generated a short-lasting reduction in the intake of energy-dense standard chow in deprived animals and energy-dense palatable chow in sated mice. Anorexigenic doses of TRP did not cause a CTA. TRP failed to affect intake of palatable yet calorie-dilute or noncaloric solutions (10% sucrose, 4.1% Intralipid or 0.1% saccharin) even for higher TRP doses that decreased water intake in thirsty mice. c-Fos analysis revealed an increase in activation of key feeding-related brain areas, especially in the brainstem and hypothalamus. Overall, intragastric TRP was found to diminish energy-driven food consumption as well as (at high doses) thirst-induced water intake and affect activation of relevant central circuits.
In the second set of experiments, I investigated whether anorexigenic and brain activation effects persist when TRP bypasses the gut, i.e., TRP is injected directly in the IP cavity in rats. The effect of IP TRP was examined in both energy- and palatability-induced feeding. 30 and 100 mg/kg IP TRP suppressed chow intake in energy deprived rats. Only a higher 100 mg/kg IP TRP dose reduced consumption of palatable chow and palatable sucrose, saccharin and Intralipid solutions in sated animals. Thirst-driven water intake was reduced after 30 and 100 mg/kg IP TRP. Neither 30 nor 100 mg/kg IP TRP caused a CTA. c-Fos analysis showed the most pronounced effect of IP TRP on hypothalamic paraventricular (PVN) and supraoptic (SON) nuclei and the nucleus of the solitary tract in the brainstem. It can be concluded that IP TRP suppresses energy deprivation-induced intake of chow and thirst-induced water intake within the same dose range, whereas higher doses are necessary to reduce consumption of palatable solutions in sated animals. IP TRP hypophagia is accompanied by activation of central circuitry that encompasses brainstem and hypothalamic sites, though changes are not as prominent as with intragastric TRP.
Intragastric and IP TRP administered at hypophagic doses increases c-Fos immunoreactivity in the hypothalamic PVN and SON. As these sites host neurons that synthesise a key satiety mediator, oxytocin (OT), the third and final set of studies explored a hypothesis that TRP’s anorexigenic action relies on enhanced activity of the OT system. By employing double-immunohistochemistry, I determined that the lowest effective dose of intragastric and IP TRP increased the activation of both PVN and SON OT neurons, although the effect was more pronounced after intragastric administration. Intragastric TRP upregulated OT mRNA in the hypothalamus. A blood-brain barrier-penetrant OT receptor antagonist, L-368,899, reversed hypophagia induced by TRP administered via both routes. Unlike the lowest effective dose of intragastric TRP which decreases only feeding, IP TRP at the lowest effective dose diminishes both food and water intake. Hence it was confirmed that L-368,899 pre-treatment does not affect TRP-driven reduction in drinking. The findings suggest therefore a functional relationship between TRP and OT in the regulation of energy-driven food intake.
Overall, the findings presented herein shed more light on the nature of anorexigenic properties of TRP. It appears that TRP acutely suppresses ingestive behaviour driven by energy, but it is a very weak inhibitor of palatability-motivated consumption. While both intragastric and IP TRP also decreased water intake, the fact that a low dose of the intragastric amino acid was sufficient to decrease feeding but not drinking, strongly suggests that a direct interaction of TRP with the gastric mucosa is a crucial contributor to reduced energy intake. TRP engages broad brain circuits relevant to feeding, especially the hypothalamus and brainstem. OT appears to be a candidate molecule potentially mediating TRP’s effect on food intake.

text: Characterisation of an acute anorexigenic action of l-tryptophan: a link with neural mechanisms regulating appetite Recent evidence suggests that individual amino acids may promote hypophagia, however, our understanding of processes underlying their anorexigenic action is extremely limited. The few human and laboratory animal studies performed to date suggest that a free essential amino acid, l-tryptophan (TRP) reduces food intake. It is unclear, however, whether TRP acutely affects consumption driven by energy needs or by palatability, and whether central mechanisms underlie TRP-induced hypophagia. This thesis provides a detailed characterisation of ingestive behavioural effects induced by TRP administered intragastrically or (in order to bypass the gut) via an intraperitoneal (IP) injection in laboratory rodents prior to a meal as well as relevant neural processes triggered by TRP.
The first set of experiments explored whether an intragastric preload of TRP affects energy- and palatability-induced feeding in mice. A conditioned taste aversion (CTA) test was used to assess whether hypophagia is unrelated to sickness. Finally, c-Fos immunohistochemistry was employed to detect changes in activation of feeding-related brain sites induced by an anorexigenic dose of intragastric TRP. TRP generated a short-lasting reduction in the intake of energy-dense standard chow in deprived animals and energy-dense palatable chow in sated mice. Anorexigenic doses of TRP did not cause a CTA. TRP failed to affect intake of palatable yet calorie-dilute or noncaloric solutions (10% sucrose, 4.1% Intralipid or 0.1% saccharin) even for higher TRP doses that decreased water intake in thirsty mice. c-Fos analysis revealed an increase in activation of key feeding-related brain areas, especially in the brainstem and hypothalamus. Overall, intragastric TRP was found to diminish energy-driven food consumption as well as (at high doses) thirst-induced water intake and affect activation of relevant central circuits.
In the second set of experiments, I investigated whether anorexigenic and brain activation effects persist when TRP bypasses the gut, i.e., TRP is injected directly in the IP cavity in rats. The effect of IP TRP was examined in both energy- and palatability-induced feeding. 30 and 100 mg/kg IP TRP suppressed chow intake in energy deprived rats. Only a higher 100 mg/kg IP TRP dose reduced consumption of palatable chow and palatable sucrose, saccharin and Intralipid solutions in sated animals. Thirst-driven water intake was reduced after 30 and 100 mg/kg IP TRP. Neither 30 nor 100 mg/kg IP TRP caused a CTA. c-Fos analysis showed the most pronounced effect of IP TRP on hypothalamic paraventricular (PVN) and supraoptic (SON) nuclei and the nucleus of the solitary tract in the brainstem. It can be concluded that IP TRP suppresses energy deprivation-induced intake of chow and thirst-induced water intake within the same dose range, whereas higher doses are necessary to reduce consumption of palatable solutions in sated animals. IP TRP hypophagia is accompanied by activation of central circuitry that encompasses brainstem and hypothalamic sites, though changes are not as prominent as with intragastric TRP.
Intragastric and IP TRP administered at hypophagic doses increases c-Fos immunoreactivity in the hypothalamic PVN and SON. As these sites host neurons that synthesise a key satiety mediator, oxytocin (OT), the third and final set of studies explored a hypothesis that TRP’s anorexigenic action relies on enhanced activity of the OT system. By employing double-immunohistochemistry, I determined that the lowest effective dose of intragastric and IP TRP increased the activation of both PVN and SON OT neurons, although the effect was more pronounced after intragastric administration. Intragastric TRP upregulated OT mRNA in the hypothalamus. A blood-brain barrier-penetrant OT receptor antagonist, L-368,899, reversed hypophagia induced by TRP administered via both routes. Unlike the lowest effective dose of intragastric TRP which decreases only feeding, IP TRP at the lowest effective dose diminishes both food and water intake. Hence it was confirmed that L-368,899 pre-treatment does not affect TRP-driven reduction in drinking. The findings suggest therefore a functional relationship between TRP and OT in the regulation of energy-driven food intake.
Overall, the findings presented herein shed more light on the nature of anorexigenic properties of TRP. It appears that TRP acutely suppresses ingestive behaviour driven by energy, but it is a very weak inhibitor of palatability-motivated consumption. While both intragastric and IP TRP also decreased water intake, the fact that a low dose of the intragastric amino acid was sufficient to decrease feeding but not drinking, strongly suggests that a direct interaction of TRP with the gastric mucosa is a crucial contributor to reduced energy intake. TRP engages broad brain circuits relevant to feeding, especially the hypothalamus and brainstem. OT appears to be a candidate molecule potentially mediating TRP’s effect on food intake.

year: 2018

title: Hā Ora: secondary care barriers and enablers to early diagnosis of lung cancer for Māori communities.

authors: Kidd, Jacquie

subjects: Barriers

abstract: BACKGROUND: Lung Cancer is the leading cause of cancer deaths in Aotearoa New Zealand. Māori communities in particular have higher incidence and mortality rates from Lung Cancer. Diagnosis of lung cancer at an early stage can allow for curative treatment. This project aimed to document the barriers to early diagnosis and treatment of lung cancer in secondary care for Māori communities. 
METHODS: This project used a kaupapa Māori approach. Nine community hui (focus groups) and nine primary healthcare provider hui were carried out in five rural localities in the Midland region. Community hui included cancer patients, whānau (families), and other community members. Healthcare provider hui comprised staff members at the local primary healthcare centre, including General Practitioners and nurses. Hui data were thematically analysed. 
RESULTS: Barriers and enablers to early diagnosis of lung cancer were categorised into two broad themes: Specialist services and treatment, and whānau journey. The barriers and enablers that participants experienced in specialist services and treatment related to access to care, engagement with specialists, communication with specialist services and cultural values and respect, whereas barriers and enablers relating to the whānau journey focused on agency and the impact on whānau. 
CONCLUSIONS: The study highlighted the need to improve communication within and across healthcare services, the importance of understanding the cultural needs of patients and whānau and a health system strategy that meets these needs. Findings also demonstrated the resilience of Māori and the active efforts of whānau as carers to foster health literacy in future generations.

text: Hā Ora: secondary care barriers and enablers to early diagnosis of lung cancer for Māori communities. BACKGROUND: Lung Cancer is the leading cause of cancer deaths in Aotearoa New Zealand. Māori communities in particular have higher incidence and mortality rates from Lung Cancer. Diagnosis of lung cancer at an early stage can allow for curative treatment. This project aimed to document the barriers to early diagnosis and treatment of lung cancer in secondary care for Māori communities. 
METHODS: This project used a kaupapa Māori approach. Nine community hui (focus groups) and nine primary healthcare provider hui were carried out in five rural localities in the Midland region. Community hui included cancer patients, whānau (families), and other community members. Healthcare provider hui comprised staff members at the local primary healthcare centre, including General Practitioners and nurses. Hui data were thematically analysed. 
RESULTS: Barriers and enablers to early diagnosis of lung cancer were categorised into two broad themes: Specialist services and treatment, and whānau journey. The barriers and enablers that participants experienced in specialist services and treatment related to access to care, engagement with specialists, communication with specialist services and cultural values and respect, whereas barriers and enablers relating to the whānau journey focused on agency and the impact on whānau. 
CONCLUSIONS: The study highlighted the need to improve communication within and across healthcare services, the importance of understanding the cultural needs of patients and whānau and a health system strategy that meets these needs. Findings also demonstrated the resilience of Māori and the active efforts of whānau as carers to foster health literacy in future generations.

year: 2021