title: “Pushing an irritational button”: Asian psychologists making sense of racialization in psychology training in Aotearoa/New Zealand

authors: Tan, Kyle K. H.

abstract: The monocultural psychology training in Aotearoa New Zealand deliberately centers White racial framing which enables those who benefit from Whiteness to uphold an imposed hierarchy of racially inferior (Māori) and superior (Pākehā) groups. In Aotearoa, we are faced with a reality that Asian (as a diverse group from East Asia, Southeast Asia, and South Asia) knowledge sources and the intake of Asian students into psychology training are scarcely prioritized. In this study, we utilized counter-storytelling as a critical race praxis to illuminate the various forms of Asianization (Asian racialization) as a subframe of White racial framing. Employing interpretative phenomenological analysis, we explored the subjective experiences of four Asian psychologists as they made sense of racism and the formation of their racialized identity within psychology training. Our analysis uncovered three main themes with subordinate themes: (1) the White mold of psychology (encountering White ideals of psychology and pursuing perceived benefits of Whiteness); (2) bearing the brunt of Asianization (ranging from being achievers yet forgotten to being perceived as a threat and unassimilable); and (3) relating to Māori (expressing identity validation and empathy yet experiencing lateral violence). We observed the manifestation of White racial framing across various cognitive (e.g., the prioritization of western knowledge and the promotion of colorblind norms), emotional (e.g., White fragility), and behavioral aspects (e.g., expectations placed on minoritized ethnic groups to assimilate), all of which contribute to Asianization archetypes (viz., the forgotten Asian, the irritational button, and the unassimilable foreigner).

text: “Pushing an irritational button”: Asian psychologists making sense of racialization in psychology training in Aotearoa/New Zealand The monocultural psychology training in Aotearoa New Zealand deliberately centers White racial framing which enables those who benefit from Whiteness to uphold an imposed hierarchy of racially inferior (Māori) and superior (Pākehā) groups. In Aotearoa, we are faced with a reality that Asian (as a diverse group from East Asia, Southeast Asia, and South Asia) knowledge sources and the intake of Asian students into psychology training are scarcely prioritized. In this study, we utilized counter-storytelling as a critical race praxis to illuminate the various forms of Asianization (Asian racialization) as a subframe of White racial framing. Employing interpretative phenomenological analysis, we explored the subjective experiences of four Asian psychologists as they made sense of racism and the formation of their racialized identity within psychology training. Our analysis uncovered three main themes with subordinate themes: (1) the White mold of psychology (encountering White ideals of psychology and pursuing perceived benefits of Whiteness); (2) bearing the brunt of Asianization (ranging from being achievers yet forgotten to being perceived as a threat and unassimilable); and (3) relating to Māori (expressing identity validation and empathy yet experiencing lateral violence). We observed the manifestation of White racial framing across various cognitive (e.g., the prioritization of western knowledge and the promotion of colorblind norms), emotional (e.g., White fragility), and behavioral aspects (e.g., expectations placed on minoritized ethnic groups to assimilate), all of which contribute to Asianization archetypes (viz., the forgotten Asian, the irritational button, and the unassimilable foreigner).

year: 2025

title: Cartesian genetic programming for trading: a preliminary investigation

authors: Mayo, Michael

subjects: Cartesian Genetic Programming

abstract: In this paper, a preliminary investigation of Cartesian Genetic Programming (CGP) for algorithmic intraday trading is conducted. CGP is a recent new variant of genetic programming that differs from traditional approaches in a number of ways, including being able to evolve programs with limited size and with multiple outputs. CGP is used to evolve a predictor for intraday price movements, and trading strategies using the evolved predictors are evaluated along three dimensions (return, maximum drawdown and recovery factor) and against four different financial datasets (the Euro/US dollar exchange rate and the Dow Jones Industrial Average during periods from 2006 and 2010). We show that CGP is capable in many instances of evolving programs that, when used as trading strategies, lead to modest positive returns.

text: Cartesian genetic programming for trading: a preliminary investigation In this paper, a preliminary investigation of Cartesian Genetic Programming (CGP) for algorithmic intraday trading is conducted. CGP is a recent new variant of genetic programming that differs from traditional approaches in a number of ways, including being able to evolve programs with limited size and with multiple outputs. CGP is used to evolve a predictor for intraday price movements, and trading strategies using the evolved predictors are evaluated along three dimensions (return, maximum drawdown and recovery factor) and against four different financial datasets (the Euro/US dollar exchange rate and the Dow Jones Industrial Average during periods from 2006 and 2010). We show that CGP is capable in many instances of evolving programs that, when used as trading strategies, lead to modest positive returns.

year: 2012

title: In vitro cell culture to study microglial inflammation

authors: Newland, Julia

subjects: CNs

abstract: Inflammation of the central nervous system (CNS) characterised by release of cytokines such as tumour necrosis factor-alpha (TNF-a) and interleukin-1 (IL-1) is an event that is often detrimental to neuronal cells and is thought to contribute to the neuronal loss observed during neurodegeneration.
One objective of this study was to investigate the potential anti-inflammatory properties of kawakawa leaf extracts using in vitro model cell systems. Kawakawa leaf extracts anti-inflammatory properties have anecdotally been documented in traditional Maori medicinal practices (Rangoa). However, before this aspect could be carried out, experiments were undertaken to investigate the effects the kawakawa leaf extracts had on the growth rates of two mammalian cell lines (HeLa and THP-1 cells).
Interestingly, the growth assays showed that the extracts to have both a stimulatory and inhibitory effect on cell growth. Toxicity of cells can be categorised as either necrotic or apoptotic cell death. In this study, HeLa cells and THP-1 cells were incubated under standard growth conditions with various concentrations (10 to 100ug/ml) of Kawakawa leave extracts prepared at room temperature or 60OC.
Growth data as seen in figures 2 and 3 typically have a long lag phase before they start to reach exponential growth between days 4 and 5. The extract having the largest stimulatory effect on HeLa cells as shown by figure 6 was 25 ug/ml at 60OC and the largest inhibitory effect seen on HeLa cells was seen at 50 ug/ml RT shown by figure 6. The extract which has the largest stimulatory effect on THP-1 cells is 25 ug/ml 60OC as shown by figure 11 whereas the extract producing the largest inhibitory effect is 25 ug/ml RT.

Apoptotic and necrotic cell death mechanisms were examined by using in vitro biochemistry techniques. Assessments were largely made based on biochemical changes of HeLa cells and THP-1 cells post treatment of Kawakawa leave extracts.
Measurement of lactate dehydrogenase (LDH assays) in the growth media of cells that were shown to be growth inhibited during exposure to Kawakawa extracts indicated that the growth inhibition resulting from exposure to the extracts was not due to necrotic cell death processes. (ie that cells maintained their membrane integrity) When compared to the control, a lower amount of cytosolic LDH was seen in THP-1 cell lines. However, HeLa cell lines produced a high level of cytosolic LDH which may be due to mycoplasma contamination. On average, Kawakawa concentrations at 12.5ug/ml and 25ug/ml yielded less lysed cells percentage across both cell lines.
The demonstrated cell growth inhibition was unlikely to be due to necrosis and because of this it was decided to see if cell death was caused by mitochondrial processes that would further support apoptotic cell death. The biochemical assay MTT indirectly measures mitochondrial dehydrogenase activity in the presence of kawakawa leave extracts.
The MTT data illustrated mitochondrial impairment where HeLa cells exposed to Kawakawa 60OC concentrations 6.25 ug/ml and 12.5 ug/ml had the lowest average mitochondrial activity. THP-1 cells exposed to Kawakawa 60OC concentrations 12.5 ug/ml and 50 ug/ml had the lowest average mitochondrial activity.
The main results of this study include, the treatment of HeLa and THP-1 cells with kawakawa extracts demonstrated that cytotoxicity was not due to necrosis. The most interesting finding of this study is when kawakawa extracts inhibit cell growth there is no increase in LDH. This is suggestive that the cellular membrane remains intact when exposed to the extract.

text: In vitro cell culture to study microglial inflammation Inflammation of the central nervous system (CNS) characterised by release of cytokines such as tumour necrosis factor-alpha (TNF-a) and interleukin-1 (IL-1) is an event that is often detrimental to neuronal cells and is thought to contribute to the neuronal loss observed during neurodegeneration.
One objective of this study was to investigate the potential anti-inflammatory properties of kawakawa leaf extracts using in vitro model cell systems. Kawakawa leaf extracts anti-inflammatory properties have anecdotally been documented in traditional Maori medicinal practices (Rangoa). However, before this aspect could be carried out, experiments were undertaken to investigate the effects the kawakawa leaf extracts had on the growth rates of two mammalian cell lines (HeLa and THP-1 cells).
Interestingly, the growth assays showed that the extracts to have both a stimulatory and inhibitory effect on cell growth. Toxicity of cells can be categorised as either necrotic or apoptotic cell death. In this study, HeLa cells and THP-1 cells were incubated under standard growth conditions with various concentrations (10 to 100ug/ml) of Kawakawa leave extracts prepared at room temperature or 60OC.
Growth data as seen in figures 2 and 3 typically have a long lag phase before they start to reach exponential growth between days 4 and 5. The extract having the largest stimulatory effect on HeLa cells as shown by figure 6 was 25 ug/ml at 60OC and the largest inhibitory effect seen on HeLa cells was seen at 50 ug/ml RT shown by figure 6. The extract which has the largest stimulatory effect on THP-1 cells is 25 ug/ml 60OC as shown by figure 11 whereas the extract producing the largest inhibitory effect is 25 ug/ml RT.

Apoptotic and necrotic cell death mechanisms were examined by using in vitro biochemistry techniques. Assessments were largely made based on biochemical changes of HeLa cells and THP-1 cells post treatment of Kawakawa leave extracts.
Measurement of lactate dehydrogenase (LDH assays) in the growth media of cells that were shown to be growth inhibited during exposure to Kawakawa extracts indicated that the growth inhibition resulting from exposure to the extracts was not due to necrotic cell death processes. (ie that cells maintained their membrane integrity) When compared to the control, a lower amount of cytosolic LDH was seen in THP-1 cell lines. However, HeLa cell lines produced a high level of cytosolic LDH which may be due to mycoplasma contamination. On average, Kawakawa concentrations at 12.5ug/ml and 25ug/ml yielded less lysed cells percentage across both cell lines.
The demonstrated cell growth inhibition was unlikely to be due to necrosis and because of this it was decided to see if cell death was caused by mitochondrial processes that would further support apoptotic cell death. The biochemical assay MTT indirectly measures mitochondrial dehydrogenase activity in the presence of kawakawa leave extracts.
The MTT data illustrated mitochondrial impairment where HeLa cells exposed to Kawakawa 60OC concentrations 6.25 ug/ml and 12.5 ug/ml had the lowest average mitochondrial activity. THP-1 cells exposed to Kawakawa 60OC concentrations 12.5 ug/ml and 50 ug/ml had the lowest average mitochondrial activity.
The main results of this study include, the treatment of HeLa and THP-1 cells with kawakawa extracts demonstrated that cytotoxicity was not due to necrosis. The most interesting finding of this study is when kawakawa extracts inhibit cell growth there is no increase in LDH. This is suggestive that the cellular membrane remains intact when exposed to the extract.

year: 2016