title: Modern life at high temperatures

authors: Daniel, Roy M.

subjects: biology

abstract: A variety of micro-organisms are now known which grow optimally above 65°C, and are defined as extreme thermophiles. As might be expected they are found in both natural and artificial hot environments. Until comparatively recently the upper optimum temperature for the growth of any living organism was about 85°C. Then in 1982 Stetter described an organism, isolated from the hot sea floor of a submarine solfatara field, which grew optimally at 105°C. Since then several other organisms have been found with optimum growth temperatures at 100"C or above and a few are capable of growth at 110*C (e.g. Huber et al., 1987; Fiala and Stetter, 1986; Zillig et al., 1987; Stetter et al., 1990).

text: Modern life at high temperatures A variety of micro-organisms are now known which grow optimally above 65°C, and are defined as extreme thermophiles. As might be expected they are found in both natural and artificial hot environments. Until comparatively recently the upper optimum temperature for the growth of any living organism was about 85°C. Then in 1982 Stetter described an organism, isolated from the hot sea floor of a submarine solfatara field, which grew optimally at 105°C. Since then several other organisms have been found with optimum growth temperatures at 100"C or above and a few are capable of growth at 110*C (e.g. Huber et al., 1987; Fiala and Stetter, 1986; Zillig et al., 1987; Stetter et al., 1990).

year: 1992

title: A Model In Vitro System to Study Heat Shock Protein 60 (HSP60) Expression in Response to Mitochondrial Impairment in Human Cells

authors: Hall, Luke

subjects: HSP60

abstract: Heat Shock Proteins (HSPs) are a class of ubiquitously expressed and functionally related proteins found in all living organisms from humans to bacteria. Their expression is increased in response to various cellular stressors in what is referred to as the heat shock response. The induction of one particular HSP, HSP60, has been found to be correlated with mitochondria specific cell stress. Recently HSP60 has been found to be secreted and expressed extracellularly, after first being thought to be strictly intracellular. However, the mechanisms of these mechanisms of translocation and secretion have not been clearly identified. 
The aim of this study was to develop a model in vitro system for HSP60 expression in human cells so that treatments which resulted in mitochondrial impairment could be investigated. 
This study looked at several aspects of high glucose, hydrogen peroxide (H₂O₂), and sodium azide treatment on human HeLa cells. At low levels, each treatment had a hormetic effect on HeLa cell growth; however at high concentrations growth was significantly inhibited. Additionally, high treatment concentrations resulted in increased cell lysis as determined by LDH assays. Treatment with concentrations of 100mM glucose, 200μM H₂O₂, and 50μM sodium azide were the only treatment concentrations that did not result in significantly different levels of cell lysis when compared to a control sample. Mitochondrial dehydrogenase activity was also found to be significantly decreased at high treatment concentrations as determined by MTT assays. Thus, 100mM glucose, 200μM H₂O₂, and 50μM sodium azide treatments were identified as optimal conditions for mitochondrial targeted cell stress, as each of these treatments impaired cell growth and inhibited mitochondrial activity while having no significant effect on the degree of cell lysis. 
The 100mM glucose, 200μM H₂O₂, and 50μM sodium azide treatments were then investigated for the intracellular reactive oxygen species (ROS) activity they induced over treatment periods of 24 hours, 3 and 7 days. After 7 days of treatment, the 200μM H₂O₂ and 50μM sodium azide treatments resulted in an approximate three-fold increase in ROS activity, while the 100mM glucose treatment resulted in almost twice as much ROS compared to a control sample.
Finally, the effects of 100mM glucose, 200μM H₂O₂, and 50μM sodium azide treatments on HSP60 and HSP70 expression was also examined over 3 and 7 day time periods. After the 7 day treatment period, the 100mM glucose treatment had induced a 2.43 fold increase in HSP60 expression and a 2.75 fold increase in HSP70 expression, the 200μM H₂O₂ induced a 3.48 fold increase in HSP60 expression and a 3.98 fold increase in HSP70 expression, and finally the 50μM sodium azide induced a 4.74 fold increase in HSP60 expression and a 5.08 fold increase in HSP70 expression. 
It can therefore be concluded that 100mM glucose, 200μM H₂O₂, and 50μM sodium azide results in the upregulation of HSP60 and HSP70 in human HeLa cells. Therefore this model may be used to investigate further aspects of HSP60 induction, such as its translocation and secretion.

text: A Model In Vitro System to Study Heat Shock Protein 60 (HSP60) Expression in Response to Mitochondrial Impairment in Human Cells Heat Shock Proteins (HSPs) are a class of ubiquitously expressed and functionally related proteins found in all living organisms from humans to bacteria. Their expression is increased in response to various cellular stressors in what is referred to as the heat shock response. The induction of one particular HSP, HSP60, has been found to be correlated with mitochondria specific cell stress. Recently HSP60 has been found to be secreted and expressed extracellularly, after first being thought to be strictly intracellular. However, the mechanisms of these mechanisms of translocation and secretion have not been clearly identified. 
The aim of this study was to develop a model in vitro system for HSP60 expression in human cells so that treatments which resulted in mitochondrial impairment could be investigated. 
This study looked at several aspects of high glucose, hydrogen peroxide (H₂O₂), and sodium azide treatment on human HeLa cells. At low levels, each treatment had a hormetic effect on HeLa cell growth; however at high concentrations growth was significantly inhibited. Additionally, high treatment concentrations resulted in increased cell lysis as determined by LDH assays. Treatment with concentrations of 100mM glucose, 200μM H₂O₂, and 50μM sodium azide were the only treatment concentrations that did not result in significantly different levels of cell lysis when compared to a control sample. Mitochondrial dehydrogenase activity was also found to be significantly decreased at high treatment concentrations as determined by MTT assays. Thus, 100mM glucose, 200μM H₂O₂, and 50μM sodium azide treatments were identified as optimal conditions for mitochondrial targeted cell stress, as each of these treatments impaired cell growth and inhibited mitochondrial activity while having no significant effect on the degree of cell lysis. 
The 100mM glucose, 200μM H₂O₂, and 50μM sodium azide treatments were then investigated for the intracellular reactive oxygen species (ROS) activity they induced over treatment periods of 24 hours, 3 and 7 days. After 7 days of treatment, the 200μM H₂O₂ and 50μM sodium azide treatments resulted in an approximate three-fold increase in ROS activity, while the 100mM glucose treatment resulted in almost twice as much ROS compared to a control sample.
Finally, the effects of 100mM glucose, 200μM H₂O₂, and 50μM sodium azide treatments on HSP60 and HSP70 expression was also examined over 3 and 7 day time periods. After the 7 day treatment period, the 100mM glucose treatment had induced a 2.43 fold increase in HSP60 expression and a 2.75 fold increase in HSP70 expression, the 200μM H₂O₂ induced a 3.48 fold increase in HSP60 expression and a 3.98 fold increase in HSP70 expression, and finally the 50μM sodium azide induced a 4.74 fold increase in HSP60 expression and a 5.08 fold increase in HSP70 expression. 
It can therefore be concluded that 100mM glucose, 200μM H₂O₂, and 50μM sodium azide results in the upregulation of HSP60 and HSP70 in human HeLa cells. Therefore this model may be used to investigate further aspects of HSP60 induction, such as its translocation and secretion.

year: 2013

title: Recognition and indigenizing official statistics: Reflections from Aotearoa New Zealand and Australia

authors: Kukutai, Tahu

subjects: Indigenou

abstract: In First World colonised nations such as Aotearoa New Zealand and Australia, population statistics form the evidentiary base for how Indigenous peoples are known and `managed' through state policy approaches. Yet, population statistics are not a neutral counting. Decisions of what and how to count reflect particular assumptions about Indigenous identity, ways of life and wellbeing. More often than not, the requirements and priorities of government take precedence over the informational needs and priorities of Indigenous communities. Whereas National Statistics Offices (NSOs) once rendered Indigenous peoples invisible in official statistics through non-recognition, the more pressing problem in the 21st century is that of misrecognition. In seeking to move beyond statistical misrecognition, we propose a set of guiding principles for bringing government reporting frameworks and Indigenous concepts of identity and wellbeing into closer proximity. We argue that a principled approach to collecting, disseminating and analysing Indigenous data not only avoids misrecognising Indigenous peoples but enhances the functionality of official statistics for Indigenous peoples and NSOs alike.

text: Recognition and indigenizing official statistics: Reflections from Aotearoa New Zealand and Australia In First World colonised nations such as Aotearoa New Zealand and Australia, population statistics form the evidentiary base for how Indigenous peoples are known and `managed' through state policy approaches. Yet, population statistics are not a neutral counting. Decisions of what and how to count reflect particular assumptions about Indigenous identity, ways of life and wellbeing. More often than not, the requirements and priorities of government take precedence over the informational needs and priorities of Indigenous communities. Whereas National Statistics Offices (NSOs) once rendered Indigenous peoples invisible in official statistics through non-recognition, the more pressing problem in the 21st century is that of misrecognition. In seeking to move beyond statistical misrecognition, we propose a set of guiding principles for bringing government reporting frameworks and Indigenous concepts of identity and wellbeing into closer proximity. We argue that a principled approach to collecting, disseminating and analysing Indigenous data not only avoids misrecognising Indigenous peoples but enhances the functionality of official statistics for Indigenous peoples and NSOs alike.

year: 2015