title: Utility Exchanger Network Design for Non-Isothermal Utility Considering Process Control

authors: Tarighaleslami, Amir Hossein

abstract: This paper investigates a preliminary control strategy based on bypass control loop of Utility Exchangers Network (UEN) for non-isothermal utilities in a Total Site Heat Integration (TSHI) system. Few details on the design and control of non-isothermal utility systems, e.g. hot water loops, that includes Total Site heat recovery are presented in the literature. Heat Exchanger Networks (HEN) can be considered as a combined Heat Recovery Network (HRN) and UEN for each individual processes within the Total Site. Control strategy presented in the current paper are based on the control of utility side in a process – utility heat exchanger match to control process stream target temperature and analyse Total Site (TS) utility system in a Process Integration point of view. Bypass control has been used in the research. A Hot Water loop as representative of a large industrial plant utility system is studied as a case study. The process stream segment target temperature to be achieved and process stream segment supply temperature and flow rate may vary up to ±15 %. The HW utility temperature in the loop is controlled by using indirect heat transfer from higher and lower level utility and by using HW loop bypass. A 24 h period has been considered for the study. Results show that the HW utility loop has a 2.4 MW heat deficit in time-average condition. By controlling the HW utility loop using the proposed heuristics, utility heating requirement may vary between 0.7 to 3.5 MW, which is supplied by the Low Pressure steam main.

text: Utility Exchanger Network Design for Non-Isothermal Utility Considering Process Control This paper investigates a preliminary control strategy based on bypass control loop of Utility Exchangers Network (UEN) for non-isothermal utilities in a Total Site Heat Integration (TSHI) system. Few details on the design and control of non-isothermal utility systems, e.g. hot water loops, that includes Total Site heat recovery are presented in the literature. Heat Exchanger Networks (HEN) can be considered as a combined Heat Recovery Network (HRN) and UEN for each individual processes within the Total Site. Control strategy presented in the current paper are based on the control of utility side in a process – utility heat exchanger match to control process stream target temperature and analyse Total Site (TS) utility system in a Process Integration point of view. Bypass control has been used in the research. A Hot Water loop as representative of a large industrial plant utility system is studied as a case study. The process stream segment target temperature to be achieved and process stream segment supply temperature and flow rate may vary up to ±15 %. The HW utility temperature in the loop is controlled by using indirect heat transfer from higher and lower level utility and by using HW loop bypass. A 24 h period has been considered for the study. Results show that the HW utility loop has a 2.4 MW heat deficit in time-average condition. By controlling the HW utility loop using the proposed heuristics, utility heating requirement may vary between 0.7 to 3.5 MW, which is supplied by the Low Pressure steam main.

year: 2018

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: Maori & Psychology Research Unit annual report 2004

authors: Rua, Mohi

subjects: Māori & Psychology Research Unit annual report

abstract: Annual report of the Maori and Psychology Research Unit (MPRU) 2004. The unit was established in August of 1997. The unit is designed to provide a catalyst and support network for enhancing research concerning the psychological needs, aspirations, and priorities of Maori people. The MPRU is well situated to draw together skilled and experienced interdisciplinary research groups by networking and establishing working relationships with staff and students within the Faculty of Arts and Social Sciences, the University, and the wider community.

text: Maori & Psychology Research Unit annual report 2004 Annual report of the Maori and Psychology Research Unit (MPRU) 2004. The unit was established in August of 1997. The unit is designed to provide a catalyst and support network for enhancing research concerning the psychological needs, aspirations, and priorities of Maori people. The MPRU is well situated to draw together skilled and experienced interdisciplinary research groups by networking and establishing working relationships with staff and students within the Faculty of Arts and Social Sciences, the University, and the wider community.

year: 2004