title: Submission from Myra Williamson to the Education and Workforce Select Committee - Enquiry into Student Accomodation

authors: Williamson, Myra Elsie Jane Bell

subjects: Student Accommodation Inquiry

abstract: This is a written submission from me to Parliament's Education and Workforce Select Committee in response to its call for submissions in relation to the Inquiry into Student Accommodation. The Education and Workforce Select Committee is, among other things, working on a permanent code of conduct to replace the interim Education (Pastoral Care of Domestic Tertiary Students) Code of Practice 2019. I made this submission electronically on 23 June. The closing date for submissions is 2 July. This is a link to Parliament's webpage with the Terms of Reference for the Inquiry into Student Accommodation. My submission addresses various pieces of legislation (including the Residential Tenancies Act 1986, the Education Act 1989, and the Education (Pastoral Care) Amendment Act 2019. It also addresses various provisions of the interim Education (Pastoral Care of Domestic Tertiary Students) Code of Practice 2019 which is available here: https://www.education.govt.nz/assets/Documents/Further-education/Interim-Code-of-Practice-as-tabled-in-the-House-of-Representatives.pdf. Finally, the Education Dept resources page regarding the interim Code is here: https://www.education.govt.nz/further-education/information-for-students/code-of-practice-pastoral-care-domestic-tertiary/.

text: Submission from Myra Williamson to the Education and Workforce Select Committee - Enquiry into Student Accomodation This is a written submission from me to Parliament's Education and Workforce Select Committee in response to its call for submissions in relation to the Inquiry into Student Accommodation. The Education and Workforce Select Committee is, among other things, working on a permanent code of conduct to replace the interim Education (Pastoral Care of Domestic Tertiary Students) Code of Practice 2019. I made this submission electronically on 23 June. The closing date for submissions is 2 July. This is a link to Parliament's webpage with the Terms of Reference for the Inquiry into Student Accommodation. My submission addresses various pieces of legislation (including the Residential Tenancies Act 1986, the Education Act 1989, and the Education (Pastoral Care) Amendment Act 2019. It also addresses various provisions of the interim Education (Pastoral Care of Domestic Tertiary Students) Code of Practice 2019 which is available here: https://www.education.govt.nz/assets/Documents/Further-education/Interim-Code-of-Practice-as-tabled-in-the-House-of-Representatives.pdf. Finally, the Education Dept resources page regarding the interim Code is here: https://www.education.govt.nz/further-education/information-for-students/code-of-practice-pastoral-care-domestic-tertiary/.

year: 2020

title: Expression of TNF- α at mRNA level in Thp-1 cells exposed to LPS and HSP60: Possible impact on diabetic vascular inflammation

authors: Azfar, Afreen

subjects: mRNA

abstract: Diabetes mellitus is a chronic disease characterized by hyperglycaemia. It occurs when the b cells of the pancreas produce either low levels of insulin or no insulin at all. The chronic hyperglycaemic condition of diabetes is associated with the dysfunction, long-term damage and failure of organs such as the heart and blood vessels. Diabetes is closely linked to the prevalence of cardiovascular diseases, which is one of the highest causes of death worldwide. In particular, the hyperglycaemic and chronic inflammatory state of diabetes has been linked with atherogenesis, which is when fatty deposits build up in the arteries and they become inflamed. It still remains unknown how diabetes contributes to atherosclerosis.
Heat Shock Protein 60 (HSP60) is an important endogenous inflammatory mediator elevated in diabetic patients. HSP60 can be released from various cell types, including monocyte cells, which are the most common cell type found in atherosclerotic plaques. The mechanism behind how HSP60 triggers endothelial cell inflammation remains unknown, but has been hypothesised to be similar to that of a Toll like receptor 4 ligand, lipopolysaccharide (LPS). Understanding the molecular mechanism of HSP60 could give insights into the pathological, cellular and molecular basis of vascular inflammation in diabetes as well as other vascular diseases such as cardiovascular disease.
It is hypothesized that monocyte-derived HSP60 has a role in causing inflammation in the diabetic vasculature through the expression of pro- inflammatory cytokines such as TNF-α, which could contribute to atherosclerosis. In this study a human monocyte cell line (Thp-1) was used to mimic monocyte behaviour. First a growth curve was established, which indicated when the cells were in their exponential phase. This enabled RNA to be extracted during the period when cells were growing the fastest.
Thp-1 cells were then exposed to LPS for 6, 12, and 24 hours to determine the expression of TNF-α. After conducting RT-PCR, a 12 hour time point was selected. Since inconsistent results were obtained using this semi- quantitative analysis, qPCR was carried out for the rest of the project.
Thp-1 cells were then exposed to 50ng/mL and 100ng/mL of LPS for 12 hours. After conducting and analysing qPCR using the delta-delta Ct method and the Pfaffl method, a ~2 fold increase was seen in the expression of a pro-inflammatory cytokine, TNF-α. These results however were not significant (determined by a Student’s T test).
In order to obtain a higher level of TNF-α expression, this experiment was repeated with 10ng/mL and 50ng/mL of LPS for 4 hours, based on previous published research. These results were analysed using the delta-delta Ct method and the Pfaffl method. The results were not what was expected; only an insignificant <1 fold increase was seen in the samples.
Thp-1 cells were also exposed to 500ng/mL and 1500ng/mL of HSP60 for 4 hours in order to see a TNF-α induction. HSP60 has been hypothesised to work through the same mechanism as LPS to trigger TNF-α , leading to an inflammatory response. However again, no significant increase in expression was seen (as determined by a Student’s T test).
The inability to detect a significant up-regulation of the expression of TNF-α at mRNA level with LPS (positive control) and HSP60 in Thp-1 cells was surprising as this is well documented in the literature. This could possibly have been due to the high passage number of the Thp-1 cell cultures used in this study; mycoplasma contamination or stability of the LPS used. The study therefore needs to be repeated with cells of a lower passage number and cells checked for mycoplasma contamination to establish appropriate time frames of exposure and concentrations of LPS and HSP60 required to see a TNF-α induction. This could then be followed by experiments using receptor antagonists, such as TAK-242, (a TLR4 antagonist) to determine if TNF-α expression levels would give an indication of whether or not HSP60 was using the same pathway as LPS, and if it indeed played a part in causing diabetic vascular inflammation.

text: Expression of TNF- α at mRNA level in Thp-1 cells exposed to LPS and HSP60: Possible impact on diabetic vascular inflammation Diabetes mellitus is a chronic disease characterized by hyperglycaemia. It occurs when the b cells of the pancreas produce either low levels of insulin or no insulin at all. The chronic hyperglycaemic condition of diabetes is associated with the dysfunction, long-term damage and failure of organs such as the heart and blood vessels. Diabetes is closely linked to the prevalence of cardiovascular diseases, which is one of the highest causes of death worldwide. In particular, the hyperglycaemic and chronic inflammatory state of diabetes has been linked with atherogenesis, which is when fatty deposits build up in the arteries and they become inflamed. It still remains unknown how diabetes contributes to atherosclerosis.
Heat Shock Protein 60 (HSP60) is an important endogenous inflammatory mediator elevated in diabetic patients. HSP60 can be released from various cell types, including monocyte cells, which are the most common cell type found in atherosclerotic plaques. The mechanism behind how HSP60 triggers endothelial cell inflammation remains unknown, but has been hypothesised to be similar to that of a Toll like receptor 4 ligand, lipopolysaccharide (LPS). Understanding the molecular mechanism of HSP60 could give insights into the pathological, cellular and molecular basis of vascular inflammation in diabetes as well as other vascular diseases such as cardiovascular disease.
It is hypothesized that monocyte-derived HSP60 has a role in causing inflammation in the diabetic vasculature through the expression of pro- inflammatory cytokines such as TNF-α, which could contribute to atherosclerosis. In this study a human monocyte cell line (Thp-1) was used to mimic monocyte behaviour. First a growth curve was established, which indicated when the cells were in their exponential phase. This enabled RNA to be extracted during the period when cells were growing the fastest.
Thp-1 cells were then exposed to LPS for 6, 12, and 24 hours to determine the expression of TNF-α. After conducting RT-PCR, a 12 hour time point was selected. Since inconsistent results were obtained using this semi- quantitative analysis, qPCR was carried out for the rest of the project.
Thp-1 cells were then exposed to 50ng/mL and 100ng/mL of LPS for 12 hours. After conducting and analysing qPCR using the delta-delta Ct method and the Pfaffl method, a ~2 fold increase was seen in the expression of a pro-inflammatory cytokine, TNF-α. These results however were not significant (determined by a Student’s T test).
In order to obtain a higher level of TNF-α expression, this experiment was repeated with 10ng/mL and 50ng/mL of LPS for 4 hours, based on previous published research. These results were analysed using the delta-delta Ct method and the Pfaffl method. The results were not what was expected; only an insignificant <1 fold increase was seen in the samples.
Thp-1 cells were also exposed to 500ng/mL and 1500ng/mL of HSP60 for 4 hours in order to see a TNF-α induction. HSP60 has been hypothesised to work through the same mechanism as LPS to trigger TNF-α , leading to an inflammatory response. However again, no significant increase in expression was seen (as determined by a Student’s T test).
The inability to detect a significant up-regulation of the expression of TNF-α at mRNA level with LPS (positive control) and HSP60 in Thp-1 cells was surprising as this is well documented in the literature. This could possibly have been due to the high passage number of the Thp-1 cell cultures used in this study; mycoplasma contamination or stability of the LPS used. The study therefore needs to be repeated with cells of a lower passage number and cells checked for mycoplasma contamination to establish appropriate time frames of exposure and concentrations of LPS and HSP60 required to see a TNF-α induction. This could then be followed by experiments using receptor antagonists, such as TAK-242, (a TLR4 antagonist) to determine if TNF-α expression levels would give an indication of whether or not HSP60 was using the same pathway as LPS, and if it indeed played a part in causing diabetic vascular inflammation.

year: 2018

title: Geographical and ethnic differences of osteoarthritis-associated hip and knee replacement surgeries in New Zealand: a population-based cross-sectional study

authors: Lao, Chunhuan

abstract: Objectives To (1) explore the regional and ethnic differences in rates of publicly funded osteoarthritis-associated hip and knee replacement surgeries and (2) investigate the mortality after surgery.

Design Population-based, retrospective, cross-sectional study.

Setting General population in New Zealand.

Participants Patients with osteoarthritis who underwent publicly funded primary hip and knee replacement surgeries in 2005–2017. Patients aged 14–99 years were included.

Primary and secondary outcome measures Age-standardised rate, standardised mortality ratio (SMR) and 30 days, 90 days and 1 year mortality.

Results We identified 53 439 primary hip replacements and 50 072 primary knee replacements with a diagnosis of osteoarthritis. The number and age-standardised rates of hip and knee replacements increased over time. Māori had the highest age-standardised rate of hip replacements, followed by European/others and Pacific, and Asian had the lowest rate. Pacific had the highest age-standardised rate of knee replacements, followed by Māori and European/others, and Asian had the lowest rate. The Northern Health Network had the lowest rate of hip surgeries, and the Southern Health Network had the lowest rate of knee surgeries. The SMRs of patients undergoing hip and knee replacements were lower than the general population: 0.92 (95% CI 0.89 to 0.95) for hip and 0.79 (95% CI 0.76 to 0.82) for knee. The SMRs were decreasing over time. The patterns of 30 days, 90 days and 1 year mortality were similar to the SMR.

Conclusions The numbers of publicly funded osteoarthritis-associated primary hip and knee replacements are steadily increasing. Māori people had the highest age-standardised rate of hip replacements and Pacific people had the highest rate of knee replacements. The Northern Health Network had the lowest rate of hip surgeries, and the Southern Health Network had the lowest rate of knee surgeries. Compared with the general population, patients who had hip and knee replacements have a better life expectancy.

text: Geographical and ethnic differences of osteoarthritis-associated hip and knee replacement surgeries in New Zealand: a population-based cross-sectional study Objectives To (1) explore the regional and ethnic differences in rates of publicly funded osteoarthritis-associated hip and knee replacement surgeries and (2) investigate the mortality after surgery.

Design Population-based, retrospective, cross-sectional study.

Setting General population in New Zealand.

Participants Patients with osteoarthritis who underwent publicly funded primary hip and knee replacement surgeries in 2005–2017. Patients aged 14–99 years were included.

Primary and secondary outcome measures Age-standardised rate, standardised mortality ratio (SMR) and 30 days, 90 days and 1 year mortality.

Results We identified 53 439 primary hip replacements and 50 072 primary knee replacements with a diagnosis of osteoarthritis. The number and age-standardised rates of hip and knee replacements increased over time. Māori had the highest age-standardised rate of hip replacements, followed by European/others and Pacific, and Asian had the lowest rate. Pacific had the highest age-standardised rate of knee replacements, followed by Māori and European/others, and Asian had the lowest rate. The Northern Health Network had the lowest rate of hip surgeries, and the Southern Health Network had the lowest rate of knee surgeries. The SMRs of patients undergoing hip and knee replacements were lower than the general population: 0.92 (95% CI 0.89 to 0.95) for hip and 0.79 (95% CI 0.76 to 0.82) for knee. The SMRs were decreasing over time. The patterns of 30 days, 90 days and 1 year mortality were similar to the SMR.

Conclusions The numbers of publicly funded osteoarthritis-associated primary hip and knee replacements are steadily increasing. Māori people had the highest age-standardised rate of hip replacements and Pacific people had the highest rate of knee replacements. The Northern Health Network had the lowest rate of hip surgeries, and the Southern Health Network had the lowest rate of knee surgeries. Compared with the general population, patients who had hip and knee replacements have a better life expectancy.

year: 2019